Transcriber’s Notes

  Text printed in italics has been transcribed _between underscores_,
  bold face printed text =between equal signs=. Small capitals have
  been replaced with ALL CAPITALS.

  Literature references are numbered and listed per chapter at the
  end of the chapter, footnotes (indicated by letters in square
  brackets) will be found directly underneath the paragraph, table or
  illustration to which they refer.

  More Transcriber’s Notes may be found at the end of this text.




LEAD POISONING AND LEAD ABSORPTION




INTERNATIONAL MEDICAL MONOGRAPHS


  _General Editors_ { LEONARD HILL, M.B., F.R.S.
                    { WILLIAM BULLOCH, M.D.

_THE VOLUMES ALREADY PUBLISHED OR IN PREPARATION ARE:_


  =THE MECHANICAL FACTORS OF DIGESTION.= By WALTER B. CANNON, A.M.,
  M.D., George Higginson Professor of Physiology, Harvard University.

  [_Ready._

  =SYPHILIS: FROM THE MODERN STANDPOINT.= By JAMES MACINTOSH, M.D.,
  Grocers’ Research Scholar; and PAUL FILDES, M.D., B.C., Assistant
  Bacteriologist to the London Hospital.

  [_Ready._

  =BLOOD-VESSEL SURGERY AND ITS APPLICATIONS.= By CHARLES CLAUDE
  GUTHRIE, M.D., Ph.D., Professor of Physiology and Pharmacology,
  University of Pittsburgh, etc.

  [_Ready._

  =CAISSON SICKNESS AND THE PHYSIOLOGY OF WORK in Compressed Air.= By
  LEONARD HILL, M.B., F.R.S., Lecturer on Physiology, London Hospital.

  [_Ready._

  =LEAD POISONING AND LEAD ABSORPTION.= By THOMAS LEGGE, M.D., D.P.H.,
  H.M. Medical Inspector of Factories, etc.; and KENNETH W. GOADBY,
  D.P.H., Pathologist and Lecturer on Bacteriology, National Dental
  Hospital.

  =THE PROTEIN ELEMENT IN NUTRITION.= By Major D. MCCAY, M.B., B.Ch.,
  B.A.O., M.R.C.P., I.M.S., Professor of Physiology, Medical College,
  Calcutta, etc.

  =SHOCK: The Pathological Physiology of Some Modes of Dying.= By
  YANDELL HENDERSON, Ph.D., Professor of Physiology, Yale University.

  =THE CARRIER PROBLEM IN INFECTIOUS DISEASE.= By J. C. LEDINGHAM,
  D.Sc., M.B., M.A., Chief Bacteriologist, Lister Institute of
  Preventive Medicine, London; and J. A. ARKWRIGHT, M.A., M.D.,
  M.R.C.P., Lister Institute of Preventive Medicine, London.

  =DIABETES.= By J. J. MACLEOD, Professor of Physiology, Western
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  _A Descriptive Circular of the Series will be sent free on
  application to the Publishers:_

  LONDON: EDWARD ARNOLD

  NEW YORK: LONGMANS, GREEN & CO.




  INTERNATIONAL MEDICAL MONOGRAPHS

  _General Editors_ { LEONARD HILL, M.B., F.R.S.
                    { WILLIAM BULLOCH, M.D.

  LEAD POISONING AND
  LEAD ABSORPTION

  THE
  SYMPTOMS, PATHOLOGY AND PREVENTION,
  WITH SPECIAL REFERENCE TO THEIR
  INDUSTRIAL ORIGIN AND AN ACCOUNT OF THE
  PRINCIPAL PROCESSES INVOLVING RISK

  BY

  THOMAS M. LEGGE, M.D. OXON., D.P.H. CANTAB.

  H.M. MEDICAL INSPECTOR OF FACTORIES; LECTURER ON FACTORY HYGIENE
  UNIVERSITY OF MANCHESTER

  AND

  KENNETH W. GOADBY, M.R.C.S., D.P.H. CANTAB.

  PATHOLOGIST AND LECTURER ON BACTERIOLOGY, NATIONAL DENTAL HOSPITAL
  APPOINTED SURGEON TO CERTAIN SMELTING AND WHITE
  LEAD FACTORIES IN EAST LONDON

  LONDON
  EDWARD ARNOLD
  NEW YORK: LONGMANS, GREEN & CO.
  1912
  [_All rights reserved_]




GENERAL EDITORS’ PREFACE


The Editors hope to issue in this series of International Medical
Monographs contributions to the domain of the Medical Sciences on
subjects of immediate interest, made by first-hand authorities who have
been engaged in extending the confines of knowledge. Readers who seek
to follow the rapid progress made in some new phase of investigation
will find therein accurate information acquired from the consultation
of the leading authorities of Europe and America, and illuminated by
the researches and considered opinions of the authors.

Amidst the press and rush of modern research, and the multitude of
papers published in many tongues, it is necessary to find men of proved
merit and ripe experience, who will winnow the wheat from the chaff,
and give us the present knowledge of their own subjects in a duly
balanced, concise, and accurate form.

This volume deals with a subject of wide interest, for lead is dealt
with in so many important processes of manufacture--in the making of
white lead; pottery glazing; glass polishing; handling of printing
type; litho-making; house, coach, and motor painting; manufacture of
paints and colour; file-making; tinning of metals; harness-making;
manufacture of accumulators, etc.

The authors bring forward convincing evidence, experimental and
statistical, in favour of the causation of lead poisoning by the
inhalation of dust. This makes prevention a comparatively simple
matter, and the methods of prevention are effective, and will
contribute greatly to the health of the workers and the prevention of
phthisis, which is so prevalent among lead-workers. Exhaust fans and
hoods, or vacuum cleaners, for carrying away the dust formed in the
various processes--these are the simple means by which the dust can be
removed and the workers’ health assured.

  LEONARD HILL.
  WILLIAM BULLOCH.

  _September, 1912._




AUTHORS’ PREFACE


Progress in the knowledge of the use of lead, the pathology of lead
poisoning, and the means of preventing or mitigating the risk from it,
has been rapid of late years, and has led to much legislative action
in all civilized countries. The present is a fitting time, therefore,
to take stock of the general position. We have both, in different
ways, been occupied with the subject for several years past, the
one administratively, and the other experimentally, in addition to
the practical knowledge gained by examining weekly over two hundred
lead-workers.

The present treatise takes account mainly of our own persona
experience, and of work done in this country, especially by members
of the Factory Department of the Home Office, and certifying and
appointed surgeons carrying out periodical medical examinations in lead
factories. The book, however, has no official sanction.

We are familiar with the immense field of Continental literature
bearing on legislation against lead poisoning, but have considered any
detailed reference to this outside the scope of our book, except in
regard to the medical aspects of the disease.

Most of the preventive measures mentioned are enforced under
regulations or special rules applying to the various industries
or under powers conferred by the Factory and Workshops Act, 1901.
Occasionally, however, where, in the present state of knowledge,
particular processes are not amenable to the measures ordinarily
applied, we have suggested other possible lines on which the dangers
may be met. We have not reprinted these regulations and special rules,
as anyone consulting this book is sure to have access to them in the
various works published on the Factory Acts.

The practical value of the experimental inquiry described in Chapter
VI., and the light it seems to throw on much that has been difficult to
understand in the causation of lead poisoning, has led us to give the
results in detail.

One of us (K. W. G.) is responsible for Chapters I., III., and V. to
XI., and the other (T. M. L.) for Chapters II. and XII. to XVII.;
but the subject-matter in all (except Chapter VI., which is the work
entirely of K. W. G.) has been worked upon by both.

Our thanks are due to the Sturtevant Engineering Co., Ltd., London;
Messrs. Davidson and Co., Ltd., Belfast; the Zephyr Ventilating Co.,
Bristol; and Messrs. Enthoven and Sons, Ltd., Limehouse, for kindly
supplying us with drawings and photographs.

  _September, 1912._




CONTENTS


  CHAPTER                                                           PAGE

     I. HISTORICAL--CHEMISTRY OF LEAD                                  1

    II. ÆTIOLOGY                                                       7

   III. SUSCEPTIBILITY AND IMMUNITY                                   27

    IV. STATISTICS OF PLUMBISM                                        44

     V. PATHOLOGY                                                     62

    VI. PATHOLOGY--_Continued_                                        81

   VII. SYMPTOMATOLOGY AND DIAGNOSIS                                 110

  VIII. EXCRETION OF LEAD                                            127

    IX. THE NERVOUS SYSTEM                                           140

     X. CHEMICAL INVESTIGATIONS                                      165

    XI. TREATMENT                                                    184

   XII. PREVENTIVE MEASURES AGAINST LEAD POISONING                   199

  XIII. PREVENTIVE MEASURES AGAINST LEAD POISONING--_Continued_      221

   XIV. PREVENTIVE MEASURES AGAINST LEAD POISONING--_Continued_      230

    XV. DESCRIPTION OF PROCESSES                                     242

  XVI.  DESCRIPTION OF PROCESSES--_Continued_                        265

  XVII. DESCRIPTION OF PROCESSES--_Continued_                        288

        INDEX                                                        305




LIST OF PLATES


                  FACING
                   PAGE

  PLATE I.      92

  PLATE II.     93

  PLATE III.    95

  PLATE IV.    276




LEAD POISONING AND LEAD ABSORPTION




CHAPTER I

HISTORICAL--CHEMISTRY OF LEAD


The use of lead for various industrial processes and for painting was
well known to the ancients. Pliny[1] speaks of white lead, and a method
of corroding lead in earthen pots with vinegar, sunk into a heap of
dung, as the means by which white lead was made for paint. Agricola
mentions three forms of lead--white lead, a compound which was probably
bismuth, and metallic lead itself. The alchemists were acquainted with
the metal under the name of “saturn,” the term signifying the ease
with which the nobler metals, silver and gold, disappear when added to
molten lead.

Colic caused by lead was also known in ancient times, and is
described by Pliny; many other writers refer to it, and Hippocrates
was apparently acquainted with lead colic. Not until Stockhusen[2],
however, in 1656, ascribed the colic of lead-miners and smelters to the
fumes given off from the molten liquid was the definite co-relation
between lead and so-called “metallic colic” properly understood,
and the symptoms directly traced to poisoning from the metal and
its compounds. Æthius, in the early part of the sixteenth century,
gave a description of a type of colic called “bellon,” frequently
associated with the drinking of certain wines. Tronchin[3], in 1757,
discovered that many of these wines were able to dissolve the glaze
of the earthenware vessels in which they were stored, the glaze being
compounded with litharge.

In our own country, John Hunter[4] describes the frequent incidence of
“dry bellyache” in the garrison of Jamaica, caused by the consumption
of rum which had become contaminated with lead. Many other writers in
ancient and historical books on medicine have written on the causation
of colic, palsy, and other symptoms, following the ingestion of salts
of lead; and as the compounds of lead, mainly the acetate or sugar of
lead, were freely used medicinally, often in large doses, opportunities
constantly occurred for observing the symptoms produced in susceptible
persons. It is not to the present purpose to examine the historical
side of the question of lead poisoning, but those interested will find
several valuable references in Meillère’s work “Le Saturnisme”[5].

Lead was used in the seventeenth and eighteenth centuries particularly,
and in the earlier part of the nineteenth, for its action upon the
blood. In view of experimental evidence of the action of lead on the
tissues, particularly the blood, this empirical use has interest. Salts
of lead were found to be hæmostatic, and were therefore used for the
treatment of ulcers because of the power, notably of lead acetate, of
coagulating albuminous tissue. It was also used in the treatment of
fevers, where again it is quite possible that the administration of a
lead salt, such as an acetate, produced increase in the coagulability
of the blood. At the same time spasms of colic and other accidents
followed its use. There is practically no disease to which the human
body is subject which was not treated by lead in some form or another.
Lead, with the addition of arsenic, was given for malaria, while its
use in phthisis was also common. The present use of diachylon plaster
is an instance of the continuous use of a salt of lead medicinally, as
also is the lotion of the British Pharmacopœia containing opium and
lead.


THE CHEMISTRY OF LEAD.


=Physical Properties.=--Lead belongs to the group of heavy metals, and
occupies a position between bismuth and thorium in the list of the
atomic weights, the atomic weight being 206·4, and density 11·85. It
is blue-grey in colour, and its softness and facility to form a mark
upon paper are well known. Lead melts at a temperature of 325° C., and
at this temperature a certain (if negligible) amount of volatilization
takes place, which vapour becomes reprecipitated in the form of an
oxide. Use is made of the volatility of the metal at the higher
temperatures, 550° C. and upwards, in the oxidation of lead from a
mixture of lead, silver, and gold; the oxide of lead, or litharge, is
partially collected and absorbed by the crucible, but the greater part
is mainly removed from the surface of the liquid metal as it is formed,
while the richer metal is left in the crucible.

Chemically speaking lead is a tetrad, and forms a number of organic
derivatives, especially through the intervention of a particular
oxide, minium. Lead forms metallic alkalies and alkaline earths,
resembling silver in this direction, and also metallic compounds
with zinc and copper; in this point it is very similar to silver.
Small quantities of lead present in other metals--as, for instance, a
small trace in gold--alter its physical qualities to a great extent;
whilst the addition of minute traces of other metals to lead--as, for
instance, antimony--cause it to become hard, a fact made use of in the
manufacture of shot.

A number of oxides of the metal are known: two varieties of protoxides
(massicot and litharge), protoxide hydrate, and bioxide. Sulphide, or
galena, represents the chief form in which lead is found in Nature, and
from which the actual metal is produced by metallurgical processes.

The salts of lead may be divided as follows:

1. The carbonates or hydrated carbonates employed in a large number
of industrial and other processes, which are the cause of much lead
poisoning.

2. The acetates, both normal and basic, which are particularly
concerned in the production of white lead--at any rate in the process
of converting metallic lead into the hydrated carbonate through the
medium of acetic acid and steam.

3. Chromate of lead, which is used as a pigment, and also in dyeing
yarns, etc.

4. The nitrates and chlorides; the chloride particularly is used as an
oxidizing agent (plumbing, soldering, tinning of metals).

5. The silicates, silico-borates, silico-fluoborates, which constitute
the many varieties of glass and crystals used in optical instruments,
and the various glazes and enamel colours used in the potteries.

There are a large number of other derivatives, but these are not of
special interest to the subject in hand.


=The Action of Water upon Lead.=--The action of water on lead was known
even to the ancients, Pliny and Galen having written on the subject.
At times, and under certain conditions, as much as 20 milligrammes per
litre have been found, as in the Bacup epidemic, and 14 milligrammes
per litre in the epidemic at Claremont. Bisserie[6] in 1900 made an
exhaustive inquiry into the action of water upon lead; he gives the
following conclusions:

1. Water and saline solutions attack lead more or less readily when it
is in combination with another metal, such as solder, copper, bronze,
iron, or nickel, the result being a hydrated oxide.

2. The maximum effect is produced with water slightly acid and with
solutions of chlorides or nitrates. With these it is not necessary to
have other metals present, and if the water is thoroughly aerated the
pure metal is attacked.

3. Bicarbonates and carbonic acid exercise by themselves an action
on wet lead, but the carbonate of lead formed in the process adheres
firmly to the surface of the metal, and prevents any further action.

4. Sulphates act in the same way, but in less degree.

5. This protective action is much diminished when the water is even
slightly charged with nitrates or organic material. Pouchet has pointed
out that lead branch-pipes fixed to iron water-pipes, thus producing an
“iron-lead couple,” set up definite electro-chemical changes, and tend
to increase the rate at which solution of lead in the pipe water takes
place.

Houston[7], in an extensive and very full report on the effect of
water upon lead, especially undertaken for the purpose of inquiry into
the contamination of supplies of drinking water by means of lead,
distinguishes two species of action--namely, plumbo-solvency, which
is brought about by the acidity of the water in contact with lead;
and a second kind of action, erosion, determined to some extent by
the dissolved air in the water. He came to the conclusion that the
plumbo-solvency and erosive action of water on metallic lead differed
considerably, and that the protective layer or plumbo-protective
substance did not always protect lead pipes from the solvent action of
water.


=Chemical Characters of Lead Salts.=--A short summary of the chemistry
of lead salts may not be out of place.

A soluble salt of lead, such as the acetate or nitrate, is precipitated
by (1) hydrogen sulphide or alkaline sulphide as a brown or black
precipitate, which is insoluble in ammonium sulphide. In dilute
solutions this sulphide is, however, appreciably soluble in mineral
acids, and may introduce errors in analysis, especially as the
solubility is distinctly increased by the presence of certain earthy
salts. The sulphide produced through the action of alkaline sulphide on
a soluble salt of lead is less soluble than is the corresponding acid
sulphide. Soluble salts of lead are at once precipitated by albumin or
peptone; the resulting precipitate has no stable composition.

Under certain conditions definite colloidal precipitates are formed,
particularly in the presence of sulphide of copper or mercury. (2)
Sulphuric acid or soluble sulphates produce a precipitate of lead
sulphate insoluble in excess of the precipitating salt or sulphuric
acid, and only slightly soluble in alkaline solutions. This method
is the one generally adopted for gravimetric determination of a lead
salt. (3) Potassium chromate produces a precipitate of chromate of
lead very little soluble in acid, but soluble in caustic alkali. (4)
Potassium iodide produces a yellow lead iodide, soluble on heating, and
reprecipitating and crystallizing on cooling. (5) Alkaline chlorides
and hydrochloric acid produce needle-like crystals of lead chloride
soluble on heating, and reprecipitating on cooling. (6) Potassium
nitrate in conjunction with a copper salt (copper acetate) produces
a precipitate of a triple copper, lead, and potassium nitrate,
crystallizing in characteristic violet-black cubes. This reaction is
one made use of in the qualitative determination of small quantities of
lead in organic fluids (see p. 167).

All the precipitates of lead salts, with the exception of the sulphide,
are soluble in fixed alkalies, in ammonium acetate, ammonium tartrate,
and ammonium citrate. It is possible to determine the presence of lead
in a large volume without evaporating down the whole bulk of fluid. By
this means liquid containing lead is treated with sulphide of copper,
sulphide of mercury, or baryta-water. Meillère states that he has
detected the presence of as small a quantity as 1 milligramme of lead
in 1,000 c.c. of water in this manner without evaporating the liquid.
Where lead is in organic combination, as is the case in the urine of
persons suffering from lead poisoning, it is not decomposed by hydrogen
sulphide, and the method is therefore not applicable in such cases, but
is useful in water examination.


=Electrolytic Reactions.=--Solutions of lead are easily electrolyzed,
and give a precipitate of lead at the cathode; simultaneously the
peroxide is produced at the anode, and the reaction is acid. In nitric
acid solutions Riche pointed out that the whole of the lead is carried
to the anode, and this is the reaction made use of in the determination
of lead present in the urine (see p. 172).

The presence of copper in an electrolyte regulates the precipitation
of lead oxide, copper alone being deposited at the cathode, and at
the same time the presence of a small quantity of copper promotes the
destruction of organic materials.


REFERENCES.

  [1] PLINY: lxxxiii., 11, N.c.v.

  [2] STOCKHUSEN: De Litharg. Fumo, etc. Goslar, 1656.

  [3] TRONCHIN: De Colica Pictonum. 1758.

  [4] JOHN HUNTER: Observations of Diseases of the Army in Jamaica.
  London, 1788.

  [5] MEILLÈRE, G.: Le Saturnisme. Paris, 1903.

  [6] BISSERIE: Bull. Soc. Pharmacol. May, 1900.

  [7] HOUSTON: Local Government Board Annual Report, 1901-02,
  supplement, vol. ii.




CHAPTER II

ÆTIOLOGY


Lead poisoning of industrial origin rarely occurs in the acute form.
Practically all cases coming under the notice of either appointed
surgeons, certifying surgeons, or even in the wards of general
hospitals, are of the subacute or chronic type. There is no reason to
suppose that lead compounds are used more frequently by the workers in
lead industries as abortifacients than by other persons.

The compounds of lead which are responsible for poisoning in industrial
processes are for the most part the hydrated carbonate, or white lead,
and the oxides of lead, whilst a comparatively small number of cases
owe their origin to compounds, such as chromates and chlorides.

The poisonous nature of any lead compound from an industrial point
of view is proportional to (1) the size of the ultimate particles
of the substance manufactured, and therefore the ease with which
such particles are capable of dissemination in the air; and (2) the
solubility of the particles in the normal fluids of the body, such as
the saliva, pharyngeal and tracheal and bronchial mucus, etc., and
the fluids of the stomach and intestine. An instance of the variation
in size of the particles of lead compounds used industrially is the
difference between ground lead silicate (fritted lead) used in the
potteries, and the size of the particles of ordinary white or “raw”
lead. By micrometric measurements one of us [K. W. G.[1]] found the
average size of the particles of fritt to be ten times that of the
white lead particles. Further, direct experiment made with equal masses
of the two compounds in such a manner that the rate of settling of the
dust arising could be directly compared in a beam of parallel light
showed presence of dust in the white lead chamber fifteen minutes
after the fritt chamber was entirely clear. It is found as a matter
of practice that where dust is especially created, and where it is
difficult to remove such dust by exhaust fans, the greatest incidence
of lead poisoning occurs. The association of dusty processes and
incidence of lead poisoning is discussed in relation to the various
trades in Chapters XV. to XVII. Fume and vapour given off from the
molten metal or compounds, such as chlorides (tinning), are only a
special case of dust.

The channels through which lead or its compounds may gain entrance to
the animal body are theoretically three in number:

  1. Respiratory tract.

  2. Gastro-intestinal.

  3. Cutaneous.

For many years most authorities have held that industrial poisoning by
means of compounds of lead takes place directly through the alimentary
canal, and that the poison is conveyed to the mouth mainly by unwashed
hands, by food contaminated with lead dust, and by lead dust suspended
in the air becoming deposited upon the mucous membrane of the mouth and
pharynx, and then swallowed. As evidence that lead dust is swallowed,
the classical symptom of colic in lead poisoning has been adduced, on
the supposition, in the absence of any experimental proof, that the
lead swallowed acted as an irritant on the gastro-intestinal canal,
thus causing colic, and, on absorption from the canal, setting up
other general symptoms. Much of the early treatment of lead poisoning
is based upon this assumption, and the administration of sulphuric
acid lemonade and the exhibition of sulphate of magnesia and other
similar compounds as treatment is further evidence of the view that the
poisoning was considered primarily intestinal.

One of the chief objections to this view, apart from the experimental
evidence, is that in those trades where metallic lead is handled,
particularly lead rolling, very few hygienic precautions have ever
been taken in regard to washing before meals, smoking, etc. Although
in these trades the hands become coated with a lead compound (oleate),
and the workers frequently eat their food with unwashed hands, thus
affording every opportunity for the ingestion of lead, the incidence of
poisoning is by no means as high or so pronounced in these occupations
as in those giving rise to lead dust, such as the white lead industry,
where special precautions are taken, and where the incidence of
poisoning is always related to the dust breathed.


=Respiratory Tract.=--In a report on the incidence of lead poisoning
in the manufacture of paints and colours, one of us [T. M. L.[2]] in
1902 laid stress on the marked incidence of poisoning in the specially
dusty lead processes. Following on that report special attention was
given to the removal of dust by means of exhaust ventilation. With the
introduction of precautionary measures, the incidence of poisoning
underwent a marked decrease, this decrease being most definite in those
industries where efficient exhaust ventilation could be maintained
(see p. 47). Experience shows that cases of poisoning in any given
trade or manufacturing process are always referable to the operations
which cause the greatest amount of dust, and where, therefore, the
opportunity of inhaling lead dust is greatest.

The investigations of Duckering[3], referred to on p. 203, show the
amount of dust present in the air in certain dangerous processes.
His results clinch the deductions made from general observation,
that dusty processes are those especially related to incidence of
industrial poisoning. Ætiologically, therefore, the relationship of
dust-contaminated air and poisoning is undeniable, and in not a few
instances on record persons residing at a distance from a lead factory
have developed poisoning, although not employed in any occupation
involving contact with lead, aerial infection through dust remaining
the only explanation. The actual channel through which the lead dust
suspended in the air gains entrance to the body is, therefore, of
especial importance; one of two channels is open--gastro-intestinal and
respiratory.

The investigations of one of us (K. W. G.) on the experimental
production of lead poisoning in animals has shown conclusively that the
dust inhaled was far more dangerous, and produced symptoms far earlier
than did the direct ingestion of a very much larger quantity of the
same compound by way of the mouth and gastro-intestinal canal. There
is no doubt whatever that the chief agent in causing lead poisoning is
dust or fume suspended in the air. That a certain amount finds its way
into the stomach direct is not denied, but from experimental evidence
we consider the lung rather than the stomach to be the chief channel
through which absorption takes place (see p. 81).

The following table gives a specific instance of the incidence of
lead poisoning in a white lead factory, and demonstrates clearly the
ætiological importance of dust. The increase in reported cases, as well
as in symptoms of lead absorption not sufficiently severe to prevent
the individual from following his usual occupation, was associated
with the rebuilding of a portion of the factory in which the packing
of dry white lead had been carried on for a large number of years. The
alterations necessitated the removal of several floors, all of which
were thoroughly impregnated with lead dust. Before the alterations were
undertaken it was recognized that considerable danger would arise;
stringent precautions were therefore taken, and the hands engaged in
the alterations kept under special observation. Notwithstanding this
there was an increase in the number of reported cases, which were all
mild cases of colic; all recovered, and were able to return to their
work in a short time.

TABLE I.--LEAD POISONING IN A WHITE LEAD FACTORY.

  The figures refer to the weekly examination of the whole of the men.
  For example, if a man was returned as suffering from anæmia on three
  occasions, he appears as three cases in Column 7.

  +-------+-------+-------+------+------+-------+------+------+------+
  |       | Total | Total | Cases| Cases|       |      |      |      |
  |       | Number| Cases |  in  |  in  |       |      |      |      |
  |       |   of  |   of  | Dusty| Other| Cases | Cases| Cases|      |
  |       | Exami-|Poison-| Pro- | Pro- |of Sus-|  of  |  of  | Blue |
  | Year  |nations|  ing  |cesses|cesses|pension|Anæmia|Tremor| Line |
  +-------+-------+-------+------+------+-------+------+------+------+
  |  (1)  |  (2)  |  (3)  |  (4) |  (5) |  (6)  | (7)  | (8)  | (9)  |
  |1905   | 5,464 |   9   |   8  |   1  |  20   | 78[B]|249[B]|311[B]|
  |1906[A]| 5,096 |  18   |  16  |   2  |   9   |256   |215   |532   |
  |1907   | 4,303 |   4   |   3  |   1  |   6   | 62   | 81   | 38   |
  |1908   | 3,965 |   4   |   3  |   1  |   5   | 40   | 25   | 11   |
  +-------+-------+-------+------+------+-------+------+------+------+

  [A] Structural alterations in progress, including cutting up “lead
  floor,” saturated with white lead dust.

  [B] These numbers for the half-year only, the inspection being taken
  over in June, 1905.

Meillère[4] goes to considerable trouble to show that absorption of
lead dust by the lung is hypothetical; that it may take place, but
that it is not a channel of absorption of practical importance. He
cites a number of opinions and experiments by various observers on the
absorption of lead through the mucous membrane of the mouth, alimentary
canal, conjunctiva, etc., and he regards the absorption of lead as one
peculiarly confined, in the majority of instances, to the intestinal
canal.

The usual view is that, in the passage of the respired dust-laden air
through the nose, the larger particles of dust are deposited first of
all upon the mucous membrane in the interior chambers of the nose;
further, a second deposit takes place on the posterior wall of the
pharynx and in the throat, where the eddies produced by the current of
air inhaled through the nostrils allow the finer particles to become
more easily deposited. Finally, should a small trace gain access to the
larynx, it is said to be deposited there upon the mucous membrane, to
be subsequently ejected, and only a very small proportion of the total
may ever find its way into the lung.

In all arduous labour, directly the respiration rate rises through
extra calls made upon the muscles of the body, an increase in the
depth of respiration takes place; yet even under these circumstances
Meillère and others incline to the view that the dust is deposited on
the mucous surfaces of the mouth and swallowed. Experimental evidence
is entirely opposed to these suppositions. In the first place, unless
particles of dust readily find their way into the lung, it is difficult
to understand how the lung itself becomes the site of so much deposit
of carbon, and of flinty material in stonegrinder’s pneumokoniosis.
The staining of the lung by means of carbon particles, particularly in
dwellers in cities, is too well known to warrant more than a passing
reference. Moreover, experimental work has shown that fine powders
suspended in the air easily reach the lung. Armit[5] has shown that
the nickel in nickel carbonyl poisoning gains direct access to the
lung, and becomes deposited there, the metallic particles being readily
demonstrated in the lung tissue itself. Further, the experiments (see
p. 84) demonstrate that white lead dust and other forms of lead dust
definitely gain access to the lung, and thus inhaled produce all the
symptoms of lead poisoning in animals subjected to the inhalation.
White lead, litharge, or red lead, are not easily suspended in water,
and long-continued mixing is necessary to make a suspension. Great
difficulty is found in “laying” lead dust by water, as the following
experiment demonstrates: Five wash-bottles are arranged in series; in
the first ground dry white lead is placed, and the other three bottles
are filled with water, and a tube laid under the surface of the water
in such a way that the air from the first bottle must pass the whole of
the water seals in each subsequent bottle. In the last bottle is dilute
nitric acid saturated with sulphuretted hydrogen. If the series is now
attached to an aspirating jar, and air drawn slowly over at the rate of
ordinary respiration, the white lead powder in the first bottle being
at the same time shaken so that the air is fully charged with finely
powdered dust, lead is quickly detected in the air passing through
the last bottle of the series, by the darkening of the solution. In
this way the presence of lead dust has been demonstrated after passing
through four 2-inch water seals and 8 feet of ¹⁄₄-inch wet rubber
tubing. Such an experiment negatives the theory that all, or even a
large quantity, of a finely divided powder becomes deposited on the
upper portion of the respiratory tract.

Particles of lead present in the air in industrial processes are
exceedingly minute, and even in ground white lead the average size
of the particle is under 1 μ. Finally, Tanquerel[6] and Stanski[7]
succeeded in producing lead poisoning experimentally by blowing lead
dust through a tube inserted in a tracheotomy opening. There remains,
therefore, no room for doubt that the lung is the pre-eminent portal
for lead absorption, particularly in industrial processes; from which
it follows, as has been extensively shown in actual practice, that
the diminution of dust in workshops and factories by means of exhaust
ventilation is invariably followed by a diminution in the number of
cases of plumbism.


=Gastro-Intestinal.=--We have dealt with absorption by way of the lung,
and have insisted that such inhalation of dust is of greater importance
in giving rise to industrial lead poisoning than gastro-intestinal
absorption. Gastro-intestinal absorption can take place, and is
by no means negligible, in ordinary industrial conditions. One of
the most interesting and important confirmatory evidences of the
absorption of lead by the gastro-intestinal canal is to be found in
the large outbreaks of poisoning in which water-supplies have been
contaminated, either at their source or locally. We have already seen
that electrolysis may play an important part in the solution of lead
in water, and also learnt from Gautier[8] that the carbon dioxide
content of water is not necessarily the sole predisposing element in
the solution of lead. In this connection an important case is described
by Thresh[9], where water by no means soft, but holding some 30 degrees
of hardness, produced lead poisoning in an isolated family. The water
in question was distinctly acid to litmus-paper, and contained a very
high percentage of nitrates; the compound or salt of lead present was
therefore one easily absorbed from the alimentary canal (see p. 86).

In all instances of water-borne lead poisoning the amount of lead
present in the water was small; but as such lead would not be
removed by boiling, the amount of water consumed per person from the
contaminated source was probably large. As the signs of poisoning
did not appear until a considerable time had elapsed, a much larger
quantity of lead was probably absorbed than would appear from the
simple statement that the water contained ¹⁄₁₀ grain per gallon.

A number of cases have been reported from use of diachylon as an
abortifacient, and the symptoms in these cases are invariably those
which occur in other severe forms of poisoning such as are met with in
industrial processes. In nearly every case colic was the first symptom,
followed later by paresis of various types--amaurosis, albuminuria,
albuminuric retinitis, melancholia, encephalopathy--and not a few of
the persons succumbed. In most of the reported cases abortion was
produced, but in some, particularly in one[10], three dozen pills
containing diachylon were taken in a month, producing acute lead
poisoning, colic, and paresis, but not abortion.

In fifteen recorded cases of the use of diachylon, fourteen showed
a lead line, in many cases distinct and broad. This point has
considerable interest, as such a line cannot have been produced by oral
contact. The drug in the form of pills would be rapidly swallowed,
and little opportunity afforded for particles to remain in the mouth.
Its presence, therefore, suggests excretion from circulating blood of
lead which has been absorbed in the intestine. The blue line will be
referred to again later (see p. 122).

Practically all cases of water poisoning and of swallowing of lead
compounds have developed colic. Further, colic is cited in all the
early recorded cases, even in the very earliest cases referred to in
the historical note, of lead poisoning; and as poisoning in those
cases had invariably taken place by swallowing the drug, it may be
presumed from this association has arisen the belief that lead must
be swallowed to produce gastro-intestinal symptoms. No attention has
been paid to the fact that a few cases of definite cutaneous absorption
of lead from the use of hair lotions have been followed by colic.
Gastro-intestinal symptoms, therefore, can be produced without the
direct ingestion of the drug, and colic is a symptom of generalized
blood-infection rather than a localized irritative action on the
intestinal mucosa. This question, again, is more related to pathology
than ætiology, and is dealt with in that section. But mention may be
made here of the fact that a number of observers, more lately Meillère,
have laid it down as an axiom that experimental production of lead
poisoning in animals gives no criterion or evidence of lead poisoning
produced in man industrially. Very grave exception must be taken at
once to such a statement. In the majority of experiments quoted by
Meillère the quantity of lead given for experimental purposes has been
large--much larger, indeed, than is necessary to produce small and
characteristic effects--and instead of chronic poisoning an acute lead
poisoning has generally been set up; and even where chronic poisoning
has supervened, the condition has as a rule been masked by the severer
initial symptoms. On the other hand, the evidence to be derived from
comparison of the various observations from animal experiments brings
out with remarkable unanimity the similarity of the symptoms to those
produced in man, and, as will be seen later in the section devoted to
Pathology, experiments by one of us (K. W. G.) have so far confirmed
this surmise; in fact, a description of a case of encephalopathy
coming on after lead poisoning of a chronic nature, described by Mott,
agrees in practically every particular with the train of symptoms as
observed in these experimental animals. Certain slight differences
as to the muscles first affected are observed, but it is practically
always the homologous muscle (the physiological action of which more
nearly resembles the human muscle) which is the one to be affected in
the animal, not the anatomical homologue. Thus, for instance, in the
cat the spinal muscles, and particularly the quadriceps extensor, is
the muscle which is first affected through the medium of the anterior
crural nerve. This extensor muscle is one which only performs a slight
amount of work in extending the knee-joint, the amount of work being,
however, disproportionate to the size of the muscle. The extensors of
the fore-feet ultimately do become weakened, but it is the hind-limb
upon which the stress first falls.

Attention has been given to the solubility of lead salts in gastric
juices, the majority of such experiments having been performed with
artificial gastric juice. The method at present in use, prescribed by
the amended rules of August, 1900, for earthenware and china factories,
is based on some, if slight, consideration of the physiology of
digestion. The method described by Rule II. states that the estimation
of the quantity of lead present in the lead fritt shall be performed as
follows:

A weighed quantity of dry material is to be continuously shaken for
one hour at room temperature with one thousand times its weight of an
aqueous solution of hydrochloric acid, containing 0·25 per cent. of
HCl. This solution is thereafter to be allowed to stand for one hour,
and to be passed through a filter. The lead salt contained in a portion
of the clear filter is then to be precipitated as lead sulphide, and
weighed as lead sulphate.

This method has been adopted on the supposition that the solubility
of a lead salt in the gastric juices is the chief source of the lead
poisoning in the Potteries, and that the hydrochloric acid content of
the solution determines, for practical purposes, the quantity of lead
dissolved out of a given sample. The temperature, however, at which
this estimation is made--namely, room temperature--is one considerably
lower than that of the body, and the quantity of lead taken up into
solution at this temperature is less than that which occurs at the
ordinary temperature of the body--37° C. Practically twice as much lead
is dissolved out of fritt at 37° C. for an hour as is rendered soluble
at the ordinary temperature of the room--about 15° C. Thomason[11], who
made some experiments in this direction, gives a figure of 2·35 lead
oxide dissolved at 15° C. and 4·54 at 37° C. In another estimation--a
matter, too, of some considerable importance--it was found that acetic
acid dissolved 1·97 per cent, at 15° C., and 3·27 at 37° C. In lactic
acid the figure was 2·28 at 15° C., and 3·53 at 37° C. It is therefore
a low estimation of the solubility of any substance by the gastric
juices if the substance is operated on at a temperature below that of
the body.

The question of the solubility of a lead salt in the gastric contents
is important in view of the small quantities of dust swallowed; and
in addition to hydrochloric acid, other substances are also present
in the gastric juice, which is by no means a simple aqueous solution
of the mineral acid. Further, the gastric juice, except in cases of
pathological type, is not acid in periods of gastric rest, unless
such acidity may be represented by the presence of fermentative
acids--acetic, lactic, and butyric.

The activity of the gastric juice on lead is directly caused by the
quantity of organic acids present in addition to the hydrochloric acid,
and by the presence of foodstuffs--(1) in the undigested and (2) in the
semidigested condition. In considering the absorption of lead products
from the gastro-intestinal canal, the normal digestive processes should
not be lost sight of--that is, the sequence of events which occur
during digestion of food. On swallowing food, no definite acidity is
present in the stomach for fifteen to twenty minutes, and even after
that time the hydrochloric acid is only commencing to be secreted. As
digestion proceeds, and the whole mass becomes partially dissolved,
such portions as are in a soluble condition are passed through the
pyloric opening at intervals, and the whole contents of the stomach do
not pass straight through the pyloric opening as through an ordinary
straight drain-pipe. As each mass of food passes onwards through the
pylorus, it comes into contact in the duodenum with pancreatic juice,
and with the bile, these alkaline fluids rapidly change the reaction,
and allow the other ferments, trypsin, etc., to become active. As the
mass proceeds onwards through the intestine, the succus entericus also
exerts its function. Finally the fluid contents of the intestine are
passed onwards through the ileo-cæcal valve. During the passage from
the pylorus to the ileo-cæcal valve, the reaction of the intestinal
contents undergoes variations, from an alkaline in the duodenum
or upper parts of the jejunum, to acid at the ileo-cæcal valve.
Practically no absorption takes place from the stomach itself; a small
quantity of water and such highly volatile fluids as alcohol may be
absorbed, but the main absorption is not commenced until the food
has left the stomach; in fact, the stomach contains no mechanism for
food absorption. The work of absorption of the products of digestion
is carried on actively through the small intestine until finally the
materials have reached the large intestine through the ileo-cæcal
valve; water is then mainly absorbed, and albuminous fluids and
substances in solution to some extent, but the amount of absorption
which takes place is infinitesimal as compared with that of the small
intestine.

These points in the physiology of digestion require to be taken
into account when discussing the absorption of lead salts in the
gastro-intestinal canal.

When human gastric juice is obtained direct from the stomach in man,
and lead is submitted to its action, definite quantities of lead pass
into solution; and, curiously enough, in the normal gastric juice lead
sulphate is as soluble as both white lead and litharge. The following
two tables give the results of the estimation of the direct action
of human gastric juice upon lead. The particular point is that the
juice was obtained by the stomach tube from persons who had been given
a simple test meal preceded by a twelve hours’ fast; the juice was
therefore in a normal condition. The tests gave the following results
in the normal stomach:

  Lead sulphate  0·080 per cent.
  White lead     0·048    „
  Litharge       0·040    „

In the second digestion, in which the analysis of the contents
showed the patient to be suffering from the condition known as
“hyperhydrochloridia,” the results were--

  Lead sulphate  0·046 per cent.
  White lead     0·042    „
  Litharge       0·340    „

A very large number of experiments have also been performed for the
purpose of determining the solubility of raw lead glaze, and white
lead, in artificial digestions, the digestions having been made up in
such a way that they resembled as far as possible in every particular
the ordinary stomach contents. The type of digestion used was as
follows:

  Dry breadcrumbs    140 grammes.
  Hydrochloric acid  5 c.c.
  Lactic acid        0·1 c.c.
  Acetic acid        0·1 c.c.
  Pepsin             1·2 grammes.
  Milk               1,200 c.c.

Digestions were performed with this mixture, and in every case the
digest was divided into two portions; each portion was retained at
body temperature, with agitation for a couple of hours, and at the
end of that time one portion was submitted to analysis. The second
portion was neutralized, sodium carbonate and pancreatic ferment added,
and digestion carried on for another two and a half hours at body
temperature. At the end of this time the pancreatic digest was examined.

Thirty-five digestions were performed. When 1 gramme of white lead
was used--that is, 0·01 per cent., containing 0·75 per cent. of lead
oxide--the quantity of lead found as lead oxide in the acid digest
varied from 2 to 3 per cent., whilst the amount found in the pancreatic
digest varied from 4 to 6·5 per cent. of the added salt. On increasing
the amount to 12 grammes--that is, 1 per cent.--the quantity returned
in the digest only increased from 1·5 to 2 per cent. In other words, in
the addition of larger quantities of material the ratio of solubility
did not rise in proportion to the quantity added. Where a direct
pancreatic digestion was performed without the preliminary digest of
the gastric contents, the amount of lead present in the digest was
only about 0·2 per cent. of the quantity added; indeed, it was very
much smaller than the amount dissolved out after preliminary acid
digestion--that is, if the normal sequence of digestion is followed,
the solubility progresses after the gastric digest has been neutralized
and pancreatic ferment has been added, whereas very slow action indeed
occurs as the result of action of the pancreatic digest alone. Some
experiments described by Thomason[12], although carried out without
special regard to the physiological question of the progressive nature
of digestion, distinctly confirm the point raised. Thus, in a digest of
gastric juice, milk, and bread, 5·0 per cent. of lead was dissolved,
whereas when pancreatic juice alone was used only 0·4 per cent. was
found to be dissolved, a remarkable confirmation of the point under
discussion.

The difficulty of estimating lead present in these gastric digestions
is a very real one, as, owing to the precipitation of lead by various
fluids of an albuminoid nature, it is difficult to determine the amount
of lead present in a given quantity of digest; moreover, in making
such a digest, much of the material may become entangled among the
clot of the milk in a purely mechanical fashion, and, in attempting to
separate the fluid from the other portion of the digest, filtration
no doubt removes any lead which has been rendered soluble first of
all, and reprecipitated as an albuminate. An albuminate of lead may be
formed with great ease in the following way: A 5 per cent. solution
of albumin in normal saline is taken, 0·02 per cent. of hydrochloric
acid is added, and 10 per cent. solution of lead chloride added as
long as a precipitate is formed. The precipitate is then filtered
off, and washed in a dialyser with acidulated water until no further
trace of lead is found in the washings. A portion of this substance
taken up in distilled water forms a solution of an opalescent nature,
which readily passes through the filter and gives the reaction of
protein with Millon’s reagent, and the lead reaction by means of
caustic potash and sulphuretted hydrogen, but very large quantities
of mineral acid are required to produce any colour with hydrogen
sulphide. Lead which gains access to the stomach, either dissolved
in water or swallowed as fine dust, becomes in all probability
converted first into a soluble substance, chloride, acetate, or
lactate, which compound is then precipitated either by the mucin
present in the stomach, or by the protein constituents of the food,
or by the partially digested food (peptonate of lead may be formed
in the same way as the albuminate described above). In this form, or
as an albuminate or other organic compound, it passes the pylorus,
and becomes reprecipitated and redigested through the action of the
pancreatic juice. A consideration of the action of artificial gastric
juices and the properly combined experiments of gastric and pancreatic
digestions suggest that the form in which lead becomes absorbed is
not a chloride, but an organic compound first formed and gradually
decomposed during the normal process of digestion, and absorbed in
this manner from the intestine along with the ordinary constituents
of food. Dixon Mann[13] has shown that about two-thirds of the lead
administered by the mouth is discharged in the fæces, and that the
remaining one-third is also slowly but only partially eliminated. This
point is of very considerable importance in relation to industrial
poisoning of presumably gastro-intestinal origin, and consideration
of the experiments quoted suggests that the digestion of albuminate
or peptonate may to some extent be the basis which determines the
excretion of so much of the lead via the fæces. This alteration of
solubility has no doubt a bearing on the immunity exhibited by many
animals when fed with lead, and probably explains the fact that many of
the experimental animals fed with lead over long periods exhibited no
symptoms of poisoning (see p. 85), whereas control animals, given a far
smaller quantity of lead by other means and through the lung, rapidly
developed symptoms of poisoning. A diversity of opinion exists as to
the effect of pepsin upon the solubility of lead. Oliver[14] considers
that the pepsin has a retarding influence on the solubility of lead in
the gastric juice, and Thomason’s experiments also support this view,
although it is difficult to see why the action of _pepsin_ alone should
be of such extreme importance. There is also the complicating fact that
other added substances in the food may mask any direct pepsin factor
that may be present. Albumose and peptone rather than pepsin are to
be regarded as the more important substance physiologically in their
reaction with lead, and it is interesting to note that Schicksal[15]
found that by exposing lead in the form of white lead in a 1 per mille
solution of hydrochloric acid in the presence of peptone produced a
greater solvent effect on white lead than did the diluted acid alone,
and the same effect was also seen on metallic lead.

TABLE II.--SCHICKSAL’S TABLE.

  +--------------------------------+---------------+------+-----------+
  |                                |               |      |  Amount   |
  |                                |               |      | dissolved |
  |                                |               |      |returned as|
  |                                |               |      | Metallic  |
  |          Solution.             |   Substance.  | Time.|  Lead.    |
  +--------------------------------+---------------+------+-----------+
  |(_a_) 1·0 per cent. peptone}100 |{White lead,   |3 days|0·1471 grm.|
  |      0·1 per cent. HCl    }c.c.|{10 grms.      |  at  |           |
  |                                |               |37° C.|           |
  |(_b_) 1·0 per cent. peptone}100 |{Metallic lead,|   „  |0·0330  „  |
  |      0·1 per cent. HCl    }c.c.|{4 grms.       |      |           |
  |                                |               |      |           |
  |(_c_) 0·1 per cent. HCl,    100 |White lead,    |      |0·0983  „  |
  |                            c.c.|10 grms.       |      |           |
  |                                |               |      |           |
  |(_d_) 0·1 per cent. HCl,    100 |Metallic lead, |      |0·0194  „  |
  |                            c.c.|4 grms.        |      |           |
  |                                |               |      |           |
  |(_e_) 0·3 per cent. Na₂CO₃      |Metallic lead, |      | None      |
  |                                |4 grms.        |      |           |
  |                                |               |      |           |
  |(_f_) 0·3 per cent. Na₂CO₃      |White lead     |      |  „        |
  |                                |               |      |           |
  |(_g_) 0·3 per cent. Na₂CO₃}     |White lead     |      |  „        |
  |      0·5 per cent. NaCl  }     |               |      |           |
  |                                |               |      |           |
  |(_h_) 0·3 per cent. Na₂CO₃}     |Metallic lead  |      |  „        |
  |      0·5 per cent. NaCl  }     |               |      |           |
  +--------------------------------+---------------+------+-----------+

The experiments referred to on p. 18 undoubtedly agree with those of
Schicksal. In addition to the presence of peptones, the effect of
carbonic acid must be also considered, as increase in solubility in
gastric and pancreatic digestions was produced when carbonic acid gas
was bubbled through the digest during the period of action. The whole
question of solubility of many materials in the fluids of the stomach
and intestinal canal requires entire revision, not only as regards
lead, but as regards a number of other metals, including arsenic.


=The Mechanism of Lead Absorption.=--The final method of absorption
of lead particles or lead solution into the animal body remains to be
considered. Experimental phagocytosis of lead particles--as, indeed, of
any minute particles of substance--suspended in an isotonic solution,
may be observed directly under the microscope. Lead particles show no
exception to the rule, and white blood-corpuscles in a hanging-drop
preparation, made by suspending them in an isotonic salt solution and
serum, may be watched englobing particles of lead, and by appropriate
means the ingested lead may be afterwards demonstrated. In such an
experiment, much of the lead absorbed by the individual corpuscles
rapidly loses its property of giving a black precipitate with
sulphuretted hydrogen, and has apparently become converted into an
organic compound, peptonate or albuminate.

In the section devoted to the Chemistry of Lead, it has been
noted that the colloidal solutions of lead are not precipitated by
sulphuretted hydrogen, and that albuminates and peptonates of lead are
presumably of colloidal form. There seems evidence, therefore, that the
direct absorption of lead takes place by means of the phagocytes of
the body, and that in them it becomes converted into a colloidal form,
in which it is probably eliminated through the kidney and intestine,
mainly the latter.

Further evidence of the englobement of lead particles by amœbic cells
may be gained if sections of the intestines of experimental animals are
examined; in the lymphoid glands particles of lead may be seen situated
in the interior of the walls, and even in the cells. It does not by any
means follow that these particles of lead sulphide present in the cells
have been formed _in situ_; more probably the lead has been converted
into a sulphide in the intestinal lumen itself, and subsequently taken
up by the amœbic cells situated in its periphery.

Another solution is possible--namely, that the particles seen in the
intestinal wall are particles of lead in process of excretion into the
intestine itself, and that the pigmentation of the vessel walls and
cells is caused by the staining of the particles of lead passing from
the blood into the lumen of the tube, which have been converted into a
sulphide during their passage.

The localization of the staining in the large intestine, especially
in the region of the appendix in animals (cats), tends to support
this theory. The large bowel near the ileo-cæcal valve, the appendix,
and even the glands in the immediate neighbourhood, are found to
be discoloured, and to contain lead in larger quantities than any
other portion of the intestine. In extreme cases the whole of the
large intestine may be stained a greyish-blue. The bloodvessels in
the mesentery in this region are also engorged. When, however, a
salt of lead, such as lead carbonate or lead oxide, gains access to
the stomach, it may be easily converted into chloride by the free
hydrochloric acid present in the stomach; and, in addition, should
there be any chronic acid-dyspepsia (hyperchlorhydria), particularly
of the fermentative type, in which free lactic acid and other organic
acids are to be found within the viscus, small quantities of lead
swallowed as dust undergo solution and conversion into chloride or
lactate. The pouring out of acid gastric juice from the stomach glands
does not take place immediately after the first bolus of food is
swallowed, and it may be twenty minutes or half an hour before the
gastric contents have an acid reaction. During this time any lead salts
previously swallowed may become incorporated with the bolus of food and
escape absorption.

Lead in solution or suspension in the stomach which becomes mixed up
with the food, and at the same time subjected to the action of various
albuminous constituents of the food in addition to acids, causes an
albuminate or peptonate of lead to be easily formed, _and as such can
never be absorbed from the stomach direct_; practically no absorption
takes place in the stomach, and the presence of food containing
albuminate precipitates any lead in solution as an organic insoluble
salt. The bolus of food impregnated with small quantities of lead
passes onwards to the intestine, where further digestion takes place.
As the mass passes through the intestine the action gradually results
in the reappearance of acidity, but at the same time a certain quantity
of sulphuretted hydrogen is produced, some of it from the degradation
of the sulphur-containing moiety of the protein molecule by ordinary
hydrolytic process and intestinal ferments, quite apart from any
bacterial action. A portion of the lead present in the chyme may be set
free again for absorption. The bile is said to assist in the solution
of lead _in vitro_.

In experiments made by one of us, which are quoted later, it has been
shown that an isolated loop of intestine allows the absorption of a
soluble lead salt (chloride) when there is no food present in the loop.
As the food mass proceeds through the length of the intestine more and
more sulphur is set free, and an opportunity arises for the fixation of
the lead as a sulphide, but even as a sulphide it is slightly soluble.
Probably, however, most of the lead becomes absorbed long before it
reaches the stage at which free sulphur or sulphuretted hydrogen
exists for the formation of sulphide. It is highly probable that lead,
in common with a number of other heavy metals, including arsenic, is
absorbed gradually in the upper part of the intestine, and re-excreted
in the lower. Such an hypothesis is undoubtedly strongly supported by
the remarkable staining of the large intestine and the ileo-cæcal valve.

The exact mechanism of the absorption of lead from its compound with
albumin or peptone as a lead peptonate or albuminate is very difficult
to state at present; lead albuminate is undoubtedly insoluble in water
or normal saline and in albumin. The process of absorption, then,
of the metal lead from the gastro-intestinal canal is very closely
related to the absorption of other heavy metals, and the fact that
animals after very large doses of lead salts administered via the mouth
show hæmorrhages in the intestinal wall, in addition to hæmorrhages in
other parts of the body, with occasional distinct ulceration, suggests
a localized coagulative action on the vessels in the wall of the
intestine as the probable origin of the ulceration. A consideration
of this problem of lead absorption from the intestine--probably only
the minutest quantity of lead, if any, is absorbed from the stomach
direct--is one of considerable importance in the prevention of such
lead poisoning as is attributable to swallowing lead. No work in a lead
factory should be commenced in the morning without partaking of food,
because if food be present the opportunities for absorption of lead are
greatly diminished, and of all foods the one to be recommended as the
most efficient is milk, or cocoa made with milk.

The absorption of dust through the lung is probably an exceedingly
complicated reaction, and Armit’s experiments with nickel carbonyl
probably give the clue. He found that in nickel carbonyl poisoning the
volatile product was split up on the surface of the lung cells, the
metallic portion passing onwards into the lung itself, to be eventually
absorbed by the serum.

From the pathological and histological investigations described on p.
81, and from the fact that particles of lead are very readily taken
up by white blood-corpuscles, we can conclude that absorption of the
finer lead particles gaining access to the lung takes place through
the medium of these phagocyte cells, as such cells are well known to
exist within the alveoli of the lung. The stored-up carbon particles
found in the lungs in dwellers in cities show that such transference of
particles from the alveoli to the inner portions of the lung trabeculæ
is a constant phenomenon, and it is therefore easily understood how
rapidly any fine particles not of themselves irritant may be easily
taken up by the tissues. Once having gained access to the interior of
the cells, the particles subjected to the action of the serum of the
blood in the ordinary process of bathing the tissues by the exuding
lymph--nay, more, actual particles of lead--may thus be actually
transferred bodily into the finer blood-spaces, and so be carried
forward to the general circulation. Such particles as remain fixed in
the lung will undergo gradual absorption, and the constant presence of
carbonic acid in the circulating blood brought to the lung undoubtedly
largely contributes to their solution, and there is no need to
presuppose the necessity of some recondite interaction of organic acid
for the solution of the inhaled lead in the lungs.

In the absorption of the substance from the intestine, it may go direct
into the blood-stream in a similar fashion through the lacteals along
the lymph channels, and so into the thoracic duct, and finally into
the general circulation. On the other hand, a certain amount, probably
not an inconsiderable portion, is taken up by the portal circulation
and transferred direct to the liver itself. Chemical analysis of the
liver supports this view, as does also the considerable amount of
stress thrown upon the liver when poisoning has taken place from the
intestinal canal on administration of massive doses of a highly soluble
lead compound. According to Steinberg[16], excretion of lead takes
place partly from the liver by the bile. This is probable, but there
is no experimental evidence at the present time to support the view.
If such an excretion does take place, the form in which the lead is
excreted is probably one in which it is no longer soluble by digestive
action. On the other hand, it may be in so soluble a form as to become
reabsorbed from the intestine, thus setting up a constant cycle. But
such a theory is one that would require a considerable amount of
experimental evidence to support it before it could be relied on.

There is no doubt that, however absorbed, lead remains stored up in
the body in minute quantities in many places, and the close analogy
to arsenic is met with in the curious elimination of the metal by the
fæces. Cloetta[17], quoted by Dixon Mann, discovered that, although
dogs were unable to take a larger dose of arsenic than 0·0035 gramme
per day without exhibiting toxic results, they could nevertheless take
arsenic in much larger doses if it were given in the solid form, and he
was able to increase the dose to as much as 2 grammes per diem without
showing any toxic symptoms. Examination of the urine and fæces showed
that as the amount of urinary excretion of arsenic diminished, so that
in the fæces increased, and in lead poisoning, even in massive doses
swallowed in error, the amount of lead excreted by the urine rapidly
diminishes in quantity, although the patient may be still suffering
from the effects of lead poisoning. The experiments, also, quoted on
p. 100 constantly pointed to the elimination of lead by way of the
intestine, and in practically all the animals that had suffered from
chronic poisoning well-marked dark staining of the upper part of the
cæcum due to lead was invariably present. This staining and excretion
of lead of the large intestine undoubtedly takes place in man. In a
case described by Little[18], where diachylon had been administered,
the administration of a large enema containing sulphate of magnesium
came away black. A more detailed result of the experiments and a
consideration of the elimination of lead are reserved for another
chapter, but it is impossible to consider the ætiology of the disease
without some reference to the general histological channels of
absorption and excretion.


=Cutaneous Absorption of Lead.=--A considerable amount of controversy
has centred on the question of the absorption of lead through the
unbroken skin. It has been shown that such drugs as belladonna applied
to the skin alone may produce dilatation of the pupil; an ointment
containing salicylic acid spread upon the skin and thoroughly rubbed in
is followed by the appearance of derivatives of salicylic acid in the
urine; mercury may be applied to the skin, and rubbed in, in sufficient
quantities to produce salivation; and a very large number of other
drugs may be cited, all of which when applied to the unbroken epidermis
with friction produce the physiological action of the drug.

There is no reason to exclude lead from the category of drugs which may
be absorbed through the medium of the skin, and, as several observers
have shown, animals may be poisoned by lead on applying a plaster of
lead acetate to the skin. Amongst these experiments may be quoted those
of Canuet[19] and Drouet[20] on rabbits. Some observers, among whom may
be mentioned Manouvrier[21], have attempted to prove that paralysis
of the hands occurs more often in the right hand in right-handed
people, in the left hand with left-handed people, and from the various
experiments showing absorption of lead through the unbroken skin they
seek to connect the lesion of the nerve with absorption direct through
the skin of the hands.

Many objections can be urged against acceptance of this theory. Lead
workers who are constantly manipulating lead in a state of solution
with bare hands do not appear as a class to be more subject to
wrist-drop than do persons who are exposed to inhalation of fumes or
dust of lead; in fact, incidence of paralysis and of nerve lesions
generally is more severe among persons exposed to prolonged inhalation
of minute quantities of lead through the respiratory tract. The greater
the exposure to dust, the greater the number of cases of anæmia and
colic, whilst in other industries, as has already been stated, where
lead exists as an oleate on the hands of the workers day in and day
out for many years, paralysis and even colic are of rare occurrence;
in other words, persons especially exposed to the absorption of lead
through their hands show a much smaller incidence of lead poisoning of
all types than do those exposed to lead dust. Further, the pathology of
wrist-drop and similar forms of paresis tends to show that the nerve
supplying the affected muscles is not affected primarily, but that the
initial cause is hæmorrhage into the sheath of the nerve, producing
ultimate degenerative change. The hæmorrhage, however, is the primary
lesion.


REFERENCES.

  [1] GOADBY, K. W.: A Note on Experimental Lead Poisoning. Journal of
  Hygiene, vol. ix., No. 1, April, 1909.

  [2] LEGGE, T. M.: Report on the Manufacture of Paints and Colours
  containing Lead (Cd. 2466). 1905.

  [3] DUCKERING, G. E.: Journal of Hygiene, vol. viii., No. 4,
  September.

  [4] MEILLÈRE, G.: Le Saturnisme, chap. iv. Paris, 1903.

  [5] ARMIT, H. W.: Journal of Hygiene, vol. viii., No. 5, November,
  1908.

  [6] TANQUEREL DES PLANCHES: Traité des Maladies de Plomb, ou
  Saturnines. Paris, 1839.

  [7] STANSKI: _Loc. cit._

  [8] GAUTIER: Intoxication Saturnine, etc. Académie de Médecine,
  viii., November, 1883.

  [9] THRESH, J. C.: The Lancet, p. 1033, October 7, 1905.

  [10] _Ibid._, January 5, 1909.

  [11] THOMASON: Report of the Departmental Committee on Lead
  Manufacture: Earthenware, China, vol. ii., appendices, p. 61. 1910.

  [12] _Ibid._

  [13] DIXON MANN: Forensic Medicine and Toxicology, p. 495. 1908.

  [14] OLIVER, SIR T.: Lead Poisoning (Goulstonian lectures). 1891.

  [15] SCHICKSAL: Die Bekämpfung der Bleigefahr in der Industrie, p.
  38. 1908.

  [16] STEINBERG: International Congress of Industrial Hygiene.
  Brussels, 1910.

  [17] CLOETTA: Dixon Mann’s Forensic Medicine and Toxicology, p. 463.

  [18] LITTLE: The Lancet, March 3, 1906.

  [19] CANUET, T.: Thèse, Paris, 1825, No. 202. Essai sur le Plomb.

  [20] DROUET: Thèse, Paris, 1875. Recherches Experimentales sur le
  Rôle de l’Absorption Cutanée dans la Paralysie Saturnine.

  [21] MANOUVRIER, A.: Thèse, Paris, 1873, No. 471. Intoxication par
  Absorption Cutanée.




CHAPTER III

SUSCEPTIBILITY AND IMMUNITY


A large number of poisonous substances, among which lead may be
included, are not equally poisonous in the same dose for all persons.
It is customary to speak of those persons who show a diminished
resistance, or whose tissues show little power of resisting the
poisonous effects of such substances, as susceptible. On the other
hand, it is possible, but not scientifically correct, to speak of
immunity to such poisonous substances. Persons, particularly, who
resist lead poisoning to a greater degree than their fellows are better
spoken of as tolerant of the poisonous effects than as being partially
immune.

The degree of resistance exhibited by any given population towards the
poisonous influence of lead shows considerable variation. Thus, in a
community using a water-supply contaminated with lead, only a small
proportion of the persons drinking the water becomes poisoned. There
are, of course, other factors than that of individual idiosyncrasy
which may determine the effect of the poison, as, for example, the
drawing of the water first thing in the morning which has been standing
in a particular pipe. But even if all disturbing factors are eliminated
in water-borne lead poisoning, differing degrees of susceptibility are
always to be observed among the persons using the water.

Lead does not differ, therefore, from any other drugs to which persons
show marked idiosyncrasies. Thus, very small doses of arsenic may
produce symptoms of colic in susceptible persons; a limited number of
individuals are highly susceptible to some drugs, such as cannabis
indica, while others are able to ingest large doses without exhibiting
any sign of poisoning; and it is well known that even in susceptible
persons the quantity of a particular drug which first produces symptoms
of poisoning may be gradually increased, if the dosage be continued
over long periods in quantities insufficient to produce marked symptoms
of poisoning. In this direction a number of experiments have been
performed with arsenic, particularly those of Cloetta[1], who found
that the dose of arsenic for dogs could be gradually raised, if given
by the mouth, to many times the ordinary fatal dose, but that if at
this point a subminimal fatal dose was injected beneath the skin acute
symptoms of arsenic poisoning followed.

We show in a later chapter that the excretion of lead in persons
tolerant of the metal takes place through the medium of the bowel, and
that probably those individuals who are engaged in what are recognized
as dangerous processes in lead industries, and yet show no signs of
illness, have established a kind of balance between the intake of the
poison and its excretion by the bowel. It is rarely possible in such
persons to find any lead excreted through the kidney. Occasionally,
however, such persons, after working a considerable time in a dangerous
lead process, become suddenly poisoned, and inquiry frequently
discloses the fact that some disturbing factor, either intercurrent
illness, alcoholic excess, etc., has occurred, or that the breathing
of a big dose of dust has precipitated the symptoms of general lead
poisoning. On the other hand, the experience of all persons engaged
in the routine examination of lead workers is that, although a worker
may show signs of lead absorption as distinguished from definite lead
poisoning during the earlier period of his employment, he later shows
less and less signs of the influence of the poisonous substance; even a
mild degree of definite poisoning in the early stages of work in a lead
process does not seriously militate against this gradually acquired
tolerance, whilst careful treatment during such a time as the man is
acquiring tolerance to the poison frequently tides him over the period,
and enables him to withstand the ordinary dangers attached to his work.

The earliest symptom of lead absorption is anæmia. The anæmia is not
very profound, and the diminution in the red blood-cells rarely reaches
as low as 2,000,000 per c.c., the hæmoglobin remaining somewhere
between 75 and 80 per cent. Some loss of orbital fat, as well as fat
in the other parts of the body, occurs, but beyond this no obvious
clinical signs of poisoning exist. Should such persons possess
unhealthy gums, a blue line rapidly makes its appearance, but where
the gums are healthy it is unusual to see any sign of deposit in this
prodromal stage.

Persons who gradually acquire tolerance go through the stage of anæmia
without exhibiting any symptoms of colic or paresis, and without any
treatment the hæmoglobin and the number of red cells gradually pass
back to a more or less normal condition. During this period--that is,
whilst the blood shows signs of a diminution in its corpuscular and
colour content--basophile granules may always be found if sought for,
but disappear as a rule when the blood-count has returned to about
4,000,000 per c.c. and an 80 per cent. hæmoglobin. Such a man has now
developed tolerance to the poisonous influence of lead, a tolerance
which may be described as a partial immunity produced by recurrent
subminimal toxic doses. On the other hand, in a number of persons
who show definite susceptibility, the blood-changes are progressive,
and do not show signs of automatic regeneration. In such persons,
even after so short time as four to six weeks’ exposure to lead
absorption, definite symptoms of colic may make their appearance. The
removal of such an individual from the poisonous influence of lead
generally clears up the symptoms in a short time, but the symptoms
may occasionally continue for several months after removal from the
influence of the poison. An individual of this type is to be looked
upon as showing peculiar susceptibility, and should not be employed in
any lead process where there is risk.

Such statistics as are available on this point show that an increased
tolerance to the poisonous influence of lead is gradually acquired
during periods of work, in that the number of attacks of poisoning
diminish in frequency very considerably in relation to the number of
years worked. As will be seen on reference to the chapter dealing with
the statistics of lead poisoning (p. 46), the greatest number of cases
occur in persons who have only worked a short time in lead. On the
other hand, the sequelæ of lead poisoning only make their appearance,
as a rule, after long-continued exposure. It is important to bear in
mind that the various forms of paresis rarely make their appearance
unless the subject has been exposed to long-continued absorption of
lead, and, further, that the blood of such persons will as a rule show,
on careful examination, evidences of the long-continued intoxication.
If measures, therefore, were taken to determine the presence of such
continued intoxication, and to diminish the amount of poison absorbed
(subjecting the individual at the same time to a proper course of
treatment), a large number of the cases of paralysis, encephalopathy,
and death, incidental to the handling and manufacture of lead, could be
eliminated.

Susceptibility may at times be shown by several members of one family.
Oliver[2] says that he has known many members of one family suffer
from and die of lead poisoning. In our experience several instances
of this susceptibility have been noticed. In one case two brothers,
working in one shift of men, developed poisoning, although no other
persons in that shift showed any signs of it. A third brother, who came
into the works after the other two had left, and who was placed under
special supervision on account of the susceptibility exhibited by his
two brothers, although given work which exposed him to the minimal
degree of lead absorption, developed signs of poisoning six weeks after
his entrance into the factory. In another factory, three sons, two
daughters, and the father, all suffered from lead poisoning within a
period of four years: the father had three attacks of colic, ultimately
wrist-drop in both hands; one daughter had one attack of colic, and
the other three attacks; whilst the three brothers all suffered from
colic and anæmia, and one had early signs of weakness of the wrist.
There was no evidence at all to show that these persons were more
careless, or had been more exposed to lead dust, than any other of the
persons with whom they worked, or that the work they were engaged upon
was more likely to have caused illness to them than to other workers.
Persons with a fresh complexion and red hair have been noted to be more
susceptible to lead poisoning than dark-haired persons.

In one factory with which we are familiar, a number of Italian
workmen are employed; these show considerably less susceptibility to
lead poisoning than do their English comrades as long as they adhere
to their own national diet. When, however, they give this up, and
particularly if they become addicted to alcohol, they rapidly show
diminished resistance; in fact, all the cases of plumbism occurring
among the Italians in this factory during the last ten years have been
complicated with alcohol. It is possible that the relatively large
quantity of vegetables in the diet of these Italians influences the
elimination of absorbed lead. There is some reason to suppose, however,
that there may be racial immunity to lead poisoning.

The following case in the same factory illustrates a point already
mentioned--namely, the gradually acquired tolerance to poisoning, and
the unstable equilibrium existing. The individual was a man of twenty
years of age. He commenced work on August 2, 1905. Six weeks later he
was under treatment for seven weeks, for lead absorption, and had a
peculiarly deep blue line round his gums, and a diminished hæmoglobin
of 75 per cent. The symptoms disappeared with ordinary routine
treatment, and his work was shifted to a position in the factory where
he was exposed to the minimum amount of lead absorption, at which work
he continued during the rest of the time he remained in the factory.
He continued quite well until June, 1906, when he was again under
treatment for two weeks, with the same blue line and anæmia, and his
blood showed the presence of basophile granules. He was under treatment
again in January and February, 1909, for five weeks, had again a
deep blue line and basophile staining of his blood. On November 7,
1911, having had no anæmia and no blue line, he had a slight attack
of colic. During this period of work his blood had been examined on
eight occasions, and on each occasion it had shown basophile granules.
The attack of colic was an exceedingly mild one. There is no reason
to suppose that he had indulged in alcoholic excess, but there was
some reason to think that for about a month he had been subjected to
increased lung absorption. No other persons working in the same shift
at the same work developed poisoning during the whole of this period.
This case illustrates initial susceptibility, partial tolerance, and
ultimate breaking down of such partially established tolerance.

During the experimental inquiry on lead poisoning by one of us [K.
W. G.[3]], the question of the subminimal toxic dose and the minimal
toxic dose was under consideration. Animals subjected to inhalation
of lead dust invariably succumbed to the effects of the poison when
the dose given represented from 0·0001 to 0·0003 gramme per litre of
air inhaled, the period of inhalation being half an hour three times a
week. On the other hand, when the lead content of the air was as low as
0·00001 gramme per litre, the symptoms of poisoning were long delayed,
and in more than one instance, after an early diminution in weight,
recovery of the lost weight took place, and the animals, whilst showing
apparent symptoms of absorption, had no definite symptoms of paresis.
These observations tend to confirm such clinically observed facts as
are given in the case cited above, but they, of course, do not form
a criterion as to the amount of lead dust which may be regarded as
innocuous to man.

Lead is peculiarly a cumulative poison, and post-mortem analyses of
viscera show that it may be stored up in certain parts of the body,
more especially in the bone and red bone marrow and brain, and to some
extent in the liver, spleen, and kidneys. Any circumstance, therefore,
that temporarily interferes with the ordinary channels through which
lead is excreted may determine the presence of a much larger quantity
than usual of the metal in circulation in the body; and if in addition
an increased quantity of the poison be inhaled, more or less acute
symptoms follow. The localization of the deposit of lead is therefore
of some importance.

Meillère and Richer[4] give an analysis of various organs of the
body, but their results are not in accord with the majority of other
observers. They found that the hair particularly contains a large
quantity of lead. They do not seem to have examined the bones. Next to
the hair, the liver seems to have contained the largest amount. Wynter
Blyth[5] found 117·1 milligrammes of lead in the brain of a person who
died of encephalopathy. In another case he found 0·6 gramme in the
liver, 0·003 in the kidney, and 0·072 in the brain. Hougounencq[6]
examined the organs of a person who died from lead poisoning, and found
the largest amount of lead in the large intestine.

  Large intestine  0·2150 gramme.
  Small intestine  0·0430    „
  Liver            0·0050    „
  Brain            0·0008    „

In the lung, stomach, kidney, and heart, only traces were found.

Dixon Mann[7] describes some experiments in which potassium iodide
was given in cases of chronic poisoning, and during the whole of the
experiments the fæces and urine were analyzed three times a week.
He found by this means that a considerable amount of lead was being
eliminated by the intestine. He therefore administered 2 grammes of
lead acetate three times a day for five days to a patient, and he found
that the fæces contained 0·1762 gramme the first day, 0·17411 gramme
the second day; the fourth day it had fallen to 0·0053 gramme, and on
the sixth day to 0·0006 gramme. The largest amount at any one time in
a day obtained from the urine was only just over 0·001 gramme; the
average amount found in the case of chronic poisoning was about 3
milligrammes, whereas the greatest amount at any one time in the urine
was only 0·9 milligramme.

The quantity of lead present in the brain necessary to determine
acute poisoning is not known, and it is probable that an extremely
minute quantity will produce very serious effects; and in support of
this may be quoted a number of observations in which search has been
made for the metal in persons who have died of diseases affecting the
brain associated with other symptoms of poisoning, and yet post-mortem
examination of the brain by chemical methods has not revealed the
presence of any lead whatever. In the case reported by Mott (see p.
71), no lead at all was recognized in the brain.

There are no reasons, therefore, for supposing that the immunity to
lead poisoning depends on the fixation and storing up of the poisonous
metal in a non-poisonous form in some special situation in the body,
and, further, the particular situation in the body richest in lead
in any given case of poisoning will depend rather on (1) the type of
compound causing the poisoning, and (2) the portal through which such
poisoning occurs.

The question of the detection of lead in the body is referred to in the
chapter dealing with Chemical Examination. It is as well to point out
in this connection that chemical investigation of the amount of lead
present in the organs of persons dying from lead poisoning should, if
possible, always be made where there is any doubt as to the diagnosis.

Certain observers--amongst them Gautier[8]--are of opinion that
traces of lead may be found in normal persons. Thus, in a rat (_Mus
decumanus_) Gautier found 2 milligrammes of lead in 60 grammes of
liver. He considers that in many persons at least 0·5 milligramme of
lead may be swallowed daily incorporated with the food, as a number of
foods are liable to contamination by lead. Tinned foods, particularly
those which are soldered up after the materials have been placed in the
tin, certain tinned fruits with acid juices, often contain small masses
of solder loose in the tins; in the case particularly of fruits the
natural acid may slowly dissolve the lead from the solder. The amount
of so-called “normal” lead, if it is to be found at all, must be very
small, and would certainly be much smaller in the case of a normal
person than in one who had been subject to definite lead poisoning.
Such experimental evidence as is forthcoming supports the clinical
observations that persons exposed to small doses of lead eventually
develop tolerance of the metal, so that they may ultimately withstand
many times the dose sufficient in the first instance to produce
poisoning.

Such circumstances are the natural factors in the prevention of
poisoning, and if due care be given to their significance, the surgeon
in charge of any lead works may by judicious treatment and alternation
of employment so assist and strengthen the natural defensive forces
that susceptibility may be diminished, and the degree of tolerance
increased to a very considerable extent. We do not imply that
efficiency in the exhaust ventilation can be in any way relaxed; all
we desire to emphasize is that certain natural defensive forces of
the body do undoubtedly exist by which susceptible persons ultimately
become less susceptible, and that by appropriate means these defensive
forces may be augmented.

Susceptibility and immunity to poisoning by lead may be considered,
according to the type of lead compound absorbed, further in its
relation to age and sex. All compounds of lead are not poisonous in the
same degree; the more easily soluble compounds are more poisonous than
the less soluble. On the other hand, compounds which appear at first
sight unlikely to produce poisoning may do so; for instance, fritted
lead or lead silicate, a substance largely used in the potteries as a
glaze, and manufactured by fusing together litharge and a silicate,
would appear at first sight to be quite an innocuous substance. Owing
to its method of preparation, however, it is not a pure compound
of lead and silica, but contains lead oxide, metallic lead, etc.,
entangled in its meshes, and experimentally one of us (K. W. G.) has
demonstrated that such a compound may be acted on by the tissues of
the body, both when injected subcutaneously and even when inhaled, and
so gradually produce definite symptoms of lead poisoning, but at a
much slower rate than the more poisonous lead compounds. The fineness
of division in which the compound of lead exists is another factor
affecting its poisonous nature; the more finely divided particles
find their way into the lung more easily than the coarser particles.
Various subsidiary matters may also determine the susceptibility in a
given individual, and of these a certain number require mention, as
they probably act as definite predisposing factors. Age and sex may
be regarded as predisposing factors to lead poisoning, and certain
diseases also.


=Age.=--Young persons are regarded as more liable to lead poisoning
than adults, although it is difficult to obtain definite figures on
the point, the duration of employment acting as a disturbing factor in
estimating the susceptibility of young persons. They may have worked in
a lead works for a year or more without showing any signs of poisoning,
but develop them later in adult life, although it is very likely that
absorption had taken place during the earlier period. In the Report
of the Departmental Committee on the Use of Lead in the Potteries
(Appendix XII.), the attack rate for the period 1899 to 1909 for young
persons is 19·3 per 1,000, and for adults 18·8 for the same period,
but the figures upon which these attack rates are based are too small
to build any conclusion. The general clinical conclusions of appointed
surgeons and certifying surgeons in the various lead factories would
be, we believe, that the susceptibility of young persons is at least
twice that of adults, and there is some ground for supposing that
the tissues of an adult when growth has ceased more readily adapt
themselves to deal with the absorption and elimination of poisonous
doses of lead than do the tissues of a young person.


=Sex.=--Women are more susceptible to poisoning by lead than men,
and in lead poisoning from drinking water the proportion of women
(especially pregnant women) and children attacked is stated to be
higher than in men, and one such epidemic is quoted by Oliver where
the rise in the number of miscarriages and premature births led to
the discovery of the fact that the water-supply was contaminated with
lead. The close relationship of lead poisoning to miscarriage has been
repeatedly made out, especially by Oliver, in the white lead industry
as carried on twenty years ago. Oliver also quotes the effect upon
rabbits[9], Glibert upon guinea-pigs[10], and in the experiments of one
of us (K. W. G.), referred to on p. 99, all the animals to which lead
was given during pregnancy aborted; and, further, with one exception
out of eight animals, all died of lead poisoning, not as the result of
the abortion, but some time later, although no further administration
of lead was made. This confirms the well-known abortifacient effect
of diachylon, and there is no doubt that the lead circulating in the
maternal blood determines the abortion. Further, observers who have
examined the fœtus in such cases have demonstrated the presence of
lead in the fœtus itself. Oliver[11] found that eggs painted with lead
nitrate did not hatch out, and on opening the eggs the embryos were
found to have reached only a limited stage of development, and to have
then died, whereas control eggs painted with lime produced live chicks.
From what is stated later with regard to the curious action of lead
upon the blood, the mechanism of abortion is easily understood; it is
probable that placental hæmorrhages are produced, as in other organs
of the body. But the effect of lead on the female is not only apparent
during pregnancy. A considerable number of women working in lead
processes suffer from amenorrhœa, and often from periods of menorrhagia
and dysmenorrhœa, which as a rule is the more striking symptom. The
effect of lead on the uterine functions, however, only exists so long
as the constant intake of the poison is taking place, and many cases
are recorded where women, after having had successive abortions while
working in lead factories, have ultimately gone through a normal
pregnancy and given birth to a living child. This circumstance bears a
strong analogy to the similar train of events in syphilis.

In the Report of the Committee on the Use of Lead in the Potteries,
some inquiry was made with regard to the possible association of lead
absorption on the male side as a predisposing cause of infant mortality
and premature birth. The tables given are not very conclusive, and
from our own observations there seems to be very little evidence for
supposing that a male lead worker is less likely to beget children,
or that his children are more likely to be unhealthy than those of
men working in any other industrial process. We are here speaking of
the effect of lead under the conditions of its general use in this
country now. In the absence of any precautions whatever as to daily
absorption of dangerous dust, the effect on the offspring, even in the
case of male lead workers, may well be evident, as has been shown by
Chyzer[12] in the manufacture of pottery as a home industry in Hungary.
One greatly disturbing factor in estimating the greater susceptibility
of the female than the male in many lead industries is that the more
dangerous work is performed by the women, such, for instance, in the
Potteries, as the process of colour-blowing and ware-cleaning.


=Predisposing Causes of Lead Poisoning.=--In lead poisoning, as in many
other diseases, a number of predisposing and contributory causes may be
cited which tend to lower the susceptibility of the individual to the
poisonous effect of the metal and its compounds, or to so modify the
functions of the body that a smaller dose of poison may produce more
profound changes than would otherwise be the case.

Certain diseases may be regarded as predisposing causes by lowering the
general resistance of the body tissues to the influence of lead, and a
consideration of the chapter on Pathology will at once demonstrate how
seriously certain diseases may contribute in this way.

The peculiar effect of lead is upon the blood and the walls of the
bloodvessels, and it will therefore follow that any disease which may
affect the intima of the bloodvessels may predispose to lead poisoning;
and, further, as the elimination of lead takes place to a certain
extent through the kidney, any disease which affects either the renal
epithelium or the general maintenance of the excretory function of
the kidney may predispose that organ to the irritative effects of the
lead circulating in the blood. In the same way, the condition of lead
absorption in which the balance of absorption and elimination of lead
remains in such a ratio that no definite symptoms of lead poisoning
appear may have that delicate balance easily upset by the introduction
of some secondary cause, which, when operating in association with lead
absorption, may precipitate symptoms attributable to poisoning by that
metal. Chronic alcoholism especially, producing as it does definite
changes in the kidney of itself--changes which it is impossible to
distinguish by the naked eye from the effects of lead poisoning--must
clearly act as a predisposing, if not even an exciting, cause of lead
kidney infection. In experiments upon animals, it was found that the
addition of alcohol to the diet of an animal which was the subject of
chronic lead absorption precipitated the attack of definite poisoning;
in other words, the latent period of lead poisoning--that is to
say, the resistance exhibited by the tissues to the toxic influence
of lead--was considerably diminished by this addition of a second
irritant, alcohol. In several experiments, also, where the form of lead
experimented with was one of the least toxic of the lead compounds, the
animals subjected to such a compound alone did not become poisoned,
but succumbed if alcohol were added to their diet. This experimental
work is amply borne out by the clinical evidence of all persons who
have had experience of industrial lead poisoning, as cases of colic
and wrist-drop are frequently observed in lead workers shortly after
alcoholic excesses. Individuals, therefore, who are suspected of the
alcoholic habit should not be employed in any process where they are
likely to run risk of absorption of lead dust.

Such diseases as syphilis and gout, by causing a heightened arterial
tension or definite disease of the intima of the bloodvessels
themselves, tend to weaken the arteries in much the same manner as
does lead circulating in the blood, and must on that account act as
predisposing causes.

In persons employed in lead trades some species of tolerance is
generally developed, and if the functions of the body progress in the
normal way the balance of elimination and absorption are equal, and, as
will be seen later, the chief channel for the elimination of lead from
the body is through the bowel. It follows, therefore, that any disease
which tends to produce constipation or chronic inactivity of the normal
intestinal functions will also tend to lower the resistance of the
individual to lead poisoning.

Of the various types of intestinal disease of a chronic nature--such,
for instance, as chronic dysentery, colitis, and the like--little need
be said; but the predisposing effect of diseased conditions of the
upper portion of the alimentary canal must not be overlooked, more
particularly affections of the oral cavity itself. This special type
of infection, often included under the term of “oral sepsis,” besides
producing anæmia, is also a constant cause of intestinal disturbance,
and as such operates as a particular predisposing cause of lead
poisoning.

With regard to gout the evidence is not so clear. It was pointed out by
Garrod[13] that gout was common among house-painters, and it has been
generally stated that lead poisoning predisposes to this complaint.
In the opinion of a considerable number of observers, however, gout
is by no means common among persons working in white lead factories
or lead-smelting works, but there seems to be some reason to suppose
that it is somewhat common among those persons employed in the painting
trades, but not among those employed in the manufacture of paints and
colours. From the experiments carried out by one of us [K. W. G.[13]].
it seems probable that the occurrence of gout among painters may be
associated with the use of turpentine, largely employed in the ordinary
processes of painting, as this substance in particular is not one
that is used by workers in other lead trades, and, from experiments
performed on animals, the inhalation of turpentine vapour was found
to produce very definite changes both in the kidney and the general
metabolism of the body.


_Malnutrition._--Malnutrition is recognized as a predisposing cause
of practically all forms of disease, and with a chronic intoxication,
such as lead poisoning, malnutrition and starvation, with its attendant
depression of all the vital forces of the body, is essentially a
predisposing cause of poisoning, so much so that even the fact of
commencing work without previously partaking of food may operate
directly as a cause of poisoning. It has been found, moreover,
experimentally by one of us [K. W. G.[14]] that an animal fed with milk
containing lead nitrate did not develop poisoning, though the control
animal developed well-marked symptoms of poisoning with a much smaller
dose given in water.


_Anæmia._--Anæmia has already been referred to as occurring with great
frequency in persons who are absorbing lead, and it usually forms one
of the chief factors in the symptom-complex of lead cachexia. As the
action of lead is particularly upon the blood and the hæmopoietic
organs, diminishing the number of red cells and the amount of
hæmoglobin, and impairing the organs from which fresh blood-cells are
produced, a disease or state associated with anæmia other than of lead
origin acts as a definite predisposing cause in the development of
toxic symptoms in a worker in an industrial lead process.

Among the anæmias, two particular types may be referred to as of
chief importance. In the first place, chlorosis, the anæmia occurring
particularly in young women, is often associated with intestinal
stasis. Lead anæmia occurring in a chlorotic person is always more
severe than simple lead anæmia. Young persons suffering from chlorosis,
therefore, should not be employed in a dangerous lead process until
the anæmia has been treated. The second type of anæmia, which, from
its frequency, may be also regarded as a predisposing cause of lead
poisoning, is chronic secondary septic anæmia. Anæmias of this type,
as was pointed out by William Hunter[15], resemble in many points the
original idiopathic or Addisonian anæmia, often termed “pernicious
anæmia,” and one of us has had occasion to inquire into the curious
type of secondary anæmia associated with septic affections of the upper
respiratory tract, particularly those related to chronic suppurative
affections of the accessory sinuses of the nose, of the gums, of the
mucous membrane of the mouth and the throat. The commonest forms of
this secondary anæmia are those due to chronic post-nasal discharge,
and to chronic infections of the gums and alveolus of the jaws, the
latter often classed together under the term “pyorrhœa alveolaris.”
This term is an exceedingly clumsy one, indicating a discharge of pus
from the gum edges and sockets of the teeth, which are often loose.
The disease commences as an infective gingivitis along the edges of
the gum, and progresses to rarefying osteitis of the alveolar process,
and often of the body of the bone. The affection rarely gives rise
to pain, and as a rule the individual is entirely unaware that any
chronic suppuration is present, and little or no notice is therefore
taken of the disease. Progressive anæmia may thus be set up without any
knowledge of its cause, partly by absorption of the actual bacteria and
their products through the alveolar bloodvessels, and partly by the
fact of the constant swallowing of pus and bacterial products, which
set up various forms of chronic gastro-intestinal incompetence. From
the discharges of the mouth, and issuing from the gum edges, numerous
bacteria have been isolated, and in more recent work one of us [K. W.
G.[16]] has succeeded in isolating and identifying certain bacteria
as a direct cause of arthritis deformans, a malady occasionally, but
without sufficient grounds, ascribed to lead poisoning. Arthritis of
various types may occur in persons engaged in lead trades, but in all
such cases we have had the opportunity of examining there has been
some obvious source of septic infection, and no evidence that the
arthritis was due to the action of lead. It is most important to draw
the attention of those engaged in the protection of lead workers from
the dangers of their occupation to these chronic septic conditions of
the mouth, and it may be taken as a general rule that, wherever the
blue line makes its appearance along the gums, such gums are in a state
of chronic infection, and the appearance of the blue line is merely
a secondary effect. It is exceedingly rare to find the blue line in
persons with intact gums and clean teeth; and although attention is
frequently drawn to the fact that a lead line exists in a person whose
_teeth_ are normal, little or no notice is taken of the presence or
absence of a suppurative condition of the gum margins. Moreover, such
a suppurative condition does not always result in obvious inflammation
of the gum edges, and very considerable destruction of the alveolus
and the interdental bone may exist without any obvious signs of its
presence, unless the case be examined carefully with a fine probe.
This particular point has been the subject of experiment by one of us.
Animals exposed to the influence of air laden with lead dust never
develop a blue line, although all the usual symptoms of lead poisoning
make their appearance. When, however, some slight suppurative lesion
of the gums was produced by an inoculation into the gum tissue of
organisms isolated from a case of infective gingivitis in a human
being, the site of inoculation and any suppurative lesion that resulted
locally at once allowed the development of a blue line, and it was only
in animals so treated that it was possible to produce experimentally
the Burtonian line.

There is no doubt that any chronic septic infection may predispose
to lead poisoning through the production of a secondary anæmia, and
it is therefore inadvisable to pass for work in a lead process of a
dangerous nature any persons suffering from an infected condition of
the mouth. It follows also that the care of the mouth and gums should
be rigorously enforced upon all persons employed in lead trades, as
the mere mechanical facilities for the accumulation of débris around
the individual teeth tends to increase the quantity of lead dust that
may be retained in the mouth. This is gradually rendered soluble and
absorbed, through the action of the bacterial acids which are always
produced along the gum margins when any entangled food is retained in
the interdental spaces.

One further point of importance attaches to the infections of the
upper respiratory tract--namely, the constant ingestion of bacteria
of a fermentative type. By this means the contents of the stomach may
be maintained in a state of hyperacidity, and any small quantities of
lead which become swallowed are thereby at once rendered soluble in the
intermeal periods.

Of the other types of anæmia which may act as predisposing causes of
lead poisoning, little need be said, as they are either associated
with other grave symptoms or are rare in this country. But as all
forms of anæmia, particularly septic anæmia, malarial fever, etc.,
are associated with destruction of the blood-cells, the presence of
basophile staining granules in the red corpuscles of such persons is
a constant feature, and must not be confounded with the basophile
staining owing its origin to the effect of lead.

In addition to the diseases mentioned which may be said to predispose
to lead poisoning, certain other diseases have been stated to be
predisposed to by the action of lead. It is no doubt a fact that where
chronic anæmia, wasting, loss of subcutaneous fat, decreased muscular
power, and general lowering of the metabolic activity of the body,
are produced, an individual so affected may be supposed to be more
susceptible to certain infectious diseases, and among these stress has
been laid on the alleged association of phthisis with lead absorption.
This point is discussed in the next chapter.

In summing up the difficult question of predisposition to lead
poisoning, together with the correlated questions of susceptibility and
immunity, certain facts may at any rate be clearly stated:

1. Undoubted individual susceptibility and immunity exist with regard
to lead poisoning in exactly the same way as individual susceptibility
and immunity may be shown to exist towards poisoning by many other
metals and drugs. Therefore, given the same opportunities for
infection, a person showing early signs of lead absorption may be
regarded as susceptible.

2. Females are at least twice, and probably three times, as susceptible
to lead poisoning as are males. Much of this susceptibility is
determined by the extra stress thrown upon the female generative organs.

3. Certain diseases predispose to lead poisoning mainly by nature of
the alterations in metabolism produced--chiefly anæmia.

4. Many persons engaged in lead industries become gradually tolerant of
the absorption of lead, and in time resist much larger doses than would
have been possible at the commencement of exposure, but in such persons
the balance between absorption and excretion upon which that tolerance
depends may become easily disturbed by intercurrent disease or sudden
increase in absorption.


REFERENCES.

  [1] CLOETTA: Dixon Mann’s Forensic Medicine and Toxicology, p. 463.

  [2] OLIVER, SIR T.: Diseases of Occupation, p. 142.

  [3] GOADBY, K. W.: Departmental Committee on Lead Poisoning, etc., in
  China and Earthenware Manufacture, Appendix No. XXV.

  [4] MEILLÈRE AND RICHER: Meillère’s Le Saturnisme. Paris, 1903.

  [5] BLYTH: Abstract of Proc. Chem. Soc., 1887-88.

  [6] HOUGOUNENCQ: Meillère’s Le Saturnisme, p. 73.

  [7] DIXON MANN: British Medical Journal, 1893.

  [8] GAUTIER: Société de Biologie, April, 1903.

  [9] OLIVER, SIR T.: British Medical Journal, May 13, 1911, p. 1096.

  [10] GLIBERT, D. J.: Le Saturnisme Expérimental. Extrait des Rapports
  Annuels de l’Inspection du Travail. Bruxelles, 1906.

  [11] OLIVER, SIR T.: Diseases of Occupation, p. 139.

  [12] CHYZER, A.: Des Intoxications par le Plomb se présentant dans la
  Céramique en Hongrie. Budapest, 1908.

  [13] GARROD: The Lancet, 1870.

  [14] GOADBY, K. W.: Departmental Committee on Lead Poisoning, etc.,
  in China and Earthenware Manufacture, Appendix XXV.

  [15] HUNTER, WILLIAM: Severest Anæmias.

  [16] GOADBY, K. W.: The Lancet, March 11, 1911.




CHAPTER IV

STATISTICS OF PLUMBISM[A]


  [A] Based mainly on reports received from certifying factory surgeons
  during the ten years 1900-1909.

Classification of notified cases of lead poisoning was carried out
on practically the same lines between the years 1900 and 1909, and
comparison of the data so collected has interest, in view of their
large number--nearly 7,000--in respect of (1) increase or decrease in
recorded amount in each one of eighteen classes of industries; (2)
severity and number of attack--_i.e._, whether first, second, third, or
chronic; and (3) main symptoms.

Notification was first enjoined by Section 29 of the Factory and
Workshop Act, 1895, which subsequently, on consolidation of the Factory
Acts, became Section 73 of the Act of 1901. This enactment requires
every medical practitioner, attending on, or called in to visit, a
patient whom he believes to be suffering from lead poisoning contracted
in a factory or workshop, to notify the case forthwith to the Chief
Inspector of Factories at the Home Office; and a similar obligation
is imposed on the occupier of a factory or workshop to send written
notice of every such case to the certifying surgeon and inspector of
factories for the district. In form there is close similarity between
this section and that requiring notification under the Infectious
Diseases (Notification) Act; but whereas the symptoms of these diseases
are, within well-recognized limits, precise, in lead poisoning the
differential diagnosis has not infrequently to be made from a variety
of common ailments--headache, anæmia, rheumatism, abdominal pain; and
there is no precise standard of what constitutes lead poisoning.

The notification of the practitioner as a rule gives no information
beyond the belief that the case is one of lead poisoning. As a matter
of routine the notification is followed up by an inquiry by the
certifying surgeon and inspector to see whether regulations already in
force have been infringed in the particular work-place or not, and as
to how far there may have been contributory negligence on the part of
the sufferer. The data supplied on the surgeon’s report form the basis
of the tabulation[1]. Brief explanation is wanted of the method adopted
in classification. Cases represent all attacks reported within a year,
and not previously reported within the preceding twelve months, so as
to make the number of persons and cases in a year the same. Where the
interval between two reports on the same person was more than twelve
months, the fresh attack was again included. The number of such second
reports on persons already included in a return numbered 284 (4·2 per
cent.), and a portion of these certainly, probably not more than 100,
have been included twice or thrice in the total 6,638 cases. Cases in
which there was obvious error in diagnosis, or in which the opinion
of the certifying surgeon was very strongly against the diagnosis
(especially when the report had been made in the first instance by
the occupier alone, and not by a medical practitioner), were excluded
from the return. These numbered 458 (6·8 per cent.). Others, again,
where there was a strong element of doubt, but not to be regarded as
more than a difference of opinion between two medical men, were marked
doubtful and included. Of these there were 424 (6·3 per cent.).

The classification of industries was designed to represent the way in
which the poisoning may be supposed to originate from (_a_) lead fumes
(1 to 4), (_b_) handling metallic lead (5 and 6), (_c_) dust from lead
compounds (7 to 14), and (_d_) lead paint (15 to 17). We attach now
only slight importance to this attempt to define causation, as it will
appear from our survey that we regard almost all cases as the result of
inhalation either of fumes or dust.

The reports describe not only the particular attack, but also the
general condition of the patient at the time of the attack. Very
frequently a combination of symptoms--colic, anæmia, and varying
degree of paralysis--are described as present, and when this is the
case each one of them has been entered under the appropriate heading.
The total number of symptoms, therefore, greatly exceeds the number
of cases, but this does not affect the correctness of the estimate of
each one as a proportion on the total number reported. The reports do
not give detailed information such as can be gained from hospital
records. Especially is this the case with the symptoms of paralysis and
encephalopathy.

Table III. shows the number of reported cases included in returns for
each of the years 1900 to 1909. On the total figures there has been
a reduction of 47·7 per cent. In the several industries the salient
feature is that the considerable diminution achieved is limited to
industries--notably white lead, earthenware and china, litho-transfers,
and paints and colours--in which, under regulations or special rules,
locally applied exhaust ventilation for the removal of dust, and
periodical medical examination of the workers, have been required.
Where, owing to the nature of the processes carried on, it has been
found impracticable, in the present state of knowledge, to apply local
exhaust ventilation, and where periodical examination of the workers is
lacking, as in smelting of metals[A] and industries using paint, there
has been tendency to increase in the number of cases. In coach-building
the increase is in part due to activity in the motor-car industry.

  [A] This is now required by the regulations dated August 12, 1911.

TABLE III.--NOTIFICATION OF POISONING BY LEAD (UNDER S. 73, 1901),
1900-1909.

  +--------------------------+---------------------------------------
  |                          |                              Reported
  |                          +--------+-----+-----+-----+-----+-----+
  |                          |  Total |     |     |     |     |     |
  |         Industry.        |1900-09.|1909.|1908.|1907.|1906.|1905.|
  +--------------------------+--------+-----+-----+-----+-----+-----+
  |            (1)           |  (2)   | (3) | (4) | (5) | (6) | (7) |
  |LEAD POISONING            |6,762²⁷⁵|553³⁰|646³²|578²⁶|632³³|592²³|
  | 1. Smelting of metals    |  412¹⁸ | 66⁵ | 70² | 28² | 38¹ | 24¹ |
  | 2. Brass works           |   75⁴  |  5  |  6  |  9¹ | 11  |  5¹ |
  | 3. Sheet lead and lead   |        |     |     |     |     |     |
  |    piping                |  109³  |  9² | 14  |  6  |  7  |  9  |
  | 4. Plumbing and soldering|  217¹² | 28  | 27  | 20² | 16⁴ | 24² |
  | 5. Printing              |  200¹⁷ | 21¹ | 30² | 26³ | 16² | 19⁴ |
  | 6. File-cutting          |  211¹⁹ |  8  |  9² | 10  | 15  | 12  |
  | 7. Tinning and enamelling|  138²  | 21  | 10  | 25  | 18¹ | 14¹ |
  | 8. White lead            |1,295³¹ | 32² | 79³ | 71  |108⁷ | 90¹ |
  | 9. Red lead              |  108   | 10  | 12  |  7  |  6  | 10  |
  |10. China and earthenware |1,065⁵⁷ | 58⁵ |117¹²|103⁸ |107⁴ | 84³ |
  |10_a._ Litho-transfers    |   48   |  1  |  2  | 10  |  5  |  5  |
  |11. Glass cutting and     |        |     |     |     |     |     |
  |    polishing             |   48⁹  |  4² |  3¹ |  4  |  4¹ |  3  |
  |12. Enamelling iron plates|   52¹  |  3  |  7  |  6  |  4  |  2  |
  |13. Electric accumulators |  285⁶  | 27² | 25¹ | 21  | 26  | 27¹ |
  |14. Paints and colours    |  422⁷  | 39² | 25  | 35¹ | 37  | 57¹ |
  |15. Coach-building        |  697⁴¹ | 95⁶ | 70³ | 70³ | 85⁷ | 56³ |
  |16. Ship-building         |  269¹⁰ | 27¹ | 15  | 22¹ | 26¹ | 32² |
  |17. Paint used in other   |        |     |     |     |     |     |
  |    industries            |  452¹⁸ | 42  | 47¹ | 49² | 37³ | 49² |
  |18. Other industries      |  659²⁰ | 57² | 78⁵ | 56² | 66² | 70¹ |
  +--------------------------+--------+-----+-----+-----+-----+-----+

  +--------------------------+-------------------------------+
  |                          |Cases.                         |
  |                          +-----+-----+-----+-----+-------+
  |                          |     |     |     |     |       |
  |         Industry.        |1904.|1903.|1902.|1901.| 1900. |
  +--------------------------+-----+-----+-----+-----+-------+
  |            (1)           | (8) | (9) | (10)| (11)|  (12) |
  |LEAD POISONING            |597²⁶|614¹⁹|629¹⁴|863³⁴|1,058³⁸|
  | 1. Smelting of metals    | 33¹ | 37² | 28  | 54³ |   34¹ |
  | 2. Brass works           | 10¹ | 15  |  5  |  6¹ |    3  |
  | 3. Sheet lead and lead   |     |     |     |     |       |
  |    piping                |  7  | 11  | 12  | 17  |   17¹ |
  | 4. Plumbing and soldering| 21³ | 26  | 23¹ | 23  |    9  |
  | 5. Printing              | 15  | 13² | 19  | 23¹ |   18² |
  | 6. File-cutting          | 20⁴ | 24² | 27¹ | 46⁷ |   40³ |
  | 7. Tinning and enamelling| 10  | 14  | 11  | 10  |    5  |
  | 8. White lead            |116² |109² |143¹ |189⁷ |  358⁶ |
  | 9. Red lead              | 11  |  6  | 13  | 14  |   19  |
  |10. China and earthenware |106⁴ | 97³ | 87⁴ |106⁵ |  200⁸ |
  |10_a._ Litho-transfers    |  3  |  3  |  2  |  7  |   10  |
  |11. Glass cutting and     |     |     |     |     |       |
  |    polishing             | --  |  4  |  8² | 11³ |    7  |
  |12. Enamelling iron plates|  3  |  4  |  3¹ |  9  |   11  |
  |13. Electric accumulators | 33  | 28  | 16¹ | 49¹ |   33  |
  |14. Paints and colours    | 32¹ | 39¹ | 46  | 56  |   56¹ |
  |15. Coach-building        | 49⁴ | 74⁵ | 63¹ | 65⁴ |   70⁵ |
  |16. Ship-building         | 48  | 24¹ | 15¹ | 28¹ |   32² |
  |17. Paint used in other   |     |     |     |     |       |
  |    industries            | 27³ | 46¹ | 44¹ | 61  |   50⁵ |
  |18. Other industries      | 53³ | 40  | 64  | 89¹ |   86⁴ |
  +--------------------------+-----+-----+-----+-----+-------+

  The principal figures are those of the cases, fatal and non-fatal;
  the small figures relate to fatal cases only.

  For the sake of completeness the figures for the years 1910 and 1911
  are given below. The grand totals are comparable with those for each
  of the years 1900 to 1909, but not the total for all of the several
  groups of industries. Thus, the name of heading No. 7 is altered to
  “Tinning of metals,” and No. 12 to “Vitreous enamelling,” because
  of regulations widening their scope, and now including cases which
  previously figured in No. 18, “Other industries.”

  +----------------------------------+-----+-----+
  |         Industry.                |1911.|1910.|
  +----------------------------------+-----+-----+
  |LEAD POISONING                    |669³⁷|505³⁸|
  |  Smelting of metals              | 48³ | 34⁵ |
  |  Brass works                     |  9¹ |  7  |
  |  Sheet lead and lead piping      | 12  |  4  |
  |  Plumbing and soldering          | 37² | 25¹ |
  |  Printing                        | 32² | 33⁴ |
  |  File-cutting                    | 18² |  9¹ |
  |  Tinning of metals               | 13  | 17  |
  |  Vitreous enamelling             | 19¹ | 17  |
  |  White lead                      | 41² | 34¹ |
  |  Red lead                        | 13¹ | 10  |
  |  China and earthenware           | 92⁶ | 77¹¹|
  |  Litho-transfers                 |  1  |  1  |
  |  Glass cutting and polishing     |  5  | --  |
  |  Electric accumulators           | 24¹ | 31  |
  |  Paints and colours              | 21  | 17¹ |
  |  Coach and car painting          |104⁵ | 70⁶ |
  |  Ship-building                   | 36  | 21² |
  |  Use of paint in other industries| 56¹ | 51³ |
  |  Other industries                | 88⁴ | 47³ |
  +----------------------------------+-----+-----+

TABLE IV.--ANALYSIS OF REPORTS ON LEAD POISONING BY CERTIFYING SURGEONS
FROM JANUARY 1, 1900, TO DECEMBER 31, 1909.

  +-----+--------------++-----------++--------------------------------++
  |     |              ||           ||     Severity of Symptoms.      ||
  +-----+--------------++-----------++----------+----------+----------++
  |     |              ||           ||          |          |          ||
  | No. | Occupation.  ||   Total.  ||  Severe. | Moderate.|  Slight. ||
  +-----+--------------++-----------++----------+----------+----------++
  | (1) |      (2)     ||    (3)    ||    (4)   |    (5)   |    (6)   ||
  +-----+--------------++-----+-----++-----+----+-----+----+-----+----++
  |     |              ||  M. |  F. ||  M. | F. |  M. | F. |  M. | F. ||
  | 1   |Smelting of   ||     |     ||     |    |     |    |     |    ||
  |     |metals:       ||     |     ||     |    |     |    |     |    ||
  |     |Cases         ||  411|   --||  104| -- |  105| -- |  197| -- ||
  |     |Per cent.     ||  100|   --|| 25·3| -- | 25·6| -- | 47·9| -- ||
  | 2   |Brass works:  ||     |     ||     |    |     |    |     |    ||
  |     |Cases         ||   70|    4||   26|   2|   20|   1|   22|   1||
  |     |Per cent.     ||  100|   --|| 37·1| -- | 28·6| -- | 31·5| -- ||
  | 3   |Sheet lead    ||     |     ||     |    |     |    |     |    ||
  |     |and lead      ||     |     ||     |    |     |    |     |    ||
  |     |piping:       ||     |     ||     |    |     |    |     |    ||
  |     |Cases         ||  102|    4||   25|   1|   29|   1|   47|   2||
  |     |Per cent.     ||  100|   --|| 24·5| -- | 28·4| -- | 46·1| -- ||
  | 4   |Plumbing and  ||     |     ||     |    |     |    |     |    ||
  |     |soldering:    ||     |     ||     |    |     |    |     |    ||
  |     |Cases         ||  186|   30||   65|   6|   49|   6|   65|  16||
  |     |Per cent.     ||  100|  100|| 34·9|20·0| 26·3|20·0| 34·9|53·3||
  | 5   |Printing:     ||     |     ||     |    |     |    |     |    ||
  |     |Cases         ||  190|    6||   55| -- |   43|   1|   82|   5||
  |     |Per cent.     ||  100|   --|| 28·9| -- | 22·6| -- | 43·2| -- ||
  | 6   |File-cutting: ||     |     ||     |    |     |    |     |    ||
  |     |Cases         ||  174|   34||   85|   8|   34|   5|   48|  21||
  |     |Per cent.     ||  100|  100|| 48·9|23·5| 19·5|14·7| 27·6|61·8||
  | 7   |Tinning and   ||     |     ||     |    |     |    |     |    ||
  |     |enamelling of ||     |     ||     |    |     |    |     |    ||
  |     |hollow-ware:  ||     |     ||     |    |     |    |     |    ||
  |     |Cases         ||   84|   53||   26|  13|   27|  16|   31|  24||
  |     |Per cent.     ||  100|  100|| 31·0|24·5| 32·1|30·2| 36·9|45·3||
  | 8   |White lead:   ||     |     ||     |    |     |    |     |    ||
  |     |Cases         ||1,167|   76||  317|  27|  235|  11|  593|  33||
  |     |Per cent.     ||  100|  100|| 27·2|35·5| 20·1|14·5| 50·8|43·4||
  | 9   |Red lead:     ||     |     ||     |    |     |    |     |    ||
  |     |Cases         ||  108|   --||   30| -- |   31| -- |   45| -- ||
  |     |Per cent.     ||  100|   --|| 27·8| -- | 28·7| -- | 41·7| -- ||
  |10   |China and     ||     |     ||     |    |     |    |     |    ||
  |     |earthenware:  ||     |     ||     |    |     |    |     |    ||
  |     |Cases         ||  490|  572||  102|  86|  158| 181|  216| 286||
  |     |Per cent.     ||  100|  100|| 20·8|15·0| 32·2|31·6| 44·1|50·0||
  |10_a_|Litho-        ||     |     ||     |    |     |    |     |    ||
  |     |transferers:  ||     |     ||     |    |     |    |     |    ||
  |     |Cases         ||   20|   28||    2|   5|    2|   8|   15|  15||
  |     |Per cent.     ||  100|  100|| 10·0|17·9| 10·0|28·6| 75·0|53·6||
  |11   |Glass cutting ||     |     ||     |    |     |    |     |    ||
  |     |and polishing:||     |     ||     |    |     |    |     |    ||
  |     |Cases         ||   47|   --||   20| -- |   11| -- |   16| -- ||
  |     |Per cent.     ||  100|   --|| 42·5| -- | 23·4| -- | 34·0| -- ||
  |12   |Enamelling of ||     |     ||     |    |     |    |     |    ||
  |     |iron plates:  ||     |     ||     |    |     |    |     |    ||
  |     |Cases         ||   38|   14||    6|   6|   19|   4|   13|   3||
  |     |Per cent.     ||  100|  100|| 15·8|42·9| 50·0|28·6| 34·2|21·4||
  |13   |Electric      ||     |     ||     |    |     |    |     |    ||
  |     |accumulators: ||     |     ||     |    |     |    |     |    ||
  |     |Cases         ||  281|   --||   58| -- |   70| -- |  151| -- ||
  |     |Per cent.     ||  100|   --|| 20·6| -- | 24·9| -- | 53·7| -- ||
  |14   |Paint and     ||     |     ||     |    |     |    |     |    ||
  |     |colour works: ||     |     ||     |    |     |    |     |    ||
  |     |Cases         ||  397|   21||  111|   2|  104|   4|  176|  15||
  |     |Per cent.     ||  100|  100|| 27·9| 9·5| 26·2|19·0| 44·4|71·5||
  |15   |Coach-making: ||     |     ||     |    |     |    |     |    ||
  |     |Cases         ||  678|    3||  176| -- |  187|   2|  293|   1||
  |     |Per cent.     ||  100|   --|| 26·0| -- | 27·6| -- | 43·2| -- ||
  |16   |Ship-building:||     |     ||     |    |     |    |     |    ||
  |     |Cases         ||  261|  -- ||   93| -- |   51| -- |  108| -- ||
  |     |Per cent.     ||  100|  -- || 35·6| -- | 19·5| -- | 41·4| -- ||
  |17   |Paints used   ||     |     ||     |    |     |    |     |    ||
  |     |in other      ||     |     ||     |    |     |    |     |    ||
  |     |industries:   ||     |     ||     |    |     |    |     |    ||
  |     |Cases         ||  405|   42||  127|  11|   97|   7|  174|  22||
  |     |Per cent.     ||  100|  100|| 31·4|26·2| 23·9|16·7| 43·0|52·4||
  |18   |Other         ||     |     ||     |    |     |    |     |    ||
  |     |industries:   ||     |     ||     |    |     |    |     |    ||
  |     |Cases         ||  528|  114||  160|  37|  117|  22|  230|  52||
  |     |Per cent.     ||  100|  100|| 30·3|32·5| 22·2|19·3| 43·6|45·6||
  |     |Total cases   ||5,637|1,001||1,588| 204|1,389| 269|2,522| 496||
  |     | „    per     ||     |     ||     |    |     |    |     |    ||
  |     |cent.         ||  100|  100|| 28·2|20·4| 24·7|26·9| 44·7|49·5||
  +-----+--------------++-----+-----++-----+----+-----+----+-----+----++

  +-----+--------------++------------------------------++
  |     |              ||       Number of Attack.      ||
  +-----+--------------++----------+---------+---------++
  |     |              ||          |         |Third, or||
  | No. | Occupation.  ||  First.  | Second. | Chronic.||
  +-----+--------------++----------+---------+---------++
  | (1) |      (2)     ||    (7)   |   (8)   |   (9)   ||
  +-----+--------------++-----+----+----+----+----+----++
  |     |              ||  M. | F. | M. | F. | M. | F. ||
  | 1   |Smelting of   ||     |    |    |    |    |    ||
  |     |metals:       ||     |    |    |    |    |    ||
  |     |Cases         ||  276| -- |  65| -- |  64| -- ||
  |     |Per cent.     || 67·2| -- |16·8| -- |15·6| -- ||
  | 2   |Brass works:  ||     |    |    |    |    |    ||
  |     |Cases         ||   40|   3|  11|   1|  17| -- ||
  |     |Per cent.     || 57·1| -- |15·7| -- |24·3| -- ||
  | 3   |Sheet lead    ||     |    |    |    |    |    ||
  |     |and lead      ||     |    |    |    |    |    ||
  |     |piping:       ||     |    |    |    |    |    ||
  |     |Cases         ||   72|   3|  17| -- |  11|   1||
  |     |Per cent.     || 70·6| -- |16·7| -- |10·8| -- ||
  | 4   |Plumbing and  ||     |    |    |    |    |    ||
  |     |soldering:    ||     |    |    |    |    |    ||
  |     |Cases         ||  114|  22|  30|   1|  32|   3||
  |     |Per cent.     || 61·3|73·3|16·1| 3·3|17·2|10·0||
  | 5   |Printing:     ||     |    |    |    |    |    ||
  |     |Cases         ||  118|   6|  29| -- |  33| -- ||
  |     |Per cent.     || 62·1| -- |15·3| -- |17·4| -- ||
  | 6   |File-cutting: ||     |    |    |    |    |    ||
  |     |Cases         ||   49|  24|  39|   4|  78|   6||
  |     |Per cent.     || 28·2|70·6|22·4|11·8|44·8|17·6||
  | 7   |Tinning and   ||     |    |    |    |    |    ||
  |     |enamelling of ||     |    |    |    |    |    ||
  |     |hollow-ware:  ||     |    |    |    |    |    ||
  |     |Cases         ||   50|  31|  18|  16|  15|   6||
  |     |Per cent.     || 59·5|58·5|21·4|30·2|17·9|11·3||
  | 8   |White lead:   ||     |    |    |    |    |    ||
  |     |Cases         ||  961|  56| 108|   9|  49|   3||
  |     |Per cent.     || 82·4|73·7| 9·3|11·8| 4·2| 3·9||
  | 9   |Red lead:     ||     |    |    |    |    |    ||
  |     |Cases         ||   90| -- |   8| -- |   8| -- ||
  |     |Per cent.     || 83·3| -- | 7·4| -- | 7·4| -- ||
  |10   |China and     ||     |    |    |    |    |    ||
  |     |earthenware:  ||     |    |    |    |    |    ||
  |     |Cases         ||  297| 469|  91|  65|  87|  17||
  |     |Per cent.     || 60·6|82·0|18·6|11·4|17·7| 3·0||
  |10_a_|Litho-        ||     |    |    |    |    |    ||
  |     |transferers:  ||     |    |    |    |    |    ||
  |     |Cases         ||   17|  27|   2| -- | -- |   1||
  |     |Per cent.     || 85·0|96·4|10·0| -- | -- | 3·6||
  |11   |Glass cutting ||     |    |    |    |    |    ||
  |     |and polishing:||     |    |    |    |    |    ||
  |     |Cases         ||   21| -- |   9| -- |  17| -- ||
  |     |Per cent.     || 44·7| -- |19·1| -- |36·2| -- ||
  |12   |Enamelling of ||     |    |    |    |    |    ||
  |     |iron plates:  ||     |    |    |    |    |    ||
  |     |Cases         ||   31|  11|   7|   2| -- | -- ||
  |     |Per cent.     || 81·6|78·6|18·4|14·3| -- | -- ||
  |13   |Electric      ||     |    |    |    |    |    ||
  |     |accumulators: ||     |    |    |    |    |    ||
  |     |Cases         ||  222| -- |  40| -- |  13| -- ||
  |     |Per cent.     || 79·0| -- |14·2| -- | 4·6| -- ||
  |14   |Paint and     ||     |    |    |    |    |    ||
  |     |colour works: ||     |    |    |    |    |    ||
  |     |Cases         ||  290|  16|  61|   3|  39|   2||
  |     |Per cent.     || 73·1|76·2|15·4|14·3| 9·8| 9·5||
  |15   |Coach-making: ||     |    |    |    |    |    ||
  |     |Cases         ||  405|   2| 127| -- | 114|   1||
  |     |Per cent.     || 59·8| -- |18·7| -- |16·8| -- ||
  |16   |Ship-building:||     |    |    |    |    |    ||
  |     |Cases         ||  181| -- |  41| -- |  24| -- ||
  |     |Per cent.     || 69·0| -- |15·7| -- | 9·2| -- ||
  |17   |Paints used   ||     |    |    |    |    |    ||
  |     |in other      ||     |    |    |    |    |    ||
  |     |industries:   ||     |    |    |    |    |    ||
  |     |Cases         ||  238|  36|  83|   4|  71|   1||
  |     |Per cent.     || 58·8|85·7|20·5| 9·5|17·5| 2·4||
  |18   |Other         ||     |    |    |    |    |    ||
  |     |industries:   ||     |    |    |    |    |    ||
  |     |Cases         ||  329|  93|  85|  14|  86|   5||
  |     |Per cent.     || 62·3|81·6|16·1|12·3|16·3| 4·4||
  |     |Total cases   ||3,800| 799| 871| 119| 758|  46||
  |     | „    per     ||     |    |    |    |    |    ||
  |     |cent.         || 67·4|79·8|15·5|11·9|13·4| 4·6||
  +-----+--------------++-----+----+----+----+----+----++

  +-----+--------------++------------------------------------------
  |     |              ||                            Main Symptoms.
  +-----+--------------++----------+----------+---------+----------
  |     |              ||          |          |         |
  | No. | Occupation.  || Gastric. |  Anæmia. |Headache.| Paretic.
  +-----+--------------++----------+----------+---------+----------
  | (1) |      (2)     ||    (10)  |   (11)   |  (12)   |   (13)
  +-----+--------------++-----+----+-----+----+----+----+-----+----
  |     |              ||  M. | F. |  M. | F. | M. | F. |  M. | F.
  | 1   |Smelting of   ||     |    |     |    |    |    |     |
  |     |metals:       ||     |    |     |    |    |    |     |
  |     |Cases         ||  325| -- |   99| -- |  18| -- |   99| --
  |     |Per cent.     || 79·1| -- | 24·1| -- | 4·4| -- | 24·1| --
  | 2   |Brass works:  ||     |    |     |    |    |    |     |
  |     |Cases         ||   57|   4|   28|   3|  16|   3|   28|   2
  |     |Per cent.     || 81·4| -- | 40·0| -- |22·9| -- | 40·0| --
  | 3   |Sheet lead    ||     |    |     |    |    |    |     |
  |     |and lead      ||     |    |     |    |    |    |     |
  |     |piping:       ||     |    |     |    |    |    |     |
  |     |Cases         ||   82|   2|   28|   1|   9|   1|   26|   2
  |     |Per cent.     || 80·4| -- | 27·5| -- | 8·8| -- | 25·5| --
  | 4   |Plumbing and  ||     |    |     |    |    |    |     |
  |     |soldering:    ||     |    |     |    |    |    |     |
  |     |Cases         ||  146|  25|   58|  14|  23|  10|   46|   7
  |     |Per cent.     || 78·5|83·3| 31·2|46·7|12·4|33·3| 24·7|23·3
  | 5   |Printing:     ||     |    |     |    |    |    |     |
  |     |Cases         ||  144|   6|   41|   3|  22|   1|   36| --
  |     |Per cent.     || 75·8| -- | 21·6| -- |11·6| -- | 18·9| --
  | 6   |File-cutting: ||     |    |     |    |    |    |     |
  |     |Cases         ||  104|  23|   50|  17|  15|   2|   80|   3
  |     |Per cent.     || 59·8|67·7| 28·7|50·0| 8·6| 5·9| 46·0| 8·8
  | 7   |Tinning and   ||     |    |     |    |    |    |     |
  |     |enamelling of ||     |    |     |    |    |    |     |
  |     |hollow-ware:  ||     |    |     |    |    |    |     |
  |     |Cases         ||   65|  49|   33|  12|   9|   3|   19|  13
  |     |Per cent.     || 77·4|92·5| 39·3|22·6|10·7| 5·7| 22·6|24·5
  | 8   |White lead:   ||     |    |     |    |    |    |     |
  |     |Cases         ||1,003|  59|  286|   8|  51|   5|  120|   7
  |     |Per cent.     || 85·9|77·6|  2·5|10·5| 4·4| 6·6| 10·3| 9·2
  | 9   |Red lead:     ||     |    |     |    |    |    |     |
  |     |Cases         ||   87| -- |   28| -- |   8| -- |   14| --
  |     |Per cent.     || 80·6| -- | 25·9| -- | 7·4| -- | 13·0| --
  |10   |China and     ||     |    |     |    |    |    |     |
  |     |earthenware:  ||     |    |     |    |    |    |     |
  |     |Cases         ||  318| 430|   93| 183|  78| 181|  147|  79
  |     |Per cent.     || 64·9|75·2| 19·0|32·0|15·9|31·6| 30·0|13·8
  |10_a_|Litho-        ||     |    |     |    |    |    |     |
  |     |transferers:  ||     |    |     |    |    |    |     |
  |     |Cases         ||   16|  25|    2|   8|   6|  14|    1|   8
  |     |Per cent.     || 80·0|89·3| 10·0|28·6|30·0|50·0|  5·0|28·6
  |11   |Glass cutting ||     |    |     |    |    |    |     |
  |     |and polishing:||     |    |     |    |    |    |     |
  |     |Cases         ||   28| -- |    9| -- |   2| -- |   14| --
  |     |Per cent.     || 59·6| -- | 19·1| -- | 4·2| -- | 29·8| --
  |12   |Enamelling of ||     |    |     |    |    |    |     |
  |     |iron plates:  ||     |    |     |    |    |    |     |
  |     |Cases         ||   37|   8|    3|   5|   2|   2|    3|   3
  |     |Per cent.     || 97·4|57·1|  7·9|35·7| 5·3|14·3|  7·9|21·4
  |13   |Electric      ||     |    |     |    |    |    |     |
  |     |accumulators: ||     |    |     |    |    |    |     |
  |     |Cases         ||  255| -- |   70| -- |  10| -- |   34| --
  |     |Per cent.     || 90·8| -- | 24·9| -- | 3·6| -- | 12·1| --
  |14   |Paint and     ||     |    |     |    |    |    |     |
  |     |colour works: ||     |    |     |    |    |    |     |
  |     |Cases         ||  344|  19|  121|   8|  36|   2|   81|   1
  |     |Per cent.     || 86·7|90·5| 30·5|38·1| 9·1| 9·5| 20·4| 4·8
  |15   |Coach-making: ||     |    |     |    |    |    |     |
  |     |Cases         ||  537|   2|  178| -- | 109| -- |  157|   1
  |     |Per cent.     || 79·2| -- | 26·3| -- |16·1| -- | 23·2| --
  |16   |Ship-building:||     |    |     |    |    |    |     |
  |     |Cases         ||  207| -- |   77| -- |  27| -- |   54| --
  |     |Per cent.     || 79·3| -- | 29·5| -- |10·3| -- | 20·7| --
  |17   |Paints used   ||     |    |     |    |    |    |     |
  |     |in other      ||     |    |     |    |    |    |     |
  |     |industries:   ||     |    |     |    |    |    |     |
  |     |Cases         ||  329|  36|  108|  21|  40|  13|  110|  12
  |     |Per cent.     || 81·2|85·7| 26·7|50·0| 9·9|31·0| 27·2|28·6
  |18   |Other         ||     |    |     |    |    |    |     |
  |     |industries:   ||     |    |     |    |    |    |     |
  |     |Cases         ||  428|  91|  161|  42|  58|  18|  121|  15
  |     |Per cent.     || 81·1|79·8| 30·5|36·8|11·0|15·8| 22·9|13·2
  |     |Total cases   ||4,512| 779|1,473| 325| 539| 255|1,190| 153
  |     | „    per     ||     |    |     |    |    |    |     |
  |     |cent.         || 80·0|77·8| 26·1|32·5| 9·6|25·5| 21·1|15·3
  +-----+--------------++-----+----+-----+----+----+----+-----+----

  +-----+--------------++-----------------------------+
  |     |              ||                             |
  +-----+--------------++----------+---------+--------+
  |     |              ||Encephalo-| Rheumat-|        |
  | No. | Occupation.  ||  pathic. |   ic.   | Other. |
  +-----+--------------++----------+---------+--------+
  | (1) |      (2)     ||   (14)   |   (15)  |  (16)  |
  +-----+--------------++----+-----+----+----+----+---+
  |     |              ||  M.|  F. | M. | F. | M. | F.|
  | 1   |Smelting of   ||    |     |    |    |    |   |
  |     |metals:       ||    |     |    |    |    |   |
  |     |Cases         ||   9| --  |  66| -- |  11|-- |
  |     |Per cent.     || 2·2| --  |16·1| -- | 2·7|-- |
  | 2   |Brass works:  ||    |     |    |    |    |   |
  |     |Cases         || -- | --  |   9|   1|   3|-- |
  |     |Per cent.     || -- | --  |12·9| -- | 4·3|-- |
  | 3   |Sheet lead    ||    |     |    |    |    |   |
  |     |and lead      ||    |     |    |    |    |   |
  |     |piping:       ||    |     |    |    |    |   |
  |     |Cases         ||   2| --  |  11|   1|   1|  1|
  |     |Per cent.     || 2·0| --  |10·8| -- | 1·0|-- |
  | 4   |Plumbing and  ||    |     |    |    |    |   |
  |     |soldering:    ||    |     |    |    |    |   |
  |     |Cases         ||  10| --  |  21|   4|   8|-- |
  |     |Per cent.     || 5·4| --  |11·3|13·3| 4·3|-- |
  | 5   |Printing:     ||    |     |    |    |    |   |
  |     |Cases         ||   8| --  |  18| -- |   8|-- |
  |     |Per cent.     || 4·2| --  | 9·5| -- | 4·2|-- |
  | 6   |File-cutting: ||    |     |    |    |    |   |
  |     |Cases         ||   7| --  |  16| -- |  20|  3|
  |     |Per cent.     || 4·0| --  | 9·2| -- |11·5|8·8|
  | 7   |Tinning and   ||    |     |    |    |    |   |
  |     |enamelling of ||    |     |    |    |    |   |
  |     |hollow-ware:  ||    |     |    |    |    |   |
  |     |Cases         ||   4|   2 |   8|   4|   1|-- |
  |     |Per cent.     || 4·8| 3·8 | 9·5| 7·5| 1·2|-- |
  | 8   |White lead:   ||    |     |    |    |    |   |
  |     |Cases         ||  59|   6 |  98|   7|  14|  2|
  |     |Per cent.     || 5·1| 7·9 | 8·4| 9·2| 1·2|2·6|
  | 9   |Red lead:     ||    |     |    |    |    |   |
  |     |Cases         ||   9| --  |  13| -- |   3|-- |
  |     |Per cent.     || 8·3| --  |12·0| -- | 2·8|-- |
  |10   |China and     ||    |     |    |    |    |   |
  |     |earthenware:  ||    |     |    |    |    |   |
  |     |Cases         ||  26|  43 |  52|  67|  39|  8|
  |     |Per cent.     || 5·3| 7·5 |10·6|11·7| 8·0|1·4|
  |10_a_|Litho-        ||    |     |    |    |    |   |
  |     |transferers:  ||    |     |    |    |    |   |
  |     |Cases         || -- |   2 |   5|   2| -- |  1|
  |     |Per cent.     || -- | 7·1 |25·0| 7·1| -- |3·6|
  |11   |Glass cutting ||    |     |    |    |    |   |
  |     |and polishing:||    |     |    |    |    |   |
  |     |Cases         ||   2| --  |   4| -- |   9|-- |
  |     |Per cent.     || 4·2| --  | 8·5| -- |19·1|-- |
  |12   |Enamelling of ||    |     |    |    |    |   |
  |     |iron plates:  ||    |     |    |    |    |   |
  |     |Cases         || -- |   1 |   6|   1| -- |-- |
  |     |Per cent.     || -- | 7·1 |15·8| 7·1| -- |-- |
  |13   |Electric      ||    |     |    |    |    |   |
  |     |accumulators: ||    |     |    |    |    |   |
  |     |Cases         ||   5| --  |  12| -- |   2|-- |
  |     |Per cent.     || 1·8| --  | 4·3| -- | 0·7|-- |
  |14   |Paint and     ||    |     |    |    |    |   |
  |     |colour works: ||    |     |    |    |    |   |
  |     |Cases         ||   8|   1 |  43|   2|   7|-- |
  |     |Per cent.     || 2·0| 4·8 |10·8| 9·5| 1·8|-- |
  |15   |Coach-making: ||    |     |    |    |    |   |
  |     |Cases         ||  16| --  |  79| -- |  23|-- |
  |     |Per cent.     || 2·4| --  |11·7| -- | 3·4|-- |
  |16   |Ship-building:||    |     |    |    |    |   |
  |     |Cases         ||   8| --  |  23| -- |   4|-- |
  |     |Per cent.     || 3·1| --  | 8·8| -- | 1·5|-- |
  |17   |Paints used   ||    |     |    |    |    |   |
  |     |in other      ||    |     |    |    |    |   |
  |     |industries:   ||    |     |    |    |    |   |
  |     |Cases         ||  10|   1 |  41|   3|   8|  1|
  |     |Per cent.     || 2·5| 2·4 |10·1| 7·1| 2·0|2·4|
  |18   |Other         ||    |     |    |    |    |   |
  |     |industries:   ||    |     |    |    |    |   |
  |     |Cases         ||  17|   6 |  43|  15|  15|-- |
  |     |Per cent.     || 3·2| 5·3 | 8·1|13·2| 2·8|-- |
  |     |Total cases   || 200|  62 | 568| 107| 176| 16|
  |     | „    per     ||    |     |    |    |    |   |
  |     |cent.         || 3·5| 6·2 |10·3|10·7| 3·1|1·6|
  +-----+--------------++----+-----+----+----+----+---+

  To reduce the size of the table, columns showing the number in each
  occupation in which (_a_) the severity of attack, and (_b_) the
  number of attack were not stated, have been omitted. Of the former
  there were 170, and of the latter 245. The total figures, however, in
  Column 3 include them.

Table IV. shows the severity of the attacks as stated by the surgeon,
the number of attack, and the main symptoms. The personal element
enters into the character of the reports, and symptoms which one
surgeon might describe as slight another might regard as moderate,
or even severe. In general, however, “slight” includes cases of (1)
colic without complication, and of comparatively short duration;
(2) anæmia in adolescence aggravated by employment; and (3) either
of the above with tendency to weakness of the extensors. “Moderate”
includes (1) a combination of colic with anæmia; (2) profound anæmia;
(3) partial paralysis; and (4) cases in which there is constitutional
debility. “Severe” includes (1) marked paralysis; (2) encephalopathic
conditions--convulsions, optic neuritis, and mental affections; (3)
grave undermining of the constitution associated with paralysis,
renal disease, and arterio-sclerosis. The reports are made during
the attack, and information is not received of the sequelæ which may
supervene, except in the event of a later report as the result of
fresh exposure to lead. Number of attack has reference to definite
occurrence of disability. Transient attacks which have preceded the
disabling condition have been usually disregarded. It was necessary
to limit the number of attacks which might be regarded as indicating
chronic plumbism, and all those included in Column 10 are either
third attacks or cases of chronic lead poisoning. Among the main
symptoms, the headings “Gastric,” “Paretic,” “Encephalopathic,” and
“Rheumatic or Arthralgic,” represent fairly accurately the relative
incidence of these in cases of lead poisoning in this country; those
under the headings “Anæmia” and “Headache” are useful in comparing
relative incidence on the two sexes, but they occur, probably, much
more frequently than the figures would indicate; those under “Tremor”
and “Other” are less valuable. Under “Other” are included “Gout,”
“Nephritis,” or “Cerebral Hæmorrhage,” so that entry under this head
indicates chronic, rather than mild, lead poisoning. The conclusions
from the table are easy to draw, as, in general, the feature which
causes severity of symptoms to be prominent leaves its mark also on
“Number of Attack” and “Main Symptoms.” Thus, in the industries in
which severe cases exceed the average (brass, plumbing, printing,
file-cutting, tinning, glass-cutting, ship-building, paints used in
other industries, and other industries), the chronic nature of the
plumbism is markedly above the average, and some severe symptom,
usually paralysis, is also above the average. An exception to this
rule is china and earthenware, where severity is considerably below
the average, but where, among men, the figures for chronic lead
poisoning and paralysis are distinctly high. It will be seen, however,
that the proportion of slight cases even in this industry is below
the average. On the other hand, severity is below the average in
smelting, white lead, red lead, litho-transfers, enamelling, electric
accumulators, paints and colours, and coach-painting, and the symptoms
in these industries are, in general, colic rather than high degree of
paralysis; but in them a severe symptom which is above the average,
in general, is encephalopathy. The explanation of these differences
depends, we believe, on two factors: (1) Duration of employment, with
which, naturally, the age of the worker is associated; (2) opportunity
of inhaling lead dust. The longer the employment, the more likely,
naturally, if absorption goes on, is the plumbism to become chronic,
and to be associated with paralysis, its prominent sign. Duration of
employment among males in file-cutting and china and earthenware, as
contrasted, for instance, with that in white lead, is very much longer,
and the same could be shown of comparatively new industries, such as
electric accumulators and litho-transfers. Thus, in one year the age
distribution and duration of employment of those attacked in three of
these industries was as follows:

  +---------------------+-------------------+-------------------+
  |                     |                   |    Duration of    |
  |                     | Age Distribution. |    Employment.    |
  |       Industry.     +---------+---------+---------+---------+
  |                     |         |         |  Under  |   Over  |
  |                     |Under 30.| Over 30.| 5 Years.| 5 Years.|
  +---------------------+---------+---------+---------+---------+
  |                     |Per Cent.|Per Cent.|Per Cent.|Per Cent.|
  |China and earthenware|   59·4  |   40·6  |   52·2  |   47·8  |
  |White lead           |   45·7  |   54·3  |   86·8  |   13·2  |
  |File-cutting         |   22·9  |   77·1  |    --   |  100·0  |
  +---------------------+---------+---------+---------+---------+

Persons employed in the manufacture of white and red lead, electric
accumulators, paints and colours, and the others named, are exposed
essentially to dust from salts of lead, which are readily absorbed.
Poisoning, therefore, if precautions are inadequate, will quickly show
itself, causing certain workers to seek other employment after one
attack. Poisoning thus produced is more likely to induce colic, or,
if the dose has been large or the individual markedly susceptible,
encephalopathic symptoms, than paralysis. On the other hand, the
slowness of the onset of symptoms in the case of brass workers,
plumbers, printers, file-cutters, and tinners, is more the result
of inhalation of fumes or of dust of metallic lead than of salts of
lead; or if the inhalation be of salts of lead, then of these in less
amount and over a long period, with, as a result, gradual undermining
of the constitution, showing itself in paralysis, arterio-sclerosis,
and renal disease. The two factors indicated obviously account for
the differences in severity and number of attack between males and
females. If second and third attacks are comparatively fewer in
females than in males, it follows that, in general, the attack will
be less severe also, and this is brought out in the figures. Cerebral
symptoms--encephalopathy, to which headache may be added--are more than
twice as frequent in females as males. This may be due to idiosyncrasy,
but it may very possibly be simply the result of short duration of
employment of young workers in processes where dust of salts of lead is
incidental.

Attacks generally are most frequent in the first or second year of
employment. Thus, of 2,195 attacks reported in the four years 1904
to 1907, as to which sufficient data are given, 898 occurred in the
first two years of employment, and of these 672 occurred in the first
year--that is, three-sevenths of all the cases were reported during
the first two years, and four-sevenths in the whole of the remaining
years of employment. It is, unfortunately, impossible to say what
is the proportion of attacks among those employed for any given age
period. In some factories--as, for example, lead smelting works--the
average duration of employment is about thirteen years. The length
of employment preceding an attack was made out from reports on cases
which occurred in the white lead industry in 1898--a time when a number
of new workers were taken on to replace the female labour abolished
in June of that year, and conditions as regards removal of dust were
entirely different from what they are now. The figures, therefore, can
only be considered to have bearing upon incidence under almost the
worst possible circumstances. Of 155 attacks, duration of employment
was stated to have been less than 1 week in 3, from 1 week to 1 month
in 8, from 1 to 3 months in 62, from 3 to 6 months in 44, from 6 to 12
months in 12, and 1 year and over in 26.

Attempt has been made to discredit the value of Section 73 of the
Factory Act, 1901, on the ground that the proportion of cases in which
some degree of paralysis is present is very high as compared with the
extent found by other observers. The points we have laid stress on--(1)
duration of employment, (2) varying kinds and amounts of lead dust and
fumes--are, we believe, quite sufficient to account for, and give value
to, the figures dealt with. To them should be added another factor,
though one of less account--namely, the extent to which particular
muscles are used. In the case of file-cutters, for instance, there is
no doubt that the cramped position of the left hand holding the chisel,
and the work thrown on the right in holding the heavy mallet, determine
the direction of the paralysis, especially on to the muscles of the
thenar and hyperthenar eminences and of the fingers.

There is, however, difficulty in deciding whether such entries on
reports as “weakness of arms and legs,” “weakness of arms,” “muscular
weakness,” etc., should be interpreted as incipient paralysis.[A]
With a disease like lead poisoning showing marked tendency to affect
the muscles supplied by the musculo-spiral and other nerves, the only
safe course was to include all these terms as equivalent to partial
paralysis. Table V. on p. 54 shows close parallelism for the six years.

  [A] During the years 1910 and 1911 cases were classified so as to
  distinguish definite paralysis, as far as possible, from the more
  indefinite terms referred to, with the result tabulated opposite. We
  have little doubt that in most of the cases included in columns (3)
  and (6) some slight degree of paresis was present.

  +--------------------+-----------------------+-----------------------+
  |                    |          1910.        |          1911.        |
  |                    +------+---------+------+------+---------+------+
  |                    |      | Weakness|      |      | Weakness|      |
  |                    |      | of Arms |      |      | of Arms |      |
  |                    |Paral-| or Loss |      |Paral-| or Loss |      |
  | Form of Paralysis. | ysis.|of Power.|Total.| ysis.|of Power.|Total.|
  +--------------------+------+---------+------+------+---------+------+
  |        (1)         |  (2) |   (3)   |  (4) |  (5) |   (6)   |  (7) |
  |Arms and   {complete|   -- |    --   |   -- |    2 |    --   |    2 |
  |legs       {partial |    4 |     6   |   10 |    1 |     4   |    5 |
  |                    |      |         |      |      |         |      |
  |Legs       {complete|   -- |    --   |   -- |   -- |    --   |   -- |
  |           {partial |    4 |     4   |   8  |   -- |     6   |    6 |
  |                    |      |         |      |      |         |      |
  |Both       {complete|   15 |    --   |  15  |   27 |    --   |   27 |
  |forearms   {partial |   19 |    30   |  49  |   20 |    44   |   64 |
  |                    |      |         |      |      |         |      |
  |Right      {complete|    8 |    --   |   8  |    5 |    --   |    5 |
  |forearm    {partial |    6 |     4   |  10  |    4 |     7   |   11 |
  |                    |      |         |      |      |         |      |
  |Left       {complete|    3 |    --   |   3  |    2 |    --   |    2 |
  |forearm    {partial |    2 |     1   |   3  |    1 |     7   |    8 |
  |                    |      |         |      |      |         |      |
  |Fingers             |    3 |    --   |   3  |    7 |    --   |    7 |
  |                    |      |         |      |      |         |      |
  |Neuritis (including |      |         |      |      |         |      |
  |numbness of hands or|      |         |      |      |         |      |
  |arms)               |    5 |    --   |   5  |    5 |    --   |    5 |
  |                    |      |         |      |      |         |      |
  |Other (including    |      |         |      |      |         |      |
  |paralysis of        |      |         |      |      |         |      |
  |deltoid, muscles of |      |         |      |      |         |      |
  |speech, locomotor   |      |         |      |      |         |      |
  |ataxy, and general  |      |         |      |      |         |      |
  |paralysis)          |    1 |    --   |   1  |    4 |     2   |    6 |
  |                    +------+---------+------+------+---------+------+
  |                    |   70 |    45   | 115  |   78 |    70   |  148 |
  +--------------------+------+---------+------+------+---------+------+

If it is difficult to distinguish rightly all the cases classed as
“paralysis,” it is even more difficult to determine what should be
included under the term “encephalopathy.” We have limited it to
epileptiform seizures, optic neuritis (uncomplicated by epilepsy), and
various forms of insanity. Table VI. on p. 54 is interesting as showing
how fairly constant the numbers are from one year to another.

Except in the one industry of earthenware and china, in which a return
of the number of persons employed according to process and kind of
ware has been made on three separate occasions, and in which the
reports of the certifying surgeons enable the cases of poisoning to be
classified in the same way, it is difficult to determine accurately
the attack rate of lead poisoning. Even in the earthenware and china
trade many things have to be borne in mind. The poisoning which occurs
is not distributed evenly over all the factories. Thus, among the 550
potteries, in the years 1904 to 1908, five potteries were responsible
for 75 cases, and 173 for the total number of cases (517), leaving 377
factories from which no cases were reported.

TABLE V.--FORMS OF PARALYSIS: 1904-1909.

  +-------------------------+------+-----+-----+-----+-----+-----+-----+
  |   Form of Paralysis.    |Total.|1909.|1908.|1907.|1906.|1905.|1904.|
  +-------------------------+------+-----+-----+-----+-----+-----+-----+
  |         (1)             | (2)  | (3) | (4) | (5) | (6) | (7) | (8) |
  |Arms and legs   {complete|  12  |   2 |   2 |   1 |   2 |   1 |   4 |
  |                {partial |  62  |  13 |   7 |   9 |  13 |   9 |  11 |
  |                         |      |     |     |     |     |     |     |
  |Legs            {complete|   3  |  -- |  -- |   1 |  -- |   1 |   1 |
  |                {partial |  25  |   5 |   7 |   1 |   3 |   5 |   4 |
  |                         |      |     |     |     |     |     |     |
  |Both forearms   {complete| 162  |  29 |  33 |  29 |  28 |  24 |  19 |
  |                {partial | 334  |  59 |  70 |  56 |  56 |  43 |  50 |
  |                         |      |     |     |     |     |     |     |
  |Right forearm   {complete|  39  |  11 |   6 |   7 |   4 |   8 |   3 |
  |                {partial |  62  |   9 |  17 |  14 |  11 |   5 |   6 |
  |                         |      |     |     |     |     |     |     |
  |Left forearm    {complete|  14  |   2 |   2 |   4 |   1 |   3 |   2 |
  |                {partial |  22  |   4 |   1 |   4 |   6 |   4 |   3 |
  |                         |      |     |     |     |     |     |     |
  |Fingers                  |  36  |   3 |   3 |   7 |  10 |   6 |   7 |
  |                         |      |     |     |     |     |     |     |
  |Neuritis (including      |      |     |     |     |     |     |     |
  |numbness of hands or     |      |     |     |     |     |     |     |
  |arms)                    |  32  |   7 |   8 |   3 |   3 |   5 |   6 |
  |                         |      |     |     |     |     |     |     |
  |Other (including         |      |     |     |     |     |     |     |
  |paralysis of deltoid,    |      |     |     |     |     |     |     |
  |muscles of speech,       |      |     |     |     |     |     |     |
  |locomotor ataxy)         |  10  |   3 |   1 |   3 |   1 |  -- |   2 |
  +-------------------------+------+-----+-----+-----+-----+-----+-----+
  |                         | 798  | 147 | 157 | 139 | 138 | 114 | 118 |
  +-------------------------+------+-----+-----+-----+-----+-----+-----+

TABLE VI.--ENCEPHALOPATHY.

  +--------------+-----+-----+-----+-----+-----+-----+-----+-----+
  |   Symptom.   |1911.|1910.|1909.|1908.|1907.|1906.|1905.|1904.|
  +--------------+-----+-----+-----+-----+-----+-----+-----+-----+
  |Epilepsy      |  6  | 16  | 12  | 15  | 14  | 11  | 12  | 15  |
  |Optic neuritis|  2  |  3  |  3  |  2  |  3  |  7  |  5  |  4  |
  |Mental defect |  5  |  2  |  2  |  1  |  6  |  3  |  1  |  2  |
  +--------------+-----+-----+-----+-----+-----+-----+-----+-----+
  |   Total      | 13  | 21  | 17  | 18  | 23  | 21  | 18  | 21  |
  +--------------+-----+-----+-----+-----+-----+-----+-----+-----+

The same state of things is found in all the other industries.
Particular factories, owing to special method of manufacture or special
manner of working, may have an incidence out of all proportion to that
prevailing in the trade generally. And it is, of course, control of
these more obvious sources of danger by the efforts of manufacturers
and the factory inspectors that has led to the notable reduction
recorded--_e.g._, in white lead works and the pottery industry.

Returns of occupiers do not lend themselves readily to exact estimate
of the number of persons exposed to risk of lead poisoning, as they do
not differentiate the processes, and in nearly all factories in which
lead is used some of those returned will not come into contact with it.

In industries, however, in which there is periodic medical examination
of persons employed in lead processes an attack rate can be made out.
It must be regarded as approximate only, as in the manufacture of
electric accumulators, for instance, medical examination is limited
to persons employed in pasting, casting, lead-burning, or any work
involving contact with dry compounds of lead, whereas the reported
attacks include a few persons engaged in processes other than those
named.

TABLE VII.--ATTACK RATE FROM LEAD POISONING IN THE YEAR 1910 IN CERTAIN
INDUSTRIES.

  +---------------------+-------------+----------+---------+-----------+
  |                     |             | Probable |         |           |
  |                     |             | Number of|Number of|Attack Rate|
  |                     |  Number of  |  Persons | Reported|    per    |
  |     Industry.       |Examinations.| employed.|  Cases. | Thousand. |
  +---------------------+-------------+----------+---------+-----------+
  |White lead           |    77,752   |   1,495  |    34   |     22    |
  |Red lead             |     8,096   |     675  |    10   |     15    |
  |Vitreous enamelling  |     3,064   |     766  |    17   |     22    |
  |Tinning of metals    |     1,475   |     492  |    17   |     34    |
  |Electric accumulators|    13,065   |   1,089  |    31   |     28    |
  |Paints and colours   |    19,081   |   1,590  |    17   |     11    |
  |Earthenware and china|    78,560   |   6,547  |    77   |     12    |
  +---------------------+-------------+----------+---------+-----------+

As has been mentioned above, the accurate information we have of the
numbers employed in the several processes in the earthenware and china
industry enable us to use the figures for that industry to illustrate,
what is certainly true of all other lead industries also, the fact of
the relative greater degree of risk in one process than another.

The fall in the number of fatal cases attributed to lead poisoning, as
is perhaps to be expected, seeing that the great majority are deaths
from chronic lead poisoning, does not run parallel with the diminution
in the number of cases. Thus, in the five years 1905 to 1909 the
deaths numbered 144, as compared with 131 in the previous five years,
although the cases fell from 3,761 to 3,001. We believe this is due
to an increasing inclination to attribute chronic nephritis, and
even (without sufficient justification in our opinion) phthisis and
pneumonia, to lead poisoning on the death certificates of lead workers.
Copies of all death certificates on which lead poisoning is entered
as directly or indirectly a cause are received by the Chief Inspector
of Factories. All of industrial origin are included in the return. Of
a total of 264 which could be followed up, encephalopathic symptoms
appeared on the death certificate in 38 (10·6 per cent.); Bright’s
disease, cerebral hæmorrhage, paralysis, or chronic lead poisoning
either alone or as a combination of symptoms closely connected, in 188
(71·2 per cent.); phthisis in 13 (5·0 per cent.); and other diseases,
such as pneumonia, etc., in 25 (9·4 per cent.). Table IX. brings out
the relative frequency in the several groups of industries, and, as is
to be anticipated, the different average age at death when due to acute
and chronic lead poisoning.

TABLE VIII.--LEAD POISONING IN EARTHENWARE AND CHINA WORKS

(CHINA, EARTHENWARE, TILES, MAJOLICA, JET AND ROCKINGHAM, CHINA
FURNITURE AND ELECTRICAL FITTINGS, SANITARY WARE).

  +-------------------------+------+-----------------+-----------------+
  |                         |      |                 | Attack-Rate per |
  |                         | Per- | Cases Reported: |     Thousand    |
  |                         | sons |     Average     |    employed:    |
  |       Processes.        |  em- |    per Year.    |Average per Year.|
  |                         |ployed+-----+-----+-----+-----+-----+-----+
  |                         |  in  |1907-|1903-|1899-|1907-|1903-|1899-|
  |                         | 1907.|1910.|1906.|1902.|1910.|1906.|1902.|
  |                         |      |     |     |     | [A] | [B] | [C] |
  +-------------------------+------+-----+-----+-----+-----+-----+-----+
  |In dipping-house:        |      |     |     |     |     |     |     |
  |Dippers               {M.|   786|   17|   18|   26|   22|   23|   34|
  |                      {F.|   150|    6|    4|    7|   40|   30|   68|
  |                         |      |     |     |     |     |     |     |
  |Dippers’ assistants   {M.|   463|    3|    3|    7|    7|    7|   15|
  |                      {F.|   397|   13|   18|   17|   33|   46|   45|
  |                         |      |     |     |     |     |     |     |
  |Ware-cleaners         {M.|   115|    1|    2|    3|    9|   20|   30|
  |                      {F.|   461|   15|   18|   30|   33|   41|   65|
  +-------------------------+------+-----+-----+-----+-----+-----+-----+
  |Total                 {M.| 1,346|   21|   23|   36|   15|   17|   27|
  |                      {F.| 1,008|   34|   40|   54|   34|   42|   58|
  +-------------------------+------+-----+-----+-----+-----+-----+-----+
  |Glost-placers         {M.| 2,291|   16|   12|   33|    7|    5|   14|
  |                      {F.|   120|    1|    1|    1|    8|   10|   14|
  |                         |      |     |     |     |     |     |     |
  |Majolica-painters     {M.|    28|   --|   --|   --|   --|   --|   --|
  |                      {F.|   358|    6|    8|   10|   13|   14|   20|
  |                         |      |     |     |     |     |     |     |
  |Ground-layers         {M.|    58|    1|   --|    1|   17|   --|   17|
  |                      {F.|   157|    1|    1|    4|    6|    5|   13|
  |                         |      |     |     |     |     |     |     |
  |Colour and litho      {M.|    14|   --|   --|   --|   --|   --|   --|
  |dusters               {F.|   143|   --|    1|    4|   --|    7|   33|
  |                         |      |     |     |     |     |     |     |
  |Enamel colour and     {M.|    51|   --|   --|    1|   --|   --|   36|
  |glaze blowers         {F.|   288|    3|    3|    2|   10|   14|   12|
  |                         |      |     |     |     |     |     |     |
  |Colour-makers and     }M.|   371|    5|    5|    6|   13|   13|   17|
  |millers and mixers of }F.|    55|    1|    1|    1|   18|   48|  114|
  |glaze or colour          |      |     |     |     |     |     |     |
  |                         |      |     |     |     |     |     |     |
  |Other persons in      }M.|   327|    2|    1|    2|    6|    5|   11|
  |contact with lead     }F.|   132|    1|    2|    4|    8|   21|   75|
  +-------------------------+------+-----+-----+-----+-----+-----+-----+
  |             {M.         | 4,504|   44|   41|   80|   10|    9|   19|
  |Grand total  {F.         | 2,361|   45|   57|   80|   19|   25|   37|
  |             {           +------+-----+-----+-----+-----+-----+-----+
  |             {(M. and F.)| 6,865|   89|   98|  160|   13|   15|   25|
  +-------------------------+------+-----+-----+-----+-----+-----+-----+

  [A] Calculated on return of employment for 1907.

  [B] Calculated on return of employment for 1904.

  [C] Calculated on return of employment for 1900.

The statistical evidence from death certificates published in the
decennial supplements of the Superintendent of Statistics[2] is of
significance, not only in enabling comparison to be made between one
industry and another, in regard to mortality from lead poisoning, but
also in determining the other causes of death most frequently entered
on death certificates of lead workers, and therefore, if they are
in high excess, as compared with male workers generally, they are
to be ascribed with some degree of certainty to deleterious effects
of lead on some of the principal organs. Thus, in Table X. a list
of occupations is given in which the mortality from plumbism in the
years 1900 to 1902 was double or more than double the standard. It
represents the mortality which would occur if the male population in
the particular industry had exactly the same age population as that of
“all males.” Further, the annual mortality among “all males” is taken
as 1,000, and that of males engaged in the several industries is stated
as a proportion of this. This “mortality figure” of 1,000 is made up
of the mortality from various causes (of which only those considered
to bear upon lead poisoning are given in the table) in the proportion
stated.

The contention that, because lead workers die from certain diseases
more frequently than “all males,” such diseases must be the sequelæ
of lead poisoning is untenable unless other recognized causes of the
diseases in question have been excluded. For excess of deaths from
phthisis and respiratory diseases the conditions of work and exposure
to inhalation of mineral and metallic dust or vitiation of atmosphere,
in pottery, spelter, printing works, and file-cutting workshops,
sufficiently account. The figures, indeed, take no account of this, and
their value, in some at any rate, is still further diminished by the
very large number of occupations (several involving no contact at all
with lead) included in the headings. With exception of the strikingly
greater proportion of deaths among lead-workers from Bright’s disease,
the figures are too contradictory to draw deductions from as to what
are “sequelæ” of lead poisoning. But this figure--160, as compared
with 35 for all males--is confirmatory evidence, if any were needed,
that chronic Bright’s disease is a sequela. And, from the pathology of
lead poisoning, we believe that the granular condition of the kidney
is due to the sclerotic change brought about in its substance by
microscopic hæmorrhages. We have very little evidence indeed in man
that this interstitial change is set up or preceded by an acute tubal
nephritis. While we do not deny that there may be some parenchymatous
change associated with lead poisoning, we do not believe that it
is of the kind which gives rise to the large white kidney, and we
should therefore exclude such disease as a sequela. But if chronic
Bright’s disease is admitted, the train of symptoms associated with
it--notably arterio-sclerotic changes resulting in cerebral hæmorrhage
and albuminuric retinitis--must be admitted also. Unless it were
established that granular nephritis were present in a lead-worker
before commencement of lead employment, we think it would be useless to
endeavour to prove that the condition was independent of lead, despite
its comparative frequency as a cause of death apart from employment.

TABLE IX.--MAIN SYMPTOMS APPEARING AS THE CAUSE IN 264 DEATH
CERTIFICATES OF LEAD POISONING.

  +-------------------------------+--------+--------+------+------+
  |                               |        |        |      |      |
  |                               |        |        |      |      |
  |                               |        |        |      |      |
  |                               |        |        |      |      |
  |                               |        |        |      |      |
  |                               |        |        |      |      |
  |       Industry.               |        |        | Cere-|      |
  |                               |        |        | bral |      |
  |                               |Encepha-|Bright’s|Hæmor-|Paral-|
  |                               |lopathy.|Disease.|rhage.| ysis.|
  +-------------------------------+--------+--------+------+------+
  |          (1)                  |  (2)   |  (3)   |  (4) |  (5) |
  |Smelting of metals             |    1   |    6   |  --  |    3 |
  |Brass works                    |   --   |    3   |  --  |    1 |
  |Sheet lead and lead piping     |   --   |    1   |  --  |   -- |
  |Plumbing and soldering         |    2   |    3   |  --  |    1 |
  |Printing                       |    3   |    3   |  --  |    2 |
  |File-cutting                   |    1   |   11   |   2  |    2 |
  |Tinning and enamelling         |   --   |    1   |  --  |   -- |
  |White lead                     |   13   |    2   |   2  |    4 |
  |China and earthenware          |    8   |   24   |  14  |    3 |
  |Glass-cutting                  |    1   |    6   |  --  |   -- |
  |Electric accumulators          |    2   |    1   |  --  |    1 |
  |Paints and colours             |    4   |    1   |  --  |   -- |
  |Coach-making                   |    1   |    8   |   5  |    6 |
  |Ship-building                  |    1   |    4   |   1  |   -- |
  |Paints used in other industries|   --   |    3   |   1  |    4 |
  |Other industries               |    1   |    2   |   1  |   -- |
  +-------------------------------+--------+--------+------+------+
  |              Total            |   38   |   79   |  26  |   27 |
  +-------------------------------+--------+--------+------+------+
  |   Average at death            |   32   |   43   |  47  |   43 |
  +-------------------------------+--------+--------+------+------+

  +-------------------------------+----+------+---------+------+
  |                               |    |      |  Pneu-  |      |
  |                               |    |      | monia,  |      |
  |                               |    |      |  Bron-  |      |
  |                               |    |      | chitis, |      |
  |                               |    |      |  Heart  |      |
  |                               |    |      | Failure,|      |
  |       Industry.               |Lead|      |  Colic, |      |
  |                               |Poi-|      |  Hernia,|      |
  |                               |son-|Phthi-|   and   |      |
  |                               |ing.| sis. |Aneurism.|Total.|
  +-------------------------------+----+------+---------+------+
  |          (1)                  | (6)| (7)  |   (8)   | (9)  |
  |Smelting of metals             |  5 |   1  |     1   |  17  |
  |Brass works                    |  1 |  --  |     1   |   6  |
  |Sheet lead and lead piping     |  1 |  --  |     1   |   3  |
  |Plumbing and soldering         |  2 |   1  |     2   |  11  |
  |Printing                       |  5 |   1  |     3   |  17  |
  |File-cutting                   |  2 |   1  |    --   |  19  |
  |Tinning and enamelling         |  1 |  --  |    --   |   2  |
  |White lead                     |  2 |   1  |     3   |  27  |
  |China and earthenware          |  6 |   2  |    --   |  57  |
  |Glass-cutting                  |  1 |  --  |     1   |   9  |
  |Electric accumulators          | -- |  --  |     2   |   6  |
  |Paints and colours             |  2 |   1  |     3   |  11  |
  |Coach-making                   | 10 |   3  |     4   |  37  |
  |Ship-building                  |  1 |   1  |    --   |   8  |
  |Paints used in other industries|  6 |   1  |     2   |  17  |
  |Other industries               | 11 |  --  |     2   |  17  |
  +-------------------------------+----+------+---------+------+
  |              Total            | 56 |  13  |    25   | 264  |
  +-------------------------------+----+------+---------+------+
  |   Average at death            | 44 |  38  |    40   |  --  |
  +-------------------------------+----+------+---------+------+

TABLE X.--COMPARATIVE MORTALITY FROM SPECIFIED CAUSES AMONG MALES
ENGAGED IN CERTAIN OCCUPATIONS: 1900-1902.

  +-------------------+------------------------------------------------
  |                   |                                Causes of Death.
  |                   +-------+-------+-----+------+------+-----+-----+
  |                   |       |       |     |      |      | Dis-| Dis-|
  |                   |       |       |     |      | Dis- |eases|eases|
  |                   |       |       |     |      | eases|  of |  of |
  |                   |       |       |     |      |  of  | the | the |
  |                   |       |       |     |      | the  | Cir-| Res-|
  |                   |       |       |     |      | Ner- |cula-|pira-|
  |                   |       |       |     |      | vous | tory| tory|
  |                   |  All  | Alco- |     |Phthi-| Sys- | Sys-| Sys-|
  |   Occupation.     |Causes.|holism.|Gout.| sis. | tem. | tem.| tem.|
  +-------------------+-------+-------+-----+------+------+-----+-----+
  |        (1)        |  (2)  |  (3)  | (4) |  (5) |  (6) | (7) | (8) |
  |All males          | 1,000 |   16  |   2 |  186 |  105 | 145 | 174 |
  |Printer            |   994 |    8  |   3 |  300 |  111 | 125 | 131 |
  |File-maker         | 1,700 |   14  |  -- |  387 |  225 | 198 | 325 |
  |Copper-worker      | 1,090 |    7  |   3 |  162 |  104 | 139 | 357 |
  |Lead-worker        | 1,408 |   38  |  -- |  165 |  134 | 222 | 309 |
  |Coach-maker        |   824 |    4  |   4 |  129 |  113 | 129 | 150 |
  |Earthenware        | 1,493 |    8  |  -- |  285 |  131 | 219 | 473 |
  |Glass              | 1,260 |    7  |   4 |  283 |  131 | 177 | 268 |
  |Painter and plumber| 1,114 |   13  |   8 |  213 |  133 | 105 | 168 |
  +-------------------+-------+-------+-----+------+------+-----+-----+

  +-------------------+---------------------------------+
  |                   |                                 |
  |                   +------+--------+-----+-----+-----+
  |                   |      |        |Other|     |     |
  |                   |      |        |Dis- |     |     |
  |                   | Dis- |        |eases|     |     |
  |                   | eases|        | of  |     |     |
  |                   |of the|        | the |     |     |
  |                   |Diges-|        | Uri-|     |     |
  |                   | tive |        | nary|     |     |
  |                   | Sys- |Bright’s| Sys-|Plum-|Acci-|
  |   Occupation.     | tem. |Disease.| tem.|bism.|dent.|
  +-------------------+------+--------+-----+-----+-----+
  |        (1)        |  (9) |  (10)  | (11)| (12)| (13)|
  |All males          |  57  |   35   |  17 |   1 |  59 |
  |Printer            |  55  |   42   |  15 |   2 |  21 |
  |File-maker         |  78  |  134   |  26 |  56 |  46 |
  |Copper-worker      |  45  |   24   |  21 |   3 |  51 |
  |Lead-worker        |  14  |  160   |  -- | 102 |  52 |
  |Coach-maker        |  46  |   39   |  14 |   8 |  29 |
  |Earthenware        |  57  |   33   |  20 |  10 |  33 |
  |Glass              |  54  |   58   |  16 |   8 |  31 |
  |Painter and plumber|  31  |   74   |  20 |  23 |  50 |
  +-------------------+------+--------+-----+-----+-----+

Other conditions which might readily be admitted as sequelæ are
optic neuritis, following on an attack of encephalopathy. No general
statement can be made in regard to mental and nervous diseases, gout,
pernicious anæmia, as sequelæ, as each must be considered in relation
to the evidence adduced in the particular case, and after exclusion, in
the first two, of syphilis as a cause.

The distinction between causation and association has to be borne
in mind before admitting as sequelæ of lead poisoning diseases of
bacterial origin, such as phthisis or pneumonia, or any disease to
which the affected person may be thought to have been rendered more
prone by reason of lead employment. The contention that a person
may have been debilitated by lead poisoning is no proof that the
enfeeblement of the constitution was the cause either of the bacillus
gaining entrance into the lung or of the ultimate fatal issue from
the engrafted disease. Such assertion in every case must rest on
supposition. Evidence that lead employment predisposes to phthisis is
not necessarily made stronger, in our opinion, by existence during
life of clinical symptoms, or, in their absence, of detection of lead
in the tissues post mortem.

In classifying causes of death, the general rule should be to select,
from the several diseases mentioned in the certificate, the disease
of the longest duration. Exceptions to this rule are that definite
diseases ordinarily known as constitutional diseases should have
preference over the other diseases mentioned. After thirty-five years
of age, certificates of death from lead poisoning are almost always
filled in in association with other diseases which are the usual causes
which lead to mortality generally. But neither phthisis, nor pneumonia,
nor any acute disease of the heart or lungs, nor valvular disease of
the heart, nor, indeed, any acute febrile condition, can have direct
relation with--_i.e._, be a sequela of--lead poisoning.


REFERENCES.

  [1] Annual Reports of the Chief Inspector of Factories since 1898,
  especially for 1909, p. 19.

  [2] Supplement to the Sixty-fifth Annual Report of the
  Registrar-General on the Mortality in Certain Occupations in the
  Three Years 1900, 1901, 1902, by Dr. John Tatham, pp. cxix-cxxii, Cd.
  2619.




CHAPTER V

PATHOLOGY


The pathology of lead poisoning has formed the subject of scientific
inquiry from the time that the association of certain pathological
symptoms was definitely correlated with poisoning by means of the metal
or its salts.

Acute poisoning, due to accidental swallowing of large doses of lead
salts or to use of lead salts criminally, generally produces a train of
symptoms different from those met with in chronic industrial poisoning.
But it is difficult to understand why so many writers upon the subject
of lead poisoning should have attempted to draw a hard-and-fast line
between the pathological symptoms in acute and chronic poisoning.
This is especially the case when the after-history of cases of acute
poisoning is traced, for in a large number of instances a case of
acute poisoning drifts on into a subacute, and finally a chronic,
stage. All the symptoms of paralysis, encephalopathy, and even kidney
degeneration, have been described in persons who were first of all the
subjects of acute poisoning.

The direct effect of a lead salt, such as the acetate, upon the mucous
membrane of the stomach, is a caustic one, and the attention of
observers seems to have been focussed on what is really a secondary
effect of the lead salt, and not one intrinsically associated with
actual poisoning by the metal itself.

A good deal of experimental work has also been performed in one way
or another--mainly by feeding with, or inoculation of, considerable
quantities of soluble lead salts--but, with one or two notable
exceptions, such experiments have not carried the knowledge of the
true pathology of lead poisoning very much farther. The statement is
not uncommonly made that no definite correlation exists between the
symptoms observed in animals and those observed in man, the reason
being that the massive doses given to animals cannot be similar to,
nor can they produce results comparable with, the slow intoxication
taking place in man; although the after-history of the majority of
cases of acute poisoning shows that the symptoms suffered are generally
identical with the severer symptoms seen in cases of chronic poisoning
of industrial origin. One of the chief reasons explaining this
remarkable point of view arises from the fact that the tissues which
come into the hands of the pathologist for post-mortem and histological
examination are as a rule derived from cases of chronic poisoning,
cases in which the acute symptoms have drifted into the subacute or
chronic stage, when any minute changes existing in the initial stages
of the poisoning have long since disappeared, or their significance has
been so far obscured by secondary changes that the primary lesions are
lost sight of.

A critical examination of the very large amount of literature published
on lead poisoning negatives the idea that acute and chronic poisoning
differ fundamentally in their pathology, and observers are found
describing identical pathological lesions resulting from acute or
chronic industrial poisoning. It is impossible to review the whole of
the existing literature. Kobert[1], in summing up the general effect of
lead upon the animal body, makes the following general statement: “Lead
affects especially the striped and unstriped muscles, the epithelium of
the excretory glands, the neuroglia of the central nervous system, and
is essentially a protoplasmic poison.”

We base our knowledge on definite experiments, so arranged that the
method of exposure was in every way similar to that in lead industries.
The only point of difference that can be urged against them is one
of degree; but as the train of symptoms produced was in every way
comparable with those suffered by man, this objection cannot be
sustained. The fact that the symptoms develop in a shorter time than
they do in industrial processes is merely a function of the intensity
of the poisoning.

An attempt will be made first to summarize the literature on the
pathology of lead poisoning, and, as such literature covers an immense
amount of ground, to group the pathological findings of various
observers, as far as possible, under four main headings--namely:

  Gastro-intestinal system.
  Nervous system.
  Excretory system.
  Circulatory system.


=Gastro-Intestinal.=--As the chief early symptom of all types of
chronic poisoning is abdominal colic, early investigators turned their
attention to the pathology in this region, and ascribed the colic to
various causes.

Oliver[2] noted that, in animals poisoned with lead, the intestine was
found to be irregularly contracted, and ascribed the pain in abdominal
colic to the irregular contraction of the intestines themselves,
supposing that the effect of lead was on the muscular tissues. He also
noted the presence in the intestine, both large and small, of staining
due to lead, and the considerable amount of lead to be found in the
large intestine. We have only met with staining by lead in the large
intestine.

Dixon Mann[3] pointed out that the fæces contain two-thirds of the
amount of lead taken by the mouth in experimental cases, and considered
that the lead was re-excreted into the intestine; and a number of other
observers hold this view. Recent work confirms the supposition, and
there is no doubt that lead is eliminated in this way.

Stockvis[4] has occasionally seen small ulcers or abrasions in the
small intestine; these he thinks may be due to small hæmorrhages.

Ménétrier[5], quoted by Meillère, describes a form of glandular
atrophy of the stomach which is met with in chronic lead poisoning. He
states that the alcoholic gastritis generally present in persons the
subject of saturnine gastritis renders the differentiation exceedingly
difficult. This observer is also in complete agreement with many others
who associate much of the chronic lead poisoning to association with
alcoholic intemperance. The particular type of gastric degeneration
Ménétrier regards as due to the effect of lead is “une sclérose
regulière, inter-tubulaire, se recontrant d’une manière diffuse et
générale dans le muqueuse gastrique.”

He further considers that this gastric sclerosis occurs earlier than
the disease of the kidneys.

Kussmaul and Meyer[6] describe a chronic intestinal catarrh with
chronic degenerative changes in the intestinal mucosa very similar to
the changes described by Ménétrier.

Tanquerel[7] inclined to the view that the colic was not associated
with spasm of the intestines, and states that no clinical evidence
could be found of intestinal spasm by rectal examination during a spasm
of colic. But, as Bernard[8] points out, intestinal spasm may occur
with “ballonment” of the rectum.

Another cause of colic is suggested by Bokai[9]--namely,
hypersensibility of the intestinal nerves--and he cites as evidence
the diminution in pain produced by the administration of morphine; and
it is not improbable that some hypersensibility of the nervous system
of the intestine goes hand in hand with the vaso-constriction that has
been shown to exist, while, in addition, many observers have found
degenerative and even subacute inflammatory changes in the sympathetic
nervous system of the abdomen, mainly in the splanchnic area and the
solar ganglion. The action of vaso-dilator drugs on the pain of colic
demonstrates the close association of vaso-motor changes with the acute
paroxysmal pain.

Riegels[10] investigated the cause of colic in 200 cases. He found
that in every instance there was reason to suppose that toxic
vaso-constriction of the vessels in the splanchnic area, due to
irritation in the vaso-constrictor nerves, was brought about by the
action of lead.

Definite gastritis has also been described in some way simulating that
caused by arsenic, with thickening in the submucosa of the stomach and
intestine. Associated with this enteritis is endarteritis, atrophy of
the glands, and Lieberkühn’s follicles. In the colon as well as the
ileum was a well-marked enteritis involving the muscular lesions of the
gut.

Various other authors describe degenerative processes with cirrhotic
changes in the gastro-intestinal tract. Amongst these, Galvini[11]
describes, in a case of death from very chronic lead poisoning, extreme
cachexia, perihepatitis, perisplenitis, atrophy of the stomach, liver,
and spleen, and chronic sclerosing peritonitis (saturnine peritonitis).
Associated with general changes in the abdominal cavity, marked
inflammation and sclerosis was found in the solar plexus. There is
said to be a very considerable correspondence between the condition of
the peritoneal cavity and its contents in lead poisoning and barium
poisoning. In some of the animals referred to in the description of the
experiments, marked inflammatory conditions of the small intestines and
colon were found, and in not a few instances definite ulceration and
signs of recent hæmorrhages were found scattered along the intestinal
tract. No sclerosis was found, however, in the peritoneal cavity,
though a common symptom of all the animals, whether poisoned by
inhalation, inoculation, or feeding, was the absence of practically all
fat from the peritoneal cavity, the omentum being represented by an
exceedingly thin membrane without any traces of fat whatever.


=Nervous System.=--Perhaps the oldest classical symptom of lead
poisoning is the potter’s palsy or wrist-drop due to interference
with the nerve-supply of the extensor muscles of the hand, leading to
inability to extend the wrist or the fingers on the arm, wasting of
the affected extensor muscles, and finally a claw-shaped hand due to
contractions produced by the pull of the unopposed flexor groups.

The origin of this extensor paralysis has been the subject of much
controversy. One party regards the lesion as of central origin,
affecting the upper motor neurons or their connections in the spinal
cord; the other takes the view that paralysis is mainly of a peripheral
type. Tanquerel[12], whose classical work on lead poisoning still
contains one of the best descriptions of the disease from the clinical
standpoint, describes an associated affection of the peripheral sensory
nerves resulting in definite anæsthesia and hyperæsthesia, and there is
no doubt that sensory nerve affection, although not very common in lead
poisoning, does occur occasionally, and is due to peripheral affection
of the nerves. Occasionally generalized peripheral neuritis is to be
met with, but even this is much less common than in alcoholism or other
toxic forms of peripheral neuritis.

In the opinion of most of the observers who regard the neuritis as of
peripheral origin, the ultimate interference with the motor nerves is
due to an ascending neuritis of the peripheral nerves affecting the
spinal ganglia, and Pal and Mannaberg[13] have described polyneuritis;
whilst Westphal[14], Dejerine[15], Eichhorst[16], Ramond[17], and
others, support particularly the primary lesion of the peripheral
nerves as the cause of the disease. Marie and Babinski[18] in 1894
evolved the central theory, and supported it by reference to the
apparent bilateral occurrence of the paresis and the analogy with many
examples of polymyelitis. Vulpian and Steiglitz[19], examining cords
of animals poisoned by lead, described vacuolation of the cells in the
anterior cornua of the cord.

The original suggestion of the spinal origin of the disease was
enunciated by Erb[20], who, without particular reference to either the
electrical or histological changes to be found in lead poisoning, based
his theory on the similarity of the lesions to polymyelitis. A few
cords of persons who have died of lead poisoning do show slight changes
in the anterior cornua.

One other theory of the nerve affections in plumbism is that
advanced first of all by Hitzig[21], and later by Boerwinkel[22] and
Eichhorst[23], who regard the initial disease as one related to the
circulation, and not necessarily to the nerve lesions themselves.
Potain[24], basing his observations on the anatomical distribution
of the blood vessels, points out that the flexor muscles, excluding
the supinator longus, are drained by the median cephalic vein, whilst
the extensors are drained by the interosseous--a peculiarity of
considerable importance, as the supinator longus escapes paralysis in
the majority of cases of wrist-drop.

The presence of paralysis in the muscles and the association of nerve
lesions to muscular paralysis led investigators to examine the nervous
system, and probably more attention has been paid to the pathology of
poisoning in this direction than in any other. Many records of isolated
cases are to be found in the literature of the subject, and the
examination of the spinal cord has been carried out in many instances;
several have been cases of generalized paralysis or dementia, with
involvement of the trunk muscles as well as those of the extremities in
the paresis.

Many observers who have made histological examinations in such
cases have found nuclear changes in the anterior columns of the
cord suggesting polymyelitis. A small number only of the total
cases of paresis, however, come under this heading. Vulpian[25],
Oppenheimer[26], Oeller[27], and others, described degenerative and
proliferative changes in the grey matter of the cord. Steiglitz[28]
by animal experiments produced inflammatory processes in the anterior
grey substance, vacuolations in the ganglion cells, and degeneration
in the anterior root ganglia. In the paralyzed muscles the changes
of degeneration are found: the muscle nuclei become spindle-shaped,
the interstitial tissue undergoes degeneration, the muscle becomes
atrophied, takes the stain badly, shows irregular striation, and the
muscle bundles become ill-defined and fused.

Scarcely any two observers are agreed as to the exact nerve lesions
which are to be found, and so at variance are the various theories
based upon the pathological findings that it is by no means uncommon to
find two sets of observers quoting the same electrical reactions and
histological appearances as proving in the one case peripheral, and
in the other the central, origin of the paralysis. On the other hand,
in the quite early observations of Hitzig[29] particular attention was
called to the bloodvessels and their possible association with the
disease. Moreover, as has been already cited, ancient physicians were
in the habit of making use of lead as a styptic and hæmostatic because
of its peculiar action on the blood.

Probably as a result of improved histological methods of examining
the nervous tissue, renewed attention was given to the nerve fibres
and nerve cells, with the result that, in the very large number of
observations recorded, many different nerve lesions are described as
the sequelæ of lead intoxication.

On the other hand, Hitzig’s observations on the associated inflammation
of the bloodvessels has received confirmation by several independent
workers. Westphal[30] cites a case of chronic lead poisoning resulting
in death from encephalopathy, and describes degeneration and œdema of
the brain following a process of chronic inflammation in the smallest
and minute bloodvessels, and also associated with degeneration of
the ganglion cells in the vicinity. Chvostek[31] also publishes a
similar case where cerebral degeneration and some œdema had occurred.
Kolisko[32], in examining the brain of a girl who had died of
encephalopathy, found chronic œdema of the brain and spinal cord,
the condition closely resembling that described by Hitzig as chronic
cerebral hypertrophy.

Quensel[33], in a man who had died of encephalopathy, found
leptomeningitis, atrophy of the cortex with degeneration of the
parenchymatous elements of the cells and nerve fibres, degenerative
changes in the vessels, nuclear destruction and pigmentation of the
cells, and œdema. Nissl[34] described granules, which bear his name,
present in the ganglion cells in the cortex, with parenchymatous
degeneration. These cases were not associated with paralysis, nor
is encephalopathy by any means always complicated with paralysis of
muscles.

Berchthold[35] describes a case of typical spastic paraplegia due to
lead, and states that the cortical neurons were but little damaged, the
weight of the poison having fallen upon the peripheral segments.

Sorgo[36] describes a case of progressive spinal muscular atrophy
traced to lead, in which degeneration of the spinal cord was a marked
feature.

Steiglitz[37], in describing the inflammatory processes produced
in animals poisoned by lead, makes special mention of a distinct
minute inflammatory change in the grey matter of the brain, with
vacuolation occurring in the ganglion cells in the anterior horns of
the spinal cord. Prévost and Binet[38], on the other hand, describe an
inflammation of the peripheral nerves occurring after administration of
lead to rabbits for one month. They produced what they describe as “a
lead polyneuritis,” with primary affection of the motor nerves. With
the brain, as with other parts of the body, various writers describe
widely differing changes. Experimentally, when the doses have been
massive and the animals rapidly poisoned, very little has been found,
and some regard this as evidence against the central origin of lead
paresis. On the other hand, in cases of chronic poisoning (mainly
chronic industrial poisoning), where an opportunity of post-mortem
examination has been afforded, marked atrophic changes have been
discovered both in the brain and spinal cord, in the motor nerves
supplying the affected muscles, and throughout the nervous system
generally, so much so that anterior polymyelitis of old origin is
described, vacuolation and degeneration of the ganglion cells, and
various other pathological changes associated with nerve degeneration.

On reviewing the literature, it becomes practically certain that in
the old and advanced cases of poisoning lesions are invariably found
in the central nervous system, while in the less advanced cases the
most marked change has been found in the peripheral nerves. In only a
very few instances have any observers noted the fact of hæmorrhages
occurring in the nervous tissues, and one of the most important
observations on this point is the careful description by Mott[39], of a
fatal case of lead poisoning in an asylum, in which distinct yielding
of the vessel walls with minute hæmorrhages was present in the cerebral
cortex. This case is quoted in full on p. 71.

In the record of the experiments by one of us (K. W. G.) on p. 95 are
described the hæmorrhages occurring in the anterior crural nerves of
cats poisoned by lead. These animals showed most distinct loss of power
in their hind-limbs, as was evidenced by their inability to jump,
and other symptoms homologous to wrist-drop in man. In these animals
no nerve degeneration or alteration in the spinal cord was found
sufficiently gross to account for the paralysis, whereas the amount of
pressure produced by the yielding of the vessel walls on the nerve
bundles and the associated exudation was evidently sufficient to cause
compression, and thereby loss of function in the nerve in question.

Now, the pathological changes described by numerous observers, such as
parenchymatous and interstitial changes in the brain, destruction of
the anterior grey matter, and, finally, the degenerative changes in
the muscle groups, the macroscopical and microscopical atrophy of the
muscle bundles with the fibrillation and other changes, are none of
them opposed to the view that hæmorrhage and exudation are the earliest
and initial change; in fact, in experimental animals minute hæmorrhages
could always be traced in the earliest stages of poisoning, frequently
before definite symptoms appeared.

Confirmation of this theory is seen in the work of Glibert[40], and the
drawings he gives showing fibrous changes in the lungs, hyperplasia,
congestion, and emphysema, cirrhotic conditions of the liver, and, as
he describes it, blood-stasis caused by elongation and dilatation of
the capillaries, are all of them highly confirmatory of the hæmorrhage
theory. Further confirmation is also afforded by the observations on
the action of lead salts upon the blood itself. From the earliest days
lead has been used as a styptic, and its empirical use has been shown
by later observation to be due to its power of readily coagulating
albumin and peptone. Further, in chronic lead poisoning there is a
marked increase in the coagulation time of the blood. Glibert, in
the work already referred to, points out the increased ductility of
the red blood-cells in lead poisoning. Quite apart from this, there
is no doubt that definite alterations in the red blood-cells occur;
a species of icterus is common in lead poisoning, the anæmia of lead
poisoning is of a destructive type, increased urobilin may occur
in the urine, and in some instances hæmatoporphyrin is present in
considerable quantities. The bone-marrow in cases of lead poisoning
undergoes distinct inflammatory change, and may possibly be the cause
of some of the curious aching arthralgias often noted as a clinical
symptom. All the pathological evidence that can be adduced points
unmistakably to the blood as suffering the initial stress in lead
poisoning, and it is therefore by no means surprising that the blood
vessels should be the next in order to undergo degenerative changes.
It is probably this degenerative change, particularly associated with
the increased coagulability, alteration in viscosity, the destruction
of the blood-cells themselves, and the permeation of the vessel
walls by definite, if exceedingly minute, quantities of lead salts,
that determines the yielding of the smaller and generally the weaker
bloodvessels. In the histological examination of the experimental
animals there was considerable evidence that the venules, rather than
the arterioles, are the first to yield.

The following case of chronic lead encephalitis, with the examination
of the nervous system described by Mott[41], is a case that has a large
bearing on the general pathology of lead poisoning, and has the merit
of being so carefully described that we cite it at length, as bringing
out some of the special features connected with the pathology of lead
poisoning.

  The patient was a coach-painter, aged forty-four. Family history of
  no particular interest. Had been a painter since a boy. No specific
  history. Treated for enlargement of liver at one time. Married. No
  children. His wife a widow; four children before married to him.

  Before the attack of encephalitis, which ultimately resulted in
  his death, he suffered from colic and obstinate constipation. The
  commencement of the final attack of lead infection was associated
  with an epileptiform fit, from which he recovered and resumed his
  work, but from this time onwards he suffered from progressive
  weakness and progressive inability to perform his ordinary work.
  Constant indulgence in alcohol did not pull him together as before;
  and although previously he had been able to indulge in large
  quantities of alcohol, a very little now affected him adversely.

  The first epileptiform attack was in July, and in November he
  commenced to have delusions, was restless, suspicious.

  On admission to the asylum he showed marked cachexia. Weight, 8 stone
  7 pounds; height, 5 feet 9 inches. There was present well-marked oral
  sepsis and blue line.

  _Mental Condition._--Restlessness; disorientation; remitting
  delirious state; periods of shouting coincident with colic, worse at
  night; auditory hallucinations.

  _Physical Condition._--Bilateral wrist-drop; extensor paralysis of
  the fingers; hand-grip and gait impaired; reaction of degeneration
  of paralyzed muscles; coarse tremors; fibrillary twitching; staccato
  articulation.

  _Sensory._--No definite change.

  _Reflexes._--Pupils normal. Sluggish reaction to light and
  accommodation.

  _Organic._--Deglutition difficult. Micturition and defæcation not
  under control.

  _Vaso-motor._--Tâche cérébrale marked.

  Eye neuro-retinitis. Unequal amaurosis.

  _Heart._--Increased action, variable; alteration during exacerbations
  of colic. Second sound in aortic area accentuated. High pressure,
  variable. Majority of arteries thickened.

  He suffered gradual mental change; the whole of the mental symptoms
  increased in severity until the patient looked like the final stages
  of a case of general paralysis. He died on December 1. Colic was
  present at intervals during the whole time.

  Post-mortem made the next day. Septic bronchitis. Hæmorrhage at the
  base of epiglottis and left vocal cord.

  _Lungs._--Septic broncho-pneumonia.

  _Pericardium._--Small amount of fluid.

  _Heart._--Striated, bluish. Weight 11¹⁄₄ ounces.

  _Ventricles._--Slight hypertrophy of left ventricle.

  _Valves._--Competent.

  _Aorta._--Atheroma near its bifurcation.

  _Arteries._--All more or less thickened.

  _Peritoneum._--Retroperitoneal hæmorrhage in region outside pancreas.
  Mesenteric glands enlarged, indurated, bluish on section.

  _Stomach._--Normal.

  _Intestines._--Vessels congested. Large bowel constricted at
  irregular intervals.

  _Cæcum._--Mucosa slate-coloured.

  _Colon._--Dark-greenish mass.

  _Liver._--Blue on section; pale yellow areas; soft in consistency.
  Weight, 47³⁄₄ ounces.

  _Spleen._--Normal.

  _Kidneys._--No fat. Cirrhotic, adherent, atrophic cortex, granular.

  _Muscles._--Generally dark in colour; wasted.

  A very complete histological examination was made of the brain and
  spinal cord, and throughout the particular changes noticed were
  proliferation of the glia, hyaline thickening of the walls of the
  vessels, both arteries and veins, and presence of congestion; and
  here and there rupture of the smallest vessels, causing miliary
  microscopic hæmorrhages into the perivascular sheaths and the
  substance of the brain. There was no infiltration with lymphocytes
  and plasma cells, as is found in general paralysis. The neuroglia
  showed a formative hyperplasia resulting from chronic irritation.

  In the cortex there was neuroglia proliferation in the polymorpho
  layer and the molecular layer. Changes were seen in the Betz cells,
  particularly in the Nissl substance, with perinuclear chromatolysis,
  such as is generally found in chronic peripheral neuritis, whether
  due to lead, alcohol, or other toxic causes.

  There was no coarse atrophy or degeneration of the fibres of the
  cortex. Neither the cerebellum nor the spinal cord at any of the
  levels examined showed fibre atrophy or degeneration, except possibly
  a slight diffuse sclerosis in the crossed pyramidal tracts of the
  lumbar region.

  Microscopical examination was made of the heart, spleen, kidney,
  liver, lung, and suprarenal gland. There was a general condition
  of angiosclerosis; in the liver a fibrotic overgrowth around the
  vessels; in the kidneys well-marked interstitial fibrosis.

  A chemical examination of the brain was also conducted by the copper
  potassium nitrite method, but no lead was found.


=Excretory System.=--A large number of observers have shown that great
stress is thrown on the kidney in the excretion of lead. Discussion
has taken place as to whether the effect is a primary interstitial
or a parenchymatous nephritis. Most observers are agreed that the
histological changes found in the kidneys of lead workers have very
little by which they may be differentiated from the effects of alcohol.

Although the kidney suffers directly from the effect of circulating
lead, the amount of lead excreted by the kidney in chronic cases is
usually small, variable in quantity, and very rarely exceeds more than
5 milligrammes in the twenty-four hours.

The chemical estimations of the quantity of lead found in the kidney of
persons who have died of lead poisoning given by different observers,
vary exceedingly. Even in cases of definite lead poisoning, where there
can be no reasonable doubt as to the diagnosis, many cases are on
record where no lead at all has been discovered in the kidney.

It is not acute nephritis which is seen in lead poisoning, but the
chronic cirrhotic variety. This probably takes a very long time to
develop; indeed, animals kept under the influence of lead for two years
show very little kidney destruction. It is quite possible that in the
kidney disease met with in lead-workers the combined effect of alcohol
with lead is really the causative factor. There is not sufficient
statistical evidence to make a definite statement on this point, and it
would only be possible by comparing the records of the autopsies of a
number of persons working in lead who do not die from lead poisoning,
and who were non-alcoholic, with a similar number of persons who, in
addition to their lead absorption, were alcoholic subjects.

It is unusual to find blood in the urine, and the condition of the
kidney does not suggest that it would be present.

Gull and Sutton[42] have described arterio-capillary fibrosis in which
the intima of the larger vessels became greatly hypertrophied, and
many of the smaller vessels are practically destroyed by obliterative
arteritis. The production of arterio-sclerosis, with attendant
thickening of the vessel walls and with the various symptoms commonly
associated with arterio-sclerosis, were regarded as secondary symptoms
of lead poisoning. The action of lead on the vessel walls themselves
thus independently proved by a large number of observers working at
different aspects of the problem suggests the pathological change
in the vessels as the common element in the cause of these diverse
symptoms of lead poisoning--colic, paralysis, mania. Generally
speaking, however, the attention of most has been rather focussed on
the kidney and the degenerative changes occurring in that organ due to
the irritative action of lead in the process of excretion than on the
vessels themselves.

Lead in the urine is by no means so common nor so definite a symptom
of lead poisoning as might be supposed, considering the extreme manner
in which the kidneys suffer in old-standing cases. Of particular
importance in this respect is the case referred to by Zinn[43], where a
woman aged thirty-three received 20 grammes of lead acetate in error.
After the first acute symptoms had passed off, the case drifted on to
one of chronic poisoning, with the usual symptoms of colic, anæmia,
and cachexia. During the whole period of the disease, both acute and
chronic stages, examinations of the urine for lead were made, using
the method of Fresenius Babo[44]; yet lead was only detected in the
urine during the early stages, and directly the acute symptoms had
passed off no further lead could be detected. This point is of some
importance, particularly when taken together with the experiments
quoted by Blum[45], who, injecting animals with lead iodide, was unable
to recover lead from the urine. The iodide only passed through the
kidney, the lead being retained in the body.

Jaksch[46] states very definitely that lead is not found in the urine
in chronic cases, but only in the acute cases, and then quite early.

With regard to the kidney two views are held--the one regarding the
disease of the kidney as primarily affecting the bloodvessels, and the
other as an initial parenchymatous change causing secondary obstruction
and alteration in the vessels themselves. There is therefore much
evidence to show that, whether the bloodvessels be primarily or
secondarily affected, almost all observers are in accord in the opinion
that at one time or another, either sooner or later, the bloodvessels
become affected through the action of lead.

Kobert[47] points out that in no case was distinct cirrhosis of the
kidney produced in experimental lead poisoning in animals; inflammation
certainly was to be seen, either interstitial or parenchymatous, but
apparently the poisoning had not progressed a sufficient length of
time for definite cirrhosis to be produced. On the other hand, kidney
changes have been found of various types, all of which may be the
precursors of the ultimate cirrhotic and fibroid change occurring in
the kidneys seen in chronic poisoning by lead as well as in chronic
alcoholism. Particular stress must be laid on the fact that cirrhotic
kidneys are so frequently the direct result of long-continued alcoholic
excess, and, from what has been demonstrated in the experimental
researches on predisposition to lead caused by alcohol, the condition
of cirrhosis of the kidney in a lead-worker is by no means indicative
of lead poisoning, as it may be an old alcoholic effect long antedating
that due to lead.

Oliver[48], Charcot[49], Gombault[50], Hoffer[51], and others, found a
certain amount of parenchymatous degeneration. Von Leyden[52], however,
was able to produce a granular condition of the kidney with glomeruli
shrunken and an arterio-capillary fibrosis. Gayler[53], on the other
hand, thinks that the arteritis of the smallest arteries is the
preliminary effect upon the kidney, whereas more recently Glibert[54]
published plates of the kidney showing definite sclerosis as well as
interstitial nephritis.

Cornil[55] and Brault[56] think the vessels are affected only
secondarily, and that parenchymatous changes are the primary lesion.
Hoffer[57], by feeding guinea-pigs with lead, produced very definite
obliterative arteritis. Klemperer[58] claims to have produced
inflammation and definite necrosis of portions of the kidney substance.

The whole of the kidney is not necessarily affected. Only portions of
it may show changes, while Kleinenberger[59] notes that in chronic
lead poisoning, at the time of acute exacerbation of the disease,
granular casts as well as red blood-cells are found; and, further, that
in cutting through them crystallized masses are occasionally found,
consisting of urates, and sometimes containing lead.

Gayler[60] considers that the effect on the kidney commences in the
muscular coats of the smaller vessels, in which endarteritis followed
by obliterative arteritis is set up.

Practically all observers, therefore, are in agreement that the kidney
suffers to a very considerable extent in chronic poisoning, and the
majority of observers are also in agreement that the bloodvessels
themselves are the primary seat of the change. Further, the presence
of blood in the urine is exceedingly rare in chronic lead poisoning,
despite Kleinenberger’s[61] statement to the contrary. It certainly may
occur during a very acute attack, but we have never seen this symptom.


=Circulatory System.=--Arterio-sclerosis occurring in lead-workers has
been known for some time, and the anæmia of saturnism has been known
for an even longer period. For some time no definite type of anæmia was
associated with lead cachexia, and the anæmia was generally regarded
as one arising from general malnutrition. Here and there through the
literature of the pathology of lead poisoning are to be found remarks
which suggest that the action upon the bloodvessels may be a primary
instead of a secondary effect. Obliterative arteritis is described by
Uhthoff[62], Pflueger[63], Oeller[64], and Pal[65], and in other cases
obliterative retinitis has been considered to be associated with the
action of the lead upon the vessel walls.

Heubel[66], and later Rosenstein[67], found that, in dogs
poisoned with lead, definite cerebral anæmia was produced, due to
vaso-constriction, and consider it to be due to the direct action
of lead upon the intima of the vessel walls. Associated with such
poisoning were symptoms of eclampsia and uræmia, and the latter author
considers that the uræmia is due to vaso-constriction of the kidney
vessels.

Oliver[68] and others have also pointed out the alteration in the
pulse-rate associated with exacerbations of colic, and a number of
observers have noted that certain drugs, such as atropin and amyl
nitrite, which are known vaso-dilators, have a distinctly calming
effect upon the paroxysms of pain.

One or two other observers have actually noted the presence of
hæmorrhages in the lesions; thus, in the case quoted by Mott[69]
definite yielding of the vessel walls and signs of old hæmorrhage
are described amongst other lesions in the brain. Seifert[70] also
describes the presence of hæmorrhages amongst the ganglion cells in
the anterior columns of the cord, both in the case of persons who
have died of lead poisoning and animals to which lead had been given
experimentally. In addition, Sajous[71] describes a case of paralysis
of the superior laryngeal nerve, associated with hæmorrhages, in the
region of the abductor muscles of the larynx. Mott’s case also showed
this laryngeal hæmorrhage.

More recently Elschnig[72], in his observations upon the eye, has
determined a close association between vaso-motor affections,
constrictions, and dilatations, and various eye lesions, such as
amaurosis and amblyopia, occurring in lead poisoning. Rambousek[73],
in summing up Elschnig’s work, points out how much his observations
tend to bridge over the gap between the action of lead upon the blood,
the bloodvessels, and the nerves. He points out that the eye is a
peculiarly favourable organ for watching the effect of a poison so
insidious as lead. The bloodvessels, the nerves, and the muscles, are
all open to inspection and actual observation to a degree not to be
found in any other part of the body. Elschnig[74], in a typical case of
sudden lead amaurosis associated with acute lead colic, found that very
definite motor spasm of the vessels of the eye, conjunctiva, and the
retina, were associated with the amaurosis. He argues from this that
the action of lead is probably directly upon the unstriped muscular
fibre of the vessel walls; that such an action may, and does, extend
to the vessels of the eye muscles, producing paralysis of the muscles
of accommodation, and a dilatation of the pupil, which may be observed
in a large number of persons employed in conditions subjecting them
to lead absorption. Elschnig further considers that the transitory
amaurosis which is often associated with lead poisoning may be due to
vaso-motor disturbances in the brain itself, as well as in the eye.

Still more recently, and due, no doubt, to a great extent to the work
of Elschnig, further attention has been drawn to the vascular system in
lead poisoning. Elschnig’s work has carried the question another stage
forward by showing the association of vaso-motor disturbances with eye
disease, whilst in this country Oliver[75] pointed out the effect upon
the pulse of abdominal colic.

At the beginning of the researches on this point described in the
next chapter, this clue running through the whole of the pathology
of lead poisoning was not appreciated. At the commencement of the
investigations there seemed to be no main general line of symptoms or
histological findings that could be adduced as characteristic of lead
poisoning; in fact, the initial experiments were performed, with the
object of examining the association of lung-absorbed lead compounds as
a possible cause of lead poisoning, as against the entrance of lead
by the alimentary canal; but as the experiments proceeded it became
clear that the stress of the initial intoxication was undoubtedly
falling upon the bloodvessels, and more particularly upon the minuter
bloodvessels, and less on the arterial side of the capillaries
(although the capillaries were to a large extent associated with the
process) than upon the venous radicles.

A general consideration of the pathology shows that lead causes
changes in the nervous system affecting both upper and lower segments,
degeneration of the ganglion cells in the cord and in the brain,
interstitial inflammation of the neuroglia, cortical degeneration,
distinct neuritis, both axial and peri-axial, of the peripheral nerves,
and also signs of change in the sympathetic nervous system in chronic
lead poisoning. Later work has, however, all tended to point out that
the chief and first effect of lead is upon the blood.

Moritz[76] first pointed out the presence of basophile granules in the
red blood-cells. The work was followed up by Emden[77], Gravitz[78],
Zinn[79], Otto[80], Silbert[81], and by Escherich[82]. All these
authors found basophilic erythrocytes in the blood associated
with blood-destruction, and Escherich in addition describes early
changes taking place in the intima of the bloodvessels associated
with vaso-constriction. The Italian author Mattirolo[83], as well as
Marchet[84] and Jores[85], came to a similar conclusion. Glibert of
Brussels[86], carrying the observations somewhat farther, and although
working with guinea-pigs, which normally show basophilic staining
in their blood-cells, was able to demonstrate one further point of
considerable value--namely, the increase in the viscosity of the blood,
with blood-corpuscles of greater toughness, elasticity, and power to
resist destruction when making films, than in normal blood.

There is thus very striking continuity in the observations of all
the various observers, despite the fact that at first sight their
descriptions may appear discordant. There seems no doubt that
practically all authors who have given attention to the subject are
agreed that the circulatory system, and primarily the blood circulating
in the vessels, is affected by lead, and, further, that the vessels
themselves undergo degeneration of various types, many of the cases
examined showing complete obliterative arteritis as the result of
long-standing irritation. Others describe no obliterative changes of
this type in the vessels, because attention was given mainly to the
nervous system, where the cells were found degenerated and showing
chromatolysis. But, on the other hand, careful observers, such as Mott,
have noted the presence, in passing, of these apparent yieldings of
the vessels here and there in the region of the degenerated nervous
tissue. Again, even the histological action of a drug such as amyl
nitrite points to involvement of the vaso-motor system. Perhaps
this curious association through all the described pathology and
bloodvessel infection would not appear so clear but for the more recent
investigations described in the following chapter.


REFERENCES.

  [1] KOBERT: Lehrbuch der Intoxikationen, 2te Aufl., 1906, p. 361.

  [2] OLIVER, SIR T.: Lead Poisoning. 1891.

  [3] DIXON MANN: Forensic Medicine and Toxicology, p. 495.

  [4] STOCKVIS: International Congress of Industrial Hygiene. Brussels,
  1910.

  [5] MÉNÉTRIER: Meillère’s Le Saturnisme, pp. 131-136.

  [6] KUSSMAUL AND MEYER: Deutsches Archiv für Klin. Med., ix., p. 283.

  [7] TANQUEREL: Traité des Maladies de Plomb, ou Saturnines. Paris,
  1839.

  [8] BERNARD: Meillère’s Le Saturnisme, p. 155.

  [9] BOKAI: Trib. Med., June 11, 1891.

  [10] RIEGELS: Kobert’s Lehrbuch der Intoxikationen, p. 363.

  [11] GALVINI: Rivista Clinica, fasc. iii., 1884.

  [12] TANQUEREL: _Ibid._

  [13] PAL AND MANNABERG: Revue Générale de Villaret, Gaz. des Hôp.,
  Fév. 16 and 19, 1903.

  [14] WESTPHAL: Archiv f. Phys. u. Nervenkr., 1874.

  [15] DEJERINE: Mém. de la Soc. de Biologie, 1879, et Exposé de
  Titres, p. 58, 1894.

  [16] EICHHORST: Ueber Bleilähmung. Virchow’s Archiv, 1890, p. 217.

  [17] RAMOND: Maladies du Système Nerveux, t. xi. 1895, 1896.

  [18] MARIE AND BABINSKI: Meillère’s Le Saturnisme, p. 193.

  [19] VULPIAN AND STEIGLITZ: Archiv für Psych., 1892, xxiv., p. 1.

  [20] ERB: Berl. Klin. Woch., 1884, p. 110.

  [21] HITZIG: Studien über Bleiverg. Berlin, 1868.

  [22] BOERWINKEL: Virchow’s Archiv, Bd. cxx., 1890.

  [23] EICHHORST: _Ibid._

  [24] POTAIN: Bull. Med., 1887.

  [25] VULPIAN: Maladies du Système Nerveux. 1879.

  [26] OPPENHEIMER: Zur Kennt. der Exp. Bleiverg. Berlin, 1898.

  [27] OELLER: Path. Anatom. der Bleilähmung. München, 1883.

  [28] STEIGLITZ: Archiv für Psychiatrie, Bd. xxiv., 1892.

  [29] HITZIG: _Ibid._

  [30] WESTPHAL: Archiv für Psychiatrie, Bd. xix., 1888.

  [31] CHVOSTEK: Neurol. Centralblatt, 1897.

  [32] KOLISKO: Die Bekämpfung der Bleigefahr in der Industrie, von
  Leymann, p. 21. 1908.

  [33] QUENSEL: Archiv für Psychiatrie, Bd. xxxv., 1902.

  [34] NISSL: Allgemeine Zeitschrift für Psychiatrie, Bd. xlv., 1892;
  Bd. iv. 1897.

  [35] BERCHTHOLD: Die Bekämpfung der Bleigefahr in der Industrie, von
  Leymann, p. 23. 1908.

  [36] SORGO: Wien. Med. Woch., 1900.

  [37] STEIGLITZ: Archiv für Psychiatrie, Bd. xxiv., 1892.

  [38] PRÉVOST AND BINET: Revue Médicale de la Suisse Romande, ii.,
  1889.

  [39] MOTT: Archives of Neurology and Psychiatry, vol. iv., p. 117.

  [40] GLIBERT: Le Saturnisme Expérimental: Extrait des Rapports Ann.
  de l’Insp. du Travail, 1906.

  [41] MOTT: _Ibid._

  [42] GULL AND SUTTON: Kobert’s Lehrbuch der Intoxikationen, 2te
  Aufl., 1906, p. 370.

  [43] ZINN: Berl. Med. Woch., 1899.

  [44] FRESENIUS BABO: Liebig’s Annalen, vol. xlix., p. 287. 1844.

  [45] BLUM: Wien. Med. Woch., No. 13, 1904.

  [46] JAKSCH: Klinische Diagnostik.

  [47] KOBERT: _Ibid._, p. 369, and general Literature, p. 376.

  [48] OLIVER, SIR T.: Lead Poisoning. 1891.

  [49] CHARCOT: Leçons sur les Maladies du Foie et des Reins. Paris,
  1882.

  [50] GOMBAULT: Archiv für Physiologie, 1881.

  [51] HOFFER: Dissertation, Freiburg, 1883.

  [52] VON LEYDEN: Zeit. für Klin. Med., 1883.

  [53] GAYLER: Ziegler’s Beitr., ii., 1888.

  [54] GLIBERT: _Ibid._

  [55] CORNIL: Journal de l’anat. et physiol., No. 2, 1883.

  [56] BRAULT: _Loc. cit._

  [57] HOFFER: _Loc. cit._

  [58] KLEMPERER: Kobert’s Lehrbuch der Intoxikationen, 2te Aufl.,
  1906, p. 370.

  [59] KLEINENBERGER: Münch. Med. Woch., No. 8, 1904.

  [60] GAYLER: _Loc. cit._

  [61] KLEINENBERGER: _Loc. cit._

  [62] UHTHOFF: Handbuch der Aug. Lief. Leipzig, 1901.

  [63] PFLUEGER: Die Bekämpfung der Bleigefahr in der Industrie, von
  Leymann, p. 21. 1908.

  [64] OELLER: _Ibid._

  [65] PAL: Zentralbl. f. innere Med. Leipzig, 1903.

  [66] HEUBEL: Path. und Symp. Chron. Bleiverg. Berlin, 1871.

  [67] ROSENSTEIN: Virchow’s Archiv. 1897.

  [68] OLIVER, SIR T.: Lead Poisoning. 1891.

  [69] MOTT: _Ibid._

  [70] SEIFERT: Berl. Klin. Woch., 1884.

  [71] SAJOUS: Archiv für Laryng., iii., 1882.

  [72] ELSCHNIG: Wien. Med. Woch., 1898.

  [73] RAMBOUSEK: Die Bekämpfung der Bleigefahr, von Leymann, p. 15.
  1908.

  [74] ELSCHNIG: _Loc. cit._

  [75] OLIVER, SIR T.: Lead Poisoning. 1891.

  [76] MORITZ: St. Petersb. Med. Woch., 1901.

  [77] EMDEN: Die Bekämpfung der Bleigefahr, von Leymann, p. 19.

  [78] GRAVITZ: Deutsche Med. Woch., No. 36. 1899.

  [79] ZINN: Berl. Klin. Woch., 1899.

  [80] OTTO: Revue Méd., 1892.

  [81] SILBERT: _Ibid._

  [82] ESCHERICH: Die Bekämpfung der Bleigefahr, von Leymann, p. 18.

  [83] MATTIROLO: _Ibid._, p. 19.

  [84] MARCHET: _Ibid._, p. 19.

  [85] JORES: Ziegler’s Beitr., Bd. xxxi., 1902.

  [86] GLIBERT: _Ibid._




CHAPTER VI

PATHOLOGY--_Continued_[A]


  [A] This chapter is the work entirely of one of us (K. W. G.)

It was thought that some light might be thrown on chronic intoxication
produced by lead salts if direct experiment were made upon animals,
resembling in the arrangement of such experiments, as far as possible,
the industrial conditions under which human beings contract lead
poisoning.

The animals chosen for the experiments were cats, as it is a fact of
common knowledge that it is impossible to keep cats in lead works,
particularly white-lead, because they rapidly become poisoned if
allowed to stray about the works. The same holds good in the case of
dogs.

From the statistics already given in Chapter IV., and from the remarks
in the chapter on Ætiology, there was no doubt whatever that dust
played a most important rôle in the production of industrial lead
poisoning. In attempting, therefore, to copy the industrial conditions,
it is essential to submit the animals experimented upon to infection
by means of air in which lead dust is suspended. A large number of
experiments have been carried out in the first place, by myself[1],
and later in conjunction with Dr. Goodbody[2], and another series of
experiments were also undertaken by myself[3]. Further experiments are
still in progress in this and other directions.

The methods of experiment adopted were as follows:


1. =Breathing Experiments=--_First Series._--A. The animals
experimented upon were placed in a large closed chamber at one end of
which an electric fan was fitted in such a way that the air was kept
in constant motion. The lead dust was introduced by means of a funnel
through the roof in a definite quantity during timed intervals. By
means of an aspirating jar and a tube inserted into the side, samples
of air were withdrawn from time to time during the experiments, and
submitted to chemical analysis to determine the quantity of lead
circulating in the air. These samples were drawn off at the level of
the animals’ heads. Great care was taken to eliminate any swallowing of
dust by the animals during the experiments, by protecting their coats
from the dust and carefully brushing them at the conclusion of each
exposure.

_Second Series._--B. In other experiments a chamber containing two
separate compartments was constructed, and lead dust suspended in
air was blown into the two compartments by means of an electric fan
situated outside. The apparatus was so arranged that the draught of
air from the fan passed through two separate boxes, in which the lead
compound under experiment was kept agitated by means of small fans
situated in the boxes and driven by a second electric motor. In this
way two different samples of lead were experimented on at one and the
same time, the air current driving in the dust through the two boxes
being equal on the two sides; the quantity of dust was therefore
directly proportional to the compound used. Samples of the dusty air
were aspirated off and subjected to analysis, as in the first series.
In this series of experiments the animals were so arranged that only
their heads projected into the dust chamber during exposure.


2. =Feeding Experiments.=--Feeding experiments were carried out by
mixing a weighed dose of the lead compound experimented with, and
adding this to a small portion of the animal’s first feed in the
morning. It was found that unless the lead was well incorporated with
the animal’s food it would not take the lead in the dry form; and in
dealing with white lead and other dust, it was necessary to give the
compound in a similar form to that in which a man would obtain it under
industrial conditions, which of course precluded the use of a solution.

The amount of lead given by the mouth as a control to the inhalation
experiments was from seven to ten times the dose which could be taken
by the animal during its exposure in the cage, and the dose was given
daily, and not every third day as in the inhalation experiments. All
the compounds used in the inhalation experiments were given to animals
by the mouth, the animals’ weights being carefully noted.

In a further series of feeding experiments a soluble salt of lead
was added to the animals’ food (water or milk), the salt in this case
being the nitrate. The quantity added was much smaller than in the dust
experiments. 0·1 gramme was given daily.


3. =Inoculation Experiments.=--As a further control to both the
breathing and feeding experiments, the various lead compounds similar
to those used in the other experiments were inoculated into animals.
The insoluble salts gave some difficulty in the technique of injection,
but by using a large needle, and making the suspension of the material
in the syringe, the difficulty was overcome. The quantity of material
inoculated varied; it was calculated in fractions of a gramme per
kilogramme body weight, the quantity of fluid used being the same in
all cases--namely, 10 c.c.--and inoculations were made subcutaneously
and intramuscularly in the muscles of the back after previous shaving.
In only one case was localized inflammation produced, and this was when
the acetate was the salt employed.

None of the animals exhibited any signs of discomfort during the
experiments from the presence of lead dust in the air; once or twice
sneezing was noticed, but this was an uncommon occurrence. This point
is of practical importance, as the lead dust contained in the air in
white-lead and other factories is not of itself irritating to the
mucous membrane of the lung. The animals subjected to this form of
experiment were no doubt absorbing much larger doses of lead than are
persons engaged in the manufacture of lead compounds.

The only ascertainable difference in the ultimate pathological lesions
produced in animals, whether inhaling large quantities or minimal
quantities of dust, was the rate at which the poisoning took place. In
certain experiments it was found that the animals maintained a kind
of equilibrium, much as do workmen engaged in dusty lead processes.
It was found, moreover, that some animals showed a certain amount of
tolerance to the effect of lead dust, in that their weights remained
almost constant, but an increase in the quantity of lead present in the
air immediately produced progressive diminution in the body weight; and
as this diminution in the body weight approached to one-third of the
animal’s initial weight, so symptoms of chronic poisoning supervened.

In addition to the animals inhaling lead dust over prolonged periods,
certain other inhalation experiments were made for the determination
of lead dust in the lung as opposed to the stomach. In the inhalation
experiments proper, where the animals were exposed to inhalation every
other day or every third day, for only an hour at a time, the quantity
of lead present in the air was not very large, and it was thought
essential to determine if, in exceedingly dusty atmospheres, any
appreciable amount of lead could be found in the stomach. Ten animals
were submitted to the inhalation of air heavily charged with various
types of lead dust. The animal was exposed to the dust for an hour
and a half to two hours; at the end of this time it was anæsthetized,
and when the respirations had ceased, and the animal was dead,
sulphuretted hydrogen was blown into the lung and into the stomach.
The animal was then rapidly dissected and staining looked for. The
tissues were further treated with acid and re-exposed to sulphuretted
hydrogen gas. In one animal only out of the ten was any staining
noticed in the stomach. In none of the others was any such staining
found, but very definite blackening was found in the larynx, trachea,
and macroscopically even in some of the bronchioles. Sections of the
lung were further submitted to histological examination, and by means
of micro-chemical tests with chromic acid and with iodine, and also
by comparing sections of the experimental animals and animals which
had not been subjected to lead dust inhalations, a very much larger
quantity of material was found present in the lungs of the inhalation
animals than in the normal animal. The dust was situated in the alveoli
and the alveolar cells, and often in the lymphatics. On examining
microscopically sections of the lungs of those animals exposed to
graduated inhalation over extensive periods, a far larger number of
blackened granules, dust, pigment, and other substances, was found than
in similar sections of animals which were under normal conditions and
had not been exposed to lead dust, although it is true such animals
show a very fair proportion of carbon particles taken up by the lung
tissue.

A further important fact was noticeable in animals Nos. 21 and 22
(see p. 101), which had been exposed to a low solubility glaze such
as is used in the Potteries. Low solubility glaze is compounded with
lead frit--that is to say, a lead glaze (or lead silicate) which has
been finely ground. The particles of this substance are much larger
than those of ordinary white lead, and in addition they are much more
angular. Of three animals exposed to this glaze, one actually died of
pneumonia (acute), and the other two suffered from some bronchial
trouble, both of them showing distinct signs of pneumonic patches and
old and chronic inflammation when examined histologically; whereas in
none of the other animals exposed to white lead dust or to the high
solubility glaze, which contained white lead as opposed to lead frit,
no such pneumonic or fibroid changes were found. This point is of some
pathological importance.

The inhalation experiments also throw some light on the quantity of
lead necessary to produce poisoning. The animals in the inhalation
experiments were exposed for varying periods, and constant estimations
made of the lead present in the air. In a number of instances samples
were taken from the cage air during the whole of the experiment, as
rapidly as possible. The quantity of lead floating in the air was found
to increase as the experiment progressed, although a large amount of
the lead introduced was caught on the side of the cage and deposited on
the floor.

In the later experiments the method of taking the samples continuously
during the experiment was abandoned, and four samples only were taken,
and the average recorded. A simple calculation will give the quantity
of lead dust it would be possible for an animal to inhale during the
whole of this period of exposure. The utmost tidal air in the case of a
cat would be taken at 50 c.c. Taking the average, about 0·27 gramme of
lead was inhaled during the half-hour of exposure.


=Feeding Experiments.=--Twelve feeding experiments of various types are
recorded. The method of experiment was as follows:

The compound under investigation was carefully weighed out each day
(0·5 to 1·0 gramme), the substance being some of the same compound
that was being made use of for inhalation experiments. In the case
of the white lead it was found essential to mix it with the animals’
food; they were given white lead in a small amount of their food, and
no further food was given for some little time after the dose of lead
had been swallowed. Low and high solubility glazes were also made
use of for feeding, and as a further experiment alcohol was given to
the animals in addition to the previous course of lead inhalation or
feeding, and the exposure to lead continued after the alcohol was
given. In addition to high solubility glazes, white lead, and flue
dust, a soluble salt of lead was also used, in one series the salt
being the nitrate. 0·1 gramme was given daily; and it is these two
nitrate animals (46 and 47) which showed distinct differences from the
white lead and other feeding experiments. In one case the lead was
given mixed with water, in the other mixed with milk. The animal which
was fed with the nitrate dissolved in water developed encephalopathy,
whereas the one in which the substance was mixed in milk exhibited no
signs, though fed for a similar period. Both the animals increased in
weight, which is an unusual effect in experimental lead poisoning.
The question of the addition of milk, which apparently prevented the
absorption of lead, is of very considerable importance, as it is highly
probable, as has been pointed out with regard to the precipitation of
lead by means of organic substances, that the albuminoid substances in
the milk precipitate the nitrate already in a state of solution; and it
may be argued from these experiments that mixing the white lead with
the food would tend to prevent the lead having a toxic or deleterious
effect, but even when the lead was given in the form of pills between
meals no poisonous effect was noticed. Further, the quantity of white
lead given was considerable, and it is highly questionable whether
the quantity of lead so taken would be dissolved by the gastric
juice excreted under normal circumstances in its entirety, as a
very considerable quantity would pass onwards through the pylorus
undissolved. Until the lead compound has become soluble it cannot react
with the albuminoid constituent of the food. Ordinary dry white lead or
litharge does not combine directly with albumin.

The majority of the experimental animals showed alteration in weight.
The most important point which is brought out by these experiments,
considering them from the point of view of inhalation, is the enormous
quantity of white lead the “feeding” animals swallowed without
producing any apparent symptoms. The quantities cited are the amounts
given per diem, whereas in the inhalation experiments the animals
were rarely exposed more than three days a week for an hour at a time
(see table, p. 101). The quantity of lead, therefore, given by the
gastro-intestinal canal was at least ten times as much, in many cases
fifteen or twenty times as much, as could be taken by the other animals
via the lung during inhalation, and yet these animals showed little or
no susceptibility to poisoning when fed with white lead or other lead
compounds, unless alcohol was given in addition.

An examination of the stomach after death showed, in the case of the
alcoholic animals, distinct evidence of gastritis, and there is some
reason to suppose that in such animals a degree of hyperacidity may
have existed, thereby promoting the rate of solution of the lead.

The increased susceptibility to lead poisoning through the agency of
alcohol is interesting. No. 6 received, in addition to its inhalations
or period of exposure in the dusty air, 50 c.c. of port wine per diem.
Symptoms of lead poisoning appeared a day sooner than in any other
animal, and if we eliminate this experiment, as the dust (flue dust
from blast-furnace) contained also arsenic and antimony, three days
sooner than the litharge animal, and twenty-five days sooner than the
other animals exposed to white lead dust. In addition, this animal was
the only one which actually died during the period of experiment; all
the other animals were killed at the end of two months and submitted
to histological examination; but the animal which had received alcohol
died with symptoms closely simulating lead encephalopathy in man. The
predisposing action of alcohol is still further emphasized by the
subsequent experiments with three animals exposed to white lead dust;
one was exposed thirty-seven and the other thirty days before symptoms
appeared, whereas when alcohol was given poisoning was apparent within
twelve days, and after only four inhalations.

In the case of animals fed with white lead, one after eight months,
and the other a year and a half, showed no signs of lead poisoning
at all, while the weights remained constant. At the end of this time
alcohol (50 c.c. of port wine) was added to the animals’ diet, and one
month after the addition of alcohol to the diet, the dose of white
lead being continued constant, encephalopathy ensued. In a second case
the animal was started on alcohol in addition to the white lead. In a
month it was showing signs of slight paresis. Again, an animal fed on
a low-solubility frit consisting of ground-up lead silicate, showed
no ill-effects after receiving a daily dose of this compound. At the
end of this time alcohol was added to its diet, and six months later
the animal developed symptoms of cerebral involvement, which continued
at intervals until a fatal attack of encephalopathy at the end of a
year. There is thus definite evidence to show that the addition of
alcohol to the animal’s diet undoubtedly hastened and determined the
appearance of lead poisoning, and this, taken in conjunction with the
inhalation experiments previously cited, is very strong evidence of the
increased susceptibility to lead poisoning produced by alcohol. This
supersensitiveness to lead through the medium of alcohol is a matter
of clinical experience to most persons who have had experience of
industrial lead poisoning, particularly those who have been engaged in
the routine examination of persons working in factories.


=Inoculation Experiments.=--In order to control both the feeding and
the inhalation experiments, and more particularly to obtain direct
information of the effect of lead upon the body tissues, resource was
had to the inoculation of the various lead compounds tested--namely:
(1) White lead, (2) litharge, (3) lead frit. These three compounds are
the three types of lead salt which are used in the Potteries, whilst
white lead and litharge are the compounds causing industrial poisoning
in the largest proportion of cases in other industries. As a further
control, the more soluble lead salts were also made use of--namely,
acetate, nitrate, and chloride--mainly for the purpose of establishing
some standard of poisoning both in rate and dose.

Several rather unexpected results were derived from the inoculation
experiments, which will be referred to.

The method of inoculation was to suspend the lead compound to be
tested in normal saline solution or distilled water. The animal was
then shaved, and the lead compound inoculated into the muscles of the
back. The corrosive action of these lead salts was avoided by using a
considerable quantity of diluent.

Lead frit is a constituent of low-solubility glaze--that is to say, a
glaze which has not more than 5 per cent. soluble lead when subjected
to the standard test of exposing 1 gramme of the glaze to a litre of
0·04 per cent. hydrochloric acid for an hour at room temperature. The
frit which was the constituent of this glaze is produced by heating
together litharge or lead and silica, the production being a yellow,
hard, glaze-like material looking very much like sugar-candy. It is not
by any means a compound of lead and silica of simple composition, as
different samples show a wide variation in their lead content; whilst,
in addition, the mode of its formation closely resembles that of an
alloy or amalgam, and allows of the formation of a eutectic entangling
in its meshes both of the constituents of which it is formed, so
that a certain amount of free lead, in addition to the silicates of
various descriptions, are present. At the same time the compound is
highly resistant to the action of mineral acids, and, of course, much
more insoluble and refractory than white lead, litharge, or other
lead oxides. The body fluids, however, particularly the fluids in the
subcutaneous and muscular tissue, definitely exert some action upon
this fritted lead, and it was found experimentally that symptoms of
poisoning could be produced in the experimental animals when even small
doses were administered. A gramme of frit was inoculated, and in all
but one case the animals showed definite signs of lead poisoning, and
in two instances actually died with symptoms of encephalitis.

By washing the frit with distilled water, a slight diminution in the
poisonousness was found, but by washing the frit with two or three
changes of dilute acetic acid (3 per cent.), and then with distilled
water, no pathological results followed inoculation. Water-washing
frit alone definitely reduces the poisonous effect, but not to the
same extent as the preliminary washing with acetic acid. On the other
hand, washing with hot water had a much greater effect than cold-water
washing.

Further evidence given by the inoculation experiments shows the
relationship between the more soluble and the insoluble lead salts.
The dose of acetate required to kill an animal was about 0·1 gramme
of acetate per kilogramme body weight. On the other hand, 0·1 gramme
of white lead produced no ill-effects, 0·5 gramme per kilogramme body
weight produced death in about two months. In addition, those animals
suffering from the more acute forms of poisoning developed definite eye
changes and retinal hæmorrhages. Tortuosity and increased size of the
retinal vessels were observed in several instances.

Besides controlling the experiments of feeding and inhalation, the
inoculation experiments play a still more important part, as they
furnish the correlation, necessarily, of the histological changes found
as the result of poisoning by means of lead. In all the animals which
have died of poisoning, certain definite trains of symptoms made their
appearance. These symptoms were in practically all particulars similar
to those observed in industrial lead poisoning in man, the onset of the
affection and its clinical course corresponding to the symptom-complex
in man, including those of cortical involvement, and often similar to
the classical Jacksonian variety.

Throughout these experiments the animals exhibited no signs of
irritation, and during the initial period, even, when loss of weight
was a noticeable feature, their appetites remained exceedingly good;
they were quite friendly, and purred loudly when stroked; but when
symptoms of poisoning became manifest, particularly the onset of
paralysis, a definite change in mental phenomena took place: the
animals became quarrelsome, highly apprehensive of danger without
cause, morose and lethargic by turns. At this stage, in more than
one instance, acute encephalopathy supervened. The mental change was
peculiarly striking in reference to Mott’s case, quoted on p. 71, as
in all respects it was exactly analogous with the train of symptoms
recorded in that case. To sum up, the symptoms produced in the
experimental animals by the lead compounds inoculated and respired, no
matter what the particular compound of lead experimented was, were as
follows:

1. Slight preliminary rise in weight at the commencement of the
experiment, lasting from one to two weeks.

2. Progressive loss of weight, mainly due to the disappearance of all
fat, subcutaneous, kidney, mesenteric, etc., with associated anæmia,
and the curious sunken and pinched faces commonly associated with
saturnine cachexia.

3. Paresis of various types.

In the cat the muscles first affected are those of the back and the
quadriceps extensor of the hind-limbs. The onset of the paralysis is
slow and insidious, but may be acute; as a rule weakness in the muscles
of the lumbar region and the spine are the first symptoms; secondly,
inability to jump, owing to the weakness of the quadriceps extensor,
while the animal tends to fall over when turning round quickly.
Encephalitis occurs, and is frequently fatal. As a rule the affection
is unilateral; complete loss of consciousness may occur, followed by
slow but complete recovery. The animals gave no evidence of suffering
pain, and, when recovered from an attack of encephalopathy, would at
once take milk, but seemed dazed and uncertain in their movements. When
the animals reached the stage of paralysis, they were destroyed under
anæsthetics, and subjected to post-mortem examination. The post-mortem
findings of a typical case were as follows:

The animal was emaciated, the fur easily pulled out, and the muscles
were exceedingly flaccid.

Rigor mortis was slow in making its appearance; the blood remained
fluid for a considerable time.

Practically no fat was to be found in the whole of the mesentery,
and the omentum was devoid of fat and shrivelled. The fat around the
kidneys had entirely disappeared. There was little orbital fat.

The peritoneum was thin and glistening, and very frail.

The whole of the mesenteric vessels, particularly in the region of the
large intestine and the ileo-cæcal valve, were engorged with blood;
whilst in the lower part of the small intestine, and often in the
duodenum, occasionally in the whole of the jejunum and ileum, traces of
minute hæmorrhages were found along the intestinal wall.

The liver was engorged with blood, as was the spleen.

The kidney capsule stripped easily, but was occasionally adherent here
and there. The whole of the cortical vessels were injected with blood,
the branching showing most distinctly.

A good deal of serous fluid was at times found underneath the kidney
capsule.

On section the cortex appeared engorged with blood, and showed here and
there, even to the naked eye, small hæmorrhages.

In the region of the appendix a few large mesenteric glands were
invariably found, whilst a few glands might also be found in the wasted
mesentery of the small intestine. In the region of the appendix the
glands were frequently dark in colour. On opening the gut, minute
hæmorrhages and ulcerated patches were to be found in the lower part of
the ileum; the ileo-cæcal valve, and the whole of the large intestine,
extending right up to the end of the appendix, was covered with a dark
slate-blue slime, in which lead could be easily recognized by chemical
processes.

Ulceration of the gastric mucous is uncommon, and only on one occasion
were any hæmorrhages found. In the thoracic cavity the lungs were
generally found to be emphysematous, and particularly in those animals
subjected to inhalation of lead frit containing angular particles of
lead glaze broncho-pneumonia was found.

The heart was flabby, and occasionally distinct roughening and
thickening of the valves was seen.

_Nervous System._--On opening the skull, hæmorrhages were frequently
found at the base of the brain, occasionally situated over the surface
of the cerebrum. Minute hæmorrhages were found often underneath the
arachnoid membrane, but the largest hæmorrhages were always found at
the base of the brain, and spreading down into the spinal canal along
the medulla.

On removing the cord, minute hæmorrhages were found along the surface,
irregular in distribution, and never very large. On section the brain
and cord appeared normal.


=Histology.=--A large number of sections were prepared from the animals
developing symptoms of poisoning; the various tissues are described
seriatim:

_Muscles._--These appear to have undergone general fatty degeneration.
The individual muscle fibres are indistinct in outline, and show
irregular areas stained by hæmatoxylin. Some infiltration may be seen
here and there between the muscle fibres, and minute hæmorrhages are
occasionally detected, the chief appearance being that of general
atrophy. The heart muscle shows similar degeneration, and the tendency
of the sarcolemma to break down and stain irregularly is apparent. In
many areas the muscle fibres stain poorly, if at all. Occasionally
minute hæmorrhages are found, passing between the muscle fibres.

_Liver._--The hepatic cells show varied degeneration; the vessels
passing between the cells are engorged with blood, the cells being
frequently much distorted from their general arrangement, and here and
there completely obliterated by small areas of exudation as well as
actual hæmorrhages.

_Spleen._--The parenchyma shows masses of irregular spaces filled with
recently-shed blood; the individual cells show a granular degeneration,
with occasional basophile staining, the general appearance being one of
chronic congestion. Here and there cloudy swelling may be seen.

_Intestine._--Sections across the small intestine show atrophy of
the intestinal wall, slight degeneration of the muscular coats, with
infiltration and minute hæmorrhages.

_Large Intestine._--Here similar minute hæmorrhages are found, in
no case large enough to be seen by the naked eye. Areas of necrotic
tissue are also seen in which considerable quantities of lead sulphide
particles are found.

PLATE I

[Illustration: FIG. 1.--SECTION OF LARGE INTESTINE OF ANIMAL POISONED
BY INHALATION OF WHITE LEAD, SHOWING EXCRETION OF LEAD BY TISSUES.
(STAINED EOSIN AND HÆMATOXYLIN.) × 250.

The whole of the large intestine was stained black, the staining
commencing at the ileo-cæcal valve. No staining is observable in the
small intestine; the line of demarcation is sharp.]

[Illustration: FIG. 2.--INTESTINAL ULCERATION IN TURPENTINE POISONING.
(STAINED EOSIN AND HÆMATOXYLIN.) × 250.]

[Illustration: FIG. 3.--SECTION OF ANTERIOR CRURAL NERVE FROM ANIMAL
POISONED BY INHALATION OF WHITE LEAD DUST, SHOWING HÆMORRHAGE IN NERVE.
(STAINED HÆMATOXYLIN AND EOSIN.) × 250.

There was paralysis of the quadriceps extensor on the right side;
the left leg was unaffected and the left anterior crural nerve was
unaffected.]

PLATE II

[Illustration: FIG. 1.--SECTION OF LUNG OF ANIMAL EXPOSED TO INHALATION
OF WHITE LEAD DUST, SHOWING MASS OF LEAD IN THE LUNG SUBSTANCE.
(STAINED HÆMATOXYLIN AND EOSIN, AND TREATED WITH H₂S.) × 250.]

[Illustration: FIG. 2.--LUNG OF ANIMAL EXPOSED TO TURPENTINE VAPOUR.
(STAINED HÆMATOXYLIN AND EOSIN.) × 250.]

[Illustration: FIG. 3.--LUNG OF ANIMAL EXPOSED TO INHALATION OF WHITE
LEAD DUST, SHOWING CHRONIC INFLAMMATION WITH EXUDATION AND CAPILLARY
LEAKAGE AND HÆMORRHAGE. (STAINED HÆMATOXYLIN AND EOSIN.) × 250.]

_Lung._--Red or grey hepatization may be found, or a general appearance
of broncho-pneumonia, where the dust used contained angular or
insoluble substances. In animals subjected to prolonged inhalation,
particles of lead could be demonstrated in the alveolar cells, and in
the tissue beyond, either by staining with chromic acid or by means of
iodine. Staining by sulphuretted hydrogen is not very satisfactory, as
most animals resident in a large city show masses of carbon situated in
various parts of the alveolar cells. If, however, a section be treated
by means of iodine or chromic acid, and watched under the microscope
during the process, the particles of carbon are easily differentiated
from those of lead compounds.

_Nervous System._--Sections of the brain and spinal cord, and of the
nerve supplying the paralyzed muscles, all exhibited the same phenomena
of minute hæmorrhages. In later cases some change in the cells is
found, but as a rule, beyond a slight increase of the intracellular
substance, little or no change is found in the cellular elements of
the brain; but in the region of the surface minute hæmorrhages may
be constantly traced, spreading over the surface of the cortex. In
the cord, sections made in various situations failed to show any very
definite degeneration, and little or no hæmorrhage was observed amongst
the cells of the cord. Hæmorrhages could occasionally be seen on the
surface.

In a number of animals the anterior crural nerves supplying the
paralyzed quadriceps extensor muscles were examined carefully both
for degeneration and for hæmorrhages. Very few degenerated nerve
fibres were found, not more than would be accounted for by the minute
hæmorrhages, which were found passing in between the nerve bundles, and
here and there producing pressure on the nerve bundles themselves.

_Kidney._--In the kidneys minute microscopical hæmorrhages, some of
them quite large, were found in the cortex. The hæmorrhages are diffuse
and irregular, and apparently due here, as in other situations in the
body, to the breaking down of minute venioles rather than arterioles.
In many cases the change is capillary. Parenchymatous nephritis may be
seen, probably resulting from the transudation taking place from the
vessel walls.

The chief view brought out in the histological examination of the
various organs is one of capillary hæmorrhage. This phenomenon is
not peculiar to lead poisoning, but, from the work of Moore of
Liverpool[4], it would seem that all heavy metals, such as bismuth,
mercury, not excepting iron, tend to produce a curious generalized
yielding of the minuter vessel walls. Armit[5] has demonstrated a
similar effect with nickel. The phenomena is, however, typically
associated with lead poisoning, and may, we think, be regarded as the
definite factor of chronic lead poisoning.

For the purposes of controlling the experiments of inhalation, two
other series of experiments were undertaken. In one instance an animal
was fed for two years on white lead; the animal was given 0·1 gramme
per day, and this was increased up to 0·5 gramme, and ultimately 1
gramme. This animal exhibited no symptoms whatever of lead poisoning,
and when it was killed, at the end of the time of experiment, showed
no apparent lesion, with the exception of very marked staining of the
colon and vermiform appendix. This staining of the large intestine
and the appendix, the engorgement of the vessels, particularly of
the omentum and mesentery, the enlargement of the lymphatic glands
in the neighbourhood of the colon, ileo-cæcal valve, and appendix,
suggest the absorption of lead in the upper part of the intestine, and
its discharge or elimination into the large intestine. That lead is
absorbed into the upper part of the intestine was demonstrated in the
following manner:

An animal was anæsthetized, an incision made, and a loop of intestine
pulled up and clamped off, a solution of lead chloride being run into
the loop by means of a hypodermic syringe. The mesenteric vein passing
from this loop of intestine was then carefully secured, a small opening
made in it, and the blood collected drop by drop until some 40 c.c.
had been collected, the time occupied being about three-quarters of an
hour. The blood thus collected was submitted to chemical examination,
and lead was demonstrated to be present. Lead therefore passes direct
from the intestine into the portal circulation.

In only one of the feeding experiments with solid compounds of lead was
any definite symptom of lead poisoning produced, and in this instance
the compound used was dust collected from the flues of a blast-furnace.
This dust was afterwards found to contain a considerable quantity of
arsenic. The experiment cannot therefore be regarded as conclusive.
With the more soluble salts of lead, however, such as the acetate,
lead poisoning may be set up by means of lead administered via the
intestinal canal: 1 gramme of lead acetate administered by means of a
hypodermic syringe through a catheter passed into the stomach of a cat
produced abortion in ten days, and death in three weeks. Four grammes
of acetate produced a similar effect in a dog in four weeks.

PLATE III

[Illustration: FIG. 1.--KIDNEY OF ANIMAL POISONED WITH WHITE LEAD
(INHALATION), SHOWING MICROSCOPICAL HÆMORRHAGES. (STAINED HÆMATOXYLIN
AND EOSIN.) × 250.]

[Illustration: FIG. 2.--KIDNEY OF MAN DYING OF CHRONIC LEAD POISONING.
(STAINED HÆMATOXYLIN AND EOSIN.) × 250.]

[Illustration: FIG. 3.--BRAIN OF YOUNG WOMAN DYING OF ACUTE LEAD
ENCEPHALOPATHY, SHOWING SMALL CEREBRAL HÆMORRHAGES. (STAINED
HÆMATOXYLIN AND EOSIN.) × 250.]

The two following cases, in which both chemical and histological
examination has been carried out on the tissues of persons who had been
employed in occupations which rendered them exposed to absorption of
lead, and who died with symptoms directly suggestive of lead poisoning,
may be added, as they confirm the experimental results given above in
all particulars:

CASE 1.--A woman aged twenty-one, employed in a litho-transfer works,
who died after a short illness during which the chief symptoms were
headache and mental clouding.

At the post-mortem examination no pathological lesions were
discoverable with the exception of a small gland which had become
calcareous, situated near the right bronchus. The brain was injected
over the left cerebral hemisphere, but no hæmorrhages were to be seen
with the naked eye. There were no other pathological signs. A portion
of the brain showing the injection and congestion were submitted to
histological and chemical analysis. Histologically the brain tissue
was found to be normal, with the exception of slight chromatolysis of
some of the larger cells; but interspersed about the whole section
in the slides examined, but more particularly in the area of the
cortex, minute microscopical hæmorrhages were found (see Fig. 3).
Here and there these hæmorrhages were seen related to the expanded
capillaries, all of which showed considerable engorgement with blood.
The arteries and veins themselves were, in addition, considerably
distended. There was no interstitial degeneration of the neuroglia
noticed. A few patches were found which apparently represented old
hæmorrhages undergoing gradual fibroid degeneration. In no case were
the hæmorrhages of a size that could be detected by the naked eye.

Two hundred and fifty grammes of the injected area of the brain were
submitted to chemical examination by the moist process described
in the chapter on Chemical Analysis. The nitric acid filtrate from
the electrolytic deposition gave a well-marked precipitate with
sulphuretted hydrogen, which was filtered off and recognized as lead.
There was only the merest trace of iron present. By colorimetric
estimation the quantity of lead found present in the brain estimated
as Pb was 0·0143 gramme. The quantity found in 250 grammes of brain
substance examined from the injected area was 0·0041 gramme.

CASE 2.--A man who had been employed in an electrical accumulator works
for a considerable time, and who had had a history of several attacks
of lead colic and one of lead paresis affecting both hands.

The man’s work in connection with lead ceased from the time of the
paresis, but some three years subsequently he died with cerebral
hæmorrhage.

Portions of the organs, brain, kidney, liver, and spleen, were examined
histologically, stained in the ordinary way with hæmatoxylin and eosin.
In the brain the same marked microscopical hæmorrhages were observed
as described in the previous case, and in addition many more areas of
old fibroid scars, very minute, but apparently corresponding to earlier
minute hæmorrhages. The kidney showed definite interstitial hæmorrhage
(see Plate III., Fig. 2), as did the liver and spleen.

A portion of the brain was further submitted to chemical examination,
and 0·0014 gramme of lead was determined as present.

The importance of this confirmatory evidence is undoubted, as the
presence of the capillary hæmorrhage existing in the tissues of a
person dying under suspicious circumstances when employed in a lead
process is confirmed by the chemical determination of lead in the
tissues.

The following tables, arranged under three headings, give some of the
experimental results obtained by submitting animals to the effect of
compounds of lead.

Table XI. gives the inoculation experiments.

The materials used in these experiments were those used in the
inhalation and feeding experiments. The experiments are also arranged
in such a manner that each series is a control one of the other.

The amount of substance used for the inoculation gives some rough idea
of the dose required to produce poisoning in an animal; but even this
question of dose in absolute quantities, administered hypodermically,
shows considerable variation in the degree of poisonous effect. The
first animal in Table XI. was inoculated with acetate, this being one
of the more soluble lead compounds, and was given it in three small
doses. The animal received 0·3 gramme per kilogramme of body weight,
whereas in No. 35 2 grammes of washed frit--that is to say, lead glaze
formed by fusing together litharge and silica--actually did produce
symptoms, but of a mild nature. Animal No. 33 only had 0·16 gramme,
being 0·05 gramme per kilogramme of body weight; and this caused acute
symptoms. 0·35 gramme of white lead in a 3·500 kilogramme animal
(No. 31) produced no symptoms at all. In the list of the inoculation
experiments, three animals only exhibited no symptoms--one of these
(No. 31) which was given white lead hypodermically, and Nos. 41 and 42,
which were inoculated with lead silicate or lead frit, which had been
previously treated with acetic acid or water.

Several practical points arise from these experiments, notably with
regard to the frits, as it is seen that a considerable amount of the
toxic properties contained in frit are removed by washing--most by
washing with acetic acid and water, but also to some extent by washing
with hot water alone, showing that in the ordinary production of
lead frit for pottery purposes a certain amount of lead in a soluble
condition as regards the body tissues was still present. This is no
doubt entangled in the true silicates in the forms of oxides, or even
as carbonate. Further, the toxicity of the lead compounds used may
certainly be arranged in the order of their solubility with regard to
the animal tissues, the acetate being the most poisonous, and the frit,
when washed, the least; but unwashed frit, even in relatively small
doses, may produce poisoning. This point is still further emphasized
in Table XIII. Animal No. 42, four months after previous inoculation,
showed no signs of poisoning. Lead nitrate in water was therefore given
in quantities of 0·01 gramme per diem; one month later this animal
developed poisoning.

Table XII. deals with the feeding experiments.

In these experiments acetate was given in one case only, and then
in the form of pills coated with keratin. It is impossible to say,
however, whether the animal ever received any soluble lead, as on one
or two occasions the keratin pills passed right through the animal
without dissolving. On the other hand, feeding with nitrate of lead
in water produced symptoms, but when the nitrate was given in milk no
symptoms appeared. It will be noticed it took a cat four months to
show any signs of poisoning taking 0·1 gramme per day; whereas the
animal receiving subcutaneous doses of 0·16 gramme of acetate showed
paralysis in fifteen days, and in twenty-two days was so ill that it
had to be destroyed under an anæsthetic. The same relationship in
time also obtains in the case of the animals fed on dry white lead.
In practically no instance did definite or severe poisoning follow
the feeding on dry white lead alone, even when quite large quantities
were taken. On reference to the inoculation experiments of Table XI.,
it will be seen that the inoculation of 2 grammes of dry white lead
produced definite symptoms, although the feeding cats had an amount
very largely in excess of this. The only animals fed on white lead or
frit exhibiting signs of lead poisoning were those which were given
alcohol in addition to the lead compound.

A comparison of the results given in Tables XI. and XII. shows that
animals which received lead compounds subcutaneously suffered much more
than the animals which received the lead via the gastro-intestinal
canal, even when the doses given via the mouth were exceedingly large.
It will follow, then, that the actual contact with the more intimate
fluids of the body, rather than the digestive juices, determines the
solubility and general distribution of the lead compound in the body.
This is confirmed by a recent paper by Straub[6].

The animals experimented upon by feeding were kept in the laboratory
under the same conditions as the inhalation animals, but were so
placed that under no circumstance could they obtain any lead dust
by inhalation. These animals were used as control to the breathing
experiments, the substance fed to the animals being in all cases the
same substance as was used for the various inhalation experiments; but
in addition a certain number of the animals were given alcohol, which
are referred to in Table XII. Alcohol was also given to animal No. 6 in
the inhalation series.

The animals fed with lead were fed with the same compound which was
used for the inhalation experiments, 0·4 to 1 gramme being given daily;
so that during the period these animals were exposed to lead dust the
other animals were taking the same compound via the intestinal canal,
but in much larger quantities, and yet they exhibited no signs of lead
poisoning.

TABLE XI.--INOCULATION.

  +----+-------+---------------------------------------------------+
  | No.|       |                                                   |
  | of |       |                                                   |
  |Ani-|       |                                                   |
  |mal.|Weight.|Total Compound used and Quantity.                  |
  +----+-------+---------------------------------------------------+
  |    |  Kgs. |                                                   |
  | 16 | 3·200 |0·91 grm. lead acetate: (1) 0·16; (2) 0·5; (3) 0·25|
  | 25 | 3·350 |Fritted lead: (1) 0·6; (2) 2·0 = 2·6 grms.         |
  | 28 | 3·050 |2 grms. white lead                                 |
  | 31 | 3·450 |0·35 grm. white lead                               |
  | 32 | 2·900 |0·3 grm. frit                                      |
  | 33 | 3·150 |0·16 grm. PbO as acetate                           |
  | 35 | 3·750 |2·0 grms. water-washed frit                        |
  | 40 | 3·050 |1·0 grm. unwashed frit                             |
  | 41 | 3·000 |1·0 grm. acetic acid and water-washed frit         |
  | 42 | 2·800 |1·0 grm. water-washed frit                         |
  | 43 | 2·900 |Lead nitrate in water: 0·01 grm. per diem          |
  +----+-------+---------------------------------------------------+

  +----+--------+---------------------------------------------------+
  | No.| Number |                                                   |
  | of |   of   |                                                   |
  |Ani-| Inocu- |                                                   |
  |mal.|lations.|Date of First Symptoms.                            |
  +----+--------+---------------------------------------------------+
  |    |        |                                                   |
  | 16 |   3    |Forty-fifth day encephalopathy                     |
  | 25 |   2    |Twenty-sixth day slight paralysis of left hind-limb|
  | 28 |   1    |Fourth day aborted                                 |
  | 31 |  --    |No symptoms                                        |
  | 32 |   1    |Eleventh day stiff joint; stepping not normal      |
  | 33 |   1    |Fifteenth day paralysis                            |
  | 35 |   1    |Ninth day aborted                                  |
  | 40 |   1    |Forty-seventh day some muscular weakness           |
  | 41 |   1    |No symptoms                                        |
  | 42 |   1    |No symptoms                                        |
  | 43 |  --    |Thirtieth day encephalopathy                       |
  +----+--------+---------------------------------------------------+

  +----+----------+-------------------+-------------------+
  | No.|          |                   |                   |
  | of |          |                   |                   |
  |Ani-|Duration. |Result.            |Final              |
  |mal.|          |                   |Weight.            |
  +----+----------+-------------------+-------------------+
  |    |          |                   | Kgs.              |
  | 16 | 47 days  |Died               |1·750              |
  | 25 | 26 days  |Killed             |3·200              |
  | 28 | 23 days  |Died               |Weight not affected|
  | 31 |  1 year  |Recovered          |3·300              |
  | 32 | 28 days  |Paralysis; died    |2·400              |
  | 33 | 22 days  |Paralysis; killed  |2·150              |
  | 35 |  1 year  |Recovered, but thin|2·900              |
  | 40 | 58 days  |Died               |2·250              |
  | 41 |  5 months|Recovered          |2·900              |
  | 42 |  4 months|Recovered          |2·950              |
  | 43 |  5 months|Died               |2·100              |
  +----+----------+-------------------+-------------------+

TABLE XII.--FEEDING EXPERIMENTS.

  +-----+-------+---------------------------+-------+------------------+
  | No. |       |                           |       |       First      |
  | of  |       |                           | Other |    Appearance    |
  | Ani-|       |                           |  Sub- |   of Poisoning   |
  | mal.|Weight.|   Compound of Pb used.    |stance.|     Symptoms.    |
  +-----+-------+---------------------------+-------+------------------+
  |     |  Kgs. |                           |       |                  |
  | 2   | 2·750 |0·5 to 0·1 grm. flue dust  |None   |Vomited fifth day;|
  |     |       |(55 per cent. PbO) from    |       |no other symptoms |
  |     |       |blast-furnace flue         |       |                  |
  | 9_a_| 3·500 |0·5 grm. dry white lead    |None   |Vomited fifth day;|
  |     |       |                           |       |no other symptoms |
  |11_a_| 3·850 |0·8 grm.                   |None   |None              |
  |     | 3·900 |After 8 months given       |50 c.c.|1 month           |
  |     |       |alcohol                    |alcohol|                  |
  |     |       |                           |(port  |                  |
  |     |       |                           |wine)  |                  |
  |12   | 3·800 |0·8 grm. dry white lead    |50 c.c.|1 month slight    |
  |     |       |                           |port   |paralysis         |
  |     |       |                           |wine   |                  |
  |13   | 3·400 |0·8 grm. dry white lead    |None   |None              |
  |14   | 3·650 |0·4 grm. low-solubility    |None   |None              |
  |     |       |frit                       |       |                  |
  |     | 3·730 |0·4 grm. low-solubility    |50 c.c.|6 months en-      |
  |     |       |frit and alcohol           |port   |cephalopathy      |
  |     |       |                           |wine   |                  |
  |23   | 4·100 |1 grm. high-solubility     |None   |None              |
  |     |       |glaze                      |       |                  |
  |     | 4·600 |Given lead nitrate, 0·01 to|None   |None              |
  |     |       |0·1 grm.                   |       |                  |
  |24   | 2·900 |1 grm. high-solubility     |None   |None              |
  |     |       |glaze                      |       |                  |
  |46   | 2·150 |0·1 grm. lead nitrate in   |None   |4 months opistho- |
  |     |       |water                      |       |tonus             |
  |47   | 2·100 |0·1 grm. lead nitrate in   |None   |None              |
  |     |       |milk                       |       |                  |
  |49   | 2·500 |2 grs. acetate in keratin  |None   |None              |
  |     |       |pill                       |       |                  |
  |15   | 2·950 |Control no lead            |None   |None              |
  +-----+-------+---------------------------+-------+------------------+

  +-----+---------+--------------------------------------+-------+
  | No. |  Total  |                                      |       |
  | of  |Duration |                                      |       |
  | Ani-|of Exper-|                                      | Final |
  | mal.|  iment. |               Result.                |Weight.|
  +-----+---------+--------------------------------------+-------+
  |     |         |                                      |  Kgs. |
  | 2   |2 months |Recovered                             | 2·000 |
  |     |         |                                      |       |
  |     |         |                                      |       |
  | 9_a_|2 months |--                                    | 3·350 |
  |     |         |                                      |       |
  |11_a_|8 months |--                                    | 3·900 |
  |     |2 months |Died (encephalopathy)                 | 1·500 |
  |     |         |                                      |       |
  |     |         |                                      |       |
  |     |         |                                      |       |
  |12   |38 days  |Died (encephalopathy)                 | 2·250 |
  |     |         |                                      |       |
  |     |         |                                      |       |
  |13   |18 months|Recovered                             | 2·950 |
  |14   |8 months |Given port wine                       | 3·750 |
  |     |         |                                      |       |
  |     |1 year   |Died cerebral symptoms                | 2·600 |
  |     |         |                                      |       |
  |     |         |                                      |       |
  |23   |1 year   |No symptoms                           |4 ·600 |
  |     |         |                                      |       |
  |     |5 months |No symptoms except loss of weight     | 3·450 |
  |     |         |                                      |       |
  |24   |6 months |Recovered                             | 4·350 |
  |     |         |                                      |       |
  |46   |4 months |Died cerebral symptoms                | 3·200 |
  |     |         |                                      |       |
  |47   |4 months |Recovered[A]                          | 2·900 |
  |     |         |                                      |       |
  |49   |3 months |Recovered[A]                          | 2·650 |
  |     |         |                                      |       |
  |15   |1 year   |No symptoms due to confinement in cage| 3·100 |
  +-----+---------+--------------------------------------+-------+

  [A] Increased in weight.

TABLE XIII.--INHALATION EXPERIMENTS.

  +----+-------+----------------------------------+-------+------------+
  | No.|       |                                  |       |            |
  | of |       |         Compound of Lead         |       |            |
  |Ani-|       |       in Dust and Average        |       | Number of  |
  |mal.|Weight.|Quantity in Air during Experiment.|Method.|Inhalations.|
  +----+-------+----------------------------------+-------+------------+
  |    |  Kgs. |                                  |       |            |
  |  1 | 3·000 |0·007 to 0·01 grm. flue dust from |   A   |11 of 1 hour|
  |    |       |blast-furnace flue                |       |            |
  |  2 | 3·580 |0·007 to 0·01 grm. litharge dust  |   A   |12          |
  |    |       |                                  |       |            |
  |  4 | 4·100 |0·001 to 0·007 grm. white lead    |   A   |12          |
  |    |       |dust                              |       |            |
  |  6 | 5·200 |0·001 to 0·007 grm. white lead    |   A   |12          |
  |    |       |(alcohol: 50 c.c. port wine daily |       |            |
  |    |       |in milk)                          |       |            |
  |  7 | 3·000 |0·001 to 0·007 grm. white lead;   |   A   |11          |
  |    |       |no alcohol                        |       |            |
  | 10 | 4·500 |0·0001 to 0·001 grm. white lead   |   B   |40 of 20    |
  |    |       |                                  |       |minutes     |
  | 11 | 3·750 |0·0001 to 0·001 grm. white lead   |   B   |40 of 20    |
  |    |       |                                  |       |minutes     |
  | 21 | 3·900 |0·001 to 0·09 grm. low-solubility |   B   |14 of 1 hour|
  |    |       |glaze                             |       |            |
  | 22 | 3·900 |0·001 to 0·09 grm. low-solubility |   B   |26          |
  |    |       |glaze                             |       |            |
  | 30 | 3·500 |0·001 to 0·09 grm. low-solubility |   B   |14          |
  |    |       |glaze                             |       |            |
  +----+-------+----------------------------------+-------+------------+

  +----+------------+--------+-----------------------+-------+
  | No.|            |        |                       |       |
  | of |   Day of   |  Dura- |                       |       |
  |Ani-|    First   | tion of|                       | Final |
  |mal.|  Symptoms. | Series.|        Result.        |Weight.|
  +----+------------+--------+-----------------------+-------+
  |    |            |        |                       |  Kgs. |
  |  1 |13 days (4  |2 months|Lead poisoning (stopped| 2·200 |
  |    |inhalations)|        |experiment)            |       |
  |  2 |15 days (5  |2 months|Lead poisoning (stopped| 3·000 |
  |    |inhalations)|        |experiment)            |       |
  |  4 |37 days (12 |2 months|Lead poisoning (stopped| 3·030 |
  |    |inhalations)|        |experiment)            |       |
  |  6 |12 days (4  |2 months|Paralysis; died        | 3·650 |
  |    |inhalations)|        |                       |       |
  |    |            |        |                       |       |
  |  7 |30 days (9  |2 months|Paralyzed; killed      | 1·700 |
  |    |inhalations)|        |                       |       |
  | 10 |120 days (30|144 days|Paralyzed; killed      | 3·200 |
  |    |inhalations)|        |                       |       |
  | 11 |120 days (30|144 days|Paralyzed; killed      | 2·750 |
  |    |inhalations)|        |                       |       |
  | 21 |42 days (14 |42 days |Acute pneumonia        | 2·700 |
  |    |inhalations)|        |                       |       |
  | 22 |60          |80 days |Killed; old pneumonia  | 2·500 |
  |    |            |        |                       |       |
  | 30 |45          |45 days |Killed                 | 2·450 |
  |    |            |        |                       |       |
  +----+------------+--------+-----------------------+-------+

The experiments definitely bring out one all-important fact--namely,
that lead dust circulating in the air is many times more dangerous than
lead actually swallowed; for even if the animals which were exposed to
the inhalation of dust swallowed the whole of the quantity contained
in the respired air, they would only obtain one-tenth of the amount
the other fed animals were getting. It is, of course, impossible to
suppose that the whole of the lead contained in the inhaled air reached
the lung. It can only have been the smaller particles which did so.
Therefore the ratio is many more than ten times between the fed and the
inhaling animal; in all probability only one-tenth of the contained
lead in the respired air reaches the lung. Under these circumstances
the ratio of poisoning via the lung to poisoning via the intestinal
canal is as 100 : 1.

Table XIII. deals with the question of inhalation.

Every care was taken during these experiments to avoid any vitiation
of such experiments by the actual swallowing of lead dust by the
animals exposed to breathing. Moreover, all the animals were carefully
controlled, in that an animal of somewhat similar weight at the same
time was subjected to the ingestion of the same lead compound, but in
much bigger quantities, via the mouth.

It will be seen immediately, on comparing Tables XI. and XII. with
Table XIII., that the rate of poisoning by means of dust is greatly in
excess of the rate of poisoning by feeding, even where poisoning by
feeding actually occurred. Also that the amount of dust present in the
air inhaled shows a marked correlation with the date of appearance of
the first symptoms of poisoning, and that where the quantity of dust is
very much reduced the poisoning was delayed longer than might have been
expected, and that when poisoning did appear the symptoms were much
less pronounced than with the more dusty atmospheres; and this although
the quantity of lead obtained would be relatively the same over the
range of time the animals were exposed.

The knowledge gained in dealing with industrial poisoning clinically
receives very strong corroboration from these inhalation experiments,
for it is a well-known fact that many persons engaged in dusty trades
exhibit a species of immunity to lead poisoning. It is true that some
susceptible persons, as has already been pointed out, very rapidly
show signs of poisoning, even with a dosage producing no effect in
other persons working under similar conditions; and it is highly
probable that these persons have arrived at a species of equilibrium by
which they are able to excrete the lead ingested, and so prevent any
accumulation and general damage to their tissues. Directly, however,
the dosage is increased, signs of poisoning come on, as in the case
of animals Nos. 10 and 11. For some seventy to eighty days little or
no sign of poisoning was seen with the small dosage commenced with. At
the end of this time, as no symptoms appeared, the quantity of lead in
the air was increased, with the result that poisoning rapidly became
manifest.

We have also in these inhalation experiments, in Cases 21 and 22,
definite evidence that a low-solubility glaze--that is to say, glaze
containing fritted lead--is capable of setting up lead poisoning when
taken via the lung, as when such glaze is inoculated, although it
produces no such symptoms when given via the mouth, except, perhaps,
when it is complicated by excessive alcohol.


=Symptoms exhibited by Experimental Animals.=--The cat is peculiarly
susceptible to lead poisoning. In lead works it is impossible to keep a
cat any length of time, as it rapidly dies of poisoning.

All the animals subjected to lead absorption, and definitely suffering
from symptoms of lead poisoning, exhibited the following symptoms:

1. Slight increase of weight over the first period of poisoning,
lasting from one to three weeks.

2. A progressive diminution in weight, progressing until the animal
exhibited definite signs of poisoning.

3. Wasting, especially of the spinal muscles (the erector spinæ and in
the lumbar region), out of proportion to the determined loss of weight;
pinched facies, with frequent exhibition of running from the eyes and
nose, even when not exposed to the action of lead dust, merely by
inoculation.

4. Various types of paralysis, particularly in the cat; the muscles of
the back and of the quadriceps extensor of the hind-legs show signs of
paralysis. In the cat the quadriceps extensor is paralyzed sooner than
the extensor communis digitorum in man. The cats show loss of power in
the hind-limbs by inability to jump. The reflexes, particularly the
knee-jerks and elbow-jerks, are first of all increased, and latterly
become lost.

The chief and main sign which was noted in the histological examination
of the animals inoculated was one of minute microscopical hæmorrhages
(this has already been referred to); these hæmorrhages were not
confined to any particular position in the body nor to any one organ.
In the animals which showed symptoms of epilepsy, occasionally
thickening of the pia mater was found, but invariably in such cases
small hæmorrhages were found immediately under the arachnoid, not
covering any great area, but apparently causing pressure upon small
areas of the cortex. In others, again, the hæmorrhages were found
lower down in the brain, and a few in the spinal cord. At times a
large amount of hæmorrhage was to be found present at the base of the
brain, spreading downwards from the medulla into the spinal canal,
but this only occurred in such animals as died with encephalopathic
symptoms. In animals which had signs of more chronic poisoning--that
is to say, gradual loss of body weight, emaciation, constipation,
contraction of the abdomen, and paresis, particularly of the hind-limbs
and the muscles of the back--hæmorrhages were found in the muscles,
liver, spleen, lung, heart, various positions in the abdomen, in the
spinal cord, in the nerve-supply of the affected muscle, and even in
the brain, none of them large enough to produce absolute destruction
of more than a very minute portion of the organ in which they were
situated.

Now, all these symptoms, and, more important still, the phenomena of
hæmorrhage, were found in all the animals which exhibited similar
symptoms, whether they were poisoned by inhalation of dusty lead
compounds or fed upon lead compounds associated with alcohol; but even
in some of the animals which were fed upon lead compounds--particularly
white lead--and which had exhibited no definite symptoms of paralysis,
or, for that matter, any symptom referable to poisoning, here and there
slight histological changes which were referable to minute hæmorrhages.

The experimental work therefore carries us very considerably forward
in correlating the symptomatology and pathology of lead poisoning. The
symptoms produced in susceptible animals by the actual inoculation
of a lead compound differ only in degree and rapidity of onset from
those produced in animals submitted to inhalation with similar
compounds. Feeding, on the other hand--that is, ingestion by way
of the gastro-intestinal canal--even in large quantities, did not
produce poisoning to any great extent, except when some material such
as alcohol was added, thereby breaking down the animal’s resistance.
Another interesting fact is given--that if lead is taken by the mouth
in addition to milk a great deal of the poisonous effect is got rid
of; thus of two animals--Nos. 46 and 47--which received lead nitrate
in their food, the one in water and the other in milk, the one
which received it in milk showed no effects even after four months’
experiment, whereas at the end of four months the animal which was
receiving the compound in its water died. This brings out a point
already insisted upon--namely, that in all lead factories it is highly
important that no work should be undertaken first thing in the morning,
before the workers have had a proper meal, and that in the absence of
a proper meal milk is the best substitute. It is highly probable that
the soluble lead salt becomes united in some form of albuminate which
is dealt with later, and perhaps turned into a sulphide and excreted
without absorption. There is no possible doubt, from the large series
of experiments which I have performed, that lead inhaled is far more
poisonous than when absorbed in any other way; further, that the
amount of poisoning produced differs somewhat according to the type of
compound inhaled, and the experiments, moreover, give some suggestion
as to the dose which is likely to produce poisoning. It is seen, where
the animal is inoculated with white lead, the dose required to produce
symptoms is below 1 gramme per kilogramme of body weight, but above 0·2
gramme per kilogramme of body weight. In feeding, 0·8 gramme, and even
1 gramme, per diem for eighteen months produces no effect, although the
same quantity plus an excess of alcohol rapidly produces the disease.
On the other hand, as small a dose as 0·1 gramme of nitrate of lead
given in water for four months produced death.

Turning to the inhalation experiments, the quantity of dust breathed
when as high as 0·0007 gramme per litre produced symptoms after only
twelve inhalations for a period of about thirty-seven days; whereas
when the dose was reduced to 0·0001 gramme per diem the time required
to produce symptoms of poisoning was 120 days; in fact, this last dose
(0·0001) for the animal under experiment was almost the lower limit, as
this animal showed an almost steady line of weight for a considerable
time, the weight remaining up for the first hundred days, a slight
variation taking place from week to week until a progressive diminution
set in.

Practically all the animals poisoned manifested a very distinct
diminution in body weight; in four only other symptoms of poisoning
appeared first. This is a fact that is often to be noted amongst
lead-workers, and if a progressive diminution in weight takes place,
there is strong reason for supposing that a considerable alteration in
the metabolism of the body has taken place; but it does not follow that
microscopical hæmorrhages or other definite effects of poisoning are
present, although such is probable.

Finally, in summing up the conclusions to be drawn from the above
experiments, it has been suggested that such experiments as
inoculation, experimental inhalation, or even feeding, are no criterion
of the circumstances under which industrial workers become infected
with lead. It is perhaps hardly necessary to refer to this point, but
for the fact that it is possible this book may be made use of by those
who are not in the habit of dealing with experimental pathology. One
of the first and most important matters in dealing with any form of
poisoning is to obtain knowledge of the actual symptoms both clinically
and physiologically, as well as pathologically, of the effects of any
drug, and to determine if the symptoms so produced in an experimental
animal conform to the symptoms as seen in man. For the purpose,
therefore, an animal is required which is susceptible to the poison,
and therefore cats were used in the foregoing experiments, as it is
absolutely impossible to keep a domesticated cat in any white lead
works, for the animals invariably become poisoned by lead.

The second point in prosecuting an inquiry into the pathology of any
disease is to determine the train of poisoning when definite dosage,
both in quantity and compound, is made use of. By feeding an animal
with a compound only, the absorption through the gastro-intestinal
canal could be studied; whereas by inoculating some of the compound--in
suspension if it be insoluble, or in solution if it be soluble--into
the subcutaneous or muscular tissue, the direct action of the
body fluids on the compound may be studied; and, furthermore, its
absorption by the membranes--that is, the cell membranes and the animal
tissues--are determined. It is necessary to give at first a dose big
enough to produce definite symptoms, and then to gradually decrease the
dose to find the minimum amount producing symptoms within a reasonable
amount of time. Inoculation experiments therefore give an answer to a
number of these questions, and are the basis upon which further inquiry
is conducted; they form a criterion from which it is possible to judge
the effect of inhalation, and the same remarks which have been made
with regard to inoculation refer to inhalation experiments. It is
essential first of all, in the experimental animals, to subject them
to rigorous enough conditions to obtain definite symptoms, and then,
by varying the experiments, to study the amount, entrance, and general
behaviour, of the poison, correlating the evidence so obtained from the
definite knowledge already gained with the previous experiments.

It is hoped that this brief note on experimental evidence will assist
in the elucidation of the foregoing experiments to those who are not
conversant with the application of experimental evidence.


=Further Experiments relating to Lead Poisoning amongst Painters.=--A
series of further experiments were made, with particular reference to
lead poisoning exhibited by painters; and as these experiments and
their results could not have been undertaken without the previous
knowledge gained of the pathology of lead poisoning due to the
inhalation of particles of dust floating in the air, their discussion
has been reserved until the previous section had been dealt with.

It has been supposed by some that surfaces painted with lead paint
give off certain emanations containing the metal lead as an organic
compound. As the incidence of lead poisoning amongst painters is
exceedingly high, as far as any statistical evidence can be obtained
(see p. 48), it would seem that the painter is peculiarly exposed to
infection by lead dust; and if, in addition, organic compounds of lead
were given off, he would be still more liable to lead poisoning.

Two methods of experiment were used:

1. The exposure of animals to the fumes given off from freshly painted
surfaces, the paints used being compounded with white lead, lead
sulphate, zinc sulphide, and zinc oxide.

Animals were exposed in a cage similar to that used in the inhalation
experiments previously described, but, instead of blowing in the
contaminated air, the cages were so arranged that boards freshly
painted with the special paint under experiment were introduced into
the cage daily, the animals remaining the whole time in the chamber.
Special precautions were taken with regard to ventilation.

2. An animal was placed in a chamber, and the compound to be tested was
heated electrically by means of a coil surrounding the glass tube in
which the compound was placed. The current was regulated by means of
resistances, so that the thermo-couple and galvanometer gave a constant
reading of 59° C. Air was constantly passed through the tube over the
heated substance and into the animal’s cage, which was efficiently
ventilated. In this way any emanations which were given off from the
normal room temperature or up to 59° C. were carried over into the
animal’s cage, and there breathed. The apparatus was so arranged that
the heating coil extended close to the point of delivery into the cage.

The result of these experiments showed that the animals confined in
cages and exposed to freshly painted surfaces, where the paint used
was white lead, zinc oxide, or lead sulphate, very soon showed signs
of poisoning, and they became emaciated and suffered from recurrent
attacks of salivation. The animals exposed in the cages in which air
was passed over either white lead paste, zinc paste, or lead sulphate
paste, showed no signs of illness, although kept in the cage and
subjected to the inhalation of any fumes which might be given off for
three months, spending the whole of the day in the cage, but being
removed during the night to separate cages.

It therefore seemed clear that, whatever illness was produced in the
animals exposed to fresh paint, they were not suffering from absorption
of lead, but of some other compound of which the paint was made.
Various constituents of the paint were therefore tried--namely, the
metallic bases, lead or zinc, and linseed-oil, with turpentine and lead
acetate mixed with turpentine. The animal exposed to the turpentine
alone very rapidly showed signs of disease--salivation, a tendency to
diarrhœa, strabismus, but the latter only after a two-hour exposure,
whilst the quantity of turpentine present in the cage air did not
exceed 10 milligrammes per litre.

The animal exposed to turpentine and lead acetate exhibited few
symptoms, but the same in kind as the animal exposed to turpentine
alone. The linseed-oil animal showed no signs of disease whatever. The
animals exposed to the metallic bases of the paint--namely, zinc oxide
or white lead--showed no signs of poisoning as long as the compound
itself was not thrown into the air in the form of dust; but when lead
dust was present in the air the animal rapidly showed the ordinary
signs of lead poisoning. The animal exposed to zinc oxide dust showed
very little sign of discomfort, but by prolonged exposure early kidney
disease was produced, and signs of chronic inflammation were detectable
in the lung.

It is interesting to note in this connection that Lehmann[7] describes
symptoms produced in cats when exposed to the vapour of turpentine.
The animals which I exposed to turpentine vapour exhibited the same
symptoms as those described by Lehmann. He gave no result of the
histological inquiry of the animals so exposed, but in no case,
apparently, was the animal killed after exposure. In my animals exposed
to the vapour of turpentine very definite disease of the kidney was
produced, the inflammation tending rather to the tubular than the
interstitial variety of nephritis. The tubules were found blocked with
débris, their contour irregular and destroyed, and their substance pale
and almost hyaline; whilst areas of cloudy swelling, together with
small hæmorrhages, were to be found scattered about the kidney. The
heart muscle was flabby, and the heart tending to dilatation; whilst
microscopically hæmorrhages could be found throughout the organ of a
minute capillary nature, and passing between and disturbing the muscle
bundles.

No changes of any sort were found in the tissues of the animals exposed
to the emanations given off from white lead paste. By analyses these
emanations were found to contain no lead, but traces of aldehyde,
formic acid, and CO₂. It follows, therefore, that the effect of
turpentine when inhaled by the painter must be to act as a contributory
cause of lead poisoning, and it is interesting in this connection to
recall the fact noted on p. 38, that Garrod has described gout as
occurring constantly among painters. The statement already quoted,
that gout is not common among workers in white lead factories, where
the exposure to lead is very much greater than among painters, points
to turpentine as the cause of the increased incidence of gout among
house-painters rather than lead absorption. The importance of dust
containing lead as a source of illness and lead poisoning in painters
must not be minimized, as in sand-papering, etc. (see p. 137). The
importance of lead dust inhaled in this way is perfectly understood. It
is, however, highly probable that the combined action of the turpentine
with the lead accounts for the fact that headache is a common symptom
of early disease in painters, which is not the case among white-lead
workers.


REFERENCES.

  [1] GOADBY, K. W.: Journal of Hygiene, vol. ix., No. 1, 1909.

  [2] GOADBY, K. W., AND GOODBODY: The Lancet, vol. ii., p. 988, 1909.

  [3] GOADBY, K. W.: Report of the Committee on Lead, etc., in
  Potteries, vol. iii., p. 478, 1910.

  [4] MOORE: Private communication.

  [5] ARMIT: Journal of Hygiene, vol. viii., No. 5, 1908.

  [6] STRAUB: Berl. Med. Woch., p. 1469, 1911.

  [7] LEHMANN: Archiv für Hygiene, vol. xxxiv., p. 321, 1899.




CHAPTER VII

SYMPTOMATOLOGY AND DIAGNOSIS


=Acute Poisoning.=--Acute poisoning by lead is not common. Industrially
it hardly ever occurs. Zinn[1] states that, out of 200 cases of
industrial lead poisoning in his clinic in Berlin, only one was to be
regarded as an acute case. In most instances the poisoning is due to
swallowing some compound of lead, either as an abortifacient or to
commit suicide.

The pathology and symptoms of such acute lead poisoning depend in
the first place upon the nature of the salt of lead swallowed, as,
for instance, after swallowing sugar of lead a burning taste is
complained of, with acute gastric pain, generally coming on within an
hour of taking the poison, salivation, metallic taste in the mouth,
acute hiccough, and griping pain in the abdomen. The mouth is stained
a whitish-grey. Later there is a great fall in blood-pressure, the
skin becomes moist, or a cold sweat may appear. The respiration and
pulse drop; finally comes vertigo, acute headache, coldness of the
extremities, anæsthesia, and death in one or two days, or the case
passes on to one of chronic poisoning. If the patient survives for
the first two or three days, retinal changes frequently make their
appearance, and occasionally acute fever may supervene. Various
paralyses also appear, and the case then becomes one of subacute or
chronic poisoning.

The lethal dose for healthy adults is probably as large as 50 grammes
for lead acetate, for lead carbonate 25 grammes; these doses are, of
course, only approximate.

Post mortem in a case of acute lead poisoning by ingestion, the mouth
and stomach show the presence of a lead salt in the mucous exudation,
together with corrosive gastritis and considerable swelling and œdema
of the mucous membrane. The large intestine is generally stained
darkly, from a light brown to a deepish black; this staining may
not appear until quite low down in the intestine. There is hyperæmia
of the liver, much engorgement of the vessels in the mesentery, the
kidney, and the brain. The rest of the intestinal viscera show signs
of engorgement. Fluid may be present in the peritoneal cavity, and
occasionally in the other serous cavities.

The histological examination of the various organs exhibits the
same microscopical hæmorrhages as are found in the cases of chronic
poisoning to be described later.

Although acute lead poisoning is rare in industrial experience, it may
occur from time to time. Several cases are on record where a workman
developed an acute attack of poisoning as a result of immersion in a
white lead beck; another case is described which followed immersion in
a tank of solution of lead acetate.

An accident of this description may conceivably occur; the treatment
of such a case should be energetic, as the poisoning is chiefly due
to lead swallowed. An emetic should be given, followed by sublimed
sulphur, or, better still, the stomach washed out with dilute hydrogen
sulphide water slightly acidulated with sulphuric acid, so as to
change any lead present in the stomach into the least soluble form.
A brisk purge should be given, and the patient encouraged to drink
considerable quantities of lemonade containing sodium or potassium
citrate. Alcohol, even during collapse, should be avoided; a hypodermic
injection of strychnine is preferable. It must be borne in mind that
lead is absorbed in the upper part of the intestine, and only in a
minute degree, if at all, from the stomach; it is re-excreted mainly
by the large bowel and by the urine; to some extent also by the sweat
and saliva. Treatment is therefore directed towards (_a_) forming an
insoluble compound as far as possible; (_b_) promoting the elimination
of the poison; (_c_) placing as little work as possible upon the
tissues most affected. Only milk should be given as food for two to
three days.

The diagnosis of lead poisoning is not in itself of any great
difficulty where any one of the classical symptoms of lead poisoning is
present, such as lead colic, paresis, or the characteristic lead anæmia
or cachexia. On the other hand, the premonitory symptoms of poisoning,
as seen by a club doctor, particularly in persons engaged in industrial
processes, are more difficult to determine; but for the appointed
surgeon, who has an opportunity of watching them from week to week,
the gradual development of anæmia, extensor weakness, and other early
symptoms, should give no difficulty. The clinical diagnosis requires
to be made earlier by the appointed surgeon than by the general
practitioner; for the appointed surgeon’s duty in a white lead works is
not only to treat lead poisoning when it is once established, but, by
carefully noting premonitory signs, to avoid the development of actual
symptoms in susceptible persons. It is convenient, therefore, to divide
the diagnosis of lead poisoning, from the clinical standpoint, into two
divisions--incipient and pronounced. Such incipient changes are for
the most part noticed amongst lead-workers, and in many cases are more
strictly signs of lead absorption than signs of lead poisoning.

The earliest symptoms of poisoning are found in the vascular system,
and the curious pallor of the face in persons who have worked in lead
for a considerable period is often pronounced, although the conjunctiva
may not show such a diminution in colour as might be expected from the
facial change, while the actual determination of hæmoglobin may be
almost normal. In addition to this, a person of fresh colour working in
lead, if susceptible, very quickly loses his florid appearance, often
heightened by the colour of the face only remaining on the cheek-bones
as a hectic flush. Such a person will also show diminution in the
colour of the conjunctival vessels, and invariably a distinct yellowish
appearance of his sclerotics, due to the pigmentation of that tissue by
broken-down blood-pigment. The yellow colour of the eyes is definite
evidence that blood-destruction is in progress.

Following on the anæmia, or, more strictly speaking, the pallor of
the face, a well-marked wasting of the subcutaneous fat takes place.
In animals poisoned with lead in small or large doses--particularly
in small doses given over a considerable period--this wasting of all
subcutaneous and other fat is a very marked feature, so much so that
practically no kidney, mesenteric or abdominal fat is to be found.
The fat is lost in a greater proportion than other body tissues. In
man the infra-orbital fat, together with the fat about the buccinator
muscle, suffers early, and a curious facial contour is produced, two
well-marked folds being seen--one the ordinary naso-labial fold, and
the other situated at the anterior margin of the masseter. This,
together with the loss of the orbital fat, gives the face a curious
pinched appearance. Such a pinched appearance is also to be found in
animals (cats) poisoned by lead. The wasting frequently precedes any
other symptoms, and it is no uncommon thing to find that a man who has
been working in a lead process exposing him to inhalation of dust for
a year is losing weight. In one case a man of 10 stone 7 pounds was
reduced in weight to 9 stone 2 pounds in fourteen months, during the
whole of which time he showed no signs at all of lead poisoning, and
only towards the latter end of the time did he exhibit any blue line
on his gums; there were no symptoms referable to lead poisoning. Such
a case is typically one of lead absorption, which, if continued, would
ultimately result in pronounced anæmia with either colic or paralysis,
probably the former. The man in question was not engaged in any lead
process, but was an electrician attending to the electric light and
motors in a smelting works. His occupation necessitated work above the
general ground-level, and therefore he inhaled the fumes and finer
dust particles detached especially from the arc lamps which required
adjustment.

In many persons who have worked in lead for long periods, wasting
does not progress beyond a certain point, and these persons may be
regarded as having established a certain degree of immunity. Men are
met with who have worked in white lead factories and in smelting
works for periods of from twenty to, in one case, forty-three years,
a considerable portion of such period being antecedent to the time at
which the regulations in force for dust removal and general protection
of the workers were established, and they must have been exposed to
much lead dust. Nevertheless they were less emaciated than many who
have only worked a year or two years in a factory under modern hygienic
conditions and special regulations. Such persons are either immune
from the commencement, or they have established a certain degree
of tolerance towards the metal; the latter supposition is the more
probable, as there is reason to think several of them suffered from a
mild degree of poisoning during the earlier years of their employment.

The rate of development of pallor and wasting are the important facts
in incipient poisoning. Anæmia, together with the presence of basophile
granules in the red cells, in a previously healthy person, and
diminution in the hæmoglobin to 75 per cent., is definite evidence that
absorption is leading on to poisoning--that is, blood-destruction--and
coincidently insidious damage to the finer bloodvessels and their
nerve-supply (see Chapter V.). Such a person may at any moment develop
a sudden attack of colic or paresis.

Associated with the wasting and pallor comes wasting of the muscles
themselves, quite apart from any nerve lesions, and with it a certain
degree of mental lethargy, slowness in comprehension, and loss of
power over individual muscles or groups of muscles, more usually the
latter. The mental lethargy shows itself in many ways--amongst others,
heaviness and drowsiness--and careful examination should be made of any
man who, previously a good time-keeper, commences somewhat suddenly
to be late in the morning. The muscles of the hands and the arms,
may show no definite wasting as compared one with another; but early
loss of power, particularly of the extensors of the wrist or fingers,
may be present for six months to a year before definite wrist-drop
makes its appearance. In two cases under our own observation, loss of
power of the extensor muscles of the wrist was present--in the one
case for eight, and in the other case eleven, months before definite
paresis occurred. In the one case the first symptom of paralysis was
inability to extend the little fingers of both hands; the case was at
once suspended from work, and was given treatment. Within forty-eight
hours both wrists were so far affected that they could not be extended.
In the second case the first symptom of paresis other than the loss
of extensor power was the inability to oppose the thumb to the first
index-finger of the left hand; within seven days complete wrist-drop of
the left hand, partial drop of the right hand, including the middle and
ring fingers, occurred. Both cases made a complete recovery.

By no means all wrists which show weakness of the extensor muscles
ultimately develop paralysis; for, on looking through the records
of the examination of three factories, only 4 per cent. of persons
whose wrists were noted as showing loss of extensor power ultimately
developed definite paralysis. In the extended position of the hands,
when the surgeon is examining for extensor weakness, note should be
made of any tremor, as fine tremor is frequently an early symptom
of ensuing paralysis. The tremor is generally fine, increased on
attempting to perform concerted acts (intention tremor); some loss of
co-ordination may be found.

Where the nerve supplying the muscle has suffered alteration in its
conductivity, as by the occurrence of a small hæmorrhage in its
sheath, gradual diminution in the nutrition of the muscle takes place;
but whether or not this is sufficient explanation for the chronic
wasting which is seen in the hands is not yet definitely proved.

In examining the hands outstretched for tremor and loss of muscular
power, wasting of the interossei may be seen before any definite
evidence of paralysis supervenes. On the palm of the hand both the
thenar and the hypothenar eminences may show flattening, and attention
should always be paid to this portion of the hand, as an early
flattening of the hypothenar eminence particularly is one of the
earlier symptoms of wrist paralysis.


=Constipation.=--Constipation is a well-known precursor of colic in
lead poisoning cases, but is by no means an invariable rule. About 15
per cent. of cases of lead colic suffer from intermittent diarrhœa.

A number of cases (see the table on p. 49) show that “rheumatic”
symptoms are amongst those associated with lead poisoning. Some of
these rheumatic symptoms, as has been explained, may be due to minute
hæmorrhages, in the muscle or elsewhere, setting up the pains of
a rheumatic nature in the part affected. One other symptom occurs
with considerable frequency both as a precursor of colic and as an
associated symptom in constipation, and even in diarrhœa associated
with lead poisoning, and often regarded as of rheumatic origin--namely,
lumbago. Complaints of lumbago in lead-workers should always be
regarded seriously, as they may be a guide in discovering an early
intoxication.

From what has been said of the excretion of lead into the large
intestine in poisoned animals, the symptom of lumbago often complained
of by lead-workers may, in some instances at any rate, owe its origin
to overloading of the large intestine, due to the inhibitory action
of lead on the intestinal muscles. It has been seen that excretion
of lead into the large intestine is the normal method of excretion
of the metal, and that concomitant congestion of the vessels in the
corresponding mesenteric area is an associated symptom in poisoned
animals. Local vasomotor spasm may also contribute.


=The Pulse.=--The pulse in lead poisoning in the incipient stage is
perhaps not so important as when poisoning has become pronounced.
Considerable variation exists amongst different observers with regard
to the blood-pressure of lead-workers. Our experience is, on the whole,
that it tends to be high, and pressures of 150 to 170 mm. Hg are
common. In an average of 100 cases we found the highest pressure to be
178, and the lowest 115, the mean 150.

Collis[2], in a special report on smelting of materials containing
lead, gives the average blood-pressure of 141 smelters as 148·2, and of
38 white lead-workers as 156·5.

Increase of tension undoubtedly takes place as lead absorption
becomes more established, and the well-known high arterial tension of
arterio-sclerosis is to be found in most workers employed in lead for
any considerable period. Even in the cases quoted above showing no
signs of lead poisoning, notwithstanding long duration of employment
in lead factories, there was a distinct increase of arterial tension,
not necessarily attributable to lead alone, but possibly also to such
incidental causes as gout, alcoholism, syphilis, etc. When colic is
present, marked diminution in the pulse-rate may be noticed during
the spasms, and even without the presence of colic a diminution in
the pulse-rate, with a definite increase of tension, as estimated by
the finger, is a matter of practical importance in the diagnosis of
absorption.

In quite early stages the pulse may be increased, and a small, rapid
pulse should be regarded as a suspicious sign. Only in the later stages
of the disease do alterations in the heart-sounds take place.

Sphygmograph tracings of the pulse of lead-poisoned persons shows the
well-marked high tension type.


=Lead Colic.=--Probably the commonest symptom, and the one for which
first and foremost relief is sought, is abdominal colic. The colic of
lead poisoning, when once seen, is rarely mistaken a second time. The
pain is generally referred to the lower portion of the abdomen, low
down, and often the sufferer points to a position immediately above the
pubes; pain may often be referred also to the right iliac fossa, and on
this account the possibility of appendicitis, or even perityphlitis or
chronic colitis, must not be forgotten.

Colic, as shown in the statistics on p. 49, is the chief symptom
complained of. No doubt, as has been previously suggested, the fact
that colic is so common a symptom induced earlier pathologists to
regard the entrance of lead through the gastro-intestinal canal as
being the portal of lead infection. We have, however, demonstrated in
the chapter on Pathology that the absorption of lead, particularly in
industrial processes, is mainly by way of the lung, and in the résumé
of the literature it has already been pointed out that strong evidence
exists for regarding colic and other abdominal symptoms associated with
pain as due to vaso-motor disturbances in the splanchnic and mesenteric
areas.

Lead colic is usually irregular, with marked exacerbations and
remissions, and in the acute form the legs are drawn upwards towards
the abdomen, the body is flexed at the hips, the face anxious and
drawn, whilst the body is covered with a cold sweat, the eyes are
staring, and convulsive movements of the limbs occur. The sufferer
often finds relief from firm pressure upon the abdomen, a point of
considerable importance in diagnosis; the pain is not increased, but
distinctly relieved, by firm pressure.

If the abdomen be digitally examined during a paroxysm of pain, the
intestines will be found contracted under the fingers, often in
an irregular fashion. In an animal acutely poisoned with lead the
intestines are found irregularly contracted during a very large portion
of their length, and when removed from the body have the appearance of
a string of sausages. There is evidence that spasmodic contraction of
the circular fibres of the muscles of the mucosa has taken place, and
the wave of peristalsis, moving forward, meets with a block at these
points of constriction, thereby causing pain.

The colic affecting the lower part of the abdomen may possibly be
related to the excretion of lead into the large intestine, and the
affection of the bloodvessels in the mesentery, and in animals poisoned
by means of lead the vessels in the mesentery, particularly in the
region of the ileo-cæcal valve and the large intestine, are engorged
with blood.

During a paroxysm the patient frequently screams in agony and rolls
about upon the bed or the floor. Temporary relief may be obtained by
leaning upon a pillow placed upon the back of a chair. The relief
afforded by such procedure is also strongly in favour of the vaso-motor
origin of the pain. During the spasm the abdomen is retracted, and
fibrillary twitching of the abdominal parietes may often be seen; a
constant desire to go to stool is generally present, but only results
in straining and, perhaps, the passage of a little mucus and blood.

Vomiting is often associated with this stage, and the patient
frequently vomits a considerable amount of thick, tenacious mucus. The
vomit is not uncommonly regarded by the patient as composed of white
lead, if he has been working in that industry. Tanquerel in 1,217 cases
noted vomiting 400 times, and marked retraction of the abdomen 649
times. Occasionally the patient complains of a sense of great weight in
the abdomen, particularly in the intervals between the spasms of pain.

During the exacerbations of colic very marked diminution in the
pulse-rate takes place, a fact that has already been referred to in the
section dealing with vaso-motor disturbances. The pulse may be as low
as 20 beats per minute, but it varies generally between 40 and 50 per
minute.

Very occasionally the first stage of colic is associated with a slight
rise of temperature. This must be regarded as an intercurrent affection
rather than as one definitely associated with lead poisoning. Probably
in such circumstances a gastritis other than the lead vaso-motor
colic is the reason for the elevation of temperature, but it may
confuse the diagnosis, suggesting rather an acute gastritis than
lead colic. Under normal conditions the temperature falls during the
colic, the extremities are cold, and the body is covered with a moist
perspiration, the temperature dropping to 96°, and even lower.

On palpating the abdomen during these acute exacerbations, it is found
that not only the gastric region, but the whole of the abdomen, is
affected. Occasionally the acute pain is referred to the navel, but
generally to the lower region of the abdomen; and very frequently the
pain is described as running down into the scrotum, whilst there may
also be pain complained of as far as the knee-joint, but this last
is unusual. There may or may not be well-marked peristalsis taking
place, but quite commonly large hardened tumours can be felt in various
situations in the abdomen, corresponding to the contracted intestinal
walls. Shifting tumours, then, may be regarded rather as a diagnostic
sign of the acute forms of lead colic.

The colic rarely commences without some slight prodromal symptoms
of dyspepsia or gastric discomfort; generally for two or three days
preceding the attack there is loss of appetite, with a distaste for
food, and obstinate constipation, particularly a general feeling of
languor associated with an unpleasant taste in the mouth. Tanquerel,
and later Grissolle[3], among others, described a form of stomatitis
which they thought was a prodromal symptom of an attack of lead colic.
Our own experience, however, does not at all coincide with these
statements.

Very occasionally the sufferer from acute colic may die during a
paroxysm due to heart failure, but we have had no experience of such a
fatality, although such an occurrence has been recorded on more than
one occasion.

After the first acute attack of colic, which generally commences
suddenly, often without previous warning, but is as a rule ushered
in by irregular and finally complete constipation, or with diarrhœa
alternating with constipation, the colic still occurs at irregular
intervals; and although the constipation be relieved by enemata or the
use of strong purgatives, paroxysmal pain will recur for days, and even
weeks. In one particular case colic recurred at intervals for eight
weeks, although the bowels were open each day and the patient had been
under regular treatment, whilst the anæmia and other general symptoms
of poisoning had disappeared.

According to the researches of Meillère[4] and others, lead is stored
up in the body in various situations, and is gradually eliminated,
such elimination taking place mainly through the fæces, and only to
a limited extent through the urine. Probably the elimination of lead
through the lower part of the intestine accounts for the recurrent
attacks of colic.

Amino[5], Chatin[6], and Harnack[7], regard this colic as due to
vaso-constriction taking place in the splanchnic area, and the rapid
action of such drugs as atropin, chloroform, and nitroglycerine,
support this view. In fact, Mayer[8] in 1881 demonstrated that in lead
colic the splanchnic vessels undergo well-marked minute inflammatory
changes. Others, from investigations carried on in persons who had
died of lead poisoning, regard the acute pain as set up by irritation
of the sympathetic nervous system, particularly of the solar plexus,
irritation of the nerves in this region presumably setting up reflex
colic.

The inhalation of amyl nitrite during an attack of colic will often
entirely relieve it, and the pulse will immediately rise to the normal
rate. It is difficult, however, in observing a case of colic, to
determine whether the colic is preceded by slowing of the pulse and the
rise of blood-pressure, or whether the colic is the immediate exciting
cause of the constriction of the vessels and the alteration of the
pulse-rate.


=Chronic Colic.=--The acute form of lead colic frequently passes on
to a chronic condition; the attacks become much less intense, and may
at times only amount to general discomfort in the abdomen, but the
symptoms may last for several weeks, and even months, with no abdominal
discomfort for a period of a week or ten days, then recurrence of pain,
gradually increasing until it has attained a considerable degree of
intensity, and then passing away, only to reappear in two or three
days’ time. In such cases of prolonged colic after an interval of two
or three weeks, small doses of strychnine or tincture of nux vomica
will determine the onset of an attack of colic, showing that the
intestinal muscular tissue remains in a state of hypersensibility long
after the attack appears to have passed away.

A particular form of colic of long duration with exacerbations and
remissions has been known for many years in the French navy, called
“seamen’s colic.” Before this time outbreaks had occurred in various
parts of the world, and John Hunter[9] described a form of _dry
bellyache_ occasioned by drinking certain West Indian wines, the wines
in question having been stored in contact with lead--in fact, the
vigorous Saxon of John Hunter peculiarly describes this chronic form of
lead colic.

Although the prodromal stages of malaise, lassitude, loss of appetite,
nausea, etc., generally precede both the acute and the chronic forms,
colic often commences suddenly. Men may be examined in the factory in
the morning, when the ordinary routine examination has elicited no
symptoms, and yet cases of acute colic have occurred later in the same
day in the very men examined.

The chief points associated with lead colic are--

1. The intermittent character.

2. The relation of the colic mainly to the lower part of the abdomen.

3. The slowing of the pulse.

4. The relief afforded by firm pressure on the abdomen.

To which may be added the action of amyl nitrite and other drugs of a
similar physiological action.


=Headache.=--Persistent headache is another of the symptoms associated
with lead poisoning, but it is not common as an early symptom. The
headache complained of by painters is probably not due to lead
poisoning, but, as has been suggested, to turpentine. The headache of
lead poisoning is invariably a later symptom, and frequently follows
an attack of colic a week or more after the abdominal pain has ceased.
The position of the headache varies; it may be of the vertex type,
almost entirely confined to the vertex and occipital regions. On the
other hand, it is frequently irregular, and neuralgic in type; but
in this type, frontal and temporal, more particularly temporal, the
patient describes the pain as if a blunt instrument were being pushed
through his head from both temporal regions at the same time. Earache,
or pain in the region of the petrous portion of the temporal bone, may
at times suggest ear disease, but this situation is not so common as
suboccipital or temporal pain.

The headache in these situations is no doubt associated with the
meningeal artery in the temporal region, and with the sinuses in
the occipital region. The headache, not unlike the colic, undergoes
remissions and exacerbations. With the exacerbations vertigo is common,
and on more than one occasion in our experience a person suffering
from persistent lead headache and vertigo has been arrested as suspect
of alcoholism. Headache and vertigo without either colic or paresis
is by no means uncommon, and may be associated with pains in the arms
and legs. These pains are generally referred to by the patient as
rheumatic, and it is a little interesting to call to mind the number of
instances in which rheumatic symptoms are returned as associated with
lead poisoning in the statistics given on p. 48. It is probable that
these pains are neither muscular nor purely nervous in origin, but are
primarily due to small lesions of the bloodvessels, as described in
the chapter on Pathology, occurring in various parts of the body, and
thereby setting up localized irritation, too minute to form an area
which can be discovered by palpation, but sufficiently pronounced to
produce irritation and reflex pain, in some respects similar to “bends”
in compressed air disease. This special type of rheumatic pain differs,
of course, from the lumbago associated with constipation.

Persistent headache is an exceedingly grave feature, and although
it may at times disappear quickly on treatment, mental clouding
and alteration of the higher functions is always to be feared;
not infrequently persistent headache ushers in a final and fatal
encephalopathy. In such a case the headache persists, becomes more and
more excruciating, the patient rapidly shows loss of mental power, and
may gradually sink into a condition of delirium. On the other hand,
an attack of acute delirium may suddenly supervene, commencing with
sudden loss of consciousness, followed by irregular movements of all
the limbs, frothing at the mouth and nose, and finally mania. Recovery
is by no means uncommon, and after a sudden attack of this description
the patients are entirely ignorant of the whole circumstance; they
may occasionally recover powers of locomotion, and wander to long
distances, unable to give an account of themselves or to remember their
names, and only after a considerable time recover consciousness of
their identity; but this type of case is comparatively rare.

The case quoted by Mott[10] gives a typical history of mental affection
due, no doubt, to lead, but partially complicated by alcohol.


=The Burtonian Line.=--Much controversy has raged around the
significance of the blue line on the gums to be seen in certain persons
working in lead, as to whether this particularly well-marked sign is to
be regarded as a diagnostic symptom of lead poisoning or not.

For a long time it was regarded, and by many is still regarded, as
sufficient evidence in itself to determine that a person is suffering
from lead poisoning. On the other hand, those who have had considerable
experience of industrial lead poisoning, particularly in the routine
examination of workmen occupied in various lead industries, do not
regard the occurrence of the Burtonian line as of more value than
that the person showing such pigmented gums has been exposed to lead
absorption.

There are two kinds of Burtonian line:

1. A fine bluish line is seen around the gingival margins, more
pronounced on the interdental papillæ of the gum, and always more
marked around such teeth as are coated with a deposit of tartar
than around teeth which are clean. This line is undoubtedly due to
the decomposition of the lead salts which have gained access to the
mouth, by the sulphuretted hydrogen produced by the decomposition and
putrefaction of food, epithelial débris, and other materials, which
have accumulated around the edges of the teeth and in the interdental
spaces. Peculiar evidence of this may often be seen in the mouths of
certain persons whose parotid glands are discharging saliva which
promotes deposits of calculus. Thus, one may often find merely the two
first upper molar teeth on both sides of the upper jaw coated with
tartar, no other teeth in the upper jaw being similarly affected. This
deposit of calcium phosphate and carbonate is exceedingly porous,
and becomes saturated with the products of decomposition, evolving
sulphuretted hydrogen in fairly large quantities. In the mouths of
such persons working in lead factories a dark bluish staining of the
cheek in apposition to the filthy tooth may be frequently seen, and
where the rest of the teeth are free from deposit no such staining
is observable. Viewed with a hand-lens, the blue line is seen to be
made up of a large number of minute granules of dark colour which are
deposited, often deeply, in the tissue. It is a matter of importance to
note that a blue line is rarely seen in the mouths of those persons who
pay attention to dental hygiene; where the teeth are clean, the gums
closely adherent to the teeth, and entire absence of pus and freedom
from deposit we have never seen a Burtonian line produced. Many of the
so-called healthy mouths with _perfect teeth_ have yet _infected gums_.

On examining sections of such a line, it is interesting to note that
at first sight the particles appear to be situated deeply in the
tissue, and mainly in relation to the bloodvessels supplying the
gum. A little closer attention shows that the particles are really
aggregated, particularly in the deficiencies between the epithelial
cells which are constantly thrown off from the surface of the gum, a
process which has its origin in an inflammatory condition, the whole
gum becoming hypertrophied, with numerous small areas of ulceration. In
these positions a certain amount of direct absorption of dust and fine
particles takes place from the ulcerated surface, and becomes converted
into lead sulphide by the sulphuretted hydrogen produced locally from
the decomposing tissue. A certain amount of pigmentation is also
referable to the mucous glands. It is well known that, in infections
of the mouth of the type of pyorrhœa alveolaris or of rarefaction
of the alveolar process, a good deal of infection coexists in the
mucous glands of the buccal membrane, especially along the gum margins
themselves, and the lead dust also becomes deposited in these glands,
and later forms a sulphide. It is possible that some blue lines are due
to excretion of lead from the blood.

Some little care is required to differentiate between the early lead
Burtonian line and the curious bluish-grey appearance of the gum edges
in cases of pyorrhœa alveolaris; when once the two conditions have
been studied, little difficulty exists, but the use of a hand-lens
will at once settle the matter. The bluish appearance of the gum in
many cases of gum disease is due to local cyanosis. A few other forms
of pigmentation of the gum edges exist, such as an occasional blue
line seen in workers with mercury, a black line in coal-miners, and so
on, but these hardly call for discussion in the present instance. Any
pigmentation of the nature discussed above is to be regarded as a sign
that the worker has been subjected to the inhalation of lead dust, and
is therefore suspect of lead absorption, in whom definite symptoms of
lead poisoning may be expected to occur if the exposure to the harmful
influence be long-continued.

2. In the second variety of blue line the pigmentation is not confined
to the gum edge or to a band rarely exceeding a millimetre in width,
as is the ordinary common blue line. In this case the whole of the
gingival mucous membrane from the edges of the teeth, and extending
some way into the buccal sulcus, five or six millimetres or even a
centimetre wide, may be seen.

When this phenomenon is present, it is always associated with a marked
degree of pyorrhœa alveolaris, the gums are soft, œdematous, and pus
oozes from their edges, the teeth are frequently loose, and the other
symptoms of disease of the os marginum are present.

Sections made from such a case suggest still more that some excretion
of lead has taken place from the bloodvessels, as the lead particles
may be seen closely related to the capillaries; but here again there is
little doubt that it is due to absorption from the externally inflamed
surfaces of the gum rather than excretion of the vessels themselves.
It is interesting to note that, in all the experimental animals, in no
instance has any Burtonian line been observed, although the animals
(cats and dogs) have been fed upon cat’s meat, which readily undergoes
putrefaction, and organisms capable of producing sulphuretted hydrogen
are invariably present in the mouths of such animals. Notwithstanding
this, the blue line has not been observed, because the animals’ gums
were entirely free from infection or pathological changes. By causing
an artificial inflammation around the canine teeth of an animal exposed
to lead infection, a definite blue line was produced in two weeks. This
line had all the characteristics of the common Burtonian line.

This form of blue line with a deep pigmentation of the whole of the
gums, although in itself not to be regarded as diagnostic of lead
poisoning alone, rarely occurs unless the person has been subjected to
such long-continued poisoning that other symptoms have already made
their appearance.

The blue line, then, whichever type is observed, cannot in our opinion
be regarded as a diagnostic sign of lead poisoning, but is merely an
indication that the person who exhibits the phenomenon has been at some
time or other subjected to lead absorption.

There is no evidence to show that lead is excreted by the salivary
glands. A number of cases of poisoning certainly complain of a metallic
taste in the mouth, and, judging from the analogy of mercury, it is
possible that excretion of small quantities of lead may take place
through the saliva; but such a point is merely of scientific interest,
and has no practical bearing on the question of lead poisoning.
Pigmentation in the salivary glands suggesting excretion of lead has
not been observed, notwithstanding the constant presence of potassium
sulphocyanide in the parotid saliva. The blue line of Burton may
occasionally be observed, in other regions of the body. From time to
time the intestine is found stained with a bluish-black deposit of lead
sulphide, and in a case of acute poisoning following the ingestion
of a large quantity of lead acetate, and in the cases described by
Oliver of the ingestion of lead oxide (litharge), black staining of
the intestines was peculiarly well marked. In all the animals referred
to it forms a constant feature in the large intestine, and in the
chapter on Pathology this blue staining of the large intestine is
more minutely described. We have met with it once in the post-mortem
examination of a man who died of lead poisoning, and when found it may,
we think, be regarded as a diagnostic sign. Macroscopical evidence is
not sufficient; it is necessary to make a histological examination of
the tissues, when the stained areas are seen to be associated with
the lymphoid tissue in the intestinal wall, and not only interstitial
portions, but actually the interior of the cells themselves, are found
to be packed with small bluish granules. Such a histological finding
would be highly characteristic of an extreme case of lead poisoning.

Where considerable quantities of lead have been taken into the
gastro-intestinal canal, a blue ring has occasionally been described
surrounding the anus.

About 85 per cent. of cases of lead poisoning with colic show obstinate
constipation as a leading symptom. The constipation generally exists
for several days preceding the onset of the colic, and may persist
for as long as twelve to fourteen days, while six to seven days is a
common period. There is very little that is characteristic about the
constipation other than its intractability; indeed, it is frequently of
the greatest difficulty to relieve this symptom. No doubt the direct
origin is due to the excretion of lead into the large intestine (see p.
94).

Palpation of the colon often shows distension, with a good deal of
pain on pressure at both the hepatic and splanchnic flexures, more
particularly the latter. Distinctly painful spots may be found in the
length of the intestine, due to small ulcers, or more probably to the
minute hæmorrhages which we have elsewhere described as associated with
lead poisoning. The remaining 15 per cent. of cases have as a prodromal
symptom diarrhœa. Further, diarrhœa is not uncommon amongst persons
who are working in a lead factory, and who do not show other signs of
poisoning; and as lead taken into the body in various ways is excreted
through the fæces in common with other heavy metals, such as iron,
bismuth, nickel, as well as arsenic, the occurrence of diarrhœa should
suggest to the surgeon the possibility of considerable lead absorption
having taken place.


REFERENCES.

  [1] ZINN: Berl. Klin. Woch., No. 50, 1899.

  [2] COLLIS, E. L.: Special Report on Dangerous or Injurious Processes
  in the Smelting of Materials containing Lead, p. 6. 1910.

  [3] GRISSOLLE: Thèse, Paris, 1835.

  [4] MEILLÈRE, G.: Le Saturnisme, p. 122. Paris, 1903.

  [5] AMINO: Archiv. Ital. di Clin. Med., 1893.

  [6] CHATIN: Province Méd., Lyon, No. 4, 1892.

  [7] HARNACK: Deutsch. Med. Woch., 1897.

  [8] MAYER: Virchow’s Archiv, 1881.

  [9] HUNTER, JOHN: Observations of the Diseases of the Army in
  Jamaica. London, 1788.

  [10] MOTT, F.: Archives of Neurology and Psychiatry, vol. iv., p. 117.




CHAPTER VIII

EXCRETION OF LEAD


=Symptomatology and Diagnosis= (_Continued_)--=Excretion of Lead.=--The
two chief channels for excretion of lead are the urine and the fæces,
while some include the saliva and the sweat.

In the case of the sweat there is not much evidence, but a few
observers, mainly French, claim to have discovered traces of lead in
the skin of lead-workers. In such a case, however, it is exceedingly
difficult to eliminate the question of surface contamination; and
although brisk peripheral circulation and transudation may possibly
carry off a certain amount of lead, the chance of this is highly
improbable.

There seems rather more evidence that the salivary glands may eliminate
lead, as a number of other substances are undoubtedly passed in this
way. Mercury certainly undergoes excretion through the salivary
glands and the mucous glands of the mouth, and it is therefore not
improbable that a metal so closely related in its chemical, and
perhaps physiological, relations may be excreted in a similar fashion.
Meillère[1] cites three instances of parotitis which were considered to
be of lead origin, and further quotes an instance where, in chemical
examination of the salivary glands after death, lead was found in small
quantities.

Chronic parotitis is not infrequently cited as a symptom in cases
of reported industrial lead poisoning, and may owe its origin to
impairment of the salivary gland by the passage of the metal. Chronic
parotitis, or even tenderness of the parotid glands, does not occur
frequently among lead-workers with symptoms of lead absorption.
Excretion, however, of lead through the salivary glands is not of
great importance, except from the occasional complaint of a metallic
taste in the mouth in chronic lead poisoning, and in such instances
possibly definite excretion of lead is taking place through the parotid
glands. A case may be cited which rather supports the view that lead
may be excreted through the salivary glands. A certain worker engaged
in a dangerous lead process from time to time, but never as a constant
symptom, showed distinct pigmentation in the internal surfaces of
both cheeks in the region of the buccal papillæ of the parotid duct.
The pigmentation was intermittent; at times a large patch of deep
blue-black pigmentation was found in the situation on both sides,
with no staining of the cheeks around or of the gum margins, although
his teeth in these regions were coated with foul tartar. If the lead
in this instance gained access through the mouth, why should it have
been deposited merely upon the cheek in this one situation, despite
the fact that several other situations in the mouth exhibited the
same conditions of bacterial decomposition for the production of
sulphuretted hydrogen? We have not observed this pigmentation in the
neighbourhood of the ducts of the submaxillary and sublingual glands,
but only in the parotid.

By far the most important organ in the excretion of lead, from the
point of view of symptomatology and diagnosis, is the kidney. Lead is
not uncommonly found in the urine of lead-workers and in the urine of
those suffering from lead poisoning. The quantity present is usually
small and in a form in which it is exceedingly difficult to detect.
Yet very pronounced changes in the kidneys may take place, with little
evidence in the urine itself that pathological changes are taking place.

The urine of workers in lead factories is frequently high-coloured; in
fact, as a general rule the degree of pigmentation is greater than is
normal, and in those persons who show some degree of icterus, with the
curious yellowish-brown colour of the conjunctivæ, hæmatoporphyrin may
be detected on applying suitable tests.

In well-established cases of chronic poisoning, albuminuria as a rule
is found, together with certain alterations in the other constituents
of the urine, such alteration frequently making its appearance before
the definite onset of albuminuria. Further, the changes in the eye,
referred to under a special heading, have been frequently described as
albuminuric retinitis of lead origin, it being true that eye changes
are often associated with chronic changes in the kidney.

In acute poisoning lead is generally found in the urine, but in chronic
poisoning it is by no means a common occurrence. From time to time
small quantities are excreted, and in the chemical analysis made of
the kidneys in cases of fatal lead poisoning a certain amount of lead
has frequently been noted. Wynter Blyth[2] found in the kidneys of two
white lead workers a total of 0·003 gramme. Peyrusson and Pillault[3],
quoted by Meillère, found a similar quantity, 0·003 gramme, while in
experimental animals Meillère himself found considerably less, only
0·0001 gramme; Stevenson, in a case reported by Newton Pitt[4], 0·0086
per cent. of lead in the cæcum and colon. Notwithstanding a small
quantity of lead which may be determined by chemical methods as present
in the urine or the kidney, very definite nephritis is set up in these
organs, obviously due to the irritative effect of the metallic poison.


=The Kidneys.=--Kidney disease of several types has been described
as associated with poisoning by lead, particularly with chronic lead
poisoning, where large quantities of a soluble lead salt have been
ingested. Very considerable strain is thrown upon the kidney, with the
result that the lead salts themselves are passed through; but, as has
been pointed out when dealing with acute poisoning, the passage of lead
through the kidneys does not continue for any considerable time, and in
lead poisoning of an industrial and chronic nature no lead at all has
been found in the urine in undoubted cases. Even when present, it may
be difficult to detect unless the electrolytic method is used (see p.
174). At the same time kidney disease undoubtedly does occur in a very
large number of workers.

All heavy metals, of which silver, mercury, iron, zinc, and finally
lead, may be quoted as examples, appear to be eliminated by the kidney
when they are present in the body in toxic doses, and often when in
small non-toxic doses, but in the latter case to a greater extent
through the bowel than through the kidney. The lead circulating in the
blood, in common with other heavy metals, may be found chemically in
the kidney, but the quantity recovered is not as large as one would
expect from the considerable amount of inflammation often present.

In the experiments on animals, subjected to poisoning over considerable
periods, the condition of the kidney in every instance showed distinct
histological changes; and the longer such animals had been subjected
to the poisonous effects of the metal, the more advanced were the
signs of degeneration in its structure. In the earliest cases the
disease partook much more of the nature of an interstitial nephritis,
and it was in the later and more chronic stages only that changes
in the glomeruli and fibroid degeneration were to be found, but in
even these earliest cases of poisoning definite minute interstitial
hæmorrhages were to be found scattered about the kidney. These minute
hæmorrhages did not cause symptoms of hæmaturia, as in none of the
experimental animals was bloody urine observed. On the other hand,
besides definite small areas of hæmorrhage, patches were discoverable,
indicative of hæmorrhage which had undergone fibroid change. Even in
the illustrations given by Glibert[5], there appears to be evidence
that hæmorrhage had taken place and had undergone fibroid degeneration,
and there is very little doubt that in cases of kidney disease, the
preliminary action of the poison determines small local yieldings
of the vessel walls, with leakage, often hardly amounting to true
hæmorrhage, at such spots. There is nothing opposed to the theory in
the findings of other observers; in fact, if the preliminary gross
effect be leakage of the description given, all the other lesions
described by various observers follow as a corollary.

In the kidney, as in the other regions of the body, the venioles rather
than the arterioles appear to be the preliminary site of destruction,
and microscopical observation of the sections leads to the view that
the intima of the vessels and not the media or the muscular coat is
the one affected in the first place. Capillary hæmorrhages under
these conditions are easier to understand than if the arterioles
themselves or their muscular or middle coats were primarily affected.
As degenerative changes progress, the whole of the vessel--external and
middle coats and intima--undergoes change, ultimately resulting in the
extreme narrowing and consequent blocking of the vessels themselves.
Further shrinkage taking place in this area produces the shrunken
sclerosed kidney.

Zinc in the form of oxide behaves in very much the same way upon the
kidney as does lead. An experimental animal, which was given 0·2 gramme
of zinc oxide per kilogramme body weight by hypodermic injection in
the muscles of the back, died in fifteen days, and the kidneys showed
extensive hæmorrhages--not merely the minute and capillary hæmorrhages
found in lead poisoning, but hæmorrhages extending right through from
the cortex.

Clinically, kidney disease, unless albumin be detected in the urine,
is not a prominent symptom during the progress of an attack of chronic
lead poisoning, and is to be regarded as a late symptom, developing as
the result of long-continued irritation. The difficulty of eliminating
alcoholic complication has been discussed, and there are no specific
symptoms or post-mortem signs which enable one to distinguish alcoholic
nephritis from the nephritis of lead poisoning.

In the chapter on Pathology, the effect of alcohol on the kidney was
cited as a common predisposing cause of kidney disease in lead-workers,
and the effect of alcoholic excess in the case of a person who is
already the subject of chronic lead absorption may determine the change
from absorption to definite poisoning, because of alteration in the
excreting-power of the kidney. So long as the ratio between ingestion
and excretion is maintained the balance is kept up, and, although the
tissues of the body may show signs of a certain amount of degeneration,
no definite disease is produced; but the gastric irritation and the
work thrown upon the kidney in removing from the blood large quantities
of alcohol may be sufficient to alter this absorption-excretory balance
and determine the attack of poisoning.

Acute nephritis is rare, and cannot be regarded as a sequela of chronic
lead poisoning. Acute nephritis occurring in a lead-worker, with the
associated symptoms of general œdema of the face, eyes, hands, feet,
is of the gravest possible moment, and such a sudden appearance of
nephritis is almost invariably fatal. In chronic nephritis, to which
most of the lead cases belong, the usual signs are to be found in
the urine. Pain is rarely a symptom; and although pain in the back
is often complained of by lead-workers, examination rarely suggests
that the backache is of kidney origin, but rather the lumbago type
associated with chronic constipation. Care, however, must be taken,
when backache is complained of, in eliminating kidney disease as a
possible origin of the pain. A quantitative examination of the urine,
with reference to the total acidity and phosphate excretion, may
assist; and although this is not possible in a routine examination
of cases of lead absorption, it may be useful in cases of suspected
poisoning, especially where there are evidences of a good deal of
blood-destruction.

For convenience of description, it is better to consider the action of
lead upon the blood under two headings:

1. That of the corpuscular and other changes.

2. The action on the vessel walls, and pathological changes secondary
to disease of the vessels.


=The Anæmia of Lead Poisoning and Saturnine Anæmia.=--From the early
days of medicine it has been known that lead produces poverty of the
blood, and the white or yellowish-white appearance of persons who have
been subjected to long-continued inhalation of lead dust or fumes
constitutes striking evidence of blood-alteration. At the same time
it is a common fact that the facial pallor does not always go hand in
hand with diminution in the hæmoglobin. The conjunctiva may be observed
as a test for colour, and here may be seen the curious vaso-motor
disturbances which are partially responsible for the facial pallor.

Facial pallor in some forms of lead cachexia owes its origin to
interference with the nerve-supply to the vessel walls, and it is
a noticeable fact that a lead-worker whose face shows unmistakable
signs of pallor rapidly flushes when spoken to suddenly or if mentally
disturbed. The anæmia of lead poisoning is, however, a very definite
fact. All observers are agreed that a marked diminution in the
hæmoglobin of the blood takes place, to as low, often, as 35 per cent.,
without necessitating abstention from work, and without any serious
interference with respiration, even when performing heavy manual labour.

In persons in whom the hæmoglobin is diminished there is frequently a
yellowish or icterous hue of the skin, particularly the conjunctiva,
due to staining of the tissues with altered blood-pigment. The
hæmoglobin derivative--hæmatoporphyrin--can also be found in the
urine of persons suffering from a marked degree of reduction in the
blood-pigment, and may be taken as confirmatory evidence of destructive
or hæmolytic anæmia. The symptom is, however, a later one than is
frequently stated by the French observers, and can only be regarded as
a later and confirmatory symptom, and not as an early one of diagnostic
importance.

As would be expected from the destruction of blood-pigment, the
morbid process leaves its imprint upon the individual red cells, and
basophile staining of a number of the red corpuscles is to be found in
a very large proportion of persons poisoned by lead. Moritz[6] first
pointed out that these alterations in the red cells were present in
lead poisoning. The basophile granules are by no means confined to
lead anæmia, but are to be found in any severe secondary anæmia where
hæmolysis has taken place, as in nitrobenzene and aniline poisoning,
carbon bisulphide, etc. In addition to the basophile-staining granules
in the blood-cells, the whole corpuscle may take on a bluish-grey tint
when stained. The best stain to demonstrate these bodies is Leishman’s
modification of Romanowski’s, and there is no occasion to stain the
blood in the fresh condition, as the presence of the granules may be
demonstrated easily, even after two or three months. Schmidt[7] thinks
that if the basophile corpuscles reach 100 per million red cells the
cause is undoubtedly lead poisoning.

Alterations are also to be observed in the structure of the red
blood-cells in addition to the basophile staining. Distinct vacuoles
appear, but as a general observation--first noted by Glibert[8]--the
blood appears to be more resistant to damage when making the films,
and the red corpuscles themselves seem to be more elastic than normal
(increased viscosity). Alteration in the shapes of the corpuscles also
takes place, and not only small varieties--microcytes--but also the
large macrocytes are to be found. Nucleated red cells are rare.

The diminution in the number of the red cells is not so pronounced as
would be supposed from the diminution in the quantity of hæmoglobin;
but in the later stages, as in other secondary anæmias of toxic origin,
the total quantity of red cells sinks to a count of a million or less
per cubic millimetre.

According to Garrod, etc., the alkalinity of the blood is decreased in
lead absorption.

The white blood-corpuscles do not show any change in their structure
by the ordinary methods of staining, but they apparently show, as do
the red cells, more resistance to injury in spreading blood-films--that
is to say, the viscosity of the blood, which is apparently increased
in lead poisoning, is also exhibited by the white cells. In the
early stages of lead poisoning, more especially in acute lead
poisoning, distinct leucocytosis may be observed, such a leucocytosis
showing itself rather in relation to the lymphocytes than to the
polymorphonuclear cells. In addition, the large mononuclear cells are
also greatly increased, and a differential blood-count from a case of
lead poisoning which also shows the presence of basophile granules
in the cells invariably brings to light a definite increase in the
percentage number of lymphocytes, and a decrease in the number of
polymorphonuclears, and this even when the total leucocyte count is
not outside the ordinary limit of normal variation. On the whole, the
number of leucocytes present in the blood of persons suffering from
lead absorption will always be found to tend rather towards the higher
than the lower limit of normal variation.

At times a considerable increase in the number of eosinophile cells
is found in films made from persons suffering from lead poisoning,
particularly when there has been prolonged obstinate constipation. The
count is never high, and is rarely more than 5 or 6 per cent. It is not
usual to find any of the other forms of white cells in the blood, and
in this way the anæmia of lead poisoning may be easily differentiated
from the other forms, such as pernicious anæmia, lymphatic leucæmia,
spleno-medullary lymphocythæmia. By examining a number of blood-films
derived from persons subjected to lead absorption, and shuffled with a
number of films from normal persons, one of us (K. W. G.) has been able
to separate out, by the above method, the blood-films taken from the
suspected persons. The criteria in the determination were--

1. The presence of basophile granules.

2. Total basophile staining and size of corpuscles--poikilocytosis.

3. Differential count, showing increase in a number of lymphocytes and
large mononuclear cells.

Determination of the presence of lead poisoning from the examination of
the blood, therefore, receives considerable support; but at the same
time it is open to some objection from the fact that it is not in lead
poisoning alone that basophile granules make their appearance in the
blood. Any cause producing destruction of the red blood-cells, and even
their depletion by prolonged hæmorrhage, is followed by an increase in
the output of the red cells from the bone-marrow[9]. During this output
of extra blood-cells from the bone-marrow, numerous cells gain entrance
to the blood, in which the nuclei are not entirely degenerated; and
it is these particular cells which give the phenomena of basophile
staining, and their presence is rather indicative of the increased
blood-formation that is progressing, following blood-destruction,
rather than direct evidence of blood-destruction itself.

In a number of forms of anæmia--in fact, in almost all forms of severe
secondary anæmia, and certainly all forms of anæmia associated with
hæmolysis--the presence of basophile granules may be demonstrated.
They are commonly found in pernicious anæmia, secondary septic anæmia,
and the anæmia of malaria. Practically, the use of basophile granules
in the presence of the blood of lead-workers is being utilized in
Leipzig for the early detection of lead poisoning. By means of the
Zeiss eyepiece enumeration disc the relative number of basophile
granule cells to normal red cells is determined; and when the number
of red cells containing basophile granules exceeds 100 per million red
cells, the individual from whom the blood is derived is regarded as in
a presaturnine condition, and given proper treatment. By this means
it has been found possible to diminish the number of persons actually
suffering from lead poisoning.

The adoption of such a method has some drawbacks, especially in view of
the fact that substances other than lead may cause the basophilia. At
the same time there is no doubt that, if all persons employed in lead
trades who showed basophilia were suspended from their employment at
the present time, a very large number of persons would be dealt with.
Yet the practical application of this method is by no means impossible
under industrial conditions, and would at any rate give a definite test
upon which diagnosis could be made, though it would be quite impossible
to expect the general practitioner or the certifying surgeon to
estimate the basophilic content. All such estimations would necessarily
have to be performed at some properly equipped pathological laboratory,
such as at the present time many municipal authorities possess.

These facts are of importance, as a differential count of the white
cells, together with a careful inspection of a blood-film for basophile
staining and alteration in the red cells, as well as other phenomena
noted, together with an estimation of the hæmoglobin contained in the
blood, are to our mind of considerably more value in the diagnosis of
lead poisoning than is the quantitative estimation of the red or white
cells. The following tables give a certain number of enumerations,
etc., made from the blood of lead-poisoned persons:

BLOOD-EXAMINATION OF LEAD ANÆMIA--DIFFERENTIAL COUNT PER CENT.

  +---+-----+---------+------+------+--+--+--+--+--+--+--+--+--+--+--+
  |No.| Hb. |  R.B.C. |W.B.C.|Index.|A.|B.|C.|D.|E.|F.|G.|H.|I.|J.|K.|
  +---+-----+---------+------+------+--+--+--+--+--+--+--+--+--+--+--+
  |   | Per |         |      |      |  |  |  |  |  |  |  |  |  |  |  |
  |   |Cent.|         |      |      |  |  |  |  |  |  |  |  |  |  |  |
  |  1| 60  |3,460,000| 7,000|  0·7 |63|20| 6| 3| 8| 0| +| -| +| -| +|
  |  2| 45  |1,707,000| 9,000|  1·4 |46|38| 8| 1| 7| 0| +| +| +| +| +|
  |  3| 55  |2,620,000|20,000|  1·0 |58|32| 4| 2| 4| 0| +| -| +| -| +|
  |  4| 60  |1,334,000|10,000|  3·0 |55|35| 8| 0| 5| 0| +| -| +| +| +|
  |  5| 54  |3,210,000| 8,000|  0·9 |52|41| 4| 2| 1| 0| +| +| +| -| +|
  |  6| 60  |1,347,000|10,000|  3·0 |59|32| 3| 2| 3| 1| +| +| +| +| +|
  |  7| 65  |3,760,000| 9,000|  0·9 |  |  |  |  |  |  |  |  |  |  |  |
  |  8| 65  |2,200,000|10,000|  0·7 |  |  |  |  |  |  |  |  | +|  | +|
  |  9| 50  |3,860,000| 8,000|  0·6 |  |  |  |  |  | -|  |  | +|  | +|
  | 10| 60  |3,420,000| 9,000|  1·0 |76|16|13| 3| 0| 0|  |  | +|  | +|
  +---+-----+---------+------+------+--+--+--+--+--+--+--+--+--+--+--+

  +---+-----------------------+------------------------------------+
  |No.|          Work.        |              Notes.                |
  +---+-----------------------+------------------------------------+
  |   |                       |                                    |
  |   |                       |                                    |
  |  1|Paint mill             | 5 years.                           |
  |  2|Paint mill             |10 years.                           |
  |  3|Paint mill             | 7 years.                           |
  |  4|Packer white lead      | 5 years.                           |
  |  5|Grinder                | 6 years.                           |
  |  6|White lead             | 8 years.                           |
  |  7|Press and stoves       | 8 years.                           |
  |  8|Zinc distillation still|20 years; double wrist-drop 2 years.|
  |  9|White lead beds        |10 years.                           |
  | 10|Packer                 |                                    |
  +---+-----------------------+------------------------------------+

  A = Polymorphonuclears.
  B = Lymphocytes.
  C = Large hyaline.
  D = Eosinophile.
  E = Transitional.
  F = Basophile.
  G = Microcytes.
  H = Megalocytes.
  I = Poikilocytes.
  J = Nucleated red.
  K = Plehn’s bodies.

  Corpuscles, Thoma-Zeiss.
  Hæmaglobin, Haldane’s instrument.
  Films, stained Leishman.

The form of lead inhaled is immaterial, and definite poisoning with
alteration in the blood may be occasioned, not only with white lead and
lead fume, but also even with lead sulphate and lead silicate.

The following table gives the result of blood-counts performed upon the
blood of persons employed in the manufacture of a paint erroneously
supposed to be innocuous, as the base consisted of lead sulphate and
oxysulphate:

DIFFERENTIAL COUNTS PER CENT. OF BLOOD-FILMS FROM LEAD SULPHATE WORKERS.

  +---+-----+--+--+--+--+--+--+--+--+--+--+
  |No.|A.[A]|B.|C.|D.|E.|F.|G.|H.|I.|J.|K.|
  +---+-----+--+--+--+--+--+--+--+--+--+--+
  | 1 |  55 |16| 5| 1| 0| +| +| -| +| +| +|
  | 3 |  57 |16|26| 1| 0| +| +| -| -| +| -|
  | 6 |  67 |23| 9| 1| 0| +| +| +| +| +| +|
  | 7 |  72 |18| 5| 5| 0| +| -| -| -| +| +|
  | 8 |  65 |26| 7| 2| 0| +| +| -| -| +| +|
  +---+-----+--+--+--+--+--+--+--+--+--+--+

  [A]

  A = Polymorphonuclears.
  B = Lymphocytes.
  C = Mononuclears.
  D = Eosinophiles.
  E = Myelocytes.
  F = Basophiles.
  G = Microcytes.
  H = Megalocytes.
  I = Poikilocytes.
  J = Vacuolated red cells.
  K = Normoblasts.

Sand-papering surfaces of painted objects, walls, coaches, etc.,
also throws a definite amount of lead dust into the air whenever
the sand-papered paint contains lead. The following table gives
the differential counts of the blood of persons employed in the
furniture-painting trades:

DIFFERENTIAL COUNTS PER CENT. OF BLOOD-FILMS FROM FURNITURE-MAKERS
(SAND-PAPERERS).

  +---+-----+--+--+--+--+--+--+--+--+--+--+
  |No.|A.[A]|B.|C.|D.|E.|F.|G.|H.|I.|J.|K.|
  +---+-----+--+--+--+--+--+--+--+--+--+--+
  | 10|  48 |39|11| 1| 1| +| +| +| +| +| +|
  | 13|  54 |35| 9| 2| 0| +| +| +| +| +| -|
  | 15|  53 |32|13| 1| 1| +| -| -| -| -| -|
  | 16|  58 |30| 9| 3| 0| +| -| -| +| -| -|
  | 19|  56 |31|12| 0| 1| +| -| -| +| +| -|
  +---+-----+--+--+--+--+--+--+--+--+--+--+

  [A]

  A = Polymorphonuclears.
  B = Lymphocytes.
  C = Mononuclears.
  D = Eosinophiles.
  E = Myelocytes.
  F = Basophiles.
  G = Microcytes.
  H = Megalocytes.
  I = Poikilocytes.
  J = Vacuolated red cells.
  K = Normoblasts.


=Circulatory System.=--A very large number of the symptoms referable to
chronic and well-defined lead poisoning are referable to circulatory
lesions, and, as has been elsewhere pointed out, the ultimate nerve
degeneration occurring in various parts of the body is probably but
a final symptom of the earlier hæmorrhage which has taken place.
Certain symptoms are, however, more closely related to the circulation
than others, and may therefore be more conveniently grouped together
under the present heading. The smaller changes, many of them connected
with special organs (such, for instance, as the eye) or particular
regions (as the mesenteric vessels), have been already referred to in
dealing with colic and eye changes. Vaso-motor changes precede the
actual change in the vessel walls themselves. On the other hand, the
alterations in the structure of the liver, lung, spleen, and more
especially the kidney, are secondary to change in the structure of the
walls of the vessels themselves.

Vaso-motor disturbances may or may not be of nervous origin, although
the former view is probably correct, and it is also equally possible
that the direct affection of the vessels is associated with the nerve
irritation. On the other hand, direct inflammation of the vessel
walls, resulting in obliterative arteritis, in arterio-sclerosis,
and degeneration and exudation in the kidney, lung, and liver,
are practically due to degenerative changes either in the intima
or the middle coats of the finer vessels. The common symptoms of
arterio-sclerosis, vertigo, headache, and pulsation in the vessels, and
of the persistent headache already referred to, all suggest changes
taking place in the vessels complicated by œdema. In the early stages
of kidney degeneration, however, it is common to find an interstitial
nephritis due apparently to exudation from the vessel walls. Such an
hypothesis is to some extent supported by the somewhat allied condition
of engorgement and fibroid change in the liver and lung, and to a
lesser extent in the spleen. In the lung, even in persons not exposed
to inhalation of lead, and in animals, as pointed out by Glibert,
secondary changes in the lung follow lead intoxication, such changes
taking the form of emphysema and generalized fibrosis; whilst the
liver is engorged with blood, and later undergoes similar degenerative
changes. The bloodvessels in these organs are found to have lost a
considerable amount of their elasticity, to have yielded here and
there, and in other places to be completely closed by obliterative
arteritis. Microscopical hæmorrhages are to be found mainly in the
veins leading from the capillaries. In the kidney such vessel changes
as are outlined are the precursors of disease, and albumin is found
in the urine, but the quantity is rarely very large. Casts are not
common, and the amount of lead present in the urine may be exceedingly
small, difficult to trace, and in many cases entirely absent.

In the later stages of chronic saturnism the heart may show
degenerative changes. Microscopical examination of the heart muscle
shows that alteration of the fibres of the muscles takes place in a
manner similar to that of the voluntary muscles. Disease of the heart
valves is uncommon; alterations in the heart sounds are infrequent; the
clinical picture of the cardiac condition is that of a “flabby” heart.


REFERENCES.

  [1] MEILLÈRE, G.: Le Saturnisme. Paris, 1903.

  [2] BLYTH, WYNTER: Proc. Chem. Soc, 1887-88.

  [3] PEYRUSSON AND PILLAULT: Meillère’s Le Saturnisme, chap. iv.

  [4] NEWTON PITT: Trans. Path. Soc, No. 42, 1891.

  [5] GLIBERT: Le Saturnisme Expérimental: Extrait des Rapports Ann. de
  l’Inspect. du Travail, Brussels, 1906.

  [6] MORITZ: Mediz. Woch., St. Petersburg, 1901.

  [7] SCHMIDT: Arch. für Hygiene, vol. lxiii., p. 1, 1907.

  [8] GLIBERT: _Ibid._

  [9] BOYCOTT: Journal of Hygiene, 1910.




CHAPTER IX

THE NERVOUS SYSTEM


=Symptomatology and Diagnosis= (_Continued_)--=The Nervous
System.=--The most definite objective symptoms of chronic poisoning
by means of lead are those of the nervous system. From the time of
Tanquerel[1] affections of the hands and fingers and the muscles of the
back have all been well known. Associated with the paralysis are local
vaso-motor effects, such as cyanosed condition of the skin over the
paralyzed muscles, cold hands, etc.; whilst later, if the paralysis be
severe and persists, atrophic changes take place in the skin, muscles,
bone, whilst definite contracture occurs from unopposed contraction of
the unaffected muscles. Paralysis will therefore be associated with two
of the great systems into which the body is divided for the purposes
of medical and physiological description--namely, the muscular and the
nervous--and, on account of the similarity of the clinical symptoms of
lead paralysis, attention has been drawn rather to the nerve changes
preceding muscular paralysis and degeneration than to other influences
affecting the nerve inflammation.

Lancereaux[2] considered that lead poisoning resulting in paralysis
takes the form of a gradual impregnation of the nervous tissue with
lead salts, until such a time as degenerative effects are set up, and
with it muscular paralysis.

Meillère[3], who has given much attention to the ætiology of lead
poisoning, as well as to the clinical study of the disease, considers
that plumbism may be divided into three periods:

(_a_) Impregnation of the tissues of the body, the nervous tissue being
the chief one affected by lead salts.

(_b_) Retardation of the general oxidation changes of the body,
resulting in malnutrition and general loss of tone.

(_c_) Establishment of intoxication, with the generalized affections,
paresis, etc.

If three such periods can be recognized, as no doubt they can, as
divisions of the time during which lead gradually affects the tissues,
the symptoms in the more severe cases would be expected to be those
associated with the more prolonged exposure. This, no doubt, is true to
a limited extent, more particularly in industrial poisoning, depending
for its development on a long-continued dosage of lead in minute
quantities, and for the most part of metallic lead. On the other hand,
with some of the salts of lead, notably the hydrated carbonate, acute
disease may take place during the first stage--namely, impregnation
of lead--the determining factor then being either the retardation of
the elimination of lead, or a suddenly increased quantity in lead
dosage, or some intercurrent disease, or even alcoholic excess,
whereby a sudden large excess of the poison is thrown into the general
circulation.

The commonest type of paralysis occurring is the one affecting the
muscles of the hands, which may for a considerable time show some
diminution in their extensor power before the actual onset of the
disease takes place. The onset of paralysis is practically always
unaccompanied by pyrexia; the only occasions in which pyrexia may be
associated with the onset of the attack are those cases in which some
secondary cause determines the paralysis, and the pyrexia in these
instances is due to the intercurrent disease, and not to the lead
infection.

Although weakness of the extensor muscles of the hands may be present
in persons subjected to lead absorption for a considerable time, the
actual onset of the disease itself is frequently sudden; but in the
majority of cases it is distinctly chronic, and is rarely, in the case
of paresis, associated with any definite prodromal symptoms. Prodromal
symptoms have been noted, such, for instance, as lassitude, general
debility, and more especially loss of weight. Cramps of the muscles
the nerve-supply of which is becoming affected, alteration of the skin
over areas corresponding to definite cutaneous nerves, hyperæsthesia,
anæsthesia, or analgesia, may occasionally be present. Neuralgic pains
have also been described, but these are inconstant, and generally of
the arthralgic type related to the periarticular tissues of joints
rather than to pain in the course of the nerves. The pain is rather
of the visceral referred type than a definite neuralgia. Tremor is,
however, frequently associated with the preliminary condition of
paresis, and in several cases variations in the amount of weakness of
the extensor muscles of the wrist have been noticed, as far as can be
estimated clinically without the use of a dynamometer. Associated with
this weakness is tremor of a fine type, often increased by movement
(intention tremor), and in every case more marked during the periods of
increased weakness. Instances have occurred where definite wrist-drop
followed after a prolonged period of weakness; in others the weakness
has temporarily cleared up for six months, and no difference could be
determined in the extensor power of the two wrists; while in others,
again, the weakness is progressive, but slight, and insufficient
to warrant the removal of the workman from his occupation. Again,
progressive weakness may remain a symptom of the wrists of workmen for
years.


=The Forms of Lead Paresis.=--The paralysis may be partial or
generalized, but the chief muscles affected are the extensors of the
wrists and the forearm, and the interossei of the hand. As a rule,
the first muscles to be affected are the extensor communis digitorum
and the extensor indicis. The muscles of the shoulder--mainly the
deltoid--come next in order, followed by the muscles of the leg,
particularly the peroneus longus and brevis, with occasionally the
interossei of the foot; the muscles of the back, neck, and abdominal
walls, are occasionally affected, as are those of the larynx and
diaphragm, and it is of interest to note that Trousseau pointed out
that among horses employed in lead works paralysis of the superior
laryngeal nerve often occurred.

Considerable difficulty is experienced in estimating the reason of the
predilection of lead for the musculo-spiral nerve, this being the nerve
mainly affected in wrist-drop. Owing to the fact that the supinator
longus receives an additional nerve-supply to the musculo-spiral,
this muscle frequently escapes paralysis when the whole of the other
extensors of the hand are involved. Moreover, the predilection for
given nerves differs in different animals, and one of us (K. W. G.) has
found experimentally that in cats the first nerve to be affected is the
anterior crural supplying the quadriceps extensor, whilst the second
group of muscles affected are the spinal muscles, particularly in the
lumbar region.

Among the speculations which have been made with regard to this
predilection for definite groups of muscles supplied by one nerve,
Teleky[4] examined forty cases of paralysis with special reference to
Edinger’s theory--namely, that the function of muscles (and of other
organs) breaks down under certain circumstances before the strain
set upon them. In this way Edinger explains paralysis following lead
poisoning as being due to excessive strain on the particular group of
muscles affected, based on a consideration of the relative volumes and
weights of the muscles of the hand and forearm, and the demands made on
the several groups, flexors, extensors, supinators, etc., by the coarse
or fine work respectively demanded of them in industrial employment. He
concludes that--

1. Of the forearm, the flexors (triceps, anconeus, extensors, biceps,
brachialis anticus, and supinator longus) possess a high degree of
capacity for work, but are not called into play mainly in the execution
of fine work; while the supinators are characterized by great mass, and
are brought into play mainly in work of coarse and heavy nature, and
not during fine manipulations.

2. The muscles concerned in pronation are of small capacity for work,
and are not called on for sustained work.

As for the muscles acting on the wrist and hand, he concludes that the
extensors (carpi radialis longior and brevior, carpi ulnaris, and the
extensors of the fingers) are powerful, and much exceed in capacity
for work the flexors (flexor carpi radialis, flexor carpi ulnaris,
the flexors of the fingers, etc.), but in all fine manual work, and
specially where close grasping movements enter into association with
the flexors, external strain is put upon them, whilst the flexors
merely support their action.

The extensor communis digitorum is the weakest of all the long finger
muscles; its volume is hardly one-fourth that of the corresponding
flexors, and while it acts only on the first of the phalanges, the
flexors act on all three. In all fine work they are called on for heavy
strain, especially the interossei and the lumbricals, but in harmony
with the long flexors when grasping movements are performed. The small
muscles of the fingers have nearly the same mass as the extensor
communis, and in all fine movements the grasping efforts are taxed
severely; but their play is under considerably more favourable physical
relations than that of the extensors, whilst in addition they are
aided in their work at times by the long flexors. The chief adductor
muscle of the thumb (extensor metacarpi pollicis) is particularly
powerful; the other extensors of the thumb are very weak, and work
under unfavourable physical conditions, but are supported in their
action by the strong abductor muscle. The muscles of the abductor,
opponens and flexor brevis, in the complicated work thrown on the thumb
in manipulation, are much exerted, so that the effects of overexertion
show themselves first in this region.

Thus, Edinger maintains that the muscle-supply of the arm is designed
for coarse heavy work, the muscles of the fingers and the hand
having to carry out more work than can be expected of them from a
consideration of their volume and their physical action.

The commonest form of lead palsy, the antibrachial type of
Déjerine-Klumpke[5], is explicable from consideration of overexertion
of the particular group of muscles named. The supinator muscle,
supplied also by the musculo-spiral nerve which serves the paralyzed
muscles, escapes because of its size, and the fact that functionally it
belongs to the flexor group, and the first-named reason also, explain
the frequent escape of the long abductor of the thumb.

Teleky[6] investigated thirteen slight cases of the antibrachial
type. In one both hands were affected, in one the left only, and in
all the others the right only--facts which he thinks bring out the
rule of causation by employment. Of fourteen painters, three had the
right forearm affected only, the other eleven both right and left, but
always more marked in the right. Amongst them he cites cases where
the shoulder muscles were paralyzed, which he considered was due to
the extra strain of unusual employment, involving a raising of the
arms above the head, or lying on the back painting the under parts of
carriages. In several of the painters the index-finger was the least
affected, by reason of the less exertion thrown on it by the position
assumed in holding the brush between the second and third fingers. The
long abductor, probably because of its size and power, is in no case
completely paralyzed.

In file-cutters he insists that the predominant share, falling on
a single or on several small muscles of the hands, makes the early
appearance of paralysis of the small muscles the characteristic sign.
In this connection we have frequently observed decrease in the size
of the thenar and hypothenar eminences amongst lead rollers; in fact,
in the majority of lead rollers who have followed their occupation for
a large number of years the flattening of both thenar and hypothenar
eminences is well marked, but it is only fair to point out that in
these cases very considerable stress is thrown on the muscle of this
part of the hand by the pressure of the lead plate in pushing it
inwards into the roller and grasping it on its appearance back again
through the roller, and that, further, the use of large and clumsy
gloves with all the fingers inserted into one part, and the thumb only
into the other, tends to produce inaction of portions of the lumbricals
and of the opponens pollicis, and may, therefore, from purely
mechanical reasons cause damage to this part of the hand.

Teleky[7] cites cases of right-sided paralysis of the adductor brevis
pollicis supplied by the median nerve, and partial paralysis of the
long extensors and of the extensor ossis metacarpi pollicis supplied
by the radial nerve, and in one or two cases complete paralysis of the
thenar muscles and adductor, whilst the extensors of the fingers and
wrists were only partially paralyzed. The cases all occurred in lead
capsule polishers. This particular selection of muscles is clearly the
result of the peculiar movement necessary in polishing the capsules
of bottles on a revolving spindle, involving specially the use of the
opponens muscle.

This observation of Teleky’s is in direct accord with the observation
quoted above of the hands of persons engaged in lead rolling.

In the lower extremity, paralysis of the muscles associated also with
paralysis of the adductor and extensors of the thumb was found by
Teleky in a shoemaker who had contracted plumbism by the use of white
lead. He explains this lower extremity paralysis by the exertion thrown
on the adductor muscles of the thigh whilst holding the shoes.

In children affected with lead palsy the lower extremities are more
frequently paralyzed than the upper, due to the relatively greater
strain in childhood on the legs than on the arms.

Edinger’s theory, supported as it is undoubtedly by Teleky’s
observations, is a matter of the greatest importance in the production
of paralysis; for if we accept the view that lead is a poison that
has a selective power on certain nerves, we have still to consider
which is the greatest force, the selection of certain groups of
muscles or the effect of functional action. The theory of muscular
overexertion certainly falls in with the type of paralysis, and Teleky
has undoubtedly shown that under certain circumstances, by special
exertion of other muscle groups not usually affected, these muscles
alone, or to a greater extent than those usually affected, are involved
in the paresis. If, therefore, lead has a selective action, which is
exceedingly doubtful, it must be very slight.

Such selective action is, of course, exceeded by a functional activity
which brings about the affection of those nerves which supply the
muscles most used. If, therefore, we judge of paralysis as being due to
the selective action of lead on certain nerves, we are met at once with
the objection that the muscles affected do not always correspond to
such a nerve distribution, and that muscles supplied by other than the
musculo-spiral nerve are affected by paralysis.

Careful consideration of the chapter on Pathology, and more
particularly of the histological findings described, in which the
preliminary action of lead is found to be typically and invariably on
the blood, setting up degenerative changes microscopical in size and
limited in area, affecting the vessel walls and producing a yielding of
the vessel, determining minute microscopical hæmorrhages distributed,
not necessarily in one position of the body, but all over the body, and
peculiarly in the case of the cat affecting those muscles called upon
to perform sudden and violent movement--namely, jumping--enables us to
regard such microscopical hæmorrhages as an adequate explanation of
the association of paralysis in muscle groups, functionally related to
various trades and industrial processes.

It may be argued, and we think with considerable reason, both from
pathological and clinical findings, that, as muscular exertion is
apparently associated with the onset of paralysis, particularly in
those muscles which may be regarded as physically somewhat inadequate
to the work they have to perform, and that, as the paralysis is
associated with definite functional groups of muscles, and to a curious
extent varies according to the trade in which the sufferer is engaged,
therefore greater stress thrown upon the muscular tissue at some period
or another during occupation determines the microscopical hæmorrhage in
the nerve supplying the muscles, or in the muscle itself, so that the
paralysis affects just such muscles as have an increased strain thrown
upon them. It does not necessarily follow that the preliminary initial
hæmorrhage occurring should be a large one--in fact, from the whole of
the histological history, hæmorrhages are exceedingly minute; neither
does it follow that it is essential for such hæmorrhages to take place
in the whole length of the nerve itself; but it is only necessary
that the finer branches of the nerve should have their venioles
or arterioles affected, and it is of course in the finer branches
particularly, as has been pointed out in relation to the venioles, that
degeneration of the intima of the vessels takes place.

Finally, the effect of early treatment on lead palsy tends to bear out
this theory. If a case of lead palsy be treated in the early stages,
the clinical course of the case is good; increased paralysis generally
takes place in the first week, and, where, perhaps, only two or three
fingers are involved when the case is first seen, spreads generally
to other regions within a week, and the whole hand is affected; but
from this moment onwards improvement takes place on the application of
suitable treatment, and, if continued, almost invariably results in the
entire recovery from the paresis.

There is little doubt that this is the true explanation of the ordinary
paresis of lead poisoning, and a very great deal more evidence is
required to combat it and to prove the selective action of lead
upon individual nerves, since the theory of hæmorrhage does not owe
its origin to conjecture, but is based on clinical and histological
examination of early cases of poisoning.

In attempting to find a cause for the paralysis of the hands so
commonly present in painters, it has been suggested that lead is
absorbed through the skin, and affects the nerves at their junction
with the muscles, setting up a peripheral neuritis [Gombault[8]]. The
theory breaks down at once when such commonly-occurring affections
as paralysis of the ocular muscles, paralysis of the peroneal type,
paralysis of the muscles of the shoulder, etc., are considered.

For the convenience of description lead paralyses are generally divided
into a series of groups, the grouping varying according to the function
of the various muscles rather than to their anatomical grouping. The
various types of paralysis have to be considered in detail:


1. _Antibrachial Type_ (_Déjerine-Klumpke_--_Remak_).--The first muscle
affected is the extensor communis digitorum, with dropping of middle
and ring fingers, while extension of the first and fourth is possible
because of their separate muscles of extension (extensor minimi digiti
and extensor indicis). Paralysis may be limited to these, and not
advance farther, but it is common to see these two muscles primarily
affected, and for other muscles to become involved after the patient
is put on treatment, although exposure to lead has ceased. Usually,
however, the paralysis advances, involving the extensors of the index
and little fingers, so that the basal phalanges of the four fingers
cannot be extended. The long extensor of the thumb is next involved,
but this may be delayed. The two terminal phalanges are still able
to be extended by the interossei (as shown by Duchenne) when the
basal phalanx is passively extended on the metacarpal. Abduction and
adduction of the fingers also remain unaffected. The wrist muscles are
affected next. The hand remains in semi-pronation, and when hanging
down forms a right angle with the forearm, the fingers slightly flexed
with the thumb towards the palm, and the hand deflected to the ulnar
side. In grasping an object the flexors remain unaffected, the wrist is
much flexed owing to the shortening of the flexors in consequence of
the extensor paralysis. The hand cannot pass the median line. The long
abductor of the thumb--that is, the extensor ossis metacarpi pollicis,
also known as the “extensor primi internodii pollicis”--is only very
rarely involved, but has been described as being the muscle alone
involved in the paralysis affecting persons engaged in polishing lead
capsules.


2. _The Superior or Brachial Type_ (_Remak_).--The muscles affected
are those of the Duchenne-Erb group--namely, the deltoid, biceps,
brachialis anticus, and supinator longus. The supra- and infrascapular
muscles are also as a rule involved, but the pectoralis major rarely.
This type of paralysis is usually found in old cases associated with
other forms of paralysis, but may be found as a primary affection (as
already noted amongst painters); sometimes the deltoid is the only
muscle affected, with diminution in electrical contractility of the
other muscles of the group.

The arm hangs loosely by the trunk, with the forearm semi-pronated. The
arm cannot be raised, nor can the forearm be bent on the upper arm.
Extension is unaffected, as the triceps is never involved. Supination
is impossible because of paralysis of the supinator brevis. Movement
effecting rotation of the shoulders is involved, due to the paralysis
of the supra- and infra-spinatus. Electrical reactions are said to be
less marked in the brachial than the antibrachial type, and complete
loss of faradic contractility is rare; but in one of the three cases
described below, in which electrical reactions were carefully tested,
the right deltoid showed entire loss of contractility to faradism.


3. _Aran-Duchenne Type._--The muscles of the thenar and hypothenar
eminences and interossei are affected. This type of lead paralysis may
be distinguished from progressive muscular atrophy by the electrical
reactions, and the fact that the atrophy is accompanied by more or
less pronounced muscular paralysis. The atrophy is almost always most
marked, and advances pari passu with the paralysis. This form may occur
alone, or be complicated with the antibrachial type, which is the most
common. It is seen in file-cutters as the result of overstrain of the
muscles in question. Moebius[9], in his observations on file-cutters,
noted in one case paralysis of the left thumb, with integrity of the
other muscles of the left upper extremity. Opposition of the thumb was
very defective; there was paralysis of the short flexor and of the
adductor and atrophy of the internal half of the hypothenar eminence.
Reaction of degeneration was noted in the muscles named, but not in
the extensors of the fingers and wrist. In another case, in addition
to feebleness of the deltoid, flexors of forearm on the upper arm, and
small muscles of hand, there was paralysis and atrophy of the adductor
of the thumb and first interosseous and paralysis of the opponens.


4. _Peroneal Type._--This is a rare type, and nearly always associated
with the antibrachial or with generalized paralysis. In the former
the paralysis is slight, especially when it affects the psoas; but
there is predilection for certain groups of muscles, especially the
peroneal and extensor of the toes, while the tibialis anticus escapes.
Hyperæsthesia, or more rarely anæsthesia, precedes the onset.

The patient walks on the outside of the feet, has difficulty in
climbing stairs, and cannot stand on the toes. The toes drag on the
ground in walking, so that the foot has to be swung round at each
step, and the inner side is lifted in excess by the action of the
tibialis anticus, with uncertainty in gait. If walking is continued,
the toes drag more, and “stepping” gait is assumed by bringing into
action the muscles of the thigh. The foot cannot be flexed on the
leg; abduction of the foot and extension of the basal phalanx of the
toes is impossible. Later the peroneal muscles, extensor communis of
toes, and extensor of great toe, are paralyzed, from which fact arises
the difficulty of walking and of descending stairs, as the whole
weight of the body is supported then by the tibialis anticus. This
type corresponds with the antibrachial type of the upper extremity.
If the tibialis anticus is paralyzed, it is in association with the
gastrocnemius.


5. _Paralysis of Special Sense Organs._--Tanquerel[10] called attention
to the aphonia of horses in lead works, necessitating tracheotomy,
and Sajous[11] described adductor paralysis of the glottis in a
house-painter. Morell Mackenzie[12] also described unilateral paralysis
of the adductors in persons suffering from lead poisoning, whilst
Seifert[13] particularly describes a curious case in which paralysis of
the transverse and oblique arytenoid muscles prevented contraction of
the cord in its posterior quarter, and in a second case of paralysis,
affecting the posterior crico-arytenoid muscles on both sides, the
adductors remained unaffected. What is still more interesting in
Seifert’s case is the fact that at the post-mortem old hæmorrhages
were found in the mucosa of the arytenoids and aryepiglottidean folds.
Occasionally sensory paralysis may be found in the special sense
organs--such, for instance, as loss of taste, loss of smell, and, in
addition, diminished power of hearing--but these defects rarely if ever
occur unless accompanied by distinct mental changes and generalized
paralysis.


6. _Eye._--Poisoning affects the eye in two ways:

  (_a_) Defects of the visual mechanism.
  (_b_) Defects of the muscular mechanism of the eye.

Lockhart Gibson[14] describes a large number of cases of paralysis of
the muscles of the eye met with amongst children in Queensland. The
cause was traced to the painted railings near which the children had
been playing. The white lead paint had somewhat disintegrated under
the action of the sun’s rays, forming an efflorescence; the children
admitted to have rubbed the paint and then sucked their fingers.

Between July, 1905, and 1908, sixty-two cases of plumbism in children
were admitted to the children’s hospital, and of these sixty-two cases
thirteen had well-marked ocular symptoms. The paralysis of the muscles
of the eye was almost invariably one of the external rectus, but other
muscles were at the same time affected; occasionally paralysis of the
whole of the oculo-motor muscles was seen with the exception of the
superior oblique. It is worthy of note that amongst these children a
very large number suffered, in addition to their eye paralysis, with
foot-drop and wrist-drop, and, on the whole, suffered from foot-drop to
a much larger extent than from paralysis of the hands.

Galezowski[15] describes paralysis of accommodation of the eye, and in
cases described by Folker[16] some amount of orbital paralysis was also
present.


7. _Generalized Paralysis._--These types do not differ in form from the
previously described types, except, perhaps, as regards their rapidity
of onset. Where the onset is slow (chronic) the subject is usually one
who has been previously affected with paralysis of the extensors of the
hand, followed by development of the paralysis in the shoulders, hand,
leg, thorax. In the acute form, paralysis may affect all the muscles
in a given limb or group, and reduce them in a few days to a complete
condition of paralysis. In extreme cases the patient lies on the back
and is incapable of rising, and sometimes even unable to eat. The
intercostals, diaphragm, and larynx, are also affected, while there is
generally dyspnœa and aphonia. The muscles of the head and neck appear
to escape. In these acute cases, pyrexia may be a common symptom.


=Electrical Reactions.=--The diagnosis of the affected muscle is
greatly assisted by careful examination of all the muscles in the
affected physiological group by means of the galvanic and faradic
currents. The battery for the purpose of testing the electrical
reactions must have an available electromotive force of over 40 volts.
A battery of thirty-two Leclanché dry cells is ample. For the faradic
current, a small induction coil operated by two Leclanché cells is
sufficient. One large, flat electrode should be used, and several
smaller ones.

The faradic current should be used first, as it stimulates the nerves
directly, and the muscles only indirectly, through their nerve-supply.
Each nerve trunk should be examined systematically. The motor points
correspond for the most part with the points of entry of the motor
nerves into the muscles which they supply. A small electrode, either a
button or a small disc about the size of a sixpence, should be used for
the examining electrode, while the larger electrode should be placed
either on the abdomen or between the shoulders. The electrodes should
be well soaked in normal saline.

The intensity of the minimum current required to produce a contraction
for each point should be noted, and compared with the effect of a
similar current on the opposite side of the body.

The reaction of degeneration of the faradic current consists in no
contraction at all being elicited, even when a very strong current
is employed. If there be unilateral wrist-drop in the left hand,
consisting of loss of power of the extensor communis digitorum on that
side, no movement of the muscle is produced at all when the electrode
is placed across the motor points of the muscle. These are situated to
the outer side of the arm when the dorsum of the hand is uppermost,
about 1¹⁄₂ to 2 inches below the olecranon. The same quantity of
current, when applied to the unaffected muscle on the opposite side,
produces a brisk reaction.

Having observed the effect with the faradic current, and the results
having been recorded, the continuous current is used, and the
electrodes made use of in an exactly similar fashion. When a small
electrode is used, the superficial nerves and muscles are more
stimulated than those lying deeply. It is necessary, therefore,
to begin with a small current and gradually increase it until the
individual muscle responds.

The strength of the current employed is registered by means of a
milliampèremeter.

With the continuous current quantitative as well as qualitative
alterations may be determined, and with the quantitative change of the
galvanic current the muscular excitability is increased, contraction
following the application of a weaker current than is necessary to
produce it in health or in the sound muscle on the other side of the
body.

With the qualitative change, the contraction is no longer sharp, but
sluggish. The anodal closing contraction is elicited with a weaker
current than kathodal closing contraction, so that ACC>KCC.

The quantitative change depends partly on the nutrition of the muscle;
the qualitative change depends on the fact that the nerve no longer
regulates the character of the contraction, and also to a small extent
is the result of changes in the muscle itself.

In a complete reaction of degeneration in an affected muscle, reaction
to the faradic current is absent, contraction to the galvanic current
is sluggish, and is produced with a smaller current in the anode than
the kathode.[A]

  [A] The kathode, or negative electrode, is attached to the zinc rod;
  the anode, or positive electrode, to the copper or carbon.

As the nerve lesion passes away, the voluntary contraction generally
begins to return before the nerves show any reaction to electrical
stimulus.

The following three cases in which the electrical reactions of the
muscles were determined, give examples of typical cases of lead
paresis. In No. 3, owing to the fact that the case was treated
immediately the paralysis occurred, complete recovery had taken place,
and, as will be seen, the electrical reactions have again become normal.

CASE 1.--Litharge and blast-furnace worker. Employed in lead works,
where a large number of different metallurgical processes associated
with the recovery of lead from the ore were carried on. Double
wrist-drop, existing for eight years, untreated until some four years
after paralysis took place, when slight improvement occurred. The
electrical reactions show that the extensor communis digitorum on the
right side is completely degenerated, whilst the first interosseous of
the right side show reactions of degeneration. On the left side the
extensor communis digitorum showed normal but very feeble reaction.
This latter point is one of considerable importance if early hæmorrhage
accounts for lead paralysis, for if the nerve itself was completely
destroyed, or if, as was the case, the muscle appeared completely
paralyzed on inspection, obviously the nerve-supply must be completely
cut off if the lesion was due to destruction of the nerve of the spinal
cord or to the destruction of the lower motor neuron. On the other
hand, the presence of small localized fibrillar contraction, found by
the galvanic current, together with the presence of a slight reaction
to faradism, suggests that some small portion of the nerve has remained
unaffected, and that for this reason certain portions of the muscle
have not undergone degeneration--a circumstance which can hardly be
expected if the cause of the paralysis is in the destruction of the
whole of the nerve-supply.

ELECTRICAL REACTIONS IN LEAD PARALYSIS. (CASE 1.)

  +----------------------+------------------------------------------+
  |       Muscle.        |                Galvanism.                |
  +----------------------+------+-----+------+----+-----------------+
  |                      |      | M.A.|      |M.A.|                 |
  |R. Deltoid (anterior  |K.C.C.|  8  |A.C.C.|  8 |                 |
  |   portion)           |      |     |      |    |                 |
  |L. Deltoid (anterior  |K.C.C.|  6  |A.C.C.|  9 |                 |
  |   portion)           |      |     |      |    |                 |
  |R. Deltoid (posterior |K.C.C.|  6  |A.C.C.|  9 |                 |
  |   portion)           |      |     |      |    |                 |
  |L. Deltoid (posterior |      |     |      |    |                 |
  |   portion)           |      |     |      |    |                 |
  |R. Supinator longus   |K.C.C.|  6  |A.C.C.| 10 |Reaction brisk   |
  |L. Supinator longus   |K.C.C.|  5  |A.C.C.|  6 |Reaction brisk   |
  |R. Extensor communis  |No reactions either A.C.C. or K.C.C.[15]  |
  |   digitorum          |      |     |      |    |                 |
  |L. Extensor communis  |K.C.C.|  8  |A.C.C.| 12 |Brisk, but feeble|
  |   digitorum          |      |     |      |    |                 |
  |R. Extensor primi     |K.C.C.| none|A.C.C.| 13 |Brisk            |
  |   internodii pollicis|      |at 13|      |    |                 |
  |L. Extensor primi     |K.C.C.|  6  |A.C.C.| 12 |Reaction brisk   |
  |   internodii pollicis|      |     |      |    |                 |
  |R. Extensor carpi     |K.C.C.|  8  |A.C.C.|  8 |Brisk Contraction|
  |   ulnaris            |      |     |      |    |                 |
  |L. Extensor carpi     |K.C.C.|  8  |A.C.C.| 12 |Brisk Contraction|
  |   ulnaris            |      |     |      |    |                 |
  |R. First interosseous |K.C.C.|  8  |A.C.C.|  6 |Contraction slow |
  |L. First interosseous |K.C.C.|  6  |A.C.C.|  6 |Brisk contraction|
  |R. Second interosseous|K.C.C.|  8  |A.C.C.| 10 |Brisk contraction|
  |L. Second interosseous|K.C.C.|  6  |A.C.C.|  8 |Brisk contraction|
  |R. Third interosseous |K.C.C.|  9  |A.C.C.|  6 |Brisk contraction|
  |L. Third interosseous |K.C.C.|  6  |A.C.C.|  8 |Brisk contraction|
  |R. Fourth interosseous|K.C.C.|  8  |A.C.C.|  6 |Brisk contraction|
  |L. Fourth interosseous|K.C.C.| 10  |A.C.C.|  9 |Brisk contraction|
  +----------------------+------+-----+------+----+-----------------+

  +----------------------+---------------+-----------------------------+
  |       Muscle.        |   Faradism.   |Remarks.                     |
  +----------------------+---------------+-----------------------------+
  |                      |               |                             |
  |R. Deltoid (anterior  |Good           |Evidently extensor communis  |
  |   portion)           |               |digitorum on right side is   |
  |L. Deltoid (anterior  |Good           |completely degenerated. First|
  |   portion)           |               |interosseous on right side   |
  |R. Deltoid (posterior |Good           |show reactions of degenera-  |
  |   portion)           |               |tion. On left side extensor  |
  |L. Deltoid (posterior |Good           |communis digitorum shows     |
  |   portion)           |               |normal but feeble contrac-   |
  |R. Supinator longus   |Good           |tions                        |
  |L. Supinator longus   |Good           |                             |
  |R. Extensor communis  |No reaction    |                             |
  |   digitorum          |               |                             |
  |L. Extensor communis  |Feeble reaction|                             |
  |   digitorum          |               |                             |
  |R. Extensor primi     |Good           |                             |
  |   internodii pollicis|               |                             |
  |L. Extensor primi     |Good (but less |                             |
  |   internodii pollicis|than right)    |                             |
  |R. Extensor carpi     |Good           |                             |
  |   ulnaris            |               |                             |
  |L. Extensor carpi     |Good           |                             |
  |   ulnaris            |               |                             |
  |R. First interosseous |No reaction    |                             |
  |L. First interosseous |Good           |                             |
  |R. Second interosseous|Slight reaction|                             |
  |L. Second interosseous|Good           |                             |
  |R. Third interosseous |Slight reaction|                             |
  |L. Third interosseous |Slight reaction|                             |
  |R. Fourth interosseous|Slight reaction|                             |
  |L. Fourth interosseous|Good           |                             |
  +----------------------+---------------+-----------------------------+

ELECTRICAL REACTIONS IN LEAD PARALYSIS. (CASE 2.)

  +---------------------+----+---------------+---------+--------------+
  |       Muscle.       |M.A.|  Galvanism.   |Faradism.|  Remarks.    |
  +---------------------+----+---------------+---------+--------------+
  |R. Deltoid           |  9 |Slow reaction  |No       |Reaction of   |
  |                     |    |A.C.C. > K.C.C.|reaction |degeneration  |
  |L. Deltoid           |  9 |Slow reaction  |Slow     |              |
  |                     |    |A.C.C. > K.C.C.|reaction |              |
  |R. Extensor communis |  9 |Slow reaction  |No       |              |
  |   digitorum         |    |A.C.C. > K.C.C.|reaction |              |
  |L. Extensor communis |  9 |Slow reaction  |No       |              |
  |   digitorum         |    |A.C.C. > K.C.C.|reaction |              |
  |Ante brachial and    |    |               |         |              |
  |brachial groups give |    |               |         |              |
  |normal reaction      |    |               |         |              |
  +---------------------+----+---------------+---------+--------------+

ELECTRICAL REACTIONS IN CASE OF RECOVERED WRIST-DROP. (CASE 3.)

  +---------------------+----+---------------+---------+--------------+
  |       Muscle.       |M.A.|  Galvanism.   |Faradism.|   Remarks.   |
  +---------------------+----+---------------+---------+--------------+
  |R. Extensor communis |  9 |Good reaction  |Good     |All muscles   |
  |   digitorum         |    |K.C.C. > A.C.C.|reaction |react well to |
  |L. Extensor communis |  9 |Good reaction  |Good     |both currents;|
  |   digitorum         |    |K.C.C. > A.C.C.|reaction |no sign of any|
  |R. Extensor ossis    |  9 |Good reaction  |Good     |reaction of   |
  |   metacarpi pollicis|    |K.C.C. > A.C.C.|reaction |degeneration  |
  |L. Extensor ossis    |    |Good reaction  |Good     |              |
  |   metacarpi pollicis|    |K.C.C. > A.C.C.|reaction |              |
  |R. Deltoid           |    |Good reaction  |Good     |              |
  |                     |    |K.C.C. > A.C.C.|reaction |              |
  |L. Deltoid           |    |Good reaction  |Good     |              |
  |                     |    |K.C.C. > A.C.C.|reaction |              |
  |R. Extensor carpi    |    |Good reaction  |Good     |              |
  |   ulnaris           |    |K.C.C. > A.C.C.|reaction |              |
  |L. Extensor carpi    |    |Good reaction  |Good     |              |
  |   ulnaris           |    |K.C.C. > A.C.C.|reaction |              |
  |R. Interossei        |    |Good reaction  |Good     |              |
  |                     |    |K.C.C. > A.C.C.|reaction |              |
  |L. Interossei        |    |Good reaction  |Good     |              |
  |                     |    |K.C.C. > A.C.C.|reaction |              |
  +---------------------+----+---------------+---------+--------------+

This case is a typical one of the anterior brachial type, showing
partial recovery of function. The man is able to grasp, although the
wrist becomes strongly flexed in so doing.

CASE 2.--We are indebted to Dr. Gossage for this case, which was
presented at the Out-patients of the Westminster Hospital; and to
Dr. Worrell, who made the electrical investigations. We are further
indebted to Dr. Worrell for the reports which are given in tabular form
of the electrical reactions of these three cases.

This is a case of brachial type, with weakness of both deltoids, and
the patient was unable to raise his right arm at the shoulder. It
will be seen that there is here also evidence that the electrical
contractility diminishes before the entire loss. It will be also
noticed that the supinators are unaffected.

CASE 3.--These are the electrical reactions of a case which had
recovered. This man showed the ordinary anterior brachial type, which
came on suddenly, although he had shown distinct weakness of wrists
when forcible flexion was performed for nine months previously, but
there had been no obvious increase in the weakness. He was immediately
removed from his work, and within seven days paralysis, which at first
only affected the extensor communis digitorum, had spread to the minimi
digiti and the extensor indicis, the opponens pollicis being also
involved on the right side. He was treated from the start with faradic
current, and was instructed to use the battery himself, which he did
twice a day for a year. At the end of two months he was sufficiently
recovered to be given light work, and at the time of taking the
reactions his wrists have so far recovered their power that we were
unable to flex them forcibly.

The progressive weakness noted in the three cases has already been
referred to, and may be a prodrome of paralysis, but there may be
recovery without paralysis supervening.


=Tremor.=--Tremor may be observed in a large number of cases of lead
poisoning, and is invariably associated with paralysis, although the
symptom of tremor by no means always progresses to definite palsy. Two
types of tremor are described--fine and coarse--and Gübler further
describes a type of tremor which is both rhythmic and intermittent. The
tremor is usually distinctly increased on attempting to grasp or point
the hand (intention tremor), but it is difficult to separate tremor
from alcoholic tremor, and, further, it must not be forgotten that
persons engaged in arduous work may show a certain amount of tremor due
to muscular fatigue. Persistent tremor, however, is a symptom that is
always to be noted and carefully watched.

Of the types of paralysis, the antibrachial is the most common, and,
secondly, probably the brachial. The least common is the peroneal. The
table on p. 54 shows the distribution of cases of paralysis, so far as
they can be made out from reports received since 1904.

Closely associated with paralysis are affections involving the brain.
Tanquerel, in his classical description of affections of the brain
associated with lead poisoning, gives the following classification:

  1. Delirium.
  2. Lead mania.
  3. Psychic depression.
  4. Coma.
  5. Convulsions, saturnine eclampsia, or epilepsy.

There is probably a very considerable relationship between insanity
and lead poisoning, as pointed out by Robert Jones[17], the resident
physician and Superintendent of Claybury Asylum.

Rayner[18] remarked that the compulsorily careful habits of life
of painters and lead-workers ought to protect them against vicious
habits, and should protect them against a too free indulgence in the
use of alcohol! Our own experience is that paralysis, and particularly
affections of the brain, occur in the majority of cases in persons
who are addicted to alcohol, and the experiments quoted in the
chapter on Pathology on the influence of alcohol in the production of
encephalitis in animals is strong presumptive evidence that alcohol is
one of the chief predisposing causes in the determination of saturnine
encephalopathy.

Encephalitis is given as a cause of death in the report already
referred to in 14·3 per cent. of 264 fatal cases. Amongst this number
encephalopathy accounted for 14·3 per cent., cerebral hæmorrhage 9·8
per cent., and paralysis 9·2 per cent. Now, all these are cases in
which cerebral lesions may be confidently stated to have existed,
which brings the total to 34·4 per cent. of deaths at least due to
brain involvement. We have already referred to the high incidence of
paralysis amongst file-cutters--40 per cent. as against 21·1 per cent.
for all industrial forms of poisoning.

When encephalitis occurs, it is usually an acute symptom, and often
develops before paralysis is set up, but as a rule is preceded by a
period of persistent headache, such headache being invariably temporal
or occipital.

Robert Jones, in his paper, states that of the 133 cases who, from the
nature of their work (painters, plumbers, etc.), were liable to lead
impregnation, 19 had signs of poisoning upon admission, whilst 22 had a
distinct history of lead poisoning at some time or other. He gives the
following analysis of the mental condition:

  Mania                            37
  Melancholia                      33
  Dementia                         19
  Dementia with epilepsy           10
  Dementia with general paralysis  24
  ? General paralysis               7
  Alcoholic mania                   3
                                  ---
                                  133

Savage[19] is of opinion that lead will produce any of the symptoms of
general paralysis of the insane, and may even be a contributory cause
of the disease, but no statistics are available of the Wassermann
reaction in these cases. Goodall[20] refers to the fact that nerve
poisons, such as syphilis, alcohol, and fevers, injury or sunstroke,
which are intermediate in fixity between alcohol and lead, seem to have
an intermediate influence in the production of general paralysis.

Jones states that the mental symptoms found in the cases are to be
grouped amongst one or other of the following varieties:

1. Of a toxæmic nature, with sensory disturbances, which tend to get
well rapidly.

2. Hallucinations of sight and hearing, more chronic in nature, which
may be permanent. The delusions in this class are almost invariably
those of being poisoned or followed about, and are in the main
persecutory.

3. Those resembling general paralysis with tremors, increased
knee-jerk, inco-ordination, accompanied with listlessness amounting to
profound dementia, but which tend to get well.


=Eye Changes.=--Two main forms of eye change are to be found amongst
lead-workers. In the first place, temporary and sudden amaurosis makes
its appearance, due no doubt to vascular change, either vaso-motor or
hæmorrhagic. The trouble may occur in one or both eyes, may come on
gradually, the patient merely being unable to distinguish letters or
faces at a distance, or he may become suddenly totally blind. In the
majority of cases the affection disappears under treatment, but in a
small number of cases total blindness persists.

Occasionally nystagmus may be seen, but is not a common symptom;
but dilatation of the pupils, quite apart from retinal changes, is
not unusual. Inequality of the pupils may be observed, but partial
dilatation of both pupils is more common, and is often associated with
early anæmia. Conjunctival hæmorrhages are to be noted from time to
time, without obvious cause, such as injury, etc., but in the majority
of cases these have been associated with other symptoms.

The first feature noticed in the eye is loss of brightness, and a
curious lack-lustre of the eyes of persons intoxicated by lead is one
of the general features making up the saturnine cachexia. Loss of
brightness of the eye is associated in many other diseases with anæmia,
but is particularly prominent in lead poisoning, much more so than is
to be accounted for alone by the degree of blood-destruction, and is a
point of which the examining surgeon should always take notice.

One other form of eye change requires attention--namely, retinal
changes due to circulatory disturbances. In an advanced case the whole
picture is one of severe albuminuric retinitis, but in the earlier
stages some engorgement of the vessels without alteration of the
surrounding tissue is seen. Elschnig[21] associated this alteration in
the vessels of the eye with vaso-motor changes caused by direct action
of the poison, producing a vascular constriction or dilatation, and
is inclined to regard the kidney disease frequently associated with
this condition of the eye as something quite apart. He would regard
the two affections as independent, and merely correlated through their
common origin--lead intoxication. It has even been suggested by some
observers that the change in the eye is secondary to cerebral œdema.
Thus Mannaberg[22] regards the encephalitis of saturnine origin as
associated with chronic œdema of the brain and spinal cord, which thus
produces reflex irritation of the nervous system of the eye. Bikler[23]
and Weber[24] consider the symptoms as circulatory. From whatever
cause the disease is set up, sooner or later changes in the form of
obliterative arteritis take place, with gradual but ultimately complete
loss of vision.

There are said to be no characteristic eye symptoms in acute cases
of lead poisoning, whereas with chronic lead poisoning in many cases
there is central and peripheral affection. The affections may be
further divided into subjective and objective. Many of the subjective
symptoms, such as loss of sight and blindness, are associated with
definite eye lesions, which may be seen with the ophthalmoscope, but
other definitely objective lesions may be present without any influence
on sight to commence with. Folker[25] describes five cases of lead
amblyopia in lead-workers from a pottery district, in all of which
there was a peculiar symptom--the gradual failing of sight associated
with colour flashes. When examined, the discs were described as white,
and the vessels small.

Lockhart Gibson[26], in describing the cases of eye disease amongst
the children in Queensland, found one symptom apparently in all the
eyes examined--namely, great swelling of the discs. This swelling of
the discs might be accompanied with no loss of sight whatever, and at
other times had been accompanied with defective sight for many months
previously. Some of the discs were excessively swollen. There were also
to be seen patches of pigment and irregular swelling of the vessels,
but no definite hæmorrhages. In the more acute cases, and particularly
those associated with complete paralysis of the ocular muscles, total
blindness usually followed.

As a rule, when complete amaurosis occurs in lead poisoning, blindness
follows through double optic neuritis or neuro-retinitis, but amblyopia
may be present without fundus changes. Occasionally the loss of
sight may be regarded as of central origin. The renal disease so
often associated with lead poisoning may cause the retinal changes
accompanying it. An albuminuric neuro-retinitis may occur without
albumin in the urine. As a rule, the eye of a lead-worker reacts to
light and accommodation. Ophthalmoscopic examination may show very
pink discs, patches of pigment scattered about irregularly outside
the discs, with occasional definite hæmorrhage. The edge of the discs
may show blurring, with further sclerosis and peri-arteritis of the
vessels, a white sheath around the arteries being often visible. The
neuritis on one or both sides may be associated with disturbances
of sight, and diffusely red and cloudy papilla, with swelling or
hæmorrhages. In choroidal atrophy pigmentation may also be seen.


=Muscular System.=--One further point may be referred to in relation
to the muscular system--namely, the occurrence of pain of a rheumatic
type. Quite a number of cases of mild degrees of lead poisoning
complain of arthralgic symptoms--that is to say, “rheumatism.” Careful
examination of such cases shows no evidence that the pain is a true
arthralgia, neither does it seem to have a true relation to gout. The
pain as a rule is referable to the muscles themselves, and in such
instances digital examination of the muscle in the region of the pain
generally exhibits deep-seated tenderness. There does not appear to be
any special marked tenderness along the trunks of the nerves supplying
the muscle, nor is there evidence of hyperæsthesia of the skin. Such
hyperæsthesia does occur in lead poisoning, but is generally associated
with cerebral lesions. The pain, therefore, must be regarded rather as
myalgic, and intercostal distribution of the pain is not infrequent;
but although the symptom is one that is often complained of, it is
an exceedingly difficult one to differentiate from other myalgias as
a definite symptom of lead poisoning. The chief point in favour of
the inclusion of this so-called lead rheumatism as a symptom of lead
poisoning is the frequency with which it is noted in the reports by
certifying surgeons. While, therefore, having no evidence to regard it
as necessarily a definite symptom of poisoning, it is one which has
been recorded in a considerable number of cases. As has been already
suggested, there is some reason to think these myalgic pains may be due
to minute hæmorrhages taking place in the muscles, thereby producing
localized irritation to some extent comparable with the “bends” of
divers.


=Post-Mortem Signs of Plumbism.=--Very real difficulty exists in
determining from naked-eye appearances at a post-mortem examination
whether the cause of death be due to chronic plumbism or not. The
changes produced by several other forms of intoxication, notably
chronic alcoholism, produce many of the same changes in the tissues as
lead. Inspection of the organs in the case of plumbism can only give
rise to a surmise that the cause of death is due to lead poisoning.

There are, however, certain macroscopical appearances at an autopsy in
the case of saturnism which should be carefully noted, and although
alone they do not constitute sufficient evidence upon which to pass a
definite opinion, they are still important as diagnostic signs in the
light of histological and chemical examination.

Particular note should be paid at an autopsy of a case of suspected
lead poisoning to the following points:

1. Mouth, for the presence or absence of blue line, which, if present,
must be examined with a lens.

2. General condition of the abdominal viscera, and particularly of
the mesenteric and perinephritic fat. In plumbism this is invariably
reduced in quantity.

3. The condition of the mesenteric vessels, as to whether or not they
are engorged with blood, or whether or not leakage appears to have
taken place.

4. General condition of the arteries, for the presence of atheroma, etc.

5. The heart muscle, which in plumbism is generally pale, flabby, and
with a tendency to general dilatation of the cavities.

6. Intestines.

(_a_) The presence of injection of the muscular coat, particularly the
lower portion of the intestine, and about the ileo-cæcal valve.

(_b_) The presence or absence of minute ulcerations, or even
hæmorrhages along the intestine, even in the mucosa of the stomach.

(_c_) The presence of dark staining in the coats of the lower
intestine, not altogether disappearing when washed under a gentle
stream of water. Should there be any evidence of this staining, it is
highly important to remove some of the fæces, as well as a portion of
the intestine, for chemical examination.

7. The condition of the liver, which in poisoning by lead, as by
alcohol, frequently shows a considerable amount of enlargement, and may
even show patches of perihepatitis due to secondary causes. But the
cirrhosis occurring in lead poisoning is not so great as in alcohol. In
lead poisoning the liver as a rule is large and soft, and engorged with
blood.

8. The kidney, for signs of interstitial rather than tubular nephritis,
adherent capsule, and blood-stained exudate.

9. If paresis of any sort has been present during the illness,
examination of the cord and brain should be made with especial care,
and in addition the nerves on the affected side supplying the affected
muscles should also be examined. In the brain definite small but coarse
hæmorrhages may be occasionally observed, but as a rule the only signs
to be found are injection of the cortical vessels, frequently over
certain definite areas, and not involving the whole of the vascular
system of the brain. Minute hæmorrhages may be also found in the spinal
cord.

For the purposes of histological examination, a portion of the
following organs should be removed and placed in a 5 per cent. formalin
solution at once: Liver, spleen, kidney, intestine, the last-named
specimen being selected from any area which shows injection, or
ulceration, or dark staining.

Smears may also be made from the bone-marrow, as in prolonged anæmia
of saturnine origin definite changes may at times be found in the
bone-marrow cells.

Where paresis has existed, a portion of the particular nerve supplying
the muscles should be obtained, and histological examination made, as
well as a portion of the cord above the lesion, and where cerebral
symptoms have been present, a portion of the brain, the portions
taken being part of that showing engorgement of the vessels. For the
nervous tissue generally, it is better to place some of the specimens
in Müller’s solution, and others in spirit. Equal parts of Müller’s
solution and formalin may be used if desired.


_Material for Chemical Examination._--For the purposes of chemical
examination, any of the organs which appear to be mainly affected
by chronic inflammation may serve, but it is usually important to
examine the brain, kidney, and liver. If any dark staining exist in
the intestine, a portion of this, together with the contained fæces,
should be removed. It is better to tie ligatures round the intestine,
and divide the coat between the ligatures, and place the whole of the
specimen in dilute formalin. Specimens thus obtained should be sent off
for examination at once. The whole of the organ need not necessarily
be despatched for examination in every case, but if only a portion is
sent, it is essential that the weight of the whole organ be accurately
taken before any portion is removed, and the total weight noted with
the specimen when sent.


REFERENCES.

  [1] TANQUEREL: Traité des Maladies de Plomb ou Saturnines. Paris,
  1839.

  [2] LANCEREAUX: Gaz. Méd., 1862; Tribune Méd., 1896.

  [3] MEILLÈRE, G.: Le Saturnisme, chap. iv.

  [4] TELEKY: Deutsch Zeitschrift für Nerven Heilk., vol. xxxvii., 1909.

  [5] DÉJERINE-KLUMPKE: Thesis on Des Polynephrites en Général et des
  Paralysies et Atrophiques Saturnines en Particulier. Paris, 1889.

  [6] TELEKY: _Ibid._

  [7] TELEKY: _Ibid._

  [8] GOMBAULT: Arch. Phys., 1873.

  [9] MOEBIUS: Ueber einige Ungewöhnliche Fälle von Bleilähmung. Cent.
  für Nervenheilk. 1886.

  [10] TANQUEREL: _Ibid._

  [11] SAJOUS: Archiv für Laryng., iii., 1882.

  [12] MORELL MACKENZIE: Brit. Med. Journ., epitome, p. 1202, 1893.

  [13] SEIFERT: Berl. Klin. Woch., 1884.

  [14] LOCKHART GIBSON: Brit. Med. Journ., vol. ii., p. 1488, 1908.

  [15] GALEZOWSKI: Jahr. f. Aug., p. 382, 1877.

  [16] FOLKER: Brit. Med. Journ., ii., p. 1556, 1898.

  [17] ROBERT JONES: Brit. Med. Journ., September 22, 1900.

  [18] RAYNER: Journ. of Mental Science, 1880.

  [19] SAVAGE: Clifford Allbutt’s Medicine, vol. vii., p. 657.

  [20] GOODALL: _Ibid._, p. 693.

  [21] ELSCHNIG: Wien. Med. Woch., Nos. xxvii, xxix., 1898.

  [22] MANNABERG: Ber. Klin. Woch., 1896.

  [23] BIKLER: Arch. für Augenheilk., b. xl., 1900.

  [24] WEBER: Thèse de Paris, 1884.

  [25] FOLKER: _Ibid._

  [26] LOCKHART GIBSON: _Ibid._




CHAPTER X

CHEMICAL INVESTIGATIONS


Very great assistance is afforded by chemical and histological
diagnosis in the determination of cases of lead poisoning, especially
when the case is likely to involve proceedings under the Workmen’s
Compensation Act. In addition, a large amount of information is
afforded to the certifying or appointed surgeon and the medical
practitioner by adoption of certain easily carried out methods of
diagnosis. It will be our purpose in the present chapter to describe
as far as possible methods by which chemical or other investigation of
a case of lead poisoning can be pursued, and the clinical methods of
diagnosis which are applied in ordinary routine.

The majority of the methods described, especially the chemical
investigation of material obtained from alleged fatal lead poisoning
for the purpose of determining the presence or absence of lead,
the histological examination of such tissues, and the examination
quantitatively of excretions for lead, are processes which can only be
carried out in a fully equipped laboratory, and certainly do not belong
to the ordinary routine of medical work. The medical practitioner
cannot be expected in the ordinary course of his routine work to
examine blood-films for basophile staining or to make differential
blood-counts. Especially is this the case in the routine examination of
large numbers of factory hands. Further, many of the processes involved
in either the chemical or histological examination of the tissues
require so much special apparatus, without which such work cannot be
undertaken, that the mere cost of the necessary instruments precludes
the investigation being carried on except in special laboratories. At
the same time, our purpose is to point out how additional methods of
research may be made use of in obscure cases, and how recourse should
be had to a well-equipped laboratory in doubtful cases. Further,
the coroner, when ordering a post-mortem examination, may ask for a
histological and chemical examination.


=Methods of Chemical Diagnosis.=--The presence of lead may require
to be determined qualitatively and quantitatively, and the procedure
may differ slightly as to which process it is necessary to adopt. The
quantitative determination of the amount of lead present in organs or
excretions of the body is of far more importance than the estimation
or determination of the fact of its presence. We have already referred
to the work of Gautier[1], who has found lead present in the tissue of
normal persons with such constancy that French observers, at any rate,
now speak of “normal lead,” to distinguish it from lead which may be
found in pathological conditions. There is, however, little doubt that
the quantity of lead existing in the human body is exceedingly small.
It is possible, with certain refined methods of chemical examination,
that qualitative traces of this substance might be found. On the
other hand, the methods of determination of lead are some of the most
difficult in toxicological analyses, on account of the presence of
other metals, particularly iron, which are exceedingly difficult to get
rid of, and may easily lead to errors.


1. =Qualitative Tests.=--The group reagent for lead is sulphuretted
hydrogen in acid or alkaline solution. Lead is precipitated by this
reagent as a black precipitate. Where no other metals are present, and
where no organic matter is present at the same time, there is very
little difficulty, and the usual method of the determination of lead in
water by means of sulphuretted hydrogen is exceedingly easy.

Potassium iodide gives a yellow precipitate soluble on warming, and
forms large crystals on the tube. Hydrochloric acid and chlorides give
needle-shaped crystals, soluble in heat, and crystallizing out when
cold. But the double chloride of potassium and lead is more soluble
in heat, and still more soluble in cold, than is the pure chloride.
This fact is made use of in the process to be described presently in
separating lead from organic mixtures.

The direct examination is rarely possible or satisfactory, but the
potassium cupric acetate method is one that may be applied to the
qualitative estimation of lead in the tissues.


_Method for detecting Small Quantities of Lead qualitatively._--Dry and
incinerate the material to be tested. Extract with hot dilute nitric
acid, after repeated incinerations, finally extracting with ammonium
acetate. Filter, incinerate, and take up the residue in dilute nitric
acid. Evaporate to dryness and add a few drops of dilute acetic acid,
and transfer drop to microscope slide.

To the drop on the microscope slide add one drop of dilute copper
acetate solution, and two to three drops of saturated solution of
potassium nitrate. Stir up the drops and well mix with a platinum wire,
allow to stand for a few minutes, and then examine with a two-thirds
objective. If lead is present, violet-black cubes of potassium copper
lead nitrate appear (K₂CuPb[NO₃]).

This test is said to give a reaction in the presence of 0·00003 gramme.


_Determination of Lead in the Urine._--The quantity of lead passed
by the kidneys into the urine is always small, even in acute lead
poisoning. Further, the lead is excreted in organic combination, and is
therefore difficult to detect. For absolute quantitative examination it
is essential to evaporate the whole bulk, using at least ¹⁄₂ gallon of
the fluid, and proceeding with the concentrate in the manner indicated
in the estimation of lead.

For the qualitative examination many methods have been suggested, but
all of them are more or less fallacious.

In certain instances in acute lead poisoning, or where a relatively
large quantity of lead is excreted by the kidney, acidulation of
the fluid with strong sulphuric acid direct will at times produce
a precipitate of lead sulphate, which may be filtered off and the
filtrate examined by the usual tests--namely:

A white precipitate with dilute sulphuric acid.

A yellow precipitate with potassium chromate, hardly soluble in nitric
acid, but soluble in alkalies.

A blue flame on heating on a platinum wire, and finally, if sufficient
substance is present, the reduction to metallic form with the blowpipe
flame.

A method has been recommended of suspending a small bag of calcium
sulphide in the sample to be examined, the supposition being that, if
the calcium sulphide in the bag showed blackening, it would be due
necessarily to lead. This is highly questionable, and in the hands of
one of us (K. W. G.) has not given satisfactory results.

A further method, which is quite simple in application, and
occasionally gives confirmatory results, may be applied in the
following manner: The urine to be examined is inoculated with the
_Bacillus coli communis_. For this purpose a small quantity of fæces
may be used. The _B. coli_ in its growth makes use of the organic
substances in the urine, and at the same time sets free sulphuretted
hydrogen. The urine left is filtered, the filtrate dissolved in 10 per
cent. nitric acid (minimal quantity), and the filtrate examined by the
usual tests. This method has occasionally given quite good results in
the hands of one of us (K. W. G.), and is, moreover, an exceedingly
easy one to carry out.

Passing sulphuretted hydrogen direct through the fluid is of no value,
as it is necessary first of all to split up the organic compound before
it will react to sulphuretted hydrogen.


_Electro-Chemical Methods._--Of all the methods at present in
use for the estimation of the presence of lead in the urine, the
electro-chemical gives by far the most satisfactory results. Several
methods are described:

The first method consists in using magnesium, which is left for some
hours in the urine, which has been previously strongly acidulated. In
this manner Marsden and Abram[2] say that they have been able to detect
1 part in 50,000 in the urine without difficulty. The method adopted is
as follows:

“A strip of pure magnesium is placed in the fluid to be examined.
Ammonium oxalate in the proportion of about 1 gramme to 150 c.c. is
added. If lead is present, it is deposited on the magnesium. A deposit
is seen within half an hour, but we have usually left it twenty-four
hours. The slip is then washed with distilled water and dried.
Confirmatory tests: (1) Warm the slip with a crystal of iodine (yellow
iodide proves lead, cadmium may be ignored); (2) dissolve deposit in
HNO₃, and apply usual tests. The magnesium can be used again after
careful washing with acid and distilled water. The surface of the
magnesium, when used, must be bright and free from oxide. The delicacy
of the method has been tested with aqueous solutions containing known
quantities of lead, also with normal urine to which known quantities of
lead have been added. In all cases a control experiment was performed
to insure the freedom of the materials from lead. Lead has been
detected when present in the proportion of 1 part to 50,000, whether in
simple aqueous solution or in urine.”

Shufflebotham and Mellor[3] describe the following method as one by
which lead may be detected in organic tissue, and in each case this
necessitated a large amount of evaporation. The method has value,
but the difficulty of dealing with large quantities of fuming nitric
acid, and the addition of this acid from time to time during the
operations, render it difficult unless a good fume chamber is at hand.
Shufflebotham and Mellor state that they obtained no reaction with the
potassium chloride-hydrochloric acid method suggested by Dixon Mann.

  “_On the Detection of Lead in Urine and Post-Mortem Specimens._--A
  piece of kidney of 20 c.c. capacity was cut up into about a dozen
  pieces. These were placed in an evaporating basin, and about 50 c.c.
  of fuming nitric acid were poured into the dish. Dense brown fumes of
  nitrogen oxides were evolved. When the action had subsided (in from
  two to three minutes), the dish was placed upon a sheet of asbestos,
  and allowed to simmer over the Bunsen flame for about an hour. If the
  frothing appears in danger of running over the sides of the dish,
  stirring with a glass rod or removal of the flame for a short time
  may be necessary. Twenty-five c.c. of the fuming acid were added at
  intervals of a quarter of an hour, and this process was repeated
  three times. The destruction of the organic matter was so complete
  that the whole of the piece of kidney passed into complete solution.
  The solution was then evaporated down to a few c.c., neutralized
  with caustic soda, filtered, and treated with hydrogen sulphide. A
  dark-brown precipitate of lead sulphide was obtained. With potassium
  chromate a yellow precipitate of lead chromate was obtained with
  the same specimen of kidney which gave a negative result with the
  KClO₃-HCl method of destroying the organic matter. Our reagents,
  dishes, etc., were then examined with a blank test, but we found no
  lead.

  “_Urine._--We then sought the presence of lead in the urine of
  Cases 2, 3, and 4. Half a gallon of urine was evaporated down to
  dryness in each of two basins. In one basin the residue was heated
  until it was charred. Both residues were then treated separately
  with fuming nitric acid, as just described. The uncharred residue
  passed into solution, and on cooling deposited a white sediment. The
  mother-liquor was neutralized and tested in the usual way. A brown
  precipitate of lead sulphide was obtained in Case 2, while in Case
  3 a well-marked black precipitate was obtained. The urine of Case 4
  gave a negative result. The charred residue did not pass completely
  into solution, and the tests for lead were not so well defined as
  when the residue was uncharred. This shows that care must be taken to
  prevent charring of the residue during evaporation.”

A method has recently been described by Hebert[4]--a modification of
Trillet’s. This method is based upon the fact that peroxide of lead,
when mixed with tetramethyl of diphenyl-methylen, gives in acetic acid
solution a fine blue coloration. Unfortunately, a number of other
peroxides give the same blue coloration, amongst them manganese,
potash, copper, magnesium. In addition, the sodium peroxide used to
convert the lead present into the peroxide also gives a bright blue
coloration with the reagent, even if present in minute quantities.

The test is made in the following manner: The substance is incinerated,
sulphuric acid added in the usual way, and the substance evaporated to
dryness. It is treated with a cold solution of sodium hypochlorite. The
hypochlorite is then removed partly by washing and partly by heating,
and the reagent is then added directly to the substance in the capsule,
and if a peroxide is present the blue colour results.

Unfortunately, this dissociation-point of the hypochlorite and the
temperature at which peroxide of lead is changed back again to the
oxide are very close together, being only about 25° C. In addition,
it is very difficult to remove the last traces of the substances
which give a blue coloration in addition to lead. One of us (K. W.
G.) has made extensive trials with this method, as, if it had been a
reliable process, it would have been one which would have considerably
facilitated the estimation of lead in small quantities. The method has
been adopted by certain French observers, who by drawing 2 c.c. of
blood from the median basilic vein, and estimating the lead present in
this small amount by means of the blue coloration, have sought to show
that at least 25 milligrammes of lead were circulating in the blood of
the body. In addition to other grave considerations, the fact that the
reagent itself is colourable by certain other peroxides which exist in
the blood-ash renders these figures entirely untrustworthy.


2. =Quantitative Methods of Estimation.=--Two methods may be used in
the detection of lead in organic substances, either in organic fluids
or in solids, and are generally termed the “wet” and “dry” methods,
from the original treatment of the substance.

In the dry method the substance is incinerated with or without the
addition of sulphuric and nitric acid; in the wet the material is
treated with hydrochloric acid and potassium chlorate. Subsequent
treatment in both cases is on the same lines.


_Method of Fresenius and Von Babo[5]--Moist Method._--The substance
which is suspected to contain the poison, if solid, is reduced to a
pulp, and is mixed with sufficient water until of the consistency of
thin gruel. The urine should be evaporated to one-fourth or one-sixth
of its volume. Fæces should be well stirred up with distilled water.
The substance is then placed in a large flask together with crystals
of potassium chlorate; each 100 grammes of the substance require 3 to
4 grammes of potassium chlorate. Pure HCl of the same weight as the
original substance is then added, the flask is placed on a water-bath
and gently heated. Care must be taken that the heating is not too
brisk, as otherwise the evolution of the chlorine peroxide takes place
too rapidly. If necessary, additional crystals of potassium chlorate
are added from time to time until the fluid becomes limpid and of a
slight yellow colour, or, if there is much organic matter, until it
assumes the appearance and colour of thin oatmeal gruel. On account of
more gradual evolution of chlorine, the chlorate that is present before
the flask is heated acts much more energetically, weight for weight,
than fragments added after the liquid is heated, as a great deal of
the gas then escapes without rendering any service. If the substance
contains sugar, starch, or alcohol, extra care must be taken to avoid
frothing over. When the fluid contents are clear or reduced to a thin
consistency, the liquid is transferred to an evaporating basin, and
allowed to remain on a water-bath until the smell of chlorine has
disappeared; it is then filtered while hot. The whole of the organic
matter is not destroyed by this process, fatty substances especially
being resistant; but if the organic matter is reduced to small
fragments, any mineral poison present will be liberated.

The objections raised against this process are that some important
poisons--such, for instance, as arsenic and antimony, specially the
former--are liable to escape partially in the form of vapour, and that
others, such as lead and silver, may remain as insoluble precipitates
on the filter. As regards the first objection, it is to be observed
that, when the hydrochloric acid is diluted with water (as in a moist
method of destroying organic matter), any arsenic which may be present
in the hot solution is not given off with its acid aqueous vapour,
arsenious chloride dissolved in hydrochloric acid being volatile
only when the solvent is concentrated. Any possibility of loss may
be avoided, however, by furnishing the flask, in which the organic
matter is being destroyed, with a condenser and receiver. The second
objection, as far as lead is concerned, is met by taking care to filter
the solution whilst hot; if only a limited amount of lead is present,
it then remains in solution as chloride so long as the liquid is hot,
and will consequently pass through the filter. A considerable quantity
is kept in solution in the cold, as it forms a combination with
potassium chloride, which is more soluble than lead chloride alone. If
a large amount is present, it will not all be found in the filtrate;
the substance left on the filter, therefore, must always be tested for
lead. In toxicological work, however, the amount of lead present is not
as a rule more than will remain dissolved in the cold. Silver chloride,
being insoluble either in hot or cold water, will not pass through the
filter; consequently the salts of silver require dealing with in a
special manner.

_Dry Method._--This is effected by heating the finely divided substance
to redness, so that it is either carbonized or completely incinerated.
When cold, the residue is drenched with nitric acid, and sufficient
heat is afterwards applied to drive off the free acid. The nitrate
of the metal is then dissolved in water, filtered, and dealt with
according to the kind of metal present.

The dry method is unsuitable in the case of the more volatile metals,
as arsenic, antimony, and, in a lesser degree, lead, tin, and zinc.
Further, it is extremely difficult and troublesome to carry out with
large masses of organic matter. It is convenient with small amounts,
and in the absence of the more volatile metals yields good results.

The following two methods are given by Glaister[6] on the one hand, and
Dixon Mann[7] on the other. Both methods are good. It will be seen that
Glaister recommends the estimation of the lead as sulphide.

When minute quantities of lead are present in combination with large
amounts of organic matter, the dry process is tedious, difficult to
carry out, and uncertain in its results. The plan adopted in the
elimination of lead by Dixon Mann is as follows:

The urine is evaporated down to the consistency of gruel, and the
fæces mixed in distilled water to a like consistency. They are then
treated by the wet method, as given above. The filtrate after cooling
is placed in a glass cell, the bottom of which consists of a sheet
of vegetable parchment; the cell is immersed to such a depth in a
deeper cell, containing distilled water acidulated with a few drops of
sulphuric acid, that the liquids in the inner and outer cells stand at
the same level. A piece of platinum-foil enclosing a surface of about
50 square centimetres, constituting the kathode, was submerged in the
liquid contained in the inner cell, a similar piece of platinum-foil,
constituting the anode, being immersed in the outer cell. The pieces
of foil are so placed as to be opposite each other, separated by the
parchment diaphragm. A current, 3 or 4 volts, is then passed through
for from six to eight hours, after which the foil is removed from the
inner cell and gently washed and dried. The metallic lead is dissolved
off the foil with dilute nitric acid aided by heat, and after driving
off most of the free acid the solution is decomposed with dilute
sulphuric acid with an equal volume of alcohol added. It is then set
aside for twenty-four hours. The precipitate of lead sulphate is washed
with water containing 12 per cent. of alcohol, until all the free acid
is removed; it is then separated by decantation, ignited, and weighed.
The amount of lead is calculated from the weight of the sulphate; 100
parts of sulphate are equal to 68·319 parts of metallic lead.

Whether the moist or the dry process is used, the residue after the
primary filtration should be tested for lead, which may be present as
sulphate and remain undissolved. If the original substance contains
lead as sulphate, the salt should be dissolved with heat in an aqueous
solution of ammonium tartrate to which a little free ammonia has been
added, then precipitated with sulphuretted hydrogen (100 parts of lead
sulphide equal 86·61 parts of metallic lead). It is better, however,
to convert the sulphide into sulphate by treating it with nitric and
subsequently sulphuric acid, after which it is ignited, weighed, and
the amount of the metal calculated by the lead sulphate factor.

Having obtained the substance by decomposing the organic matter, two
methods of estimation may be made use of:

(1) Colorimetric; (2) gravimetric.

Where the estimation is to be made gravimetrically, the substance is
always obtained as a sulphate, and the lead estimated by weighing as
a sulphate. This process is an exceedingly tedious one when a large
number of small samples have to be estimated, as in the determination
of the amount of lead dust present in the air. On the other hand, it
is probable that the use of the balance in the estimation of lead as
sulphate is more accurate where larger quantities up to 10 milligrammes
are present; but where only 2 or 3 milligrammes are present in the
amount of substance examined, the experimental error in washing is
too large to warrant the expenditure of time required in this form of
estimation, and the colorimetric method is used.


=Detection of Lead in Organic Mixtures.=--Acidulate the organic
substances, reduced to fine proportions, with nitric acid, heat for
some time, then permit to cool; filter, wash residue, and mix washings
with filtrate; concentrate filtrate; pass H₂S; place mixture in warm
place to allow precipitate to settle; after which decant supernatant
fluid, collect precipitate on tared filter, thoroughly wash, dry on
water-bath, and weigh. One part of sulphide is equivalent to 0·9331
part of lead oxide and 1·5837 parts of acetate of lead.

The electrolytic method is better adapted for the detection of
minute quantities of lead, as, for example, in the urine or fæces or
in vomited matter. The urine may be evaporated to a viscous state;
the others, finely broken up, are treated in the same way, after
HCl is added, as recommended above, the mixture heated, and pinches
of powdered chlorate of potash added, as necessary, to break down
organic matter. The heating is continued until the odour of chlorine
disappears, after which it is filtered and the filtrate allowed to
cool. The filtrate is then placed in the outer cell of a two-celled
arrangement, not unlike a dialyser, the bottom of which is formed
of vegetable parchment, the outer cell containing distilled water
acidulated with H₂SO₄. Into the inner cell is placed a piece of
platinum-foil measuring about 50 square centimetres of exposed
surface, which is connected with the kathode or negative pole of four
Grove cells, and into the outer cell is placed a like-sized piece
of platinum-foil connected with the anode or positive pole. These
pieces of foil are so placed in relation to one another that they
are only separated by the parchment. The galvanic circuit being now
closed for some hours, any lead in the filtrate will be deposited
on the platinum-foil connected with the kathode in the inner cell.
The foil is then removed, carefully washed, and the metallic lead
dissolved by dilute nitric acid aided by heat, after which the solution
is concentrated until most of the free acid is driven off; dilute
sulphuric acid is added to throw down the sulphate, alcohol being also
added to expedite precipitation. The precipitate is allowed to settle
for twenty-four to thirty-six hours, filtered on a tared filter, washed
with water containing 12 per cent. of alcohol, dried, ignited, and
weighed. One part of sulphate is equivalent to 0·68319 part of metallic
lead and to 1·25 parts of acetate of lead.

The estimation of the lead, especially if the amount be small, may
be more accurately made by the volumetric colorimetric method. The
metallic lead deposited on the platinum-foil is dissolved in nitric
acid, and distilled water added, and an aliquot portion placed in a
Nessler glass. A few drops of freshly-prepared H₂S water, or H₂S gas
itself, may be added to or bubbled through the contents of the glass so
as to form lead sulphide. The colour formed is now matched in a similar
glass, using a standard solution of lead nitrate, and forming the lead
sulphide as before.

Some have advocated the magnesium wire deposition test, originally
devised by von Jaksch, and modified by Hill Abram, for the detection
of lead in the urine of persons who are suspected to be suffering from
chronic lead poisoning (see _ante_).

  The colorimetric method of estimating lead has been made use of with
  very great success by Duckering in the estimation of lead in the air
  of potteries. The method is that devised by Mr. Vernon Harcourt[8],
  with a few modifications. The whole of the method is given, as
  observation on the quantity of lead present in the air of lead
  factories helps greatly in suggesting rational methods of precaution.

  “After drying and weighing the filters, the following is the method.
  Solutions required:

  “_Nitric Acid._--One part of pure concentrated nitric acid to three
  parts of water.

  “_Caustic Soda._--One hundred grammes of pure caustic soda dissolved
  in 250 c.c. of water.

  “_Sugar._--A saturated solution of sugar in water.

  “_Sulphuretted Hydrogen._--A saturated solution of sulphuretted
  hydrogen in water.

  “_Coloured Solution._--Cotton-wool dissolved in concentrated nitric
  acid and evaporated to dryness, and the residue dissolved in a little
  water and filtered; the solution is deep yellow in colour.

  “_Standard Lead._--A solution of lead acetate or lead nitrate made up
  to contain exactly 0·0001 gramme of lead per c.c. of solution.

  “The bulk of the dust in the filter was removed to a beaker (No.
  1), by gently tapping the inverted funnel. The cotton-wool was then
  removed from the funnel, and the upper one-third, containing the
  remainder of the dust, was cut off and added to the dust in beaker
  No. 1. The remainder of the cotton-wool was placed in a second beaker
  (No. 2); 2¹⁄₂ c.c. of hot nitric acid was dropped on the dust in
  beaker No. 1 from a pipette, a little water added, and the whole
  heated. The solution was filtered into a 50 c.c. Nessler glass, and
  the liquid remaining in the cotton-wool also removed by squeezing the
  wool with a glass rod against the side of the beaker. The cotton-wool
  in beaker No. 2 was similarly extracted with 2 c.c. of nitric acid,
  and the solution added to that remaining in beaker No. 1. The
  liquid was heated, the cotton-wool macerated in it and filtered as
  before. The wool was then washed with hot water about three or four
  times, and the liquid filtered into the Nessler glass. A number of
  standards were then made up by running into Nessler glasses, from a
  burette, varying amounts of standard lead solution covering a fair
  range. Usually five standards were made up, containing 0·5, 0·8,
  1·0, 1·2, and 1·4 c.c. lead solution, depending on the volume of
  the air aspirated and the quantity of lead expected in the known
  weight of dust found. To each standard 4¹⁄₂ c.c. nitric acid was
  added, and 5 c.c. of the caustic soda solution and 4 c.c. of the
  sugar solution were run into all the six solutions--_i.e._, one test
  and five standards--from pipettes. It was invariably found that the
  test was coloured faintly yellow, and if this is not allowed for in
  the standards high results are obtained. Hence a drop or two of the
  coloured solution (see solutions required) was added to the standards
  placed on white paper till they matched the test. Lastly, to the
  contents of each of the six glasses was added 4 c.c. of sulphuretted
  hydrogen solution, and the liquid in each made up to the 50 c.c.
  mark, and the whole well stirred. Usually it was found that the
  colour of the test came somewhat deeper than that of one standard,
  and a drop or two of lead solution was added to the standard till its
  colour matched that of the test. The elaborate method of making up a
  number of standards was adopted because it was found that any other
  way gave high results. In the way described many trial experiments
  were made, and they were invariably correct within half a drop of the
  standard solution.”

The estimation of the quantity of lead present in organic fluids,
with the disturbing influence of the presence of other metals, is a
factor which always complicates the use of the sulphuretted hydrogen
colorimetric estimation. It is almost impossible, when dealing with
fæces, with blood, or, on the other hand, with artificial digests
containing bread and milk, to eliminate the disturbing influence of
iron. Further, if steps are taken to remove the iron and other metals,
so much loss takes place in the manipulations necessary that the
results arrived at are not satisfactory. Whenever dealing with organic
matter, such as urine and fæces, it is best to make a blank test with a
similar quantity of the substance under examination obtained from other
sources, and to subtract the error found due to iron, when a rather
closer approximation may be arrived at.

So far as can be estimated, the minimal quantity of lead required to
produce poisoning is 0·005 gramme per kilogramme of body weight; but,
on the other hand, persons who have swallowed much larger doses than
this have exhibited no symptoms of poisoning. There is every reason to
suppose that lead absorbed through the lung produces a maximum toxic
effect, and, from the estimation of the quantity of lead found in
the body after death, it is highly probable that exceedingly minute
quantities of lead have, when absorbed over long periods, produced
changes not only by their actual presence in the tissues, but also have
set up degenerative changes which progress even after the elimination
of the metal from its local position.


=Histological Examination.=--In addition to the chemical examination
of tissues from a person who has died of suspected lead poisoning,
it is of the highest importance to make histological examinations,
as the naked-eye appearance of post-mortem examination is frequently
insufficient to give any clue to the cause of the poisoning. Moreover,
in a large number of instances the necropsy may exhibit a number of
signs of disease, such, for instance, as granular kidney, cirrhosis of
the liver, and so forth, which are associated with diseases other than
lead poisoning, and, in the absence of any present or past evidence of
definite hæmorrhages found associated with the other lesions already
mentioned, an ordinary autopsy must be inconclusive. It is true that
such pathological conditions are consistent with poisoning by lead; and
if the individual has been a lead-worker, it is easy, but frequently
erroneous, to conclude that the symptoms owe their origin to the
worker’s occupation. We are entirely in sympathy with the remarks of
King Alcock[9], who says:

“I plead none the less for an impartial investigation of the symptoms
presented by a lead-worker, before assigning full or even partial
responsibility of the disease to the occupation. If any and every
departure from the normal in a lead-worker is at once assigned--the
occupation being known--to plumbism, early diagnosis naturally presents
very few difficulties to the exponents of such methods. And however
severely we may condemn in the abstract such a careless, unscientific
attitude, the tendency has, in practice, to be reckoned with and
combated. The balance of probabilities would possibly suggest that
the occupation is, after all, responsible, in one sense or another,
for the more usual illnesses classically associated with the poison;
nevertheless, the attending practitioner is in duty bound to take into
consideration, and to estimate the relation of, all the concurrent
causes of such symptoms.”

On the extremely unsatisfactory position the certifying surgeon may
find himself in at a coroner’s inquest King Alcock says:

“The problem, from a strictly scientific point of view, is
complicated--one might almost say that the truth is stifled--by the
fact that the ætiological relations of the symptoms of any suspended
worker are swamped by the insistent legal relations under which he
claims and receives compensation.

“When once a formal certificate of suspension has been issued, which
has embodied a recognition of lead as a cause of certain existing
symptoms, then it becomes almost hopeless ever to reopen the question
of causation of these or other supervening troubles, be their origin
independent of lead or not. The doctor, in a legal cross-examination,
is, in scientific honesty, bound to admit at last the bare possibility
of any fantastic chain of remote sequelæ; and his protests against the
probabilities of such sequelæ are of no avail, as opposed to his own
admission. The _post, ergo propter_, appeal carries the day easily.”

For the purpose of histological examination it is essential that
portions of the brain, spinal cord, liver, kidney, and intestine,
should be examined microscopically. The nervous tissue should be placed
in formalin and Müller’s fluid, and a portion in alcohol for the
examination of the fibres. The liver, kidney, etc., should be placed in
5 per cent. formaldehyde. The tissues are then treated by the ordinary
histological methods, and sections prepared. With nervous tissue it
is essential that those prepared for the examination of the cells
should be made by the celloidin method; the others may be treated by
imbedding in paraffin. The points to be sought for in the tissues are
sufficiently indicated in the chapter on Pathology and Symptomatology,
but may be briefly recapitulated:

In the _brain_, as well as in all the tissues, careful search should
be made for minute microscopical hæmorrhages, and for evidences of
old hæmorrhages in the form of small masses of fibrous tissue, etc.
Parenchymatous degeneration, chromatolysis of nuclei, etc., nerve
degeneration.

The _arteries_ and _veins_ should also receive close scrutiny, as the
presence or absence of arteritis should be noted.

In the _kidney_ particularly, search should be made for both
interstitial and parenchymatous nephritis.

The _liver_ frequently shows signs of microscopic hæmorrhage, and it is
as well, in taking a portion of tissue for examination, to choose those
portions which appear to be specially congested.

In the _brain_ and _spinal cord_ and _nervous tissue_, search is to
be made for the same hæmorrhages as already noted. In addition, the
condition of the nerve fibres should be noted, the presence or absence
of periaxial neuritis, as well as degeneration of the axis cells, and
the various ganglion cells both in the brain and spinal cord should be
closely examined for chromatolysis and nuclear atrophy.

No evidence is afforded by micro-chemical tests of any of the sections
thus obtained, except those of the lung. It may be possible in the case
of the lung to determine the presence of lead granules in the alveolar
cells, and attention should be paid to this. It is possible also that
some evidence may be afforded by examination microscopically of the red
bone-marrow.

The intestinal walls should be examined for evidence of lead particles.

If any dark staining, deep or superficial, be found in the intestine,
it should be removed for chemical analysis. Necrotic areas of the
intestinal wall should be sought for.


=Hæmatology.=--For all practical purposes, the best stain for detection
of basophile granules in the erythrocytes is Wright’s modification of
Romanowski’s stain. This stain may be obtained in appropriate tablets,
and may be prepared immediately before use, although a stain which has
been standing for ten days or a fortnight gives much better results
than a quite new stain. The stain consists of a solution of polychrome
methylene blue, together with eosin in methyl alcohol, and the method
of procedure is as follows:

Blood is obtained by a small puncture, and slides smeared and allowed
to dry. Immediately on drying the slip is flooded with the stain,
and allowed to remain for two minutes. This causes fixation. At the
end of the two minutes the stain is diluted with an equal volume of
distilled water, and allowed to remain on for a further three minutes.
At the end of this time the stain is poured off, and the slip washed in
distilled water for another three minutes, or until the characteristic
purple-violet appearance is produced. It is better to examine such
films with an oil-immersion lens, the oil being placed directly upon
the films, and not covered with a cover-slip, as the action of Canada
balsam tends to decolorize the blue. If such specimens are required
to be kept, the oil may be washed off with xylol. It is possible to
observe basophile staining with a good sixth, but an oil-immersion
lens gives much the best result. The typical staining produced by this
means gives darkish bodies scattered about the red corpuscles, staining
sometimes deeply as the nuclei of the white corpuscles. In other cases
the appearance is like that of fine dust scattered throughout the cell.
In addition to these two forms, the whole red cell may take on a slight
generalized lilac tint, the normal cells remaining free from granules,
and stained red by the eosin. Search of 100 fields of the microscope
should be made, and if no basophile granules are found in such fields
it is unlikely that they will be found.

Basophile staining is not more pathognomonic of lead poisoning than of
any other form of anæmia, but may be regarded as a highly important
confirmatory diagnostic sign.

A differential count of the leucocytes present may be also made on
the same film in which basophile staining is observed; 300 should be
counted at least. In a typical case of lead poisoning it is found that
diminution in the polymorphonuclear leucocytes has taken place with
a corresponding increase of the lymphocytes, and possibly also the
large mononuclears, and probably a slight increase in the number of
eosinophiles.

This hæmatological method of diagnosis is of the utmost importance
in lead poisoning. A differential count such as is given on p. 137,
showing a large diminution in the polymorphonuclears, an increase in
the lymphocytes, evidence of changes in the red cells, consisting
of basophile staining, alteration in the shape of individual cells,
poikilocytosis, with vacuolation, is strong presumptive evidence of
lead absorption.

To complete the hæmatological examination, the hæmoglobin should
be estimated. This is best performed with Haldane’s instrument--an
exceedingly simple one to use. The estimation of the number of red
cells and white cells present is useful, but does not by any means give
such valuable information as does the differential count and search for
basophile granules.


=Blood-Pressure.=--Several methods are available for the estimation
of the blood-pressure. The pressure may be roughly estimated as too
high or too low by means of the finger. The presence of thickening of
the arteries may be also estimated in this way, but for determining
the absolute blood-pressure it is necessary to use one or other of
the instruments on the market. The estimation of blood-pressure
is an important point in relation to the suspected presence of
arterio-sclerosis, and should be performed wherever possible.
Sphygmographic tracings may also be taken. Such a tracing in a case of
typical poisoning gives a peculiar form of curve, which, however, may
be present in alcoholism and heavy work, and arterio-sclerosis of many
types.


=Urine Examination.=--In suspected cases of lead poisoning the
examination of the urine may reveal the presence of lead. In addition,
albumin is frequently present, especially in the early stages of
kidney inflammation. The ordinary tests for albumin should be carried
out, and it is also advisable to examine the urine spectroscopically,
as at times hæmoglobin, methæmoglobin, hæmatoporphyrin, may be
present in small quantities, each of which can be detected by means
of spectroscopic examination. Blood is not common in the urine of
lead-poisoned persons, although microscopically hæmorrhages undoubtedly
take place in the kidney. These hæmorrhages are interstitial, and as a
rule do not cause any blood-pigment to be passed in a quantity that can
be determined. It is as well, however, to centrifugalize the urine, and
examine the deposit for red blood-cells.

The presence of hæmatoporphyrin, as suggested by Steinberg[10], is
probably due to hæmorrhages in the intestine, and its presence in the
urine should be regarded with suspicion in a lead-worker.

Where a lead-worker is suffering from continued absorption of lead,
even without the manifestation of other symptoms, a change has been
noted in the acidity of the blood--namely, a loss of normal alkalinity.
The estimation of the alkalinity or acidity of the blood direct is an
exceedingly difficult process, but much information may be obtained by
careful estimation of the acidity of the urine, and of the acidity of
the urine in relation particularly to the phosphates.

Joulie[11] has pointed out the extreme value which may be obtained from
a knowledge of the urinary constituents by the means of estimation of
the acidity with suchrate of chalk. The reagent is made by slaking
lime in such a way that the resulting compound is practically dry.
A quantity of this--about 25 grammes--is then thoroughly shaken up
with 10 per cent. solution of cane-sugar, allowed to stand, and the
solution titrated against decinormal acid until it is of one-twentieth
normal. The urine is then estimated directly, the suchrate is run
into the 25 c.c. of urine until a faint white flocculent precipitate
appears. The number of c.c. of the solution of suchrate is then noted,
and multiplied by the factor of the solution. This gives the acidity
related to the phosphate and other organic acid contents, and is
similar to the method used to determine the acidity of wines.

The second estimation consists of estimating the phosphates present by
means of a standard solution of uranium nitrate, using either potassium
ferrocyanide or cochineal as an indicator. The specific gravity of the
urine is also determined. The result is then expressed in terms of
this specific gravity, or, rather, in the terms of the density of the
urine in relation to distilled water, and the whole answer returned per
litre. By this method it is not necessary to obtain a twenty-four hours
sample of the urine, the urine passed first thing in the morning being
taken for examination.

By using this density figure the quantity of acid and phosphate is
expressed in relation to the density, the equation being--

  The observed acidity
  ---------------------  =  Acidity per litre.
  The density per litre

The phosphate content is expressed in the same manner, while the ratio
of phosphate to acidity gives the ratio of excretion of phosphate to
acidity.

There is in lead-workers a considerable diminution in the amount of
phosphate excreted, and, as has been pointed out by Garrod and others,
lead apparently produces alteration in the solubility of the uric acid
content of the blood, and may therefore allow of its decomposition.
Probably lead as a urate is stored up in the tissues. For further
particulars of this method of the estimation of the urine, the reader
is referred to “Urologie Pratique et Thérapeutique Nouvelle,” by H.
Joulie.

An examination of the fæces of persons suspected of lead poisoning
may often give definite results both of the presence of lead and
hæmatoporphyrin. If small hæmorrhages have occurred high up in the
intestine, the presence of hæmatoporphyrin in the fæces may result.
The substance may be easily determined by means of the characteristic
absorption bands. A quantity of fæces is taken and extracted with acid
alcohol, and the filtrate examined spectroscopically. Urobilin bands
are commonly present, and, particularly, where much constipation exists
these bands are very well marked. There is no difficulty whatever,
however, in distinguishing them from the characteristic bands of acid
hæmatoporphyrin.


=Examination of the Fæces for Lead.=--The moist method or chemical
examination given above is the best one to apply for the determination
of lead in the fæces. As has already been pointed out, lead is commonly
excreted in the fæces, and, if only about 2 milligrammes per diem are
being excreted by the fæces in a lead-worker, the quantity cannot be
regarded as indicative of poisoning. One of us (K. W. G.) has at times
found as much as 8 to 10 milligrammes of lead excreted in the fæces of
persons engaged in a lead factory, and exhibiting no signs or symptoms
whatever of lead poisoning. If, however, the quantity of lead in
the fæces rises to anything above 6 milligrammes per diem, there is
definite evidence of an increased absorption of lead, and if at the
same time clinical symptoms be present, suggesting lead poisoning, such
a chemical determination is of the first importance.

In estimating the presence of lead in fæces, it may be necessary
to deal with the separation of iron, which may be precipitated as
phosphate and filtered off, the quantitative estimation being proceeded
with in the filtrate.

Lead is much more commonly present in the fæces of lead-workers than in
the urine, and it is better to examine the fæces rather than the urine
in suspected cases.


REFERENCES.

  [1] GAUTIER: Meillère’s Le Saturnisme, p. 74.

  [2] MARSDEN AND ABRAM: The Lancet, vol. i., p. 164, 1897.

  [3] SHUFFLEBOTHAM AND MELLOR: _Ibid._, vol. ii., p. 746, 1903.

  [4] HEBERT: Comptes Rendus, tome cxxxvi., p. 1205, 1903.

  [5] FRESENIUS AND VON BABO: Liebig’s Annalen, vol. xlix., p. 287,
  1884.

  [6] GLAISTER: Medical Jurisprudence and Toxicology. 1910.

  [7] DIXON MANN: Forensic Medicine and Toxicology, p. 496.

  [8] VERNON HARCOURT, A.: A Method for the Approximate Estimation of
  Small Quantities of Lead--Transactions of the Chemical Society, vol.
  cxvii., 1910.

  [9] KING ALCOCK, S.: Brit. Med. Journ., vol. i., p. 1371, June 24,
  1905.

  [10] STEINBERG: International Congress Industrial Hygiene. Brussels,
  1910.

  [11] JOULIE, H.: Urologie Pratique et Thérapeutique Nouvelle.




CHAPTER XI

TREATMENT


In laying down the general lines of treatment for both lead poisoning
and lead absorption, it is essential in the first place to distinguish
carefully between the two states; for although lead absorption may
gradually drift into definite lead intoxication and lead poisoning,
with all the classical symptoms associated with the saturnine cachexia,
a large number of cases, particularly those in industrial processes,
do not and should not progress beyond the early symptoms of lead
absorption. The treatment, therefore, will depend in the first place on
whether the case be one so constantly met with in industrial processes,
where generalized symptoms of lead absorption are manifest without any
definite and disabling symptoms traceable and sufficiently pronounced
to enable a diagnosis of lead poisoning to be made.

The facts given in the chapter on Pathology, on the methods of entrance
of lead, on the toxic manifestations, and the blood-changes, and, above
all, the facts relating to microscopical hæmorrhages and other profound
changes in the bloodvessels, point clearly to the lines along which the
general treatment for amelioration, prevention, or cure of poisoning
should be undertaken.

The treatment of the so-called “presaturnine state,” or what is
preferably termed the “state of lead absorption,” is one that the
appointed surgeon or certifying surgeon in lead factories or other
processes in which lead is manufactured or used, is constantly called
upon to treat. Lead poisoning is a definite entity as a disabling
disease, whereas lead absorption, although the prodromal stage of
such disease, cannot be defined as actual lead poisoning, as in many
instances persons may show signs of continued lead absorption, but
their powers of elimination can be maintained at such a level that the
ratio of absorption to elimination remains in equilibrium.

With the preventive treatment of lead poisoning we have dealt in
another place (see p. 199). What is particularly required here is the
medicinal treatment, which may be helpful in preventing lead absorption
passing on to definite lead poisoning.

For many years it has been customary in the treatment of men employed
in lead works to give occasional purgatives, and it is, moreover, a
common and proper precaution to keep a stock of some simple aperient
medicine, preferably saline composed of sodium sulphate and magnesium
sulphate, at the works in charge of the foreman, so that any man who
so desires may obtain a dose of an ordinary aperient mixture. We
have seen from the pathological evidence that the largest proportion
of lead is excreted by the bowel, and that, therefore, the sweeping
away of the bowel contents--particularly where constipation is set
up--will naturally tend to remove from the body a good deal of the
lead which has been already excreted into the intestine and which
may presumably become reabsorbed unless it be swept away. In a large
electric accumulator factory Epsom salts in the form of the granular
effervescing preparation is much appreciated. In winter 50 per cent.,
and in summer 90 per cent. of the men are said to take a daily
dose. In an important white-lead works chocolate tablets containing
hypo-(thio-)sulphite of sodium are supplied to the workers.

Another medicine made use of in lead works is the sulphuric acid
lemonade, this being acidulated with sulphuric acid and flavoured
with lemon. It is very questionable whether this substance has any
definite effect in the special direction in which it is supposed to
work--namely, that of forming an insoluble sulphate of lead in the
stomach and so preventing its absorption. The use of this drug was
suggested on the presumption that lead poisoning as a rule took its
origin from the dust swallowed and converted into a soluble form in
the stomach. As we have seen, there is very little evidence that this
entrance of lead is of much importance, although it does occasionally
take place. Furthermore, from the experiments of one of us [K. W.
G.[1]], it has been found that the sulphate of lead is at any rate as
soluble as other lead salts, such as white lead or litharge, when acted
upon by normal gastric juice.

With regard to the drinks supplied to workers in lead factories, it
is highly important that some form of fluid should be supplied which
the men may drink without harm, particularly in the more laborious
forms of employment, and, above all, in the factories where smelting,
desilverizing, etc., of lead is carried on. In these factories
the use of some type of lemonade containing sodium citrate is to
be recommended, as it has been shown that one of the pathological
effects of lead absorption is to produce an increased viscosity of
the blood, and the use of such drugs tends to some extent to diminish
this. A drink containing a few grains of sodium citrate to the ounce
and flavoured with lemon is freely drunk by workmen engaged in the
laborious processes.

Finally, as a general routine treatment, it is advisable to keep at
the factory some form of mixture containing iron, which may be given
to those persons who are showing signs of slight anæmia, generally
associated with some degree of constipation, and it is therefore better
to use a form of iron cathartic. This medicine should also be kept in
the care of the foreman, who will see that it is administered to the
men properly. In this way any persons who at the weekly examination
exhibit signs of anæmia may be promptly treated, and what is more, the
surgeon is assured that the workmen in question actually obtain the
medicine prescribed regularly.

During the routine weekly or monthly examination, or at whatever
intervals the medical examination takes place, particular attention
should be paid to the records kept of the state of health of the
various persons, and whenever possible alteration of employment should
always be enjoined when early signs of anæmia make their appearance.

The surgeon should spare no pains to determine if any of the workmen
are confirmed alcoholics, and such persons should be removed from
work in dangerous processes, while at the same time care should also
be taken to eliminate any persons suffering from those diseases which
are known to be predisposing causes of lead poisoning. The card system
of registration of any symptoms noted or treatment given facilitates
supervision of the health of the men.

In times of stress where some particularly dangerous process is in
operation, as, for instance, where portions of a building which
has become thoroughly impregnated with lead dust is being pulled
down, or where machines are being altered, removed, or rebuilt,
especial care should be exercised with the workmen so employed, and
it is advisable in such cases to adopt preventive measures on the
supposition--generally correct--that such persons are absorbing a
larger quantity of lead owing to their peculiarly dusty employment than
they were under normal circumstances. At such times, also, it may be
advisable to administer some form of mild iron cathartic to all persons
employed in the factory for, say, a week at a time. It must not be
supposed, however, that these methods of treatment in any way supersede
the precautions for the prevention of lead poisoning by mechanical and
hygienic means; they are merely additional precautions which may be put
in force under special circumstances.


=The Treatment of Lead Poisoning.=--The treatment of definite lead
poisoning, as the treatment of lead absorption, is directed towards
the elimination of the poison, the promotion of repair to the damaged
tissues, and special treatment directed towards those special organs
which suffer mostly in lead poisoning. At the same time, special
treatment of urgent symptoms may be called for; but in the treatment of
the urgent symptoms the fact of the general elimination of the poison
must not be lost sight of.

We have already seen that the channel through which the poison leaves
the body is mainly the fæces. Treatment must therefore be directed,
as in the former instance (lead absorption), towards eliminating the
poison by this means as much as possible, both by the use of enemata,
and later the use of sulphate of magnesia, which may be added to the
ordinary fluid enema; and it is far better in obstinate cases of
constipation and colic to give enemata than to continue with the huge
doses of salines or other aperients, such as croton-oil, elaterinum, or
castor-oil.


=Colic.=--Lead colic may be simple, acute, recurrent, or chronic and
continued. In whatever form colic appears pain is invariably referred
to the lower part of the abdomen, frequently into the groins, and
occasionally to the umbilicus. The pain has to be distinguished
particularly from acute gastritis, and occasionally from appendicitis,
and sometimes from that of typhoid fever. Acute colitis--not common in
this country--and dysentery, may, to some extent, simulate the pain of
lead colic, but John Hunter’s[2] original definition of “dry bellyache”
conveys very vividly the type of pain. Occasionally diarrhœa may be met
with, but as a rule obstinate constipation is present. In continued
colic, or chronic colic, sometimes lasting for several months,
obstinate constipation is the rule. In the simple acute colic the pain
passes off in the course of five or six days, generally disappearing
about four days after the lower intestine has been thoroughly cleared.

The pain of lead colic is relieved by pressure upon the abdomen,
whereas that of gastritis and most other forms of abdominal pain
may be generally elicited along the descending colon and splenic
flexure; mucus is commonly found in the stools, especially the first
evacuation, after obstinate constipation occasionally of several
days’ duration associated with an ordinary attack of lead colic.
Blood may be passed, but this symptom is not common. The pain in the
acute form is paroxysmal; it is rarely persistent, being typically
intermittent. During the paroxysm distinct slowing of the pulse-rate
with an increased blood-pressure takes place, and the administration of
vaso-dilators--such, for instance, as amyl nitrite--during a paroxysm
rapidly relieves the pain and lowers the blood-pressure, and in this
way distinguishes acute colic of lead poisoning from, say, subacute
appendicitis.

Vomiting may or may not be present, though the patient usually
complains of feeling sick, but there may be at times vomiting of a
frothy mucus.

It is unusual for a patient to die from acute colic, but acute
paroxysms have been recorded in which yielding of the blood-vessels of
the brain has occurred.

Recurrent colic is as a rule less severe than the simple acute form,
but may last for several weeks, clearing up for three or four days at
a time and then recurring with little diminution in violence from the
first attack. Such cases are probably due to the gradual excretion of
lead by the intestine, and should be treated on this supposition.

In the continued or chronic colic the pain may persist for as long as
two months, during the whole of which time the patient complains of
uneasiness and even constant pain in the lower part of the abdomen,
which becomes considerably worse after each evacuation, and almost
invariably is associated with exceedingly obstinate constipation. It is
this type of case that olive-oil or liquid paraffin relieves, while in
the acuter forms drastic purgatives such as castor-oil, croton-oil, or
pulv. jalapæ comp. may be administered.

For the treatment of pain in colic one of the various vaso-dilators
should be used, as, in addition to the spasm of the intestine, a very
considerable vaso-constriction of the whole of the vessels in the
mesenteric area occurs. Amyl nitrite gives immediate relief, but the
effect passes off somewhat rapidly, whilst scopolamine, although taking
somewhat longer to act, is better for continuous use, as its action is
longer maintained. Sodium nitrite, liquor trinitrini, and antipyrin are
also of use. Atropin may be used, but it is perhaps better given in
conjunction with magnesium sulphate.

Whatever form of purgative is given, some form of anodyne should be
combined. Drissole and Tanquerel[3] are said to have obtained excellent
results with croton-oil; one drop is given, followed seven or eight
hours later by another, and then by an enema of 2 pints of normal
saline. After two or three days the croton-oil may be again given, one
drop at a time each day. In addition, Tanquerel made use of belladonna
and opium together, finding that their combined action was better than
that of opium alone, as the physiological effect of belladonna probably
assists in preventing the intestinal cramp.

Hoffmann[4] recommends the use of olive-oil and opium, giving 3 to
4 ounces of olive-oil. He says that this relieves the spasm of the
pylorus, and is of particular use where severe vomiting is associated
with the colic. This use of olive-oil, first suggested by Hoffmann
in 1760, and revived by Weill and Duplant[5] in 1902, is somewhat
interesting, in view of the modern tendency to administer paraffinum
liquidum in the treatment of chronic constipation.

Briquet[6] recommends 4 grammes of alum and 4 grammes of dilute
sulphuric acid three times daily, with the addition of 0·05 gramme of
pulv. opii at night. Briquet says that although the purgative method
rapidly diminishes the colic, the elimination of the poison does not
take place as rapidly as by means of the treatment he recommends,
though it is open to doubt whether the use of either of these two
drugs is likely to produce any further neutralization or excretion of
absorbed lead than sulphate of magnesia. It is quite certain that the
magnesium sulphate does not act as a neutralizer of the poison, as in a
factory where sulphate of lead is manufactured some cases of definite
lead poisoning occurred, in which at least half must have been due to
the inhalation of lead sulphate dust. Under these circumstances it
seems hardly worth while to attempt to form a sulphate of lead in the
body. The action of magnesium sulphate and other salines, however,
in promoting the flow of fluid towards the intestines, and rapidly
diluting and washing out the contents, tend to eliminate such lead as
has already been excreted into the bowel.

A number of other drugs have been given from time to time for the
purpose of forming an insoluble compound with the metal in the
intestine, such, for instance, as sulphur in many forms, which is still
much used in French hospitals. Peyrow[7] advises sulphide of soda,
whilst Meillère prefers potassium sulphide as being less irritating.
He considers sulphuretted hydrogen a proper prophylactic against
reabsorption. Both experimental work and clinical observation show
that a change to sulphide does take place in the lower bowel, and that
staining of this part of the intestine is due to lead sulphide; but
as the figure on Plate II. shows, the lead may exist in the form of
granules of a dark nature, deeply embedded in the intestinal wall,
besides being situated in the exterior.

Stevens[8] suggests the use of ¹⁄₂-grain doses of calcium permanganate
thrice daily to relieve pain.

A certain number of other drugs may be also made use of from the point
of view of diminishing the pain, and one French observer advocates the
hypodermic injection of cocaine, but it is doubtful whether any good
would follow from such a procedure. Hypodermic injections of morphia
should be given whenever the pain is great, and diaphoretics as well
as diuretics should also be given, such, for instance, as ammonium
acetate, citrate of potash, or soda. Chloroform water and chloral and
bromine water may be also used, and when no other drug is at hand, the
inhalation of chloroform will rapidly relieve the acute vaso-motor
spasms associated with colic.

During the attack of colic, and for at least a day subsequent to its
disappearance, the patient should be kept on a fluid diet; milk is
best, and 10 grains of sodium citrate should be added to each glass of
milk. After the colic has subsided, a light farinaceous diet should
be given, and it is better not to give meat until at least a week has
elapsed. Alcohol is to be avoided.


=The Anæmia of Lead Poisoning.=--As has been pointed out in Chapter
VIII (p. 135), the anæmia of lead poisoning is one due to the
destruction of the red blood-cells. This is evidenced not only
by the curious sallow complexion, by the occasional presence of
hæmatoporphyrin in the fæces and urine, and often by the curious
yellow of the sclerotics, but also by an increase in the viscosity of
the blood itself. Moreover, the urine of persons suffering from lead
poisoning is invariably highly coloured, and may even show the presence
of methæmoglobin. As the anæmia is generally a symptom of continued
lead absorption for a long period, and does not necessarily occur with
every case of colic--in fact, acute colic may often supervene without
any symptoms of continued anæmia--the persons suffering from lead
anæmia should be removed from their direct contact with the dangerous
processes, and should be given, if possible, work in the open air.
Iron and arsenic may be used, preferably in combination, whilst the
iodide of iron often gives good results. Whatever preparation of iron
is given, care should always be exercised in avoiding any constipating
effect, and the free action of the bowel should be maintained, together
with a liberal supply of milk. Potassium iodide may be also given.

With regard to the action of potassium iodide, there is division of
opinion amongst various physicians as to the efficacy of the drug in
the elimination of lead from the body. At the same time a very large
number of persons hold that the administration of fairly large doses of
potassium iodide in the case of a person suffering from chronic lead
absorption may at times be associated with sudden exacerbation of the
disease, and that the drug apparently may determine the production of
acute symptoms, such as encephalopathy or paralysis, when these have
not been previous features of the case. Our experience supports this
statement, and on more than one occasion one of us (K. W. G.) has seen
a distinct increase of symptoms follow the administration of large
doses of potassium iodide. From a comparison with other cases it seems
that these symptoms would have been unlikely to make their appearance
without some secondary cause. Against this point of view must be quoted
further experiments already referred to by Zinn[9], who found that
when lead iodide was administered to experimental animals iodine alone
was found in the urine; but it must be pointed out that no estimations
were made of the fæces, and it is possible that a certain amount of
lead was eliminated in this way. What exactly is the action of iodide
on the solubility of lead in the body it is difficult to say; yet the
use of iodine compounds has been followed with considerable success
in a number of chronic inflammatory diseases, and it is possible that
it may have the action of splitting off the particular lead compound
from its organic association with the tissues, especially as it is
well known that iodine plays a very important rôle in the process
of cell metabolism. Another point which tends to support the use of
iodine is the fact that the other two halogens, bromide and chloride,
both of which enter largely into cell metabolism, also have a slightly
beneficial effect on the excretion of lead. The dose of the iodine
given should not be large to commence with, 3 grains three times a day
is sufficient, the dose being run up to some 30 or 40 grains per diem,
the symptoms meanwhile being carefully watched.

Other symptoms often associated with the anæmia of lead poisoning are--


_Rheumatic Pains._--These pains are suggestive of muscular affection,
and are possibly due to minute hæmorrhages occurring in the muscle
tissue, which have been discovered in the muscles of experimentally
poisoned animals. For the rheumatic pains diaphoretics and citrates of
soda and potassium may be given.


_Lumbago._--The lumbago constantly complained of in chronic lead
poisoning and even in the early stage of lead absorption, is very
generally related to chronic constipation rather than to a definite
affection of the lumbo-sacral joints.


_Nephritis._--Affections of the kidney associated with lead poisoning
are almost entirely confined to sclerosis. The presence of albumin
in the urine is not a very common symptom. As has been pointed out
already, the presence of lead in the urine is by no means a regular
feature of lead poisoning, though it may at times be present, and the
urine should always be examined for changes in the kidneys; but as a
number of cases of chronic lead poisoning are associated with alcohol
poisoning, the changes in the kidney cell are almost certain to be
present. On p. 95 the illustration showing the disease in the kidney
produced by experimental dosage with lead, and the kidney of a fatal
case of lead poisoning in a man who at the same time had a strong
alcoholic history, shows fairly definitely the difference between these
two points.

Acute nephritis occurs so rarely in the course of industrial lead
poisoning that it cannot be considered to be a disease due to lead.

In chronic nephritis treatment should be along the ordinary lines and
the same remark applies to enlargement of the liver.


_Heart._--Symptoms due directly to disease of the heart are rarely
caused by lead alone. The heart muscle may suffer in the same way
as the other muscles of the body, and in lead poisoning in animals
distinct hæmorrhages are found between the muscular fibres in the heart
muscle, and it is therefore probable that a form of myocarditis may
exist in lead poisoning. This, together with the increased arterial
tension, may cause dilatation, but the symptoms are those related
more to the general condition of arterio-sclerosis than to any direct
heart lesion, and as a rule these symptoms do not call for any special
treatment.


=Treatment of Nervous Manifestations in Lead Poisoning.=--With one
or two exceptions, the diseases of the nervous system associated
with lead intoxication only appear when actual lead poisoning is
established. Certain evidences of affection of the nervous system
are occasionally seen in the prodromal stage, or stage of lead
absorption. These may be merely temporary and disappear often under
treatment, by change of employment and reduction in the quantity of
lead absorbed. Thus, dilatation of the pupils--the reaction to light
being extremely sluggish or absent--is often a feature of the later
stages of the condition of lead absorption. Tremor may also be a
symptom, the outstretched hands exhibiting a fine undulatory movement,
often increased on attempting to perform some act such as touching the
nose, or touching the two fingers together, and when these symptoms
occur they must always be regarded as of somewhat grave import. But it
must be remembered that tremor may occur as a common complication of
alcoholic cases, and further, follows excessively hard manual work,
though there is usually little difficulty in distinguishing between the
various forms.

The symptomology of nervous diseases associated with lead poisoning has
already been carefully set out in Chapter IX., and the pathological
changes underlying these symptoms in Chapter V.

Of the general treatment, little needs to be added to what has
already been stated for the treatment of lead anæmia and general lead
intoxication. Iron and arsenic (not strychnine, especially in presence
of colic), and other similar drugs, should be employed together with
iodides either as potassium iodide or as an injection in the form of an
organic compound, of which there are several varieties on the market.

The injection of normal serum has been advised, as well as saline
injections, and in some instances venesection has been practised,
but it is doubtful whether anything is to be gained by this form of
treatment.

Further, it has been stated that some lead is excreted through the
skin, and for this reason sulphur baths, bathing in sulphuretted
hydrogen water, etc., have been recommended to neutralize any lead that
has gained access to the skin. Serafini[10] has claimed that by means
of electrolytic baths a certain amount of lead can be found present
in the water after continuous passing of a current, and it has been
supposed by these observers that the lead has been actually driven out
of the body under the action of the electric current. It is, of course,
possible that such lead as is discoverable in the water was merely that
which had already become incorporated with the patient’s skin through
mechanical contact.

Whatever form of treatment be adopted of a general type, the patient
must certainly be removed from the chance of any further lead
absorption; a person who is suffering from wrist-drop or other form of
paresis should not be employed in any portion of a lead works where he
may come into contact with any form of lead or its compounds for at
least a year after the paresis has disappeared, and even then it is
inadvisable for such a person to return to any form of dangerous lead
work.

The electrical treatment of the injured nerves and muscles should be
undertaken energetically; both the galvanic or faradic currents may
be used. Probably the best form is the galvanic. A small medicinal
battery may be utilized, the method of application being as follows:
One pole of the battery should be placed over the affected muscle, and
the other pole placed in a basin of water into which the patient’s hand
is dipped. The current should then be passed. It is better not to use
a current of too great intensity, particularly at the start, although
it is found in practice that a much greater current can be borne in
the early stages of the treatment than when the muscles and nerves
commence to recover. As a rule the patient experiences no inconvenience
whatever from a considerable current during the first week of his
affection, but at the end of a fortnight or three weeks less than
one-third of the initial current can be borne. The current should not
be passed continuously, but should be used for a short time and then
shut off, being again switched on for five or six minutes, and then
again shut off. The applications may also be modified by placing one
hand in the vessel of water and stroking the affected muscle and nerve
with the free electrode. The application of the current should be for
not more than half an hour at a time, and may be applied twice in the
twenty-four hours. It is quite easy to instruct the patient to perform
the electrical treatment for himself in this manner when the paresis is
affecting either the upper or lower extremity.

With the faradic current the circuit should be closed while the current
is at a minimum, and then the quantity of current raised to some 15 to
20 milliampères.

For affections of the lower extremity the application may be made by
means of one of the usual baths in which the foot is immersed, the
other electrode being placed on the back or other suitable position.
If both the lower extremities are involved, then both feet should
be placed in a bath into each of which the source of electricity is
connected.

Ionization by means of the faradic current may also be made use of.
For this purpose one of the halogens, preferably iodine or chlorine,
should be used, it being remembered that chlorine and iodine ions enter
from the negative pole, so that in such a case the bath in which the
affected limb is placed must be connected with the negative pole of the
battery.

Subsequently, with either form of electrical treatment, the part
should be well rubbed, and passive movements as well as massage are an
advantage in promoting the return of normal function. As the muscles
gradually return towards their normal state, graduated muscular
exercises should be used.

When treated in the first week or two of the onset, lead paresis
frequently recovers, and in a person suffering from lead palsy for the
first time, confined only to the hands or to a group of muscles in the
shoulder, prognosis is good. The prognosis of palsy of the lower limbs
is not so good.

Paralysis of the facial nerve is occasionally seen in lead poisoning,
and where this occurs it should be treated as previously recommended,
by means of iodides in association with localized electrical treatment.
One pole of the battery should be placed below the external auditory
meatus, and the other one passed over the face on the affected side.

In long-standing cases where no attempt has been made at treatment
in the early stages of the disease, and where considerable muscle
degeneration has already taken place, the prognosis as a rule is
very bad. Efforts should always be made in an early case by passive
movements and massage of the affected muscles to improve their
nutrition as far as possible. The diet should be light, and alcohol
should not be given at any time.


=Affections of the Central Nervous System.=--The typical form of
affection of the central cerebral nervous system caused by lead, is
lead encephalopathy. The disease may be insidious in its onset, and may
be preceded by a long stage of chronic headache with slight or total
remissions. Headaches may last for several months before the actual
acute stage of the disease is reached. In the examination of several
brains of persons who have died from lead encephalitis, microscopic
sections of the brain have shown signs of hæmorrhages which must have
taken place some considerable time prior to death, and were no doubt
associated with the headache that had been complained of for some
time previously, before the onset of the fatal illness. (See Plate
III.) Persistent headache occurring in a lead-worker should always be
regarded with grave suspicion, and such a case should be treated on the
assumption that it is an early case of lead encephalitis. Bromides and
iodides should be given, and the patient placed in quiet surroundings,
and fed on light, nutritious diet, and every attempt made to produce
elimination of the poison.

In the acute attacks vaso-motor spasm is no doubt partially accountable
for the symptoms, and various dilators, previously noted in discussing
colic, may be made use of, such, for instance, as amyl nitrite,
scopolamine, etc., whilst pyramidon, antipyrin, phenacetin, and other
similar drugs may be given between the attacks. Under no circumstances
should any person who has suffered from encephalitis or other cerebral
symptom of lead poisoning be allowed to resume work in a lead industry.

The treatment of eye affections in lead poisoning requires little
comment, as the essential treatment must be the same as in other cases,
mainly devoted towards the elimination of the poison. Attempts may be
made to treat paresis of the ocular muscles by means of mild electric
currents, but of this we have had no experience. About 50 per cent. of
cases of lead amaurosis and amblyopia recover, but a number progress to
total and permanent blindness, and prognosis in such cases must always
be guarded.


=Prognosis.=--The prognosis of the first attacks of lead poisoning of
simple colic or even slight unilateral paresis is good; practically all
cases recover under proper treatment. It is unusual for a person to
succumb to a first attack of simple colic, or paresis.

In most cases the serious forms of poisoning only make their appearance
after three or four previous attacks of colic, but a single attack of
paresis is much more frequently followed by a severe form of poisoning,
such as encephalitis.

A limited number of persons are highly susceptible to lead poisoning,
and these persons rapidly show their susceptibility when working in
a dangerous lead process. Lead poisoning occurring in an alcoholic
subject is more likely to result in paretic and mental symptoms than
in a person who is not addicted to alcohol, and the prognosis of lead
poisoning in an alcoholic is much less favourable than in the case of a
normal person.

Mental symptoms very rarely follow from a single attack of lead colic,
and as a rule do not become established under three or four attacks at
least.

A small number of persons exposed to excessive doses of lead absorption
through the lungs develop mental symptoms, such as acute encephalitis,
without any prodromal stage. The prognosis in such cases is always
exceedingly grave.

Sudden generalized forms of paralysis are not common in the early
stages, but are invariably of grave import. A few cases of paresis,
particularly those of the peroneal type, and affecting the lower limbs,
become progressive, and eventually develop into a condition resembling
progressive muscular atrophy with spinal cord degeneration.

The prognosis of simple colic in women is about as good as for males,
but if an attack of abortion is associated with lead poisoning,
eclampsia often supervenes and permanent mental derangement may follow.
In the dementia associated with lead poisoning the prognosis is not
so grave as in other forms of dementia, especially alcoholic, but
depression is an unfavourable symptom. The mania of lead poisoning is
not so noisy as that of alcoholic mania, but where there is suspicion
of alcoholic as well as lead poisoning the prognosis is exceedingly
grave.

As a rule the prognosis of cases of lead poisoning occurring in
industrial conditions is more favourable when colic is a marked feature
than when it is absent, and there is no doubt that the prognosis
in cases of industrial lead poisoning at the present time is more
favourable than it was before the introduction of exhaust ventilation
and general medical supervision--a fact no doubt to be explained by the
relative decrease in the amount of lead absorbed.


REFERENCES.

  [1] GOADBY, K. W.: Journ. of Hygiene, vol. ix., 1909.

  [2] HUNTER, JOHN: Observations of Diseases of the Army in Jamaica.
  London, 1788.

  [3] DRISSOLE AND TANQUEREL: Meillère’s Le Saturnisme, p. 164.

  [4] HOFFMANN: Journ. de Méd., October, 1750.

  [5] WEILL AND DUPLANT: Gazette des Hôpitaux, lxxix., 796, 1902.

  [6] BRIQUET: Bull. Thérap., Août, 1857.

  [7] PEYROW: Thèse de Paris, 1891.

  [8] STEVENS: Bulletin of Bureau of Labour, U.S.A., No. 95, p. 138,
  1911.

  [9] ZINN: Berl. Klin. Woch., Nr. 50, 1899.

  [10] SERAFINI: Le Morgagni, No. 11, 1884.




CHAPTER XII

PREVENTIVE MEASURES AGAINST LEAD POISONING


=Amount of Lead Fume and Dust in the Atmosphere Breathed.=--Lead fuses
at 325° C. and boils at between 1450° and 1,600° C. It is volatile when
heated to a cherry-red colour--about 550° C.

Experiments[A] carried out in the laboratory of a lead smelting works
in London to determine the temperature at which leady fumes rise
from the surface of open baths of molten lead, showed that unless
pure lead is heated to about 500° C., and at the same time stirred,
no appreciable fume comes off, and that from lead, at the same
temperature, under ordinary working conditions, little or no lead
in the form of oxide passes into the air. From lead that has been
unrefined or which contains zinc--that is, lead in the earlier stages
of its manufacture (in the reverberatory furnace)--leady fume was not
given off at temperatures less than 760° C. even when stirred, because
at a temperature of 600° C. the surface of the molten metal became
covered with fluid slag, which will not allow any oxide to be given
off. Impurities such as tin or antimony prevent the oxidation of molten
lead at lower temperatures, and give it a bright, shiny colour. When
heated to about 600° C., these impurities form a slag on the surface
of the lead containing antimoniates and stannates of lead, which do
not evolve lead fumes unless heated to temperatures never likely to be
reached in open lead pots. The reason why molten refined lead can give
off lead fume more readily than those named is because the oxide formed
on the surface is a dry powder and not in the form of slag. Hence, when
the bath is stirred, some of the dry oxide is broken up and may rise
into the air. When a bath of molten lead is not stirred at all, it can
be heated to over 740° C. without finding oxide in the air aspirated--a
temperature not obtained under ordinary working conditions.

  [A] In these experiments air was aspirated through an iron funnel
  having an area of 113 square inches (12 inches diameter), placed at
  a height of 1¹⁄₂ inches above the molten metal, and connected to an
  iron tube 3 feet in length and ¹⁄₂ inch in diameter. Inside the iron
  tube was a glass tube, one end reaching own to the top of the funnel
  and the other connected with a tube containing pure loose asbestos
  wool, and continued down to a tightly stoppered bottle holding
  dilute sulphuric acid. Another glass tube connected this bottle with
  an aspirator. The asbestos tube was weighed before and after each
  test, and the asbestos then treated with nitric acid, and the lead
  determined volumetrically. In none of the tests made was lead found
  in the bottle containing sulphuric acid.

Were there nothing else to consider but escape of lead fume from a pot
or bath of molten metal, obviously hooding over of the bath and removal
of the fume from the atmosphere of the workroom would be unnecessary
until this temperature was reached. Usually, however, the bath is kept
standing exposed to the air, and the oxide which forms on the surface
has to be skimmed off periodically, and whenever the ladle is emptied
a small cloud of dust arises. Or at times, in certain processes,
chemical interaction takes place in the bath, as in the dipping of
hollow-ware articles previously cleaned in hydrochloric acid, with
evolution of fume of volatile chloride of lead. Any vessel, therefore,
of molten metallic lead in which skimming is necessary, or in which
chemical action gives rise to fume, requires a hood and exhaust
shaft, even although the temperature is little, if at all, above the
melting-point--unless, indeed, a separate exhaust can be arranged for
the removal of the dust immediately above the point where the skimmings
are deposited.

Of many samples of dust collected in workrooms where there are baths
of molten lead, it is impossible to say definitely how much of the
lead present is due to fume, and how much to dust. Thus, a person
tempering the tangs of files was attacked by plumbism, and a sample of
dust collected from an electric pendent directly over the pot, at a
height of 4 feet from the ground, was found to contain 15·6 per cent.
of metallic lead. Similarly, a sample taken above a bath for tempering
railway springs contained 48·1 per cent. metallic lead[1]. And,
again, a sample collected from the top of the magazine of a linotype
machine contained 8·18 per cent. Such analyses point to the necessity
of enclosing, as far as possible, the sources of danger--either the
fume or the dust, or both. Determination of the melting-point of the
molten mass will often help in deciding whether there is risk of fume
from the pot, and, if there is not (as in the sample of dust from the
linotype machine referred to), will direct attention to the sources of
dust in the room. Proceeding on these lines, S. R. Bennett[2], using
a thermo-electric pyrometer which had been previously standardized and
its rate of error ascertained, and checking the results in some cases
by a mercury-in-glass thermometer (the bulb of which was protected by
metal tubing), determined the temperature of the various pots and baths
of molten lead used in the Sheffield district. As was anticipated,
temporary cessation of work, stirring up of metal, recoking of
furnaces, and other causes, produced fluctuations of temperatures from
minute to minute in the same pot, and in its different parts. The
compensated pyrometer used gave for file-hardening pots a maximum of
850° C., and a minimum of 760° C., the average mean working temperature
being about 800° C. The variations of temperature of lead used for
tempering tangs of files and rasps was found to be high, and largely
unrestricted from a practical standpoint. The maximum was 735° C.,
and the minimum 520° C., the average mean working temperature being
650° to 700° C., varying more than this within a few hours in the same
pot. Spring tempering is carried out at some comparatively constant
temperature between a maximum of nearly 600° C. and a minimum of 410°
C., depending on the kind of steel and the purpose for which the steel
is to be employed. Generally, the temperature required rises as the
percentage of carbon in the steel is diminished. As these baths are
larger than file-hardening pots, the temperature range is higher at
the bottom than at the top unless well stirred up. Some lead pots are
set in one side of a flue, and the temperature in the mass is then
greater on the furnace side. From further observation of these pots
during experiments, he was inclined to believe that the lead did not
volatilize directly into the atmosphere, as heated water does, but that
the particles of coke, fused oil, etc., which rise from the surface,
act as carriers of the rapidly oxidized lead particles which cling to
them.

Similar experiments were carried out in letterpress printing works. The
average temperature was 370° C. in the stereo pots, and in the linotype
pots at work 303° C. Scrap lead melting-pots when hottest registered
424° C., but registered as low as 310° C., according to the amount of
scrap added, the state of the fire underneath, etc. The best practical
working temperature depends largely on the composition of the metal
used. That at some factories is the same for stereo drums as for lino
pots--viz., 81·6 per cent. lead, 16·3 per cent. antimony, and 2·0 per
cent. tin, added to harden the lead. On the other hand, some printers
use a higher percentage of antimony in the lino than in the stereo
metal. Lead melts at 325° C., and antimony at 630° C., but by adding
antimony to lead up to 14 per cent. the melting-point is reduced at
an almost uniform rate to 247° C., after which further addition of
antimony raises the melting-point. This explains why temperatures as
low as 290° C. are practicable for linotype pots. The molten eutectic
has a specific gravity of about 10·5, whereas the cubic crystals
average 6·5 only; therefore in these pots the latter float on the top,
and excess of antimony is to be expected in the skimmings or on the
surface.

Administration of certain sections of the Factory and Workshop Act,
1901, would be simplified were there a ready means available for
determining the extent of contamination of the air--especially of
Section 1, requiring the factory to be ventilated so as to render
harmless, as far as practicable, all gases, vapours, dust, or other
impurities, generated in the course of the manufacturing process, that
may be injurious to health; of Section 74, empowering an inspector
to require a fan or other means if this will minimize inhalation of
injurious fumes or dust; of many regulations having as their principal
object removal of dust and fumes; and of Section 75, prohibiting meals
in rooms where lead or other poisonous substance is used, so as to give
rise to dust or fumes. Unfortunately, owing to the difficulty hitherto
of accurate collection, only a very few determinations of the actual
amount of lead dust and fume present in the atmosphere breathed have
been made. This lends peculiar value to a series of investigations by
G. Elmhirst Duckering, which have thrown much light on the amount of
lead fume present in the air of a tinning workshop, and the amount of
lead dust in the air during certain pottery processes, and the process
of sand-papering after painting. Incidentally, also, they help to
determine the minimal daily dose of lead which will set up chronic lead
poisoning[3]. Aspirating the air at about the level of the worker’s
mouth for varying periods of time, he determined the amount of lead
in the fume, or in the dust, per 10 cubic metres of air, and from
knowledge of the time during which inhalation took place he calculated
the approximate quantity inhaled per worker daily. We have summarized
some of his conclusions in the table on pp. 204, 205:

Duckering’s experiments as to the presence of fumes containing
compounds of lead in the atmosphere breathed were carried out in a
workshop for the tinning of iron hollow-ware with a mixture consisting
of half lead and half tin. The process of manufacture and the main
sources of lead contamination in the air (knowledge arrived at from
these experiments) are explained on p. 59. As the result of laboratory
experiments designed to show the effect of the violent escape of vapour
produced below the surface of molten metal in causing contamination of
the air, and the nature of the contaminating substances, he was able
to conclude that the chemical action of the materials (acid and flux)
used, and subsequent vaporization of the products of this action, was
a much more important factor than the mechanical action of escaping
vapour. Subsequently, experiments carried out on factory premises gave
the results which are expressed in the table as to the relative danger,
from lead, to (_a_) a tinner using an open bath; (_b_) a tinner working
at a bath provided with a hood and exhaust by means of a furnace flue;
and (_c_) the nature and extent of air contamination caused by the
operation of wiping excess of metal (while still in a molten state)
from the tinned article. In all three experiments aspiration of air
was made slowly: it was maintained at the rate of 3 to 4 cubic feet
an hour in the first experiment for between seven and eight hours; in
the second for twenty-eight to twenty-nine hours; and in the third for
twenty-four to twenty-five hours. The person engaged in tinning at the
open bath was shown to be exposed to much more danger than one working
at a hooded bath, while the wiper was exposed to even more danger than
the tinner using an open bath, since not only was he inhaling fume from
the hot article, but also fibre to which considerable quantities of
metallic lead and tin adhered.

Analysis of samples of dust collected in different parts of the
workroom bore out the conclusions derived from analysis of the
fumes. Thus, samples collected from ledges at varying heights above
the tinning bath containing the mixture of tin and lead contained
percentages of soluble lead (lead chloride) in striking amount as
compared with samples collected at points in the same room remote from
any source of lead fume, while the insoluble lead present, as was to be
expected from the fact that it consisted of lead attached to particles
of tow floating in the air, was less variable.

TABLE XII., SHOWING QUANTITIES OF LEAD (PB) IN THE ATMOSPHERE AT
BREATHING LEVEL.

(G. E. DUCKERING’S EXPERIMENTS.)

  +------------------------------+-------------+--------+--------------+
  |                              |             |  Esti- |              |
  |                              |             |  mated |              |
  |                              |   Present   |Time (in| Approximate  |
  |                              | in 10 Cubic | Hours) |  Quantities  |
  |                              |  Metres of  | during | of Lead (Pb) |
  |                              | Air (Milli- |  which | expressed in |
  |                              |  grammes).  |   In-  | Milligrammes |
  |                              +-----+-------+halation|   inhaled    |
  |                              |Total| Lead  |  took  |  by Worker   |
  |         Occupation.          |Dust.| (Pb). | place. |   per Day.   |
  +------------------------------+-------------+--------+--------------+
  |              (1)             | (2) |  (3)  |   (4)  |      (5)     |
  |Tinner using open bath        |  -- |  37·79|  5¹⁄₂  |     10·70    |
  |                              |     |       |        |              |
  |                              |     |       |        |              |
  |Tinner using bath covered by  |  -- |   6·36|  5¹⁄₂  |      1·80    |
  |hood, and having fumes        |     |       |        |              |
  |exhausted by draught of       |     |       |        |              |
  |furnace                       |     |       |        |              |
  |Wiping off (tinning)          |  -- | 124·31|  5¹⁄₂  |     35·20    |
  |furnace                       |     |       |        |              |
  |furnace                       |     |       |        |              |
  |furnace                       |     |       |        |              |
  |furnace                       |     |       |        |              |
  |Earthenware dipping (pottery) |  38 |   1·80|  7¹⁄₂  | 0·69 (average|
  |                              |     |       |        |of 4 expts.)  |
  |Earthenware dipping (pottery) |  84 |   6·27|  7¹⁄₂  | 2·40 (single |
  |furnace                       |     |       |        |expt.)        |
  |furnace                       |     |       |        |              |
  |China dipping (pottery)       |  36 |   2·12|  7³⁄₄  | 0·83 (average|
  |                              |     |       |        |of 4 expts.)  |
  |                              |     |       |        |              |
  |Rockingham ware dipping       |  44 |   2·26|  7¹⁄₂  | 0·86 (single |
  |(pottery)                     |     |       |        |      expt.)  |
  |                              |     |       |        |              |
  |                              |     |       |        |              |
  |                              |     |       |        |              |
  |Earthenware cleaning (pottery)|  47 |   2·29|  7¹⁄₂  | 0·88 (average|
  |                              |     |       |        |of 7 expts.)  |
  |China ware cleaning (pottery) | 123 |  13·34|  6     | 4·08 (single |
  |                              |     |       |        |expt.)        |
  |                              |     |       |        |              |
  |                              |     |       |        |              |
  |                              |     |       |        |              |
  |Earthenware drying (pottery)  |  25 |   2·19|  8     | 0·92 (average|
  |                              |     |       |        |of 3 expts.)  |
  |Earthenware glost placing     |  34 |   2·08|  8³⁄₄  | 0·93 (average|
  |(pottery)                     |     |       |        |of 3 expts.)  |
  |China glost placing (pottery) |  30 |   1·08|  9     | 0·50 (single |
  |                              |     |       |        |expt.)        |
  |China glost placing (pottery) |  21 |   0·32|  9¹⁄₂  | 0·16 (single |
  |                              |     |       |        |expt.)        |
  |Majolica-painting of tiles    |  61 |   9·11|  7¹⁄₂  | 3·48 (single |
  |(pottery)                     |     |       |        |expt.)        |
  |                              |     |       |        |              |
  |                              |     |       |        |              |
  |                              |     |       |        |              |
  |                              |{206 |  53·70|   --   |      --      |
  |Sand-papering and dusting     |{    |       |        |              |
  |railway coaches               |{241 | 116·10|   --   |      --      |
  |                              |{    |       |        |              |
  |                              |{    |       |        |              |
  |                             {| 453 |  83·10|   --   |      --      |
  |Sand-papering                {|     |       |        |              |
  |coach wheels                 {|1343 |1025·60|   --   |      --      |
  |                             {|     |       |        |              |
  |Sand-papering motor-car body  | 600 | 278·30|   --   |      --      |
  |                              |     |       |        |              |
  |                              |     |       |        |              |
  |                              |     |       |        |              |
  |                              |{ 88 |  38·70|   --   |      --      |
  |                              |{    |       |        |              |
  |Sand-papering                 |{    |       |        |              |
  |motor-car wheels              |{    |       |        |              |
  |                              |{ 35 |   4·70|   --   |      --      |
  |                              |{    |       |        |              |
  |Sand-papering van wheel       | 494 | 143·80|   --   |      --      |
  |                              |     |       |        |              |
  |                              |     |       |        |              |
  |                              |     |       |        |              |
  |Burning off old paint         |  52 |   3·40|   --   |      --      |
  |                              |     |       |        |              |
  +------------------------------+-------------+--------+--------------+

  +-----------------------------+-----+--------------------------------+
  |                             |     |                                |
  |                             |     |                                |
  |                             |     |                                |
  |                             | Per-|                                |
  |                             |cent-|                                |
  |                             | age |                                |
  |                             |  of |                                |
  |                             | Lead|                                |
  |                             |  in |                                |
  |         Occupation.         |Dust.|            Remarks.            |
  +-----------------------------+-----+--------------------------------+
  |              (1)            | (6) |                (7)             |
  |Tinner using open bath       |  -- |The whole inhaled in the form of|
  |                             |     |vapour of lead or similar       |
  |                             |     |compound.                       |
  |Tinner using bath covered by |  -- |The whole inhaled in the form of|
  |hood, and having fumes       |     |vapour of lead or similar       |
  |exhausted by draught of      |     |compound.                       |
  |furnace                      |     |                                |
  |Wiping off (tinning)         |  -- |14·1 milligrammes of metallic   |
  |furnace                      |     |lead inhaled as lead chloride,  |
  |furnace                      |     |and 21·1 milligrammes as        |
  |furnace                      |     |metallic lead adhering to       |
  |furnace                      |     |floating fibres of tow.         |
  |Earthenware dipping (pottery)| 8·30|Dipping boards not used.        |
  |                             |     |                                |
  |Earthenware dipping (pottery)| 7·42|Very dirty dipping boards used. |
  |furnace                      |     |Work very rapid, and much       |
  |furnace                      |     |shaking of ware after dipping.  |
  |China dipping (pottery)      | 5·43|China glaze usually contains    |
  |                             |     |about two-thirds as much lead as|
  |                             |     |that of earthenware.            |
  |Rockingham ware dipping      | 4·37|Dirty dipping boards in use.    |
  |(pottery)                    |     |Glaze contains three times as   |
  |                             |     |much lead as ordinary earthen-  |
  |                             |     |ware glaze, but the ware is not |
  |                             |     |shaken after dipping.           |
  |Earthenware cleaning         | 5·90|Cleaning done in or at front of |
  |(pottery)                    |     |exhaust hood.                   |
  |China ware cleaning (pottery)|10·85|Very defective exhaust; hood so |
  |                             |     |arranged that cleaning had to be|
  |                             |     |done outside. Glaze contains    |
  |                             |     |about two-thirds as much lead as|
  |                             |     |that for earthenware.           |
  |Earthenware drying (pottery) | 8·58|Filter placed at breathing level|
  |                             |     |in centre of drying stillage.   |
  |Earthenware glost placing    | 6·58|                                |
  |(pottery)                    |     |                                |
  |China glost placing (pottery)| 3·64|Boards used were fairly dirty.  |
  |                             |     |                                |
  |China glost placing (pottery)| 1·50|One man only working.           |
  |                             |     |                                |
  |Majolica-painting of tiles   |15·00|Tiles cleaned, while still damp,|
  |(pottery)                    |     |with knife. Much dry waste glaze|
  |                             |     |on wooden floor, and much       |
  |                             |     |traffic. Several cases of lead  |
  |                             |     |poisoning in this room.         |
  |                             |26·10|Passenger fish truck after one  |
  |Sand-papering and dusting    |     |coat of lead colour.            |
  |railway coaches              |48·10|Railway coach after one coat of |
  |                             |     |lead colour on filled and faced |
  |                             |     |surface.                        |
  |                            {|18·30|After two coats of quick-drying |
  |Sand-papering               {|     |white lead paint.               |
  |coach wheels                {|76·40|Old cream-painted wheel before  |
  |                            {|     |repainting.                     |
  |Sand-papering motor-car body |46·40|Door of motor body after one    |
  |                             |     |coat of lead colour and quick-  |
  |                             |     |drying sand-paper stopping.     |
  |                             |     |Urgent work.                    |
  |                             |44·00|Wooden motor wheels after two   |
  |                             |     |coats of lead colour and sand-  |
  |Sand-papering                |     |papering between. Exhaust not   |
  |motor-car wheels             |     |running.                        |
  |                             |13·30|Same point, but with exhaust    |
  |                             |     |running.                        |
  |Sand-papering van wheel      |29·10|After one coat of quick-drying  |
  |                             |     |permanent red on two coats of   |
  |                             |     |flesh colour (sand-papering     |
  |                             |     |after each coat).               |
  |Burning off old paint        | 6·50|White paint of London and North-|
  |                             |     |Western coach. Gas-burner used. |
  +-----------------------------+-----+--------------------------------+


=Dust.=--Reference to the table shows that the conditions in the
pottery workrooms, as stated in Column 7, are reflected in Columns 3
and 5. Further details from his experiments may be useful. Thus, in a
dipping room where low-solubility glaze was in use, the amount of lead
in the dust collected per 10 cubic metres of air was 0·70 milligramme.
The average of four experiments where there were no dipping boards
was 1·80 milligrammes, and where dipping boards were used, 3·75;
_i.e._, 1·95 milligrammes of lead in the dust per 10 cubic metres of
air is added by the use of dirty dipping boards. As the result of his
experiments, Duckering believes that approximately 1·95 milligrammes of
lead per 10 cubic metres of air was due to the fine spray given off in
the shaking of the ware. In bright sunlight, he says, the spray can be
seen dancing high above the dipping tub. In a dipping house where work
was done slowly by two occupants only, the proportion of lead in the
measured quantity of air was also low--0·58 milligramme per 10 cubic
metres. Where, in the absence of special provision made for admission
of fresh air to a fan, the air was drawn from a neighbouring room in
which lead processes were carried on, the amount of lead rose to 5·76
milligrammes at the level breathed by the gatherer at a mangle. In
ware-cleaning the average of all his observations where lead was used
(eleven) was 3·44 milligrammes; and he concluded that “wet cleaning of
ware causes less direct contamination of the atmosphere, even where
no local exhaust is applied. A still more important result of wet
cleaning, however, is that the overalls keep much freer of dust.” The
highest results were obtained when the process of ware-cleaning was
done outside the influence of the exhaust draught. In one instance,
where the ware was cleaned at a distance of 6 feet from the exhaust
opening, 13·34 milligrammes per 10 cubic metres of air were found.
Subsequently at the same point, after the exhaust system of ventilation
had been remodelled, 0·95 milligramme only was present. Even in a
stillage room in which no work was done other than the placing on and
removal of the boards from the racks, the lead content per 10 cubic
metres of the air was 1·08 milligrammes. In glost-placing, the average
of four experiments was 1·83 milligrammes--no doubt the result of glaze
on the boards. As much as 9·11 milligrammes of lead was found per 10
cubic metres of air in the centre of a large majolica-painting room,
with wooden floors and much traffic in it. Wooden floors generally
appeared to influence the results, as determinations of the lead
present were higher in rooms with them than with tiled floors.

In coach-painting the proportion of lead found by Duckering in the air
breathed during the actual time of sand-papering explains the severe
incidence of poisoning in this class of work. The table shows the
amount of lead in the air to be enormous, and in many cases much in
excess of the amount found in the air when wiping off in the tinning
of hollow-ware. The work of sand-papering is, however, very rarely
continuous, the time occupied in it being, for the painter, about one
to two hours daily; for the brush hand, two to three and a half hours;
and for the painter’s labourer, four to five hours.

Knowing intimately the processes at which the estimations recorded
in the table were made, the relative frequency of cases of plumbism
reported among those employed at them, and the duration of employment
prior to attack, we believe that, if the amount of lead present in the
air breathed contains less than 5 milligrammes per 10 cubic metres of
air, cases of encephalopathy and paralysis would never, and cases of
colic very rarely, occur. And this figure is a quite practical one in
any process amenable to locally-applied exhaust ventilation. Somewhere
about 2 milligrammes, or 0·002 gramme, of lead we regard as the lowest
daily dose which, inhaled as fume or dust in the air, may, in the
course of years, set up chronic plumbism.


=Local Exhaust Ventilation.=--In considering preventive measures
against lead poisoning, precedence must be given to removal of fumes
and dust by locally-applied exhaust ventilation, as, unfortunately, the
wearing of a respirator is neither in itself a sufficient protection,
nor, if it were, could the constant wearing of one be enforced. A
respirator is of no use against lead fume. In the case of dust, the
conditions which it must fulfil to be effective are, first, that the
air breathed is freed from dust, and, secondly, that it should not
incommode the wearer. Further, it should be simple in construction,
easily applied, and allow of frequent renewal of the filtering medium.
No existing respirator of moderate price conforms quite satisfactorily
with these requirements. The more closely to the face it is made to
fit, and the more effectually the air is filtered, the greater is the
inconvenience experienced when it is worn. This inconvenience is due to
the exertion (showing itself in increase of the respiratory movements
and pulse-rate) caused in aspirating the air through the filtering
medium, and rebreathing some portion of the expired breath, containing
a much greater proportion of carbonic acid gas and of moisture at
a higher temperature than are present in fresh air. Respirators,
therefore, except for work lasting a short time--half an hour to
an hour--cannot be considered an effective or sufficient means of
protecting the worker against dust. If a respirator must be worn, the
simplest form is a pad of ordinary non-absorbent cotton-wool (absorbent
wool quickly becomes sodden and impervious), about 3 inches by 4
inches, placed over the mouth and nostrils, and kept in position by
elastic bands passed round the ears. The pad should be burnt after use.

With a smooth, impervious floor, however, and ventilation designed to
remove the fumes and dust at, or as near as possible to, the point of
origin, lead poisoning would become very rare in most of the industries
to be described. The essential points of such a system are--(1) The
draught or current of air set in motion either by heat or by a fan; (2)
the ducts along which the current travels; (3) the hoods or air-guides
designed to intercept and catch the fumes and dust at the point of
generation; (4) inlets from the outside air into the room to replace
continuously the air extracted, and, in many cases, (5) a suitable dust
filter or collector.


_Exhaust by Heat._--Processes giving rise to fumes or to dust liberated
on stirring or skimming, which can be dealt with by the draught created
in the furnace flue or over a bath of molten metal provided with
adequate hood and duct up which the heated air travels, are--Smelting,
refining, spelter manufacture, and the numerous operations
necessitating the melting of lead, such as tinning with a mixture of
tin and lead, sheet lead and lead piping, stereo pots in letterpress
printing, pattern-making, tempering springs, file-hardening, etc. The
dusting of red-hot metallic surfaces, as in vitreous enamelling, might
possibly also be dealt with in the same way. The disadvantage of the
exhaust by heat is the uncertainty and inequality of the draught, and
the size of the duct necessary to cope with the volume of rarefied air
from above the molten vessel.

The closer the hood is brought down over the point where the fumes
escape, the less risk is there of cross-currents deflecting them into
the workroom. Hence all baths of molten metal should have the sides
and back closed in, leaving as small a space open in front as is
practicable in view of necessary skimming or other operations.

In the case of tinning baths, Duckering[4] describes completely
successful results when from the top of the hood a shaft at least 24
inches in diameter was carried vertically upwards into the open air to
a height of 18 feet, and the top of the shaft fitted with a wind screen
in the form of a very large cone, having its lower edge below the upper
edge of the shaft, and its nearest point at least 8 inches from the top
of the shaft. Smoke produced in large quantity at any point 6 inches
outside the front of the hood was entirely drawn into it. As, however,
the inrush of air caused an eddy of the fumes at the upper edge of
the opening, the edges of the hood were turned inwards, so that the
operation of wiping was done in a sort of short tunnel. In general, it
may be said that the diameter of pipes leading from hoods to the outer
air (on the efficacy of the draught in which success depends) is much
too small. Frequently mere increase in size will convert an indifferent
draught into a good one. The height of the hood also--_i.e._, the
distance between its lower border and the point where it joints
the duct--is of importance. The shorter this distance is, the less
serviceable does it become for the removal of fume. Indeed, it may even
retain the fume which, were the hood not present, would rise to the
roof. Sometimes safety is increased by making the hood double, leaving
a space between the two sheets, and so concentrating the draught at
the centre and at the margin. With a fan, ducts of less diameter can
be used than when dependence is placed on heat alone. A duct carried
into a chimney-stack has the advantage of dispersing the fume at a safe
distance from the workroom.

The variableness of the draught produced by heat makes it unsuitable
for removal of dust, except such as arises from skimming. The
receptacle for the skimmings should always be kept inside the canopy of
the hood. We have, however, seen the dust given off in the heading of
yarn dyed with chromate of lead successfully carried away under hoods
connected up by branch ducts with the main chimney-stack.

[Illustration: FIG. 1.--DAVIDSON’S SIROCCO PROPELLER FAN.]


_Exhaust by Fans._--The draught for removal of dust, and frequently
also of fumes, is produced by a fan, of which there are two types:
(1) low-pressure volume fans and (2) high-pressure centrifugal fans.
In the first the draught is created by the rotation of a wheel with
inclined vanes, causing the air to be driven transversely through the
wheel parallel to the axis of rotation (Fig. 1). During a revolution
a portion of the air is cut off from one side of the wheel, and
transferred through the wheel to the other. Such fans are light, run
easily, and are cheap. They are of many forms, both with regard to the
number of blades--from two to eight--and general manner in which they
are arranged. Some closely resemble the screw-propeller of a ship,
while others have blades turned over and fastened on an outer rim.
Their main defect is inability to overcome any but slight resistance
in the course of suction behind, as from constriction in, or friction
along the sides of, the ducts and right-angled bends, or of outflow in
front, as from wind-pressure. Under favourable conditions, however, and
when carefully fitted, a volume fan will exhaust dust and fumes through
a system of ducts several feet in length, as, for example, from mono
and linotype machines and electro melting-pots in letterpress printing
works. But, in order to avoid resistance from friction, the ducts have
to be somewhat larger in diameter than when a centrifugal fan is used.
With nine[A] linotype machines connected up to a 14-inch propeller
fan, the branch ducts should be about 4 inches in diameter, and the
main duct 12 inches, increasing from 12 to 15 inches within 2 feet of
the fan-box. The shorter and straighter the course of the duct to the
propeller fan, the more efficiently it works. Wind-guards are necessary
to overcome resistance from this source in front, but their position
requires to be carefully considered, so as to prevent the screen itself
crippling the outflow.

  [A] If gratings are also inserted in the same duct for general
  ventilation the number of machines must be decreased _pro ratâ_.

All fans require frequent cleaning, and in this respect propeller fans
have the advantage over centrifugal, in that they are usually more
accessible.

[Illustration: FIG. 2.--DAVIDSON’S DUST CENTRIFUGAL FAN.]


_Centrifugal Fans._--Generally, in the removal of dust, a strong
suction has to be set up in a system of narrow ducts by means of a
centrifugal fan--_i.e._, a fan-wheel formed by a number of vanes
attached to an axle mounted in a spiral-shaped casing--so that when
the wheel rotates air is carried along by the vanes, and flies off
tangentially into the space between the blades and the casing, and
thence to the outlet (Fig. 2). The air inlet or junction of the fan
with the exhaust duct is at the centre of the fan, an arrangement by
which the kinetic energy created by the rapid motion of the air leads
to increase of draught instead of being wasted in production of eddies
in the surrounding spaces. They are made in many different patterns,
according to the nature of the work to be done. Their advantage over
the propeller type in the removal of dust lies in the fact that they
overcome greater internal resistance, and a uniform high velocity in a
complicated system of pipes can thus more easily be maintained.

[Illustration: FIG. 3 shows adjustable hoods and ducts fitting closely
over rollers for mixing coloured inks, and serving not only to prevent
inhalation of lead dust by the workers, but also the colour from one
machine affecting that on another. In the particular room where the
installation is fitted there are thirteen separate sets of rollers; the
diameter of the branch duct of each machine is about 5 inches, and that
of the main duct close to the fan about 20 inches. The special points
we have considered as to entrance of all branch ducts into the main
duct tangentially, gradual tapering of the main trunk, and collection
of the dust in filter-bags, are noticeable. Further, when one set of
rollers is not in use the raising of the hood automatically cuts off
the draught through it. (Drawing supplied by the Sturtevant Engineering
Company, Limited, London.)]


_Ducts._--The main duct should be of metal (steel, sheet-iron, or
zinc); it should be circular in shape, have as straight and short a
course as possible, and be tapered in such manner that the area of
cross-section at any point shall equal the combined areas of all the
branch pipes which have entered it at that point (Fig. 3). Proper
dimensions must be studied in relation to the size of the fan and the
work to be done. Wooden ducts, unless chosen for specific reasons,
such as the presence of acid in the fumes to be removed, are very
unsatisfactory, as it is difficult to maintain them in an air-tight
condition or to make branch pipes enter with rounded junctions. Where
several branch ducts enter a main duct, situation of the fan midway
between them has advantage, not only in saving metal in piping, but
also in causing the distance of the fan from the farthest branch
duct to be only half what it would be were the fan placed at the end
of the system (see Fig. 7, p. 217). Further, the sectional area of
the two collecting ducts will be less than that of one main duct, and
greater uniformity of flow thereby secured. Where the two ducts join
up into the single duct of the fan, the bends must be easy; otherwise
the draughts would collide and neutralize one another. Branch ducts,
if they cannot be made tangential to a rounded curve, should enter
the main duct at an angle of 30 degrees, as by so doing equalization
of the draught at different openings is made fairly uniform. The very
common defect of a right-angle joint diminishes the draught by nearly
one-half. Branch ducts should never be made to enter a main duct on the
outer side of a bend, because at this point the pressure of the current
of air inside the duct is increased. They should join up on the inside
of a bend, where the pressure is reduced.


_Hoods and Air-Guides._--As the object of hoods is to concentrate the
draught on the fumes or dust to be removed from the worker, position
in regard to origin of the fumes or dust requires first consideration.
The more restricted the opening consistent with unimpeded work, the
more effective is the draught, and the less disturbed will it be by
cross-currents in the workroom. Pendock lays it down as a useful
principle that the area of the front opening into the hood should not
be more than four times that of the exhaust throat--_i.e._, the point
of junction of the hood and duct (Fig. 4). Not less important is it
that the draught should operate below the breathing level. Preference
as to the direction to be given to the exhaust current should be in the
order named: (1) Downwards; (2) downwards and backwards combined; (3)
backwards and upwards combined; and (4) upwards only. Use should be
made, for the removal of the fumes or dust, of any initial current of
hot air set up from a bath of molten metal or from a heated metallic
surface, as in vitreous enamelling. Hence under such circumstances only
(3) and (4) need be considered. Generally hoods applied err in having
too wide an opening, or they are placed too far away from the source of
danger. They require sometimes to be adjustable to suit different-sized
articles. Care is necessary to see that, when a hood has been adjusted
for large articles, it is readjusted for smaller-sized articles. The
principle of ventilation downwards and backwards is recognized as right
for grinding and polishing on a wheel, since the tangential current set
up by the wheel in its rotation is utilized. Pug-mills in paint-works
are perhaps best ventilated by applying the exhaust to a dome-shaped
hood covering the posterior half of the mill. Edge-runners must be
encased, with an exhaust pipe attached to the casing and sliding
doors or shutters for introduction or removal of material (Fig. 5). A
small negative pressure inside the casing is all that is necessary,
so as to insure passage of air inwards and not outwards. Branch ducts
must protect the casks out of which material is scooped, and the
receptacle into which it is discharged. In scooping out dry colour
from a barrel, it is unwise to attempt to remove the dust created at
every displacement of air on removal of a scoopful by means of a hood
suspended over the barrel. Instead, the last joint of the duct should
be a telescopic one, so that it can be lowered into the barrel, and be
kept at a distance of about 6 inches above the material. The air is
thus drawn downwards into the barrel (Fig. 6).

[Illustration: FIG. 4 shows a well-designed arrangement of hoods,
duct, and fan, in the packing of white lead, and the filter-bags for
collecting the dust so removed. An additional safeguard is introduced,
as the casks stand upon grids through which a down-draught is
maintained by connecting the space underneath with the exhaust system.
(Drawing supplied by the Sturtevant Engineering Company, Limited,
London.)]

Processes such as colour-dusting, aerographing, ware-cleaning,
enamel-brushing, and the like, are best carried out at benches under
hoods with glass tops. Air will enter from in front, and carry the dust
or spray away into the exhaust duct placed at the back of the bench.

[Illustration: FIG. 5 shows a pan mill with edge runners fitted with
casing (partially open). The casing is connected to a powerful fan,
and branch ducts with telescopic terminal sections control the dust
in scooping out from the barrel, in feeding into the mill, and at the
point where the ground material is discharged.]


=Collection of Dust.=--Frequently no heed is paid to the collection
of the dust. Sometimes a dust chamber is arranged to intercept it on
the far side of the fan, or attempt is made to blow the dust into
a tank of water. The fine dust of which we are speaking cannot be
satisfactorily collected by either of these methods, nor even by a
cyclone separator, so useful for the collection of many kinds of dust.
In lead works generally, the dust removed by the fan is best collected
in filter-bags made of some porous fabric. Various efficient filters
constructed on these lines by Messrs. Henry Simon, Ltd.; Messrs. Beth
and Co., Ltd.; and the Sturtevant Engineering Company, Ltd., are on the
market.

[Illustration: FIG. 6 shows an arrangement of piping with balanced
telescopic joints fitted to a Sirocco dust fan for removal of dust, in
an electric accumulator works, when scooping out litharge from a cask
into the receptacle prior to emptying the weighed quantity into the
mixing machine, also under a hood connected with the exhaust system.
(Illustration supplied by Davidson and Company, Limited, Belfast.)]

In collecting the dust, care must be taken to provide an adequate
outlet for the spent air, so as to prevent creation of a source
of friction in front which might destroy the effectiveness of the
installation.

[Illustration: FIG. 7.--EXHAUST VENTILATION ON THE PATENT “PENTARCOMB” PRINCIPLE
APPLIED TO LINOTYPE AND MONOTYPE MACHINES IN PRINTING WORKS, AS
INSTALLED BY THE ZEPHYR VENTILATING COMPANY, BRISTOL.

P, Patent “pentarcomb” for equalizing exhaust; V, patent “pentarcomb”
for general ventilation; D, main and branch ducts; F, fan; U, upcast
from fan; M, hoods over metal-pots of monotype machines, constructed
to raise and lower, and swing out and in with metal-pot; L, hoods over
metal-pots of linotype machines, constructed to raise and lower.

In the illustration “pentarcomb” grids connect the branch ducts over
the metal-pots of mono and linotype machines with the main duct. The
“pentarcomb” grids are arranged also elsewhere in the main duct itself
to assist in the general ventilation of the workroom. The hoods over
the metal-pots are constructed to be raised and lowered, and to swing
out and in radially with the melting-pot arm. (Drawings supplied by the
Zephyr Ventilating Company, Bristol.)]

In order to secure equality of flow from a number of branched ducts,
the Zephyr Ventilating Company apply a special grating of curved and
slanting inlets--the “pentarcomb”--to each branch duct. The air
passing through the comb is split up into numerous small columns, and
the inclination of the curve which each is made to take is such as to
reduce friction to a minimum. By means of this device we have found,
in a trunk with twenty branches, the draught at the one farthest from
the fan as serviceable as that next to it. The method is illustrated
applied locally to remove the fumes from linotype machines, and
generally in the main duct for removal of foul air near the ceiling.

Where electricity is available as a motive power for driving the fan,
some modification in the views expressed as to the curvature of the
pipes and system of installation can be allowed. In a red lead plant,
for instance, it may be desirable to have the pipes leading to the
sifter or packing machine with sharp angles, so as to prevent tendency
of such heavy dust to collect in them. The electric current allows a
fan to be installed at any point desired; and if applied with knowledge
that the increased friction due to an acute angle has to be overcome,
the result may be quite satisfactory.

The various forms of vacuum cleaning apparatus with mouthpieces
designed to aspirate the dust from different surfaces are sure
to be increasingly used. In our opinion, wherever electric power
is available, they will obviate barbarous methods involving use
of hand-brushes to collect dust from machines, such as those for
litho-dusting or for sweeping lead dust from benches and floors, or use
of bellows to blow out the dust from compositors’ cases.

Finally, the carrying out of lead processes by automatic methods and
with the interior of the casing under a negative pressure, so that
the material is transported from one process to another by means of
worms or conveyors, is everywhere to be aimed at. Or, again, it has
been found possible on a commercial scale, by means of compressed air
in a closed system of receivers and pipes, to force material in very
fine state of division from one place to another, as, for instance, of
litharge from the cask into the mixing machine for preparation of the
paste for manufacture of accumulator plates, without risk of contact.

Indication of the efficiency of the draught may be gained by holding
smoke-paper at the orifice of the hood. The definition of efficient
exhaust in some regulations for the removal of fumes, as in the Tinning
Regulations, is that it shall not be deemed to be efficient unless
it removes smoke generated at the point where the fume originates.
Accurate gauging, however, of the draught can only be done with an
anemometer, so as to determine the number of linear and cubic feet
passing through the throat per minute. Only rarely does one find an
occupier alive to the value of the use of such an instrument. The
importance of this point has been recognized in the Regulations for
Heading of Yarn, by the requirement that the speed of each exhaust
opening shall be determined once in every three months at least,
and recorded in the general register. We prefer to use Davis’s[A]
self-timing anemometer, which gives readings in feet per second without
the need of a watch. Other useful anemometers--Casella’s or Negretti
and Zambra’s--require to be timed.

  [A] It is not available for velocities exceeding 1,200 linear feet
  per minute.

The details of all routine observations on localized exhaust
ventilation might well be entered on a card hung up in the workroom.
Such a card drawn up by our colleagues, Miss Lovibond and Mr. C. R.
Pendock, has the following headings:

  FIRM............................... PROCESS...........................

  FANS:  No..... Kind................ Size....... Maker.................
                 Motive power........ H.P........ Method of driving.....
                 Other load..........             Condition of driving..
                 Screen.............. Dust col-
                 Direction........... lection....
                 Periodic cleaning...

  HOODS: No..... Kind................ Size.......
                 Structure...........
                 Distance between each..

  DUCTS: No..... Kind................
                 Size................ Length..... Section...............
                 Structure...........
                 Periodic cleaning...

  FRESH-AIR
  INLETS: No.... Kind................
                 Position............
                 Size................
                 Fixed or temporary..

  +-------+--------+--------------------+-------+------------+---------+
  | Hood: |Position|Date................|Date................|         |
  | Refer-|   of   |                    |                    |         |
  |  ence | Anemo- |External            |External            |         |
  |Number.| meter. |Conditions..........|Conditions..........|Remarks. |
  +-------+--------+-------+-----+------+-------+-----+------+---------+
  |       |        |       |Speed|Volume|       |Speed|Volume|         |
  |       |        |Area of|  F. | C.F. |Area of|  F. | C.F. |         |
  |       |        |Throat.| p.m.| p.m. |Throat.| p.m.| p.m. |         |
  +-------+--------+-------+-----+------+-------+-----+------+---------+
  |       |        |       |     |      |       |     |      |         |
  |       |        |       |     |      |       |     |      |         |
  |       |        |       |     |      |       |     |      |         |
  |       |        |       |     |      |       |     |      |         |
  |       |        |       |     |      |       |     |      |         |
  +-------+--------+-------+-----+------+-------+-----+------+---------+

Frequent cleaning and inspection of exhaust installations are very
important, as accumulation of dust greatly impedes the flow of air
at all points of the system. The person employed in cleaning the fan
should wear a respirator. Hoods and ducts should always be cleaned with
the exhaust in full action.


REFERENCES.

  [1] Annual Report of the Chief Inspector of Factories for 1910, p.
  172.

  [2] _Ibid._, pp. 172, 173.

  [3] G. ELMHIRST DUCKERING: A Report on an Experimental Investigation
  into the Conditions of Work in Tinning Workshops, and Appendices.
  Included in Special Report on Dangerous or Injurious Processes in the
  Coating of Metal with Lead or a Mixture of Lead and Tin. Cd. 3793.
  Wyman and Sons, Ltd. Price 1s.

  G. ELMHIRST DUCKERING: The Cause of Lead Poisoning in the Tinning of
  Metals. Journal of Hygiene, vol. viii., pp. 474-503, 1908.

  G. ELMHIRST DUCKERING: Report on an Investigation of the Air of
  Workplaces in Potteries. Included as Appendix XLIX. in Report of
  the Departmental Committee appointed to inquire into the Dangers
  attendant on the Use of Lead, and the Danger or Injury to Health
  arising from Dust and Other Causes in the Manufacture of Earthenware
  and China, vol. ii., pp. 93-113, 1910. Cd. 5278. Price 1s. 9d.

  [4] G. ELMHIRST DUCKERING: Annual Report of the Chief Inspector of
  Factories for 1910, p. 47.

  [5] C. R. PENDOCK (one of H.M. Inspectors of Factories): Report on
  Systems of Ventilation in Use in Potteries. Included as Appendix
  XLVIII. in vol. ii. of Potteries Committee’s Report referred to
  under[3].

  C. R. PENDOCK: Second Report of the Departmental Committee appointed
  to inquire into the Ventilation of Factories and Workshops, part i.,
  and especially part ii., 1907. Cd. 3552 and 3553. Price together, 4s.
  8d.

  Other works referred to include--Construction des Usines au Point de
  Vue de l’Hygiène, by Ingénieur-Architecte Maniguet. Ch. Béranger,
  Paris, 1906; Hygiène Industrielle, by MM. Leclerc de Pulligny,
  Boulin, and others. J. B. Baillière et Fils, Paris, 1908; and many
  excellently illustrated trade catalogues issued by ventilating
  engineering firms, such as the Sturtevant Engineering Company, Ltd.,
  London; Henry Simon, Ltd., Manchester; Davidson and Company, Ltd.,
  Belfast; John Gibbs and Son, Liverpool.




CHAPTER XIII

PREVENTIVE MEASURES AGAINST LEAD POISONING--_Continued_


=Periodical Examination.=--In various codes of regulations a surgeon
is required to make periodical medical examination of the workers.
The term “surgeon” is defined as the “Certifying Factory Surgeon of
the district, or a duly qualified medical practitioner, appointed
by written certificate of the Chief Inspector of Factories, which
appointment shall be subject to such conditions as may be specified
in that certificate.” The wording of the regulation varies somewhat
in different codes, but the intention in all is the same, and the
following example from the Tinning Regulations will indicate the
purpose and scope:

  “Every person employed in tinning shall be examined by the surgeon
  once in every three months (or at such shorter or longer intervals as
  may be prescribed in writing by the Chief Inspector of Factories),
  on a day of which due notice shall be given to all concerned. The
  surgeon shall have the power of suspension as regards all persons
  employed in tinning, and no such person after suspension shall be
  employed in tinning without written sanction from the surgeon entered
  in the health register.

  “Every person employed in tinning shall present himself at the
  appointed time for examination by the surgeon. No person employed
  in tinning shall, after suspension, work at tinning without written
  sanction from the surgeon entered in the health register.”

Under the Special Rules for white-lead works, examination is required
at weekly intervals; under the Special Rules for Earthenware and
China, Manufacture of Litho-Transfers and Red Lead, and under the
Regulations for Electric Accumulators, and Paints and Colours, monthly;
under the Regulations for Tinning, Yarn dyed with Chromate of Lead,
and Enamelling, at quarterly intervals, subject to the limitation or
extension specified in the regulation quoted.

The limitation as to quarterly examination is useful to meet
conditions, on the one hand, where special incidence calls for
increased safeguards; and, on the other, relaxation, by reason of
adoption of special processes or measures lessening risk. Thus, in
a yarn-dyeing factory, in consequence of occurrence of six cases
within five months, a weekly instead of a quarterly examination was
prescribed. After eight months, as no further cases were reported, a
monthly examination was substituted for the weekly, and eventually,
with continued absence of illness, the normal quarterly examination was
resumed.

An appointed time for the surgeon’s attendance at the factory has been
found necessary, because, in conformity with the literal wording of the
regulation, the occupier should not continue to employ a worker who,
for one reason or another, has not been examined by the surgeon during
the prescribed interval. With knowledge of the date and hour posted
in a conspicuous place in the factory, excuse for absence becomes
difficult. Alteration by the surgeon of his appointed time should,
whenever possible, be given beforehand. Surgeons in the past frequently
made examination of the persons employed with the view of taking them
unawares, and so of precluding special preparation beforehand--a
practice which had its advantages; but they are outweighed by the
hardship inflicted on workers who were unavoidably absent, as, for
example, night-workers. A health register is supplied to all occupiers
where periodical medical examination is enjoined, the headings of which
and manner of entry are indicated later on in this chapter.

The objects which the surgeon should have in mind in making his
examination are:

1. To prevent lead poisoning and minimize lead absorption.

2. To obtain information for the occupier and Inspector of Factories of
the relative danger of one process and another with a view to adoption
of remedial measures.

In safeguarding the health of the workers, he should make effort to
gain their confidence, in order to be able to attach proper value to
statement as to subjective symptoms. Suspicion in their minds that the
examination is made solely in the interests of the employer militates
against success, and increases inclination to conceal symptoms and
to give untruthful answers as to the state of health since the last
examination. In our opinion, the surgeon will best carry out the first
object by attention to the second. The study of thousands of reports
on cases of lead poisoning convinces us that 90 per cent. at least are
due to inhalation of dust and fumes. The surgeon, therefore, should
utilize the earliest sign of lead absorption to warn the occupier and
inspector of conditions favourable to the development of plumbism, and
due probably either to some unguarded spot in the manufacturing process
whereby dust or fumes are not being removed completely, or to ignorance
or carelessness (often excusable in the absence of proper instruction)
on the part of the worker. He should direct, therefore, especial
attention to new workers, not only because of their need for guidance
as to precautions to be observed and greater liability to attack
during the first year of employment, but also because development of
signs in them constitutes the surest guide to defects in the process
of manufacture. Occasionally symptoms in a worker may be so menacing
as to demand immediate suspension, but generally before the power is
exercised attempt to rectify the condition which gives rise to them
should be made. The surgeon can do much by influencing the foremen and
forewomen, who will necessarily come before him for examination, in
insisting on the supervision by them of care and cleanliness by the
workpeople under their charge. Should suspension, despite attention in
the manner suggested, be necessary, he will recognize that transference
to a non-lead process, if feasible, is preferable to entire cessation
from work in very many cases. The surgeon, therefore, should know what
departments are possible alternatives to lead work.

The fact that an examination is made on factory premises, is directed
to detection and prevention, treatment taking a subordinate place, and
is often made on persons who, unlike hospital patients, seek to conceal
their symptoms, causes it to be an examination _sui generis_. Hence
the surgeon must trust his sight more than his hearing. A surgeon with
experience of such work has said: “The worker in lead must be surveyed
as an individual, and idiosyncrasies must be carefully studied and
allowed for; the ‘personal equation’ is of vital importance”[1].

For the examination a well-lighted room affording privacy is essential.
While it is desirable for the surgeon periodically to see the processes
and conditions under which work is carried on, systematic examinations
of workers should not be made elsewhere than in a private room. The
custom of marshalling workers in a queue, although perhaps unavoidable
in many cases, is liable to detract from the seriousness of the
proceedings, a sense of which it should be one of the aims of the
examination to arouse. In discussing the method of interrogation and
usual examination, Dr. King Alcock[2], Certifying Factory Surgeon of
Burslem, says: “Note the general manner assumed in answering questions
and any indications of carelessness in dress and toilet. Inquire
into the state of digestion, existence of colicky pains, regularity
of bowels, menses, history of pregnancies and miscarriages, whether
before, in the intervals of, or during lead employment; existence of
headache, diplopia, or amaurosis. Note the type, facies, state of teeth
and nails, complexion, speech, tongue, strength of grasp (if possible,
with dynamometer), any tremor in outstretched hand, resistance to
forcible flexion of wrist.... If strabismus is present, note whether of
old standing or recent; and if ocular troubles seem imminent, examine
for optic neuritis, either at once or at home (this is very important,
as cases of acute and serious optic neuritis still baffle examination
by their intermensual development).” He recommends the surgeon, apart
from entry in the health register, which must necessarily be very
brief, to keep a private notebook, and to enter in it as a matter of
routine such details as name, process, age, duration of employment,
condition (married or single), pregnancies, state of bowels and menses,
dental toilet, and any special point worthy of note in individual
workers. A card index, if in use, might conveniently serve for such
entries.

In the actual routine examination it may be useful to describe the
procedure where a large number of workers pass before the surgeon in a
white-lead works every week. The points noted are:

1. The general appearance of the man as he walks forward, especially
the face with regard to anæmia, which in the majority of cases of early
lead absorption is not a true anæmia, but is due to vaso-motor spasm
of the arterioles of the face and eyes. Frequently, on speaking to a
lead-worker, the face, apparently anæmic, flushes directly.

2. The brightness of the eyes, state of the pupils, and condition of
the conjunctiva and of the ocular muscles.

3. The mouth should next be examined, and search made for any evidence
of blue line around the gum.

4. The gait should be watched both on advancing to, and retiring from,
the surgeon. If necessary, the man should be made to walk a few steps.
Although the peroneal type of palsy is extremely rare, the possibility
of its occurrence should never be absent from the mind of the surgeon.

5. The man should then be directed to stretch his hands out in front
of him, with wrists extended and fingers widely spread. Presence
or absence of tremor should be looked for, and the condition of the
finger-nails, as to the practice of biting, etc. The extensor power
should then be tested, firstly of the fingers. While the hands of the
workman remain outstretched, the surgeon places the forefinger of his
hand in the outstretched palm of the workman, and the ball of the
thumb upon the extreme tip of each finger, and by gently pulling it
down, noting the spring present in the muscles. This test is probably
the most delicate there is for detection of early extensor paralysis.
The condition of the lumbricals and interossei are noted on movement
of the fingers. The extensors of the wrist are then further examined,
the workman being directed to flex his arm at the elbow and strongly
pronate the wrist, so that the palm of the hand is directed forwards.
He is then told to close the fist when the surgeon endeavours to flex
the wrist, the workman at the same time resisting by forcible extension
of his wrist. Ordinarily the extensor communis digitorum and minimi
digiti are sufficiently powerful to resist a very powerful pull upon
the wrist; and if the wrist is found to yield, it is a sign that the
muscles are affected. Sometimes the strength of the wrists and fingers
is judged by the surgeon placing his palms on the dorsum of the
patient’s outstretched hands, and seeing whether the patient can be
prevented from lifting them without flexing the wrists or finger-joints.

The test detects (1) paralysis which has been recovered from to a large
extent; (2) commencing partial paralysis; and (3) weakness of muscular
power, especially in those who have worked in lead for a number of
years. This weakness appears to be an effect of lead upon the muscular
tissue or dependent on debility, the result of lead absorption, and
independent of nerve implication. We have known the condition to remain
unaltered for years, and also to undergo alteration, being at times
absent for months together. Occasionally reports of definite paralysis
refer to pre-existing weakness.

6. The pulse is next noted. The pulse-rate need not ordinarily be
counted, but if it is either very slow or fast careful examination at
the conclusion of the general inspection should be made.

It is well to make all these points before asking any questions. After
they are completed inquiry as to regularity of the bowels, existence
of pain or discomfort, would follow. The speech should be noted, as
slurring or hesitating speech is occasionally associated with early
lead poisoning.

All these points can be gone through quite rapidly, and at the
conclusion of the general examination, if judgment is in suspension,
careful examination in the routine medical manner should be made.

In some factories all new workers are examined by the surgeon before
they commence work in dangerous processes. At any rate, a list of such
persons should be given to the surgeon at his visit, as naturally
the question of personal fitness for employment should be decided
at his first examination. Conditions which should lead to rejection
are tubercular disease of every kind, idiopathic epilepsy, all forms
of mental disease or weakness (hysteria, feeble-mindedness, and
neurasthenia), obvious alcoholism, women who are pregnant or who give
a history of repeated miscarriages prior to work in lead, persons with
marked errors of refraction unless corrected by glasses, kidney disease
of all kinds, evidence of previous chronic saturnism, and bad oral
sepsis. Special attention will have to be paid to casual labourers, and
it should be the aim of the surgeon to discourage this class of labour
in lead industries. Work under special rules or regulations requires
to be carried out under strict discipline, and this it is extremely
difficult to maintain on other than regular workers, who recognize the
need for cleanliness and observance of regulations.

Other aids to diagnosis cannot be carried out as a matter of
routine, but will necessarily be used in particular cases, such as
ophthalmoscopic examination of the fundus, electrical reactions of
muscles, analysis of the urine, and examination of the blood-pressure.

A few words may be added on the significance of the two commonest
signs--the blue line and anæmia. It cannot be too strongly insisted
on that presence of the Burtonian line on the gums is, as a rule,
indicative of lead absorption, and not of lead poisoning. As a
danger signal its value is immense, and hardly less so its value in
clinching diagnosis in doubtful cases. Whenever the line is seen risk
is imminent, and poisoning (not necessarily of the individual in whom
it is pronounced) among the workers is inevitable in the absence of
adoption of precautions. Unfortunately, careful dental toilet, which
the surgeon will necessarily lay stress on, may prevent development,
or the practice, when adopted, cause disappearance of the line after
the lapse of a few months. Under these circumstances, the merest trace
will have all the significance of the fully-developed line in a worker
neglectful of care of the teeth. Among new workers a commencing blue
line should be strong evidence of the need for dust removal at some
point in the process of manufacture. The line, in our experience, is
dense in occupations giving rise to fumes or to dust of compounds of
lead, but comparatively rare in those handling metallic lead or its
alloys, as compositors, tea-lead rollers, solderers, and the like.

Some degree of pallor is so commonly met with in adolescence that it
is the progressive development of the anæmia which the surgeon must
especially watch for. As a danger signal, therefore, it has the same
significance nearly as the blue line; but when lead absorption has
affected the elements in the blood, progressive anæmia in new workers,
attributable to the employment, and showing no tendency to improve
after watching for a few months, is an indication for suspension or
transference to other work. In older workers, with a duration of
employment of five years or more, there may be a quasi-pathognomonic
pallor which does not vary from year to year. In them it must be
supposed that an equilibrium has been established, and development of
other symptoms, such as tremor, wrist weakness, or albuminuria, becomes
significant. Attention has already been directed to the distinct
saturnine facies associated with anæmia, and characterized by loss of
fat, particularly noticeable in the orbit and buccinator region of the
face. “So far as the question of any worker’s suspension is concerned,”
says Dr. King Alcock, “I prefer to make my instinctive _primâ facie_
distrust of a saturnine pallor the basis for action. The pallor of
plumbism cannot be summed up in hæmoglobin and corpuscular content;
it is the expression of a complex toxæmia resulting from defective
assimilation and excretion”[3].

The knowledge the surgeon should gain of the idiosyncrasies of the
workers by his periodical examination will enable him to appraise at
their proper value the nature and degree of the symptoms in notified
cases.

Sometimes a rule is made that no lead-worker who has suffered from an
attack of plumbism should be allowed to resume work. This we consider
too harsh a measure. It may be true for painters, but when remedial
measures, such as locally applied exhaust ventilation, can be applied,
with consequent removal of the danger in the process at which the
poisoning has arisen, prohibition of employment seems an unnecessarily
drastic measure.

The health register in general use where periodic medical examination
is required in pursuance of special rules and regulations is divided
into two parts, in each of which entries by the surgeon are required at
each visit.

PART I.

  +--------------------------------+-------------------------------+
  |List of Persons Employed in     |  Particulars of Examination.  |
  |                      Processes.|                               |
  +---+--------+--------+----------+-------+-------+-------+-------+
  |   |        |        |   First  |       |       |       |       |
  |   |        |        | Employed |       |       |       |       |
  |   |        |        |  in such |       |       |       |       |
  |   |Worker’s|        | Process. |  Date |  Date |  Date |  Date |
  |   |  Name, |        +----+-----+-------+-------+-------+-------+
  |No.|in full.|Process.|Age.|Date.|Result.|Result.|Result.|Result.|
  +---+--------+--------+----+-----+-------+-------+-------+-------+
  |(1)|   (2)  |   (3)  | (4)| (5) |  (6)  |  (7)  |  (8)  |  (9)  |
  |   |        |        |    |     |       |       |       |       |
  |   |        |        |    |     |       |       |       |       |
  |   |        |        |    |     |       |       |       |       |
  |   |        |        |    |     |       |       |       |       |
  +---+--------+--------+----+-----+-------+-------+-------+-------+

PART II.

  +----------+------------+---------+---------------------+---------+
  |          |            |         | Particulars of any  |         |
  |          |            |         | Directions given by |         |
  |          |            |         |the Surgeon. Any Cer-|         |
  |          |            |         | tificate of Suspen- |         |
  | Reference|            |         | sion or Certificate |         |
  |to Part 1.|            |Number of|permitting Resumption|Signature|
  +-----+----+  Date of   | Persons |   of Work must be   |    of   |
  |Page.|Col.|Examination.|Examined.|entered here in full.| Surgeon.|
  +-----+----+------------+---------+---------------------+---------+
  | (1) | (2)|     (3)    |   (4)   |         (5)         |    (6)  |
  |     |    |            |         |                     |         |
  |     |    |            |         |                     |         |
  |     |    |            |         |                     |         |
  |     |    |            |         |                     |         |
  +-----+----+------------+---------+---------------------+---------+

In Part I. of the register the surgeon should, at the times of
examination, enter the date at the head of one of the columns numbered
6 to 9; and in the space below, opposite the name of each person
examined on that date, a brief note (see next page) of the condition
found.

In Part II. he should again enter, in Column 3, the date of
examination, with a statement of the total numbers examined on that
occasion (Column 4); and in Column 5 any certificate of suspension from
work, or certificate permitting resumption of work, and particulars of
any other direction given by him, appending his signature in Column 6.

It is the duty of the occupier to enter in Part I. the following
particulars with regard to each person examined: (1) Name in full
(Column 2); (2) the process in which he or she is employed (Column
3); (3) age when first employed (Column 4); and (4) date of first
employment in that process (Column 5); and these particulars, in
respect of each person so employed, must be entered immediately on
commencement of work in the process named.

Various methods of noting the state of health of the workers have
been adopted. Use of the words “Good,” “Very fair,” and “Fair,” is
common as indicating the state of general health, with special note in
addition, often in the form of a symbol, of the presence and character
of definite ill-effects. The object of the register, however, is to
keep a record intelligible not only to the Certifying Surgeon, Factory
Inspector, and occupier, but also to the workers. Entries, therefore,
on a uniform system are desirable, taking account of the two aspects of
the health of every lead-worker, which must be considered (_a_) that
indicative of specific effects from the occupation, and (_b_) that of
general health uninfluenced by the employment. With this in mind, the
following system of entry in the health register has been adopted:

  The entries should be made upon a uniform system, as below,
  indicating degrees of deviation from normal health, and
  distinguishing (by use of _numerals_) those attributable (or possibly
  attributable, in whole or part) to work in lead, from those not
  so attributable, for which latter _letters_ should be used. The
  conclusion is perhaps best expressed as a fraction

   1    2
  ---, ---,
   A    C

  and so on.

  The numerals should be taken to mean:

  1. Passed without comment (no observed effect of lead).

  2. Blue line (or indication thereof).

  3. Marked (quasi-pathognomonic) anæmia, or other signs of impairment
  of health. (Albuminuria, or slight deficiency in tone of the extensor
  muscles of the forearm, would, and miscarriage, or other suspicious
  history of illness between examinations, might, come under this head.)

  4. Suspension or transfer, by reason of impairment of health from
  effects of work in lead. (In such cases the surgeon would be prepared
  to entertain an application for a certificate under the Workmen’s
  Compensation Act.)

  Except in the case of a worker whose exposure to lead is only recent,
  renal disease should always be indicated by a numeral.

  Letters should bear the following meaning:

  A. No comment (_i.e._, fair general health).

  B., C. Increasing degrees of impairment of general health.
  (Pregnancy, if without suspension, should be entered as C.)

  D. Suspension or transfer, for reasons other than impairment of
  health from effects of work in lead.

  X. Carelessness, or neglect of precautions, or unsuitability for work
  in lead. (Suspensions for such reasons should be marked DX.)

  Such entries of numerals and letters will in general suffice for the
  intended purpose; but the surgeon may, of course, find it desirable
  to make other notes for his own information, and it is within
  his discretion to supply further details to occupiers or workers
  concerned.


REFERENCES.

  [1], [2] S. KING ALCOCK, B. M. BOND, A. SCOTT and others, in
  discussion on the Value of Systematic Examination of Workers in
  Dangerous Trades. Brit. Med. Journ., vol. ii., pp. 741-749, 1902.

  [3] KING ALCOCK: The Early Diagnosis of Industrial Lead Poisoning.
  Paper contributed to the Second International Congress for the Study
  of Industrial Diseases held at Brussels, 1910.




CHAPTER XIV

PREVENTIVE MEASURES AGAINST LEAD POISONING--_Continued_


=Overalls and Head Coverings.=--Stress has been laid on the wearing
of overalls and head coverings in processes giving rise to dust or to
splashes of glaze or paint in special rules and regulations in the
past. With the improvement that has taken place in exhaust ventilation,
they have become less important. Indeed, the aim of all manufacturers
and ventilating engineers should be to render processes so free of dust
as to make them altogether unnecessary. Increasing knowledge of the
insidious manner in which lead dust can arise has shown that from this
point of view overalls of the cotton or linen material ordinarily worn
constitute a real source of danger. Splashes of glaze dry on them, and
at every movement involving rubbing of the surface dust is generated.
Some operations almost oblige the worker to press the article worked
upon against the chest, so that chance of inhalation of dust from
this source alone is considerable. Taking them off creates dust, and
after this is done a reprehensible practice exists of either shaking
or beating them against a post. In large factories they are usually
washed on the premises, and the water in which this is done will become
a solution containing some lead in suspension. Hence, even when washed
and dried ready for wear, overalls may not be quite free of lead. Apart
from the general obligation recognized that an employer should provide
and maintain everything necessary to guard against danger contracted
in his factory, we think that the risk run by a worker in taking the
overall home and washing it there is negligible, and offers advantages
in the ultimate cleanliness of the overall over washing on factory
premises. Laundresses shaking overalls prior to washing them have been
known to contract plumbism.

Where work with the arms is incessant, as in the heading of yarn,
overalls are burdensome, and for this reason and the fact that with
efficient exhaust ventilation there should be practically no dangerous
dust, the regulations for the heading of yarn enjoin provision of them
only on written certificate of the Chief Inspector of Factories.

Protection for the clothing, however, where splashing is incidental to
the operations, cannot be dispensed with. Hence either the overalls
themselves or the front of them should be made of some light ventilated
waterproof material, or a waterproof apron worn over overalls of the
kind at present in use. Daily sponging would then take the place of
washing.

If lead dust be visible on the hair of workers, there must be a defect
in the conditions of work to be rectified by other means than cumbering
the head. In our opinion, head coverings ought never to be necessary.
We cannot think that an attack of plumbism can ever be precipitated by
the amount of lead dust inhaled on brushing the hair.

A common provision in regulations for overalls is:

  “Overalls shall be provided for all persons employed in lead
  processes, and shall be washed or renewed every week.

  “The occupier shall provide and maintain for the use of all persons
  employed in lead processes--(_a_) A cloakroom or other suitable place
  in which such persons can deposit clothing put off during working
  hours, and separate and suitable arrangements for the storage of
  overalls required by regulation; (_b_) a dining-room, unless all
  workers leave the factory during meal-hours.

  “All persons employed in lead processes shall wear the overalls
  provided ... and shall deposit such overalls and any clothing put off
  during working hours in the places provided under the regulations.
  The overalls shall not be removed by persons employed from the
  factory or workshop.”

General sense of propriety--and it is on this ground, and not from
danger attaching to non-observance, that we press it--suggests that
overalls should be kept apart from working clothes, and preferably
outside any room in which a lead process is carried on. So long as
actual contact between the two sets of garments is prohibited, we
do not see objection to the same cloakroom sufficing for both. The
best arrangement that we have seen is a room in which each worker
has two lockers--one for the storage of overalls, and the other for
clothing put off during working hours. This presupposes supervision
and effective discipline. We think that all reasonable need in the
provision to be made is met by numbered pegs on one side of the room
or wide passage for clothing, and on the other pegs correspondingly
numbered for the overalls. Means for heating and drying the clothes
should not be overlooked (see Fig. 8).

[Illustration: FIG. 8 shows a good arrangement in a white-lead
factory, by which, as is best, cloakroom, meal-room, and washing and
bath accommodation, are all under one roof. The men on entering hang
up their clothes in the private clothes lobby, and pass through the
swinging doors to the lobby where the overalls are hung. On leaving the
factory and at midday they enter by the door leading into the lobby
for storing overalls, and from that pass to the lavatory and bathroom.
Having washed and put on their ordinary clothes, they enter the
meal-room. The building throughout is lined with white glazed bricks.]

[Illustration: FIG. 8A.--WELL LIGHTED MESS-ROOM IN A SMELTING WORKS.]


=Meal-Room Accommodation.=--Wherever lead processes are carried on the
provision of a mess-room is called for in a part of the factory remote
from possible contamination from lead dust. This we hold on general
grounds of cleanliness and self-respect, and not because we think the
eating of meals in rooms where lead is used would noticeably increase
the number of cases. The more conveniently situated in relation to the
workrooms the mess-room is, the more will it be used. Set out briefly,
the requirements of a mess-room are that it should be--

1. Well ventilated, warmed, and lighted.

2. Not less than 10 feet high, and with floor-space ample for each
person likely to occupy it at any one time.

3. Have walls the surface of which is smooth and impervious to a height
of at least 4 feet from the ground.

4. Have pigeon-holes or other arrangement in which each person can
deposit his food separate from that of others.

5. Have means of warming and cooking food.

6. Be kept properly clean and dry.

No part of a factory becomes so unsightly in the absence of daily
cleaning as a mess-room, especially where provision has only to be made
for five or six workers.

Reid[1] has suggested the following scale of floor-space per person in
mess-rooms:

  6 persons and under     10¹⁄₂ square feet per person.
  Over  6 and up to 12     7¹⁄₂    „       „       „
   „   12     „     20     6       „       „       „
   „   20     „     28     5¹⁄₂    „       „       „
   „   28 and any number   5       „       „       „

In a factory well known to us for manufacture of white lead there is
a restaurant originally started in connection with the sick club of
the factory. For fivepence the workman obtains a hot meal of meat,
bread, and vegetables. Any profits go to the sick fund. Since this has
been started improvement in the physical condition of the men has been
marked; several cases of anæmia and malnutrition have entirely cleared
up. No workman, as has already been emphasized, should commence work in
a lead factory unless he has had a good meal--that is, unless there is
some food at least in the stomach--particularly albuminous food, such
as milk, cocoa made with milk, or _café au lait_. The most suitable
foods generally for lead-workers are those containing proteids--meat,
eggs, milk, cheese, and fatty foods. Acids--vinegar, pickles, and the
like--are especially to be avoided.

Section 75 (2) of the Factory and Workshop Act, 1901, requires that,
where lead or other poisonous substance is used so as to give rise to
dust or fumes, meal-room accommodation shall be provided. The question,
as a rule, is easily decided, but there are border-line cases where
doubt may arise, as, for example, in letterpress printing factories
in regard to dust, and in soldering operations in regard to fume.
Operations in the composing-room undoubtedly give rise to dust, and in
stereotyping and casting the débris trodden underfoot causes dust to
rise. In linotype rooms, however, in the present state of knowledge, a
difficult burden of proof would rest on the person who sought to show
that dust or fumes were present to such an extent as to justify action
under the section. And the same view holds, in our opinion, in regard
to soldering.


=Lavatories.=--The usual requirement for this in nearly all regulations
is:

  The occupier should provide and maintain in good repair for all
  persons employed in lead processes--

  (1) Suitable lavatory accommodation, including at least one lavatory
  basin for every five such persons, fitted with a waste pipe, or
  placed in a trough having a waste pipe, and having a constant supply
  of hot and cold water laid on; or alternatively troughs of enamel or
  similar smooth impervious material, fitted with waste pipes without
  plugs, and having a constant supply of warm water laid on, and
  affording a length of at least two feet of trough for every five such
  persons.

  (2) Soap, nail-brushes, and a sufficient supply of clean towels,
  renewed daily.

Discipline, and responsibility placed on some one person to see to
the cleanliness of the lavatory appliances and adequate supply of the
necessary means for washing, can alone insure proper use of them by
the persons employed. The workman has so narrow a margin of time in
which to get his breakfast and dinner that he cannot be expected to
wash if facilities for doing so fail. The alternative of an enamelled
iron trough with jets of warmed water is in our experience much the
most satisfactory installation where the number employed is more than
five or six. Provision of soft soap or of soap in the form of powder,
and nail-brushes nailed to the table, hinder peculation. Wooden stands
for holding wash-basins present almost invariably a most uninviting
appearance unless covered with sheet lead.

Well-equipped wash-hand basins with hot and cold water laid on close
to the work-place are sometimes provided in addition to the lavatory
proper. If looked after they are valued and used, but if not they
become converted into receptacles for oddments.

[Illustration: FIG. 9.--GOOD WASHING AND BATH ACCOMMODATION IN A LEAD
SMELTING WORKS.]

[Illustration: FIG. 10.--WASHING TROUGH, DOUCHE BATHS, AND CLOTHES
CUPBOARDS.

Type common on the Continent.]

Roller towels should be at least 15 square feet in area for every three
persons employed, and renewed daily.

The merits of soluble sulphides in “akremnin” soap have been advanced
on the ground that the lead is converted into the insoluble black
sulphide, which is thereby made visible to the eye, and the sight of
which will, it is hoped, still further stimulate the desire to wash.
Probably such lead as remains on the hands after well washing with soap
is so closely adherent to the skin as to render risk of contamination
of the food in this way negligible. Dr. Robertson, Chemist of the Royal
Gunpowder Factory at Waltham Abbey, has found that results as good
as those to be obtained from use of akremnin soap (and without any
discoloration of the skin) are obtained from use of a solution made up
as follows: Sal ammoniac added to saturation to a solution containing
8·5 c.c. of commercial hydrochloric acid (specific gravity, 1·15) per
100 c.c. of water. The procedure adopted at Waltham Abbey is--(1) Usual
washing with soap, water, and a nail-brush; (2) scrubbing with the
special solution by means of a nail-brush dipped in it; (3) rinsing in
water; and (4) washing with soap and water.

Sommerfeld[2], from his wide experience, considers that pumice-soap,
with the addition of turpentine, is the best cleansing material
lead-workers can use.


=Baths.=--Provision of bath accommodation is required under the special
rules for white-lead factories and the regulations for electric
accumulators. In several factories, however, baths are provided
for the use of the workers. They naturally make for improvement in
general health, but we cannot regard provision of them, any more than
cloakrooms and mess-rooms, as likely to influence materially incidence
of lead poisoning in a factory. The three requisites of (1) convenience
and quickness, (2) comfort, and (3) regular use, can best be secured
by the use of shower baths in place of slipper baths. The advantage
they have are--(1) Initial cost of installation is less; (2) economy
in space; (3) economy in water; (4) economy in time required for
bathing; (5) no worker comes into contact with water used by another;
(6) cleansing must be from the head downwards. Danger of scalding can
be absolutely excluded by use of valve levers, so placed in relation to
one another that steam cannot be turned on until the cold-water valve
has been opened, and the heater can be so arranged that the water is
not raised above a definite temperature.


=Separation of Processes.=--Lead processes should, as far as possible,
be carried on in such a way that there is aerial disconnection of one
process from another. Separate workrooms, although desirable unless
very small, may not always be possible, but by exhaust ventilation
processes may be arranged so that dust is not a source of danger to
persons working elsewhere. Instances could be given where, in paint and
colour works, persons employed in the grinding of earth colours, in
which no lead entered, succumbed to attacks of plumbism from contiguity
of the plant with that for grinding lead colours. Threading up of
castor runners on a wire previous to dipping used to be done, prior to
1901, in the dipping-house itself, with the result that some severe
cases of poisoning occurred. By the rules of 1901 the process was
required to be done in a place separate from any place where dipping
(or other scheduled process) was carried on, and very few cases have
occurred since. And if exhaust ventilation is relied on, Duckering’s
experiments (p. 206) show the attention to detail necessary to prevent
air charged with lead dust being drawn to the spot by the fan. The need
for separation of processes becomes less in proportion as the cubic
space of the room increases, and dust and fumes are locally removed.


=Age of Employment.=--The same considerations as have been stated
above govern this point also. Wherever lead dust or fumes arise,
whether exhaust ventilation is applied or not, persons of either sex
under eighteen years of age are probably rather more susceptible to
attack by reason of natural failure to appreciate the risk run. When
periodical medical examination in addition to exhaust ventilation has
been adopted, the age limit can safely be reduced to sixteen. Where
handling only of metallic lead and ordinary soldering with an iron are
done, risk of contracting plumbism is so remote that an age limit may
be unnecessary.


=Wall Surface.=--Wherever walls are likely to be splashed, as in
dipping rooms and enamelling workshops, the inner surface of the walls
should be of glazed bricks or tiles or enamelled plates, any of which
help also in increasing the light necessary in such rooms. If, on
account of the cost, such perfectly smooth material is impracticable,
the walls should be painted with oil colour, which will enable them
periodically to be wet-cleansed. Dusting the walls is to be deprecated.
Hence accumulations of dust and débris on ledges, rafters, beams,
roofs, etc., should, in our opinion, only very occasionally be cleaned
down. We consider that the risk from one big cleaning down is less than
that from repeated small ones. (See p. 218).


=Floors.=--These should be smooth and impervious. Wood flooring can
hardly be regarded as coming within this category; it is unsuitable
where lead processes are carried on. Preference must be given to floors
of concrete and the like material, which can be washed down easily
rather than swept. Frequently the dust raised in sweeping the floor
has determined an attack of lead poisoning. No objection can be raised
to wooden grids and iron roll matting placed on the concrete floor for
the workers to stand on. Cold feet and transference of lead dust by the
boots are lessened by their use. Where traffic is heavy, as is often
the case in lead works, vibration is set up with wooden floors, and
dust disseminated. In smelting works cast-iron plates are serviceable
as flooring.


=Instruction of the Worker.=--Too much stress cannot be laid on this
point. To insist upon it, however, is useless unless the occupier has
installed the necessary exhaust ventilation, and equipped his factory
with the other essentials for enabling the workman to guard against
dust and free his hands of adhering lead, in whatever form. When this
has been done, then the worker himself can do something.

Often he creates dust unnecessarily. In shovelling out of a cask with
spade or trowel, in order to get out the last trace of the material to
be transferred, he generally gives it a knock, which causes dust to
fly so sharply as to escape the exhaust; or he removes the implement
quickly from the exhaust, before it has been completely emptied and
while dust is still being given off. He will use a brush to clean his
bench in preference to cleaning it by a wet method. The printer may
hold type between his teeth. Many workers bite their nails. Moustache
and beard may be fingered, and because of this workers may even be
advised to be clean-shaven. They may chew or smoke constantly while at
work, and will frequently eat with unwashed hands.

Notices enjoining care and cleanliness may be, and often are, hung
up in the workrooms, or a leaflet, such as the one here printed, is
handed to the worker on his first examination by the surgeon. Nothing,
however, can take the place of actual verbal instruction from occupier,
foreman, and fellow-worker impressed with the importance of the matter.


  LEAD POISONING: HOW CAUSED AND HOW BEST PREVENTED.

  Unless great care is taken, work in lead and lead compounds is
  injurious to health, because the lead enters the system and causes
  lead poisoning.

  Danger is greatest from breathing leady dust or fume, but eating with
  unwashed hands, and biting nails or putting such things as sweets or
  pipes into the mouth while the fingers are soiled with lead, all help
  to cause poisoning.

  Many workers in lead have a blue line round the edge of the gums,
  but the first actual symptoms of the injurious action of lead on the
  system are costiveness, colicky pains in the stomach, headache, and
  marked paleness. Occasionally headache is associated with epileptic
  fits, a very serious condition, which may be followed by loss of
  sight. “Wrist-drop,” loss of power in the muscles moving the fingers
  and wrist, results sometimes from lead poisoning, and may cause
  permanent disablement from work. It does not usually come on until
  after a person has worked in lead for some years.

  Lead, even if absorbed in small quantities, has a tendency to remain
  in the system, and if care be not taken it will go on accumulating,
  so that in time the health may become permanently damaged, even
  without any definite attack recognized as lead poisoning.

  Girls and boys, because they are not so likely to observe the
  necessary precautions as grown-up people, should be closely watched.
  Women should be especially careful, as the injurious effect of
  lead in them may seriously interfere with the healthiness of their
  children.

  As lead does not enter the system through the pores of the skin, it
  can in great measure be avoided by--

  1. Taking special care to avoid raising dust. It is to the interest
  of everyone to see that ventilating arrangements are in order for
  carrying dust away at the point where it is produced.

  Any little cloud constantly made at work is sure, if breathed, to set
  up lead poisoning. Where lead colours are used wet, danger arises
  from the splashing of the material and its subsequent drying into
  dust.

  2. Paying scrupulous attention to cleanliness of the hands, face,
  teeth, and clothing. The hands and nails should always be cleaned
  with soap and nail-brush before food is eaten, and it is a wise
  practice also to wash out the mouth. The teeth should be brushed at
  least once a day, preferably before the evening meal.

  3. Never commencing work on an empty stomach. Food containing fat,
  such as bacon and milk, is suitable.

  Overall suits, if worn, should never be shaken to rid them of dust.
  They require washing at least once a week.

  Aperient medicine, such as Epsom salts (one or two teaspoonfuls
  in water), can be taken once or twice a week with advantage by
  lead-workers.

  Experience shows that the habits and home life of the workers
  influence their liability to lead poisoning. Intemperate persons are
  the first to fall victims. Those who begin work on an empty stomach
  incur additional risk by so doing.

  Carefulness while at work, and cleanliness, offer the best means of
  escaping attacks of lead poisoning.

  Those who work in lead should keep in mind every hour of every
  working day the importance of not breathing lead dust and not
  carrying lead to the mouth in any way.

  Medical advice should at once be obtained if signs of lead poisoning
  present themselves.


REFERENCES.

  [1] GEORGE REID: Memorandum on Mess-room Accommodation: Appendix XXV.
  of the Potteries Committee’s Report, vol. ii., 1910. Cd. 5278.

  [2] TH. SOMMERFELD: Die Bekämpfung der Bleigefahr, edited by Leymann,
  p. 76.




CHAPTER XV

DESCRIPTION OF PROCESSES

  Lead smelting--Red and orange lead and litharge--Letterpress
  printing--File-cutting--File-hardening--Tinning of metals--Plumbing
  and soldering--Brass.


=Lead Smelting and Silver Refining.=--Lead poisoning very rarely occurs
in lead mining in Europe, as galena (sulphide of lead), the principal
ore in which the metal is found, is insoluble. Galena always, and other
lead ores very often, contain a small proportion of silver, ranging
from 0·001 to 1 per cent., and at times traces of gold. Owing to the
great affinity of lead for silver, lead smelting is necessarily a
process preliminary to the extraction of silver and gold from it[1].

Lead ores, drosses, etc., on arrival at the factory, are, after
sampling, deposited in bins or heaps (often in the open air), and
watered to prevent dust. All ores may, and refractory ores (containing
over 4 per cent. silica) and dross must, be smelted in a blast furnace
by aid of coke. The bulk of the charge in a blast furnace may consist
of more or less complex ores of the precious metals, especially silver.

When galena is treated in a blast furnace, preliminary roasting is
indispensable, and in many smelting works its treatment takes place in
a reverberatory or open-hearth furnace, and not in a blast furnace.

The three principal methods applicable to extraction of lead from ores
are--(1) The roast and reaction method; (2) the roast and reduction
method; and (3) the precipitation process.

By the _roast and reaction method_ a part of the galena is first
converted into oxide and sulphate of lead with access of air.
Subsequently, on shutting off the air-supply and increasing the
temperature, a reaction takes place. The sulphur in the unchanged
sulphide combines with the oxygen of the oxide and sulphate to form
sulphur dioxide, which is carried away by the draught into the bricked
flue, leaving metallic lead behind. The process is carried on in a
reverberatory or open-hearth furnace.

In the _roast and reduction method_ the first portion of the process
is carried out in a reverberatory furnace, the galena being roasted
pretty completely to lead oxide and sulphate, which are then--usually
in a blast furnace--reduced to the metallic state with coke and other
reducing agents, such as iron.

By the _precipitation process_ galena was decomposed at a high
temperature by means of metallic iron, forming a mixture of iron and
lead sulphide. This method was only applicable to rich lead ores, and
is now given up.

The three methods are hardly ever independent of one another, as the
rich slag or residues, for instance, which are obtained by the first
method are retreated by the second, and the second is, as has been
stated, almost always combined with the first.

On tapping the blast or reverberatory furnace, the lead is drawn
off into a lead well or sump, from which, when cool, it is ladled
into moulds, while the slag is run into movable metal pots or along
specially-prepared channels. The slag run off from the reverberatory
furnace contains much lead locked up as silicate, which requires to be
retreated, usually in the blast furnace. During the roasting process
much raking of the material is necessary. The slag from the blast
furnace should contain less than 1 per cent. of lead.

On the Continent and in America, the Huntingdon-Heberlein process has
been extensively adopted, with lessened incidence of poisoning, the
result of mechanical methods of working, obviating hand labour, and the
low temperature (diminishing risk from lead fume) at which the roasting
is carried on. In this process the crushed ore is desulphurized by
first mixing with lime and heating in presence of air in a revolving
furnace, provided with automatic rabble, at moderate temperature (about
700° C.). Subsequently the roasted material is conveyed from closed
bins, into which it falls automatically, by dust-proof elevators to
a converter, in which atmospheric air at slight pressure is forced
through it. The agglomerated mass so formed, when tipped out of the
converter (in doing which there is risk from dust), is well damped,
broken by hand, and charged with coke in the usual way into the blast
furnace.

In some lead-smelting works the material arrives on the premises
in the form of ingots of base bullion--_i.e._, impure lead rich in
silver--the product of previous smelting of the ore where it is mined
in Australia or Spain. And one of the main objects of the blast-furnace
smelting of galena in the factory is to produce a base bullion rich
in precious metals. The lead so obtained requires further softening
or refining to get rid of copper, antimony, arsenic, and tin. This
is effected in a reverberatory furnace, first at a low temperature
to allow of formation of furnace dross, which is removed through
the working doors, and secondly with increase of heat and access of
air to oxidize, in the order named, the tin, arsenic, and antimony.
Finally the lead is tapped into kettles or pots. If free from silver,
such lead, when poured into moulds, is ready for the market; but if
rich in silver, it is treated for the recovery of that metal either
by (_a_) Pattinson’s process, depending on the higher temperature of
crystallization of lead than of an alloy of lead and silver, which
enables a separation of one from the other to be made by a process
of ladling the crystalline from the liquid portion; or, much more
commonly, by (_b_) Parkes’s process, depending on the formation,
on addition of zinc to a pot of molten lead, of crusts consisting
of an alloy of silver, lead, and zinc. The crusts obtained in the
latter process, after cooling, are broken up, placed in a crucible,
and the zinc driven off at a temperature of 1,000° C. in a dezincing
Faber du Faur retort. The rich bullion, retained either in the last
kettle by the Pattinson process, or remaining in the crucible after
dezincing, next undergoes cupellation--_i.e._, exposure to a blast
of air in a furnace. The lead is oxidized into litharge, which drops
into a receptacle below the furnace, leaving the silver behind. In all
lead-smelting works the draught from the furnace carries much dust of
ore and fuel, and fume, consisting of sulphide, sulphate, and oxides of
lead, into the flues. The dust is easily collected in dust chambers,
but the fume requires ducts of great length--sometimes a mile or
more--in which to deposit.


_Dangers and Prevention._--The risk from dust in general labouring
work, in depositing the ores in bins, in removing them to, and charging
them into, the furnace, can only be controlled by watering, preferably
by a spray. From the blast furnace lead fume and carbon monoxide may
escape at the point where charging is done, if there is back pressure
from blockage in the flues, or if the furnace blast is not working
perfectly. In tapping the lead and in manipulations such as charging,
drossing, and skimming, conducted through the doors of furnaces of all
descriptions, hoods, extending at the sides down to the floor level,
require to be arranged over the working doors, and connected either
with ducts passing vertically through the roof or directly with the
exhaust created in the furnace or flue itself. Dross and skimmings
removed through the working doors should be received into iron trolleys
capable of being covered, and not be allowed to fall on to the floors,
to be shovelled up later on to barrows. Before such dross or slag from
reverberatory furnaces is broken up for further treatment it should be
well watered.

Lead absorption among the men actually employed in the Pattinson
and Parkes’s processes is comparatively rare, as the temperature of
the molten metal does not exceed 450° to 500° C. When, however, the
zinc-silver-lead and gold alloy is removed for treatment in special
furnaces for distillation off of the zinc, prior to cupellation, the
lead from the Parkes’s pot, now free from silver, but containing traces
of zinc, antimony, and other impurities, is run in some works into
what are termed “market pots” for a final refining. Air and steam are
blown through to oxidize the impurities. The pot is skimmed twice,
the first dross containing antimony, etc., and the second a fine dust
consisting of lead (60 per cent.) and zinc. The risk of poisoning at
this point is considerable, although an exhaust fan connects up the
cover of the pot with a cyclone separator, to carry away the fume when
the steam is blown through. In other works this dezincing is done in
a refining furnace, the material being then in a slaggy state, thus
hindering development of fumes. After the condensation of the zinc in
the distillation of the silver-lead and zinc crust the cover of the
pot is raised, and the remaining metal, containing 80 per cent. of
lead at a temperature of about 2,000° F., is ladled out into moulds
for treatment in the cupelling furnace. The temperature at which this
ladling operation has to be done makes the work impossible for those
unaccustomed to it. Exhaust ventilation in the operation of emptying
the pot, and cutting off the heat by a water-cooled jacket, suggest
themselves as means to combat the undoubted risk.

In cupellation the temperature is high (about 2,000° C.), and fume will
escape from the working door and from the opening where the rich lead
is fed into the furnace. The danger here is sufficiently recognized
by hoods and ducts placed in front of the furnace, but the draught,
unless the ducts are connected up with a high-pressure fan, may prove
inadequate to carry away all the fume.

Flue-cleaning, carried out usually at quarterly or half-yearly periods,
is dusty work, as much of the dust is in so fine a state of division as
to repel contact with water.

Smelting of other metals when the ores contain appreciable amounts
of lead is equally productive of plumbism. Thus, in the year 1901
fourteen cases were reported from an iron works for the manufacture of
spiegeleisen, the ore (now no longer used) coming from Greece[2]. In
previous years it would appear to have been even greater. A remarkable
feature of all the reported cases from this factory was that the form
assumed was colic, and never paralysis. The poisoning was due to
vaporization of the molten lead by the very high temperature to which
it was raised as the molten iron flowed out of the furnace on tapping.
The danger from fume was limited to the first few feet of the channel,
as the heavier molten lead gravitated down between loose brickwork into
a pit. Dust collected above the point where the furnace was tapped
contained 39·77 per cent. of lead monoxide, and the flue dust 4·22 per
cent.[3]. A flannel respirator worn once only by one of the furnace men
contained lead equal to 16 milligrammes of lead monoxide. In 1906 three
cases were reported in the extraction of copper. The persons affected
were employed in charging ore into the cupola[4].

Heavy incidence of poisoning (twelve cases in two months) in a smelting
works (now closed) led to examination of sixteen men. The gums of
only one man were free of a blue line--in most it was particularly
dense--eight were anæmic, one had paralysis of the wrists, and five
others weakness. Analysis of the air was made at different points
in the factory by the chemist of the works, G. D. Cowan, with the
following results:

  The samples from the cupola were taken from inside the hood (about
  5 feet above the men’s heads). The gas was filtered through
  cotton-wool, so that all solid particles were retained, and the
  remaining gas was treated separately. The solid particles will be
  called “dust,” and the gas, after filtration, “fume.”

  The cupola samples on being examined gave--

  Dust, first sample    0·08152 grain of lead per cubic foot.
   „    second sample   0·07297   „         „          „
  Fume, first sample }  0·00526   „         „          „
   „    second   „   }

  The samples from the lead well were taken 12 inches above the molten
  metal at the end of the lead siphon, and gave the following results:

  Dust  0·05653 grain per cubic foot.
  Fume  Nil.

  The briquetting machine samples were taken from the platform where
  all the ore and fluxes are mixed before briquetting.

  The results obtained here were as follows:

  Dust                             0·95715 grain of lead per cubic foot.
  Fume, or fine dust that passed
  through filter                   0·01314     „         „        „

  The reason for these high results was owing to dust raised when
  waggons of ore were tipped prior to mixing.

Assuming that 20 cubic inches of air pass in and out of the lungs at
each respiration, a man in eight hours would inhale and exhale 94·4
cubic feet. This amount of air, inhaled at the position in the cupola
where the sample was taken, would contain 7·3818 grains of lead; at
the lead well, 5·3064 grains; and at the briquetting machines, 91·5953
grains. Although the condition of the air where the men actually worked
must have contained much less than these amounts, the analyses quite
serve to explain the heavy incidence.

Collis[5] quotes the following analysis of dust and fumes from Hofman’s
“Metallurgy of Lead.”

LEAD SMELTING: ANALYSES OF DUST AND FUMES (FROM HOFMAN’S “METALLURGY OF
LEAD”).

  +--------------------------------+---------------------------------+
  |                                |         Percentage of--         |
  |                                +------+------+-----+------+------+
  |                                |      | Arse-|     | Lead | Lead |
  |                                |  Ar- | nious|     |Monox-| Sul- |
  |      Material Analysed.        |senic.|Oxide.|Lead.| ide. |phate.|
  +--------------------------------+------+------+-----+------+------+
  |            (1)                 |  (2) |  (3) | (4) | (5)  |  (6) |
  |All dust collected in ten years,|  --  |  --  | 25·6|  --  |  --  |
  |average                         |      |      |     |      |      |
  | Dust from--                    |      |      |     |      |      |
  |  Downcomers of eleven blast    |  --  |  --  | 47·5|  --  |  --  |
  |  furnaces                      |      |      |     |      |      |
  |  Roof of blast-furnace building|  --  |  --  | 27·1|  --  |  --  |
  | Fumes from--                   |      |      |     |      |      |
  |  Slag pot while boiling        |  --  |  4·8 |  -- | 41·0 | 26·2 |
  |  Reverberatory settling furnace|  2·3 |  --  |  -- | 31·0 |  --  |
  | Flue dust--                    |      |      |     |      |      |
  |  Friedrichshütte, Silesia      |  --  |  --  |  -- | 62·8 |  --  |
  |                    { A         |  7·5 |  --  | 26·2|  --  |  --  |
  |  Freiberg, Saxony  { B         | 37·5 |  --  | 21·3|  --  |  --  |
  |                    { C         | 46·4 |  --  | 16·2|  --  |  --  |
  |  Pribram, Bohemia              |  --  |  1·0 |  -- | 45·5 |  --  |
  +--------------------------------+------+------+-----+------+------+

Collis[6] estimated the attack rate in lead-smelting works at 30, and
in spelter works at 10, per 1,000 per annum. In one factory he found
it 80 per 1,000, and in a spelter works five cases occurred in a few
months among seven workers.

The distribution of the reported cases from year to year was as follows:

  +--------------+-----+-----+-----+-----+-----+-----+-----+
  |  Process.    |1900.|1901.|1902.|1903.|1904.|1905.|1906.|
  +--------------+-----+-----+-----+-----+-----+-----+-----+
  |Lead smelting |  21 |  26 |  13 |  13 |   7 |  10 |  16 |
  |Desilverizing |   1 |   3 |   9 |  10 |  16 |   6 |   9 |
  |Spelter       |   5 |  11 |   3 |   4 |   4 |   5 |   9 |
  |Other (copper,|   7 |  14 |   3 |  10 |   6 |   3 |   4 |
  |iron, etc.)   |     |     |     |     |     |     |     |
  |              +-----+-----+-----+-----+-----+-----+-----+
  |              |  34 |  54 |  28 |  37 |  33 |  24 |  38 |
  +--------------+-----+-----+-----+-----+-----+-----+-----+

  +--------------+-----+-----+-----+-----+-----+------+
  |  Process.    |1907.|1908.|1909.|1910.|1911.|Total.|
  +--------------+-----+-----+-----+-----+-----+------+
  |Lead smelting |  21 |  31 |  28 |  21 |  33 |  240 |
  |Desilverizing |   4 |   3 |   6 |  -- |   3 |   70 |
  |Spelter       |   2 |  31 |  25 |  12 |  11 |  122 |
  |Other (copper,|   1 |   5 |   7 |   1 |   1 |   62 |
  |iron, etc.)   |     |     |     |     |     |      |
  |              +-----+-----+-----+-----+-----+------+
  |              |  28 |  70 |  66 |  34 |  48 |  494 |
  +--------------+-----+-----+-----+-----+-----+------+


=Spelter (Zinc) Manufacture.=--Lead is present in zinc ores in a
proportion of from 1 to 10 per cent. (usually 3 per cent.). Despite
this small proportion, incidence of chronic plumbism among those
engaged in the manufacture is high, as in the present state of
knowledge the lead fume given off in distillation of the zinc cannot
be efficiently removed. Blende (zinc sulphide) is first calcined, and
the residue, after mixture with calamine (zinc ashes) and anthracite,
forms the charge for the furnace. The retorts are arranged in long
rows one above the other, and frequently back to back in the furnace,
so that there may be 250 or more to each furnace, and of the furnaces
there may be several in a shed. Attached to the retort is a fireclay
receptacle (condenser) into which the zinc distils, and an iron nozzle
(prolong) to prevent oxidation in the condenser. While distillation
goes on the carbonic oxide gas evolved burns brightly, tinged with the
greenish-white colour imparted by the zinc. The products of combustion,
with traces of lead fume from the hundreds of prolongs, are discharged
into the atmosphere of the sheds, where temperature is high. The
latest design of prolongs, however, has an exit at which the products
of combustion escape near the furnace, so that the greater portion
pass up into the ventilating hoods. Periodically--three times to each
charge--the workman removes the prolong, ladles out such zinc as has
condensed, and pours it into moulds. Finally, when distillation is
completed, the contents of the retorts are raked out, and it is in the
fuming hot residues so deposited on the floors that much of the danger
arises. In distilling furnaces of modern design the hot residues fall
through openings in the window of the furnaces into “pockets,” in
which they cool off considerably before they are drawn out into iron
skips. In another form of furnace used in the manufacture of spelter
(Silesian), the workman after charging can leave the furnace until the
time for tapping arrives. The two operations involve work for six hours
a day only.


_Dangers and Prevention._--During distillation the detrimental effect
of a current of air (formation of zinc oxide) on the zinc is an
obstacle to the removal of the fume by exhaust ventilation locally
applied over the prolongs of the condensers. Exhaust ventilation of
a kind can, however, be arranged, except under unfavourable weather
conditions, by erecting hoods of material such as galvanized iron right
across the roof of the shed over, and parallel with, the furnaces, up
which the heated current of air from the furnaces travels. Lofty, roomy
sheds assist materially in the escape of the fumes. Various forms of
modification in the condensers, designed to lessen escape of fume, and
so recover more zinc, are being tried.

Samples of fume condensed as a grey powder, and collected by Collis
from different kinds of prolongs, showed 1·3 to 2·7 per cent.[7]
of metallic lead respectively, and a sample of dust deposited from
material containing 10 per cent. of lead, 3·25 per cent.[8].


=Manufacture of Red and Orange Lead and Litharge.=--These processes
are frequently carried on as part of lead-smelting works. Red lead is
produced by oxidation, first, of metallic pig-lead, in a reverberatory
furnace at dull red heat, into massicot (yellow monoxide). During the
process the material is constantly raked. The massicot is withdrawn
from the furnace, and subsequently, after drying and sieving, is again
subjected to similar treatment at slightly lower temperature. Orange
lead is made by treating white lead in the manner described.

During the ten years 1900-1909 the number of reported cases from the
manufacture of red lead was 108, of which 47 were attributed to work at
the furnaces, 43 to packing and sieving, and 16 occurred among general
labourers, part of whose duty it was to sweep up the floors. Collis
estimates the attack rate in the five years 1905-1909, in a certain
number of factories employing 171 persons, at 50 per 1,000. Reference
to the table on p. 48 shows that the proportion of those suffering from
encephalopathy is higher than in any other industry--an observation
previously noted by Layet[9].


_Dangers and Prevention._--Danger is practically limited to escape
of dust in (1) raking the charge out from the hearth on to iron
trolleys, (2) sieving, and (3) packing. In all these operations exhaust
ventilation is essential, and for sieving and packing the installation
requires to be designed with especial care, so as to be able to keep
within the sphere of the exhaust the spading and shovelling of the
material, in very fine state of division, into the cask. Sometimes the
material is elevated from pits, and eventually packed by mechanical
means into barrels resting on a jolter. Unless the elevators are
quite dust-proof, and the collar hermetically seals the connection of
the shoot with the barrel, the vibration of the heavy machinery and
pressure of air inside the casing will cause dust to escape.

Red lead can be, and is, now made on an extensive scale in such a way
that all operations, from commencement with pig-lead to the final
packing, are carried out by mechanical means so entirely closed in that
the worker does not come into contact with the material. The person
who then may be affected is the fitter attending to repairs of the
machinery. The pig-lead is melted, stirred, and mixed in a covered-in
melting-pot. The massicot which is formed is drawn off by an exhaust
into a hopper, from the bottom of which it is fed mechanically on to
the floor of the furnace. Mechanical rabbles stir it from the centre
to the outside of the furnace floor, from where it is conveyed, under
negative pressure, to the hopper of a grinding mill. From here it is
again similarly fed into another furnace. The exhaust pipe from this
furnace collects the finished product, carrying it mechanically to a
hopper which automatically feeds the red lead into casks. Negative
pressure throughout prevents escape of dust.


=Manufacture of Litharge.=--Pig-lead is placed in a cupellation
furnace, and constantly stirred and raked over to cause entire
oxidation, and then is either raked out or run out from the furnace
hearth into moulds, and allowed to cool in the form of large balls.
These balls, of a roughly crystalline nature, are deposited on the
floor, where they are exposed to the air. Disintegration is accelerated
by breaking up the large fragments by hand. Subsequently the material
is placed in a disintegrator for fine division and packed.


_Dangers and Prevention._--Manufacture of litharge may cause a greater
amount of dust than any other process with which we are familiar. The
nature of the operations is such that it is impossible at all stages
to control this dust. Danger is greatest in the early operations of
shovelling up the disintegrated powdery material from the floors into
receptacles, and in discharging the contents into the disintegrating
machine. The work is heavy, and a respirator is with difficulty worn.
A movable hood attached to a flexible duct in connection with an
exhaust which could be moved from place to place on the floor suggests
itself, but when tried it has not effectively controlled the dust,
owing to both the trouble involved and the difficulty of bringing
the exhaust near enough to the work. When once the material reaches
the disintegrator, exhaust over the hopper, and in connection with
the enclosed sifter and grinder and packing machine, can readily be
secured. Bins should be provided for the litharge lumps, so as to
avoid trampling the powder underfoot, and covered barrows for removing
the semi-powdered material. Alternation of employment lessens risk,
and should be always arranged. In any new plant the possibility of
automatic methods of carrying out the process as far as possible should
be considered.


=Sheet Lead and Lead Piping.=--This industry also is not infrequently
carried out on smelting premises. To make lead piping, molten refined
lead is run into a cylinder containing an adjustable mandrel in its
centre. The cylinder is forced by hydraulic pressure against a hollow
ram having an adjustable orifice to form the desired thickness of pipe.
In the case of sheet lead the thick plates are gradually reduced to the
desired thickness by pressure of heavy steel rollers.


_Dangers and Prevention._--Little risk attaches to handling the clean
sheet lead or drawn lead. Danger is in the early stages. Old oxidized
lead piping, lead cisterns, tea lead, old accumulator plates, etc., lie
in heaps on the premises. These cannot be handled without generation
of dust. When melted and stirred, copious fumes arise, carrying up
dust, from which, and from that raised in drossing the surface of the
metal, absorption of lead is inevitable unless the melting-pot is
fully protected from side-draughts and provided with a hood and duct
leading into the main chimney-stack. Doors in front of the hood serve
still further to confine the fumes. The skimmings from the pot require
to be placed in a receptacle under the hood. Of 109 cases reported
in the ten years 1900-1909, operations at the melting-pot accounted
for at least 47. We are in agreement with Dixon Mann, who remarks:
“Workers in metallic lead do not suffer unless they are frequently in
the presence of large quantities of the molten metal, or inhale fine
particles of solid lead or its oxide whilst manipulating old metal.
Lead, though not usually classed amongst the volatile metals, is
capable of volatilization at a high temperature, and in the form of
vapour may be taken into the system through the respiratory tract, and
also into the stomach. One of the worst cases of chronic lead poisoning
I ever saw was that of a man who bought the sheets of lead linings of
old tea-chests, and melted them down into pig-lead. He did the work in
a small room, without any contrivance for ventilation, and attended to
the whole process himself”[10].


=Letterpress Printing.=--In this industry account has to be taken of
contact with--

1. Molten lead in (_a_) casting the type in different kinds of
machines, including the monotype and linotype; (_b_) in stereotyping;
and (_c_) in recasting into moulds the line or single type after it
has been once used, together with débris from the stereo machine and
sweepings from the floor.

2. Metallic lead in handling and dressing the type, and subsequent
use of it by the compositor. The type metal itself usually consists
of--Lead, 75 per cent.; antimony, 23 per cent.; and tin, 2 per cent.

During the ten years 1900-1909, 200 cases were reported--92
compositors, 71 stereotype and linotype operators, and 37 in subsidiary
processes, mainly in the casting-room. Thus, apparently, operations
involving contact with molten metal are more likely to cause lead
poisoning than actual handling.


_Type-Casting._--In letter founding and in the monotype letter-casting
machine the molten metal, heated by a coal fire in the former and
Bunsen burner in the latter, at regular intervals fills the matrices at
a point where it is cooled by a jet of compressed air, and the formed
letter is then mechanically ejected into a receptacle. The temperature
of the molten metal has to be carefully regulated, and does not usually
rise above 400° to 450° C.--a temperature at which it is extremely
doubtful if lead fume can be produced. Sommerfeld[11] states that in 60
cubic metres of air aspirated close to a type-casting machine no trace
of lead was found, because vaporization does not take place below 550°
C. Such skimming as must occasionally be made of the small surface
of molten metal is in a slaggy state, and does not appear to contain
much oxide. This is deposited usually in a small box and removed to be
remelted once a day. What fume, often of unpleasant odour, is noted is
probably due to acroleic acid vapour from the grease and dirt.

The letters having been cast, the type may be rubbed on sandstone or
on a file, by which small quantities of metallic dust are given off;
set up on setting-boards so that all letters face the same way (work on
which female young persons are usually engaged); certain portions of
letters undercut so as to make them lie perfectly parallel; dressed,
planed, and examined, so as to be of precisely the same height; and
finally assorted into founts and packed in the warehouse. In all these
operations the fingers necessarily get blackened by contact, and there
must be slight dislodgment of metal particles to account for the cases
reported.

In the linotype machine, matrices are brought down from the magazine
by touching the corresponding letters on the type indicator until
they are arranged so as to form the line; a lever then carries them
sideways into position, so as to allow the molten metal to flow into
the mould and cast the line. Another lever then raises the matrices,
which are carried into the magazine again, the slab of metal with the
cast line upon it falling into a receptacle. Here, again, danger of
lead fume is hardly in question. As the matrices drop down from the
magazine, particles of lead which they have gathered when in contact
with the metal are detached, and are visible on every linotype machine
at this point. The brass cover of the magazine, if not frequently
cleaned, soon becomes coated with fine dust. Although lead fume may
not be given off, it is none the less necessary to remove the products
of combustion from the heating apparatus, in order to prevent constant
vitiation of air and to reduce the temperature in the neighbourhood of
the machines. Monotype machines give off much heat. Exhaust ventilation
by hoods reaching well over the pots, and branch ducts entering the
main duct in connection with a fan tangentially, can alone accomplish
this satisfactorily. Hoods and ducts leading merely into a shaft
running up the side of the building fail to prevent condensation of
the water vapour, which in consequence trickles back. Wherever a
well-thought-out system of exhaust ventilation has been installed,
reduction in temperature and comfort to the operatives has been
secured. Temperatures above 65° F. must incommode a linotype operator.

[Illustration: FIG. 11.--EXHAUST VENTILATION ON THE PATENT “PENTARCOMB”
PRINCIPLE APPLIED TO METAL MELTING-POTS, ETC., IN PRINTING FOUNDRY, AS
INSTALLED BY THE ZEPHYR VENTILATING COMPANY, BRISTOL.

P, Patent “pentarcomb” for equalizing exhaust; D, main and branch
ducts; U, upcast from fan; F, fan; H, hoods over melting-pots and dross
drums; S, stereo metal melting-pots; B, boxes or drums for dross.

The illustration shows exhaust ventilation applied to the melting
and stereo pots and dross drums in a letterpress printing foundry.
The draught over each pot is equalized at the point where the branch
ducts join the main duct by insertion of a patent “pentarcomb” grid,
which breaks up the columns of air into numerous smaller channels by
specially curved metal plates so as to minimize friction. The ducts are
graduated, and the exhaust is provided by a volume fan.]

In the foundry the recasting of old used type, etc., is effected, and
periodically scraps and sweepings are melted down. These melting-pots
should have telescopic hoods so balanced that they can readily be
lowered, so as to enclose the bath of molten metal and allow the
fume to be drawn by the fan into a duct of such width as to offer no
obstacle to escape. A duct too narrow to deal with the great expansion
the heated air undergoes is a defect very frequently found. A principal
source of danger is the skimming of the melting-pot for sweepings,
etc., and deposit of the large amount of dross by the side of the pot.
Receptacles for the dross in connection with the exhaust system are
imperatively needed.

Exhaust, where practicable, over the often large melting-pot for
stereotype casting is desirable, in order to secure a reasonable
temperature. Here there is the danger of splashing of molten metal,
which is subsequently trodden underfoot.


_Compositors’ Work._--The letters are distributed in the small
compartments of the type cases. From attrition dust may lie thick in
the compartments, and when at work there is always tendency for small
quantities of this dust to be dispersed. While this is the principal
source of poisoning, inasmuch as dust containing lead must adhere to
the fingers, lead may thus enter the system with food or when smoking.
It is quite as easy, also, to believe that lead poisoning may result
from solvent action of the blood and tissue fluids on small spicules of
lead type which penetrate the skin as to credit the well-substantiated
cases of plumbism ensuing on retention of bullets or shot in the body.
Compositors sometimes contract the habit of holding type between their
teeth.

The old dangerous method of blowing out the dust on the staircase by
means of a bellows should before long be entirely supplanted by use
of suction bellows or use of printers’ case dust-extractors. In the
Clements apparatus the cases are placed on a shelf, which is made to
oscillate; air is forced into the compartments from numerous jets, so
as to raise the dust, which is removed by suction and collected. The
cases are thus cleaned with great saving of time in the composing-room
itself, and without contamination of the general atmosphere by dust.

The dust removed from a composing box by a vacuum cleaner was found in
the Government laboratory to contain 9·8 per cent. of metallic lead,
and that collected from the top of the magazine of a linotype machine
8·18 per cent.

Regulations issued in 1911 in Austria require, among other things--(1)
Melting-pots, and, so far as is practicable, linotype pots also, to be
provided with hoods and ducts to carry the fumes to the outside air or
into a chimney; (2) the type cases to fit either close on to the floor
or with a sufficient space below the lowest drawer to enable the floor
underneath to be easily cleaned; (3) the interior of all compositors’
boxes to be cleaned at least once every three months--if possible,
by means of a vacuum suction apparatus; and (4) quarterly periodical
medical examination to be made of persons employed in casting,
stereotyping, linotyping, assorting type, and composing.

Sommerfeld[12] believes that in Berlin 1·07 per cent. of the
compositors suffer from lead poisoning every year, and that 2·5 per
cent. of all the diseases they suffer from are due to lead. Among 3,641
printers applying for sick relief, Silberstein[13] found 65 suffering
from lead poisoning (1·7 per cent.). Where, however, diagnosis of
lead poisoning is based upon examination of the blood, as in Leipzig,
the amount of compensation paid by the Sickness Insurance Society has
diminished considerably. Thus, of 207 compositors who were either sent
by medical men as cases of, or went themselves suspecting that they
were suffering from, lead poisoning, only 17 (8·2 per cent.) showed
basophilia to such degree as to warrant the diagnosis. The proportion,
on the other hand, among letter founders and electrotypers was 28·6 per
cent.

Printers suffer extensively from phthisis, their comparative mortality
from this cause as compared with the figure for all occupied males
being 290 : 175[14]. This high mortality is probably due mainly to the
vitiation of the atmosphere, and reluctance, on account of extreme
sensitiveness to draughts, to admit fresh air. This closing of windows
by persons employed should be an additional reason for checking the
vitiation from Bunsen burners in connection with linotype and monotype
machines by the only practicable means of preventing perceptible
draught--namely, exhaust ventilation.


=File-Cutting[15].=--The steel file to be cut is placed on a stone
block in the centre of which is inserted a smaller steel block, called
a “stiddy.” The worker holds in his right hand a hammer, weighing
sometimes 7 or 8 pounds, and in his left, closely gripped, a chisel.
Each tooth in the file--and there may be as many as 3,800 teeth to be
cut--is the result of a blow on the chisel, and we have counted as many
as 120 blows with a 7-pound and 200 with a 4-pound hammer per minute.
To offer resistance to the blow and yet prevent a recoil, the file (in
the case of the finer kinds) is placed on a lead bed--that is, a thin
strip of metallic lead. With attrition from repeated impact the lead
bed becomes worn away in the course of a few days, and part of what is
so worn away necessarily takes the form of lead in fine particulate
state.


_Dangers._--Absorption of lead follows from the dust generated by each
blow, from brushing the dust off the cut file, and from licking the
finger and thumb holding the chisel. Other conditions predisposing
to plumbism before the present regulations came into force, and not
altogether without effect still, were--too close proximity of one stock
to another, defective ventilation of the (frequently) small shed in
which the work was done, overcrowding, accumulation of dust on the
benches, uneven floors, inadequate washing facilities, and, apparently,
lack of appreciation of the danger.

The remarkable feature of plumbism in this industry is the long
duration of employment before pronounced symptoms manifest themselves
(see p. 51). The insidious onset is, however, accompanied by an
undermining of the constitution, showing itself eventually in atrophy
of the muscles, especially of the thenar and hypothenar eminences
of the hand, and of the lumbricals and interosseous muscles of the
fingers, the result of continual gripping of the hammer and chisel,
chronic interstitial nephritis, with its associated arterio-sclerotic
changes, and heavy incidence of phthisis.

Provision of locally applied exhaust ventilation has never been
suggested for this industry, owing to absence of power to drive a fan
in the small workshops, and because no lead dust is seen to be given
off. Diminution in the number of cases is due to the fact that machine
file-cutting (with zinc as the bed) has been substituted for hand
file-cutting for coarse files. In hand cutting, in some instances, beds
of pewter, or of alloys with comparatively small proportion of lead,
have replaced the use of lead beds. The remedial measures prescribed in
the regulations have also played a part.

At the time the regulations came into force, in 1903, there were about
708 file-cutting shops in the United Kingdom, of which 517 were in
Sheffield. Immediately after they came into force 126 certificates of
exemption were granted for use of beds containing less than 5 per cent.
of lead, and every year fresh applications are received[16]. There does
appear, however, to be difficulty in securing beds which conform to the
standards laid down. Thus, in the four years 1907-1910, of 23 samples
submitted as containing less than 5 per cent., 16 were in excess.

The number of reported cases of poisoning in the five years 1900-1904
was 151, and 51 in the five later years 1905-1909. The attack rate is
about 10 per 1,000, but, although this may be low compared with other
trades, the much greater severity of the attacks has to be borne in
mind.


=File-Hardening.=--The process consists in keeping the files in a bath
of molten lead at high temperature, covered with charcoal. The file is
removed when red-hot, straightened if necessary, and plunged into a
solution of brine.


_Dangers and Prevention._--Poisoning is attributable to fume given
off by the molten lead (a temperature of 850° C. was recorded by S.
R. Bennett--see p. 201), risk of which can only be met by efficient
hooding and exhaust unless an alternative method of hardening is
adopted, dispensing with the lead bath--_e.g._, by exposure to heat on
a hearth, in a gas furnace, or by other means. In this small industry
in and around Sheffield three cases were reported within a year,
each involving partial or complete paralysis of the extensors of the
forearm. Of ten men employed at the work, three showed presence of
a blue line, three were cachectic, and one had weakness of the arms
and wrists. In two of the three factories attempts had been made
unsuccessfully to carry the fumes away by a hood and duct[17].

Hardening of forks and similar articles in the same manner has also
given rise to poisoning.

We are informed that methods of hardening and tempering drills, tools,
etc., by the use of fused metallic salts, are being adopted in some
works. By mixing together two or more salts in definite proportions,
suitable fusing-points can in all cases be produced. These baths can
be raised to any desired melting-point to suit the requirement of
different steels. For example, sodium nitrate and potassium nitrate in
certain proportions give melting-points from 220° to 340° C., and can
be used for tempering baths up to 600° C. For tempering above 600° C.
mixtures of sodium chloride and potassium chloride can be used, whilst
for hardening, sodium chloride or barium chloride give adequate ranges
of temperature. Similarly, mixtures of sodium sulphate (melting-point,
890° C.) and lithium sulphate (860° C.) can be made to give any
melting-point from 605° to 860° C.


=Tinning of Metals[18].=--Cheap hollow-ware vessels such as kettles
and frying-pans are often coated with a mixture of (usually) half lead
and half tin by dipping them into a bath of the molten metal, after
cleaning in hydrochloric acid.


_Danger and Prevention._--Duckering has shown (see p. 203) that fumes
of chloride of lead are given off which are especially noticeable
when the dipped article is removed to a stand to have the superfluous
metal wiped from it with tow while still in a molten state. Detailed
reference is made on p. 204 to the nature of the fume given off and the
amount of lead present in the atmosphere breathed and inhaled daily by
the worker.

The danger from fumes can be in great measure removed, both from the
bath and from the wiping stand, by locally applied exhaust ventilation,
which may be secured by utilization of the draught from the fire under
each melting-pot, or by a hood and duct carried vertically through
the roof if arranged as described on p. 209. Danger from dust arises
also from the skimmings, if not deposited in a receptacle within the
hood, from dust and débris on the floor, and possibly from traces of
metallic lead and lead chloride attached to particles of tow floating
in the air. Risk of lead absorption is less in later processes, such
as affixing the spout and handle (mounting), and hammering or denting.
Occasionally roughnesses are removed by rubbing the coating with emery
paper.


_Harness Furniture._--Hames, buckles, bits, etc., are usually coated
with nickel or copper, more rarely with silver. The process is in the
nature of soldering, and the steel, prepared in the same way as has
been described for hollow-ware, has a mixture of two parts tin and
one part lead poured over it on a hearth. The strip of thin nickel
sheeting is passed through a similar mixture, and is wiped with
tow--the operation to which such poisoning as occurs in this industry
is mainly due, in consequence of the difficulty of efficiently removing
the vapour of lead chloride from the molten metal upon the long strip
of nickel. Subsequently the prepared steel article and the strip of
nickel or copper are made to unite under pressure of a soldering-iron.
In silver plating danger from fume is slightly less, as the steel
portion (for example, the hame) only is tinned. In the final operation
of polishing on a mop danger arises from dust, unless locally applied
exhaust is provided.


_Iron Drums and Kegs._--Use of a tinning mixture of lead and tin in
this industry is obviously in the nature of soldering. The body of
the drum is made either of black sheet-iron or of terne (lead-coated)
sheet. In order to unite the seam and to fix the bottom sheet, the drum
is made to stand in a shallow bath and laid on its side. The danger
from lead chloride vapour is considerable, and the method of prevention
is precisely of the kind described above.

Similar coating of articles first cleaned in hydrochloric acid is
met with, as, for example, of the component parts of radiators of
motor-cars, of steel bars, and of wire. Incidence of poisoning has not
occurred to an extent to make necessary more than the application of
locally-applied exhaust to remove the fumes.


_Manufacture of Terne Plates._--The manufacture of lead-coated sheets
for roofing purposes is carried on in a few works in South Wales along
with the manufacture of tin plates. Lead poisoning in the industry
is practically unknown. We can only recollect occurrence of one
case, despite the fact that the mixture contains from 65 to 95 per
cent. of lead. For cleaning the plates prior to passing them through
the concentrated zinc chloride flux into the molten mixture, dilute
sulphuric acid is used, and not hydrochloric acid. As to the remarkably
different results on health of the two processes, Duckering concludes:

“The absence of lead poisoning among terne-plate workers and tinners
would appear to be explained by--(1) The use of cleaning agents and
a flux of such a nature, and in such a way, as to involve a minimum
contact with the tinning metals, and under such conditions as to
inhibit extensive interaction between them, and also under such
conditions as to inhibit production of fume or vapours, even if
any interaction occurs; (2) use of a scientifically prepared flux
containing no uncombined acid or excess of water in such a way as to
prevent introduction of these substances, or of ferrous compounds
coming into intimate contact with the tinning metal; (3) so conducting
the operation of tinning that any chlorides possibly adhering to the
plates are removed before the plate reappears in the open air, under
conditions preventing them from appearing in the air as vapour, but
it is very doubtful whether any chlorides could adhere to the plates;
and (4) absence of any manual work on the plates before the metallic
coating is set and hard. On the other hand, the existence of widespread
lead poisoning in tinning of hollow-ware is explained by--(1) Use of
cleaning agents and flux in such a way as to bring these materials into
intimate contact with the tinning metals under conditions eminently
favourable to chemical interaction and vaporization of resultant
compounds; (2) use of an unscientifically prepared flux containing
a large excess of water and much free acid; (3) so conducting the
operations as to favour the escape into the atmosphere of vapours of
soluble lead compounds, such as lead chloride, and of metallic lead and
soluble lead compounds, carried mechanically by fibres of tow during
processes subsequent to tinning, as in wiping; and (4)--a minor point
not to be lost sight of--possibility of contamination of the hands by
soluble lead compounds, due to manipulating the material with which the
articles are wiped.

“It should be added that while use of a scientifically prepared
flux [(2) above] in hollow-ware tinning would no doubt lessen the
possibility of the production of fumes, it is not to be anticipated
(unless a flux containing no chlorides were used) that this would do
away with lead poisoning. In other words, the method of use is, as
indicated above, a far more important factor.”

In the ten years 1900-1909 the number of reported cases in tinning
hollow-ware was 93 among about 200 persons employed, in harness
furniture 23 among about 150 persons employed, and in iron drums and
kegs 47 among about 250 persons employed.


=Plumbing and Soldering.=--The figures included in the table on p.
47 have reference only to these processes as carried on in factory
premises. House plumbers, when reported, are included with house
painters. The figures are made up of two classes--(1) Those handling
white and red lead paste, and (2) those engaged in soldering and lead
burning. The number of cases reported in the ten years 1900-1909 was,
in the first class 122, and in the second 95.

Any worker using red lead as a jointing paste who is not a house
plumber or a coach or ship builder is included under the first heading,
as, for example, electricians, persons engaged in mechanics’ workshops,
lead-light making where red lead cement is brushed between the lead
lines and the glass to render them water-tight, and such occupations
as placing strips of canvas coated with red lead between sheets of
iron work before riveting, so as to afford protection against rust. In
several reports there is reference to the dust created in the breaking
up of old joints with aid of hammer and chisel before proceeding to
recaulk them.

Dust in making up the paste is the principal source of danger. This is
crudely done, and unless large quantities of paste are made exhaust
ventilation is never provided, in view of the intermittency of the
work. The wearing of a respirator should be possible, but it would
be unsafe to recommend that as a sufficient means of prevention.
Installation, whenever possible, of localized exhaust ventilation at
the mixing bench is most desirable. Personal cleanliness is important,
as the hands become ingrained with the paste.

The heading “Soldering” includes in the main (_a_) the soldering of
tins of all descriptions, bicycle lamps, etc., with a stick of solder,
either held in the hand or lying on the bench, which is touched by the
hot soldering-iron, the surface to be soldered having previously been
cleaned with “killed spirit”--_i.e._, zinc chloride flux; and (_b_)
lead burning, by means of a hydrogen or oxy-hydrogen blowpipe flame, of
lead-lined boxes, vats in sulphuric acid and other chemical works. Some
cases are included which occurred in the manufacture of solder itself.
Green wood is held at the bottom of the pot of molten metal, and the
gases distilled from the wood pass upwards through the metal and escape
at the surface, carrying small quantities of lead into the atmosphere
of the workroom.


_Dangers and Prevention._--It can be confidently said of soldering
that, bearing in mind the very large number of persons employed, the
number of cases reported is remarkably small, and it is difficult
to assert generally, as can easily be asserted of tinning, that
inhalation of soldering fumes must necessarily set up lead poisoning.
Moreover, examination of persons employed in soldering for signs of
lead absorption is almost always negative, a blue line on the gums even
being rarely visible.

On the other hand, the process of soldering is so analogous to that of
tinning that such poisoning as occurs is probably due to inhalation
by susceptible persons of lead chloride fumes. And this is borne out
by the results of analysis in the Government laboratory of a sample
of deposit collected from a duct where exhaust ventilation had been
applied to take away the fumes.

  The material was a black mass, obviously containing a large
  proportion of carbon.

  On completely extracting with water, the solution was found to show
  an acidity equal to 0·20 per cent. of hydrochloric acid calculated
  on the original sample, and in this solution the following metallic
  substances were present--viz.:

                                            Percentage on
                                         Original Substance.
  Zinc, calculated as zinc chloride            19·53
  Copper, calculated as copper chloride         1·77
  Lead, calculated as lead chloride             0·19

Tin and arsenic were both absent, and the chlorine present closely
corresponded with the proportion of chloride shown above.

The portion of the substance which was insoluble in water was found to
contain the following metallic substances:

                                         Percentage on
                                      Original Substance.
  Tin, calculated as tin oxide              6·09
  Lead, calculated as lead oxide            1·33
  Copper, calculated as copper oxide        0·57
  Zinc, calculated as zinc oxide            0·20

  This portion of the sample was also free from arsenic.

We believe that where soldering is done by several persons in a
workroom, inhalation of the fumes is prejudicial to health, and that
the usual methods of localized ventilation are desirable. Where this
has been done the result has been in every way satisfactory.

In lead burning the heat from the blowpipe flame is sufficient, if kept
long enough in contact with the lead sheet, to cause volatilization
of the metal, and, as the worker’s face must necessarily be close to
the flame, inhalation of fume is inevitable. Such work, however, has
often, unfortunately, to be carried on in confined spaces where exhaust
ventilation cannot be applied.


=Brass[19].=--The malady the brass caster has suffered from in the past
is _par excellence_ brassfounders’ ague. Lead, however, is introduced
(rarely exceeding 10 per cent.) for the purpose of softening the alloy
of copper and zinc. Of 77 cases of lead poisoning in the ten years
1900-1909 included under the heading “Brass,” 38 were polishers, 28
casters and others, and 11 chandelier fitters. Cases occur among the
casters probably from inhalation of the fumes in pouring, and among the
polishers from inhalation of the small proportion of lead in the dust
given off in the absence of adequate exhaust. In a factory where there
were two emery wheels, one with a hood and fan to carry the dust away,
while the other remained unprotected, the worker at the unguarded wheel
suffered from lead poisoning. In filing and dressing the article is
held in a clamp with leaden claws, which gradually become worn away,
just as does the lead bed used by the file-cutter. This may account for
the poisoning reported among filers and dressers.

A sample of dust taken from under a calico mop for brass polishing was
found in the Government laboratory to contain 2·1 per cent. of lead.

The joints of chandelier fittings are sealed with a white lead paste.
Instead of always testing the completeness of the seal by means of an
air pump and pressure gauge, the fitter frequently tests it by applying
his lips to the unsealed end and blowing through the pipe. All the
cases among chandelier fitters are caused in this way--perhaps the
clearest instance of poisoning by absorption through the alimentary
canal, as distinguished from absorption through the lungs, that can be
cited. While use of an air pump and immersion of the joint in water or
pressure gauge only is an entire protection, and should be provided
wherever this work is done, constant supervision as to its use is
called for. The sealing of the joint can be done with a material known
as “caulkite,” containing neither white nor red lead.

  For references, see end of Chapter XVII.




CHAPTER XVI

DESCRIPTION OF PROCESSES--_Continued_


=Manufacture of White Lead[20].=--The usual method in this country is
that known as the “Dutch process,” although the German chamber process,
precipitation processes, and others, are all practised.


_Dutch Process._--A layer of spent tan is placed on the floor of the
stack (a chamber with walls of brick some 25 feet high, and a vertical
opening from top to base through which the men enter), upon which are
arranged earthenware pots partially filled with dilute acetic acid.
Strips of lead are then placed on small square “cockney” pots, or more
rarely in the form of folded grids, inside deep, long “castle” pots,
and the whole covered with boards, resting on special “bearer pots”
containing dilute acetic acid. Ten to fifteen of such layers (blue
beds) one on the top of the other are built into the stacks to a height
of some 20 feet. When completed, the stacks remain for 80 to 100 days
before being emptied. During this period the temperature rises to 75°
to 80° C., considerable evolution of carbonic acid gas takes place, and
the lead is converted first into acetate and subsequently the white
basic carbonate. The layers (white beds) are uncovered and the corroded
strips (corrosions) collected by hand. They are placed in trays and
carried to heavy steel rollers by means of which and subsequent raking
in wash becks the carbonate is detached from the uncorroded central
core of blue lead. In many factories corrosions are now conveyed
from the stacks to the wash becks or rollers by travelling cranes.
The recovered blue lead is removed in a wet state to be remelted and
recast. The corrosions, after passing through the rollers and wash
becks, are shovelled on to a picking-board and transferred gradually
to the grindstones. From the stones the ground pulp passes to the
settling becks through several gratings of fine copper mesh. In the
form of pulp the material is ladled by hand into bowls for conveyance
to the drying stoves. When dry, the contents of the bowl are emptied
into barrels and headed, or into hoppers, from whence the material is
conveyed to be packed either by hand or automatically by mechanical
packers, or to be converted into paint.


_Dangers and Prevention._--In casting the strips, risk does not arise
from lead fume, as the temperature at which this is effected (350°
C.) is too low for appreciable fume to be given off. Danger here is
from skimmings and deposit of them on the floor or into a receptacle
unprovided with exhaust draught. Pots in which remelting of the
uncorroded cores (returns) is done should be provided with hoods and
exhaust, because of the dust given off in stirring and skimming and the
spurting which occurs as they are thrown in wet. In making the blue
beds, dust arises from particles of white lead adhering to the pots
and in the tan bark. Pots, on removal from the white beds, should have
all white lead inside them removed by washing in a tank. Screening of
the bark should be dispensed with. Emptying the white beds accounts,
perhaps, for the largest number of cases, owing to the impossibility,
in the present state of knowledge, of dealing with the dust by means
of exhaust ventilation, or quite adequately by watering or wearing of
respirators. Watering by means of a hosepipe with rose attached is,
however, the main safeguard. Substitution of the square cockney pots
for the long castle pot is also of moment, as the flat plates of lead
form a denser and more porcellanous corrosion than that of the grids in
the castle pots. Moreover, in stripping the beds the flat corrosions
can be lifted into trays without creating dust, whereas to dislodge the
contents of the castle pots may require a sharp tap, and the unglazed
portion of the interior surface of the latter retains some carbonate
when moistened. Watering requires to be thorough and done with care,
or else the softer material of the corrosion may be washed into the
tan. No less important is it to water the layers of tan, and at a time
while they are yet warm and slightly damp, otherwise the tan becomes so
dry that the water runs through, and does not adequately prevent dust
formation on its removal. A requirement of the special rules is that
the trays for collecting the corrosions shall not stand directly upon
the beds. When corrosions contain an undue proportion of lead acetate,
they are termed technically “floury,” and much dust may arise from
them on watering unless this be done with a very fine rose.

Dust at the rollers and wash becks is usually checked by preliminary
immersion of the tray of corrosions in a trough of water, but the extra
weight of the water causes this sometimes, in the absence of mechanical
arrangements for immersion, to be done perfunctorily. Where there
are rollers, the tray is inserted in a small opening above them, the
contents saturated by a spray, and then tipped over. This method also
may fail to control the dust, as, unless the men engaged in washing the
corrosions in the wash beck keep the mass tipped in from piling up in
a heap, the contents of the trays are discharged on to the heap, and
not into water. In some factories exhaust ventilation at the rollers or
wash becks has been necessary.

During subsequent wet processes of grinding danger is mainly from
splashing. From the settling tanks the white lead is pumped into
filter presses, and the resulting cake is dried. Here the considerable
risk from splashing is again almost unavoidable. Concrete floors are
necessary. Emptying the stoves involves much handling, with inevitable
creation of dust, especially when the bowls are withdrawn from the
racks. Risk has been greatly lessened by reducing the height of
the shelves to 10 feet and prohibiting the piling of one bowl upon
another. Mechanical drying stoves into which men need not enter either
for filling or drawing are now commonly met with. Of these there
are various types--(1) Horses similar to those common in laundries,
which can be withdrawn on rails; (2) small chambers built up one upon
another somewhat in the form of gas retorts in a gasworks, heated by
steam jackets and coils, each chamber containing only two or three
cakes of white lead pulp, the cakes themselves being removed by a
mechanical process from the press into the drying chambers; (3) bogies
carrying the white lead in bowls on racks made to pass through the
tunnel-like stove; (4) drying machines--_i.e._, closed cylinders fitted
with a series of platforms so arranged that they may be charged with
white lead on one side, and so fixed as to be turned round by means
of mechanical appliances. When dry, the material is discharged into
a chute by a series of scrapers into a small enclosed compartment,
holding the barrel to be filled. With the drying machine, however,
there is considerable risk of dust leakage, especially when the doors
are opened. In packing by hand, safety depends on efficient exhaust
ventilation when the contents are tipped into the barrel, but a danger
constantly present is that, to get through the work quickly, the bowls
may be withdrawn from the influence of the exhaust before the last
traces of dust have been removed from the bowl. Mechanical packing, by
means of a large bladed screw forcing the white lead into the barrel,
which as it becomes filled is lowered automatically, is everywhere
desirable. An essential condition of this method is that a dust-proof
collar should connect the automatic packer with the barrel. Some dust
almost inevitably escapes, and a hood and exhaust should be provided,
however perfectly the machine is said to act.

Much of the white lead is converted into paint on the premises,
being ground in oil either in pug mills, Torrance mills, or under
edge-runners. A negative pressure must be maintained inside the casing,
which must enclose the stones. Here the conditions are precisely those
described under the manufacture of paints and colours. In some white
lead works conversion into paint is done without the dangerous process
of stove drying, either by drying under a vacuum or by mixing the white
lead directly with oil. In the process of grinding the oil incorporates
itself with the white lead, and the water is forced out, running away
in a clear stream.


_Chamber Process._--In this method, almost universally used in Germany,
and adopted in at least one large white lead works in this country,
a chamber arranged with numerous sets of parallel bars on which the
thin strips of lead are set saddle-wise takes the place of the stack
in the Dutch process. Carbonic acid gas and acetic acid vapour act
on and corrode the strips. In a period of from eight to ten weeks
the corrosions mostly fall to the ground. Such of the strips as do
not fall have to be lifted off the bars, having been previously well
saturated with water from a hosepipe, and are dropped on to the floor
of the chamber. We are not satisfied that working in the dark, confined
chamber by artificial light is less dangerous than working on the
stacks. Chamber-made lead undergoes practically the same subsequent
processes as have been described.


_Precipitation Processes._--These also dispense with stacks and the
consequent risks attending work on the blue and white beds, but they
substitute another--namely, use of oxide of lead (litharge or the
suboxide) as the initial product to be carbonated, with the inevitable
danger, in the absence of mechanical contrivances entirely closed in,
of shovelling dusty material. In many of these methods, however,
mechanical arrangements obviate hand labour or contact with dust in all
but the first process.

The Brimsdown process[21], for instance, is automatic and free from
dust, except in the initial stage of preparation of litharge in
cupellation furnaces. The great risk from the disintegration of this
material (see p. 250) by turning it out on the floors is obviated
by allowing disintegration to take place in the pots (which must
not, therefore, be completely filled), and tipping these when cooled
directly into a breaker under powerful exhaust draught. From the bin
into which it falls the material is conveyed by dust-proof elevators
to (_a_) screens and packing arrangements when the object is flaked
litharge, or (_b_), in the case of the bulk of the material for
manufacture of white lead, by enclosed conveyors to reducers and mixing
mills, where reduction and hydration take place. It is then charged
automatically into weak solution of acetic acid, and by agitation with
carbonic acid gas converted into basic carbonate of lead. From the
carbonators pumps force it into filter presses, where the acetate is
drained off and washed out by pure water. The cakes of white lead are
fed into mixing machines and pugged with linseed-oil until the water
has been entirely removed, and finally passed through the roller mills
to be packed in casks.

Dry white lead is made by feeding a metal travelling lattice with pulp
white lead inside a drying chamber entirely closed in. When dry, the
white lead is automatically brushed off, elevated, and automatically
packed in a chamber under efficient exhaust draught. In this part of
the process, therefore, risk to the workers is very small.

The stringent Special Rules for the White Lead Industry show
what other precautions, in addition to exhaust ventilation, are
necessary--especially personal cleanliness. The effect of one other
factor--casual labour--however, must be referred to. The condition at
the present time is very different from that which existed twelve years
ago. From one factory in 1899, depending much on casual labour, 111
cases were reported, and from another 72. In an inquiry made by one of
us in 1898, information was obtained of the actual number employed on
any one date, and of the total number passing through the factories in
a year.

Among the firms with regular employment at that time, the incidence of
lead poisoning was 60 per 1,000 on the average number employed, and in
those with casual employment 390 per 1,000. Work in lead had secured a
bad name, and no one who could get employment elsewhere would take to
it. Consequently, the class of men applying for work was a low one--men
discharged from other employment and those unfitted for skilled labour.
Not a few were addicted to alcohol. The work was unskilled, and had the
additional advantage to men of that class that much of it was piece
work, paid at a good rate, which could be finished as a rule by three
o’clock in the afternoon.

Diminution in the number of cases from 399 in 1899 to 34 in 1910 has
been brought about mainly by--(1) Improved structural conditions;
(2) adoption of mechanical means (cranes, rails, hoists, etc.) for
conveyance of material in substitution for hand carrying; (3) exhaust
ventilation, where dust arises as in packing and paint-mixing; (4)
periodical medical examination; (5) diminution in height of the stoves
or adoption of mechanical drying stoves; (6) conversion of white lead
into paint by means of direct mixture with oil while in the pulp
stage; and (7) substitution of small, square, glazed pots--cockney
pots--requiring the lead strips to be placed on them, for the deep
castle pots into which the lead grids are folded in the white beds.
Prohibition of female employment in the dangerous processes was made
prior to the Special Rules of 1899. Their greater susceptibility as
compared with men, the special effect of lead on the uterine functions,
and the unsuitability of much of the work for women, fully justified
the step recommended by the White Lead Committee in 1898.


=Earthenware and China[22].=--The industry includes the manufacture of
earthenware, china, tiles, majolica ware, Rockingham ware (teapots),
sanitary ware, china furniture, and electrical fittings, and any other
articles made from clay; but of the total 6,865 persons employed in
lead processes in the whole of the United Kingdom in 1907, 5,834
are included in the manufacture of the first three. And even in the
manufacture of earthenware, china, and tiles, the poisoning which
occurs is not distributed evenly over the whole of the factories.
These number 550, and, taking the period 1904-1908, 5 potteries were
responsible for 75 cases, 17 for 119, and 151 for 323, leaving 377
factories out of the 550 from which no case was reported. Incidence
seems to depend more on the scale and rapidity of the output of cups,
saucers, plates, and tiles, in everyday use, than on anything else.

The number of reported cases year by year from 1900 to 1909 has been as
follows:

ALL LEAD-WORKERS IN PLACES UNDER EARTHENWARE AND CHINA SPECIAL RULES.
WHOLE OF UNITED KINGDOM (INCLUDING NORTH STAFFORD).

NUMBER OF PERSONS EMPLOYED.


  +-------+----+------+------+-----+-----+------+-----++-------+-------+
  |       |    |      |      |     |     |      |     ||       |       |
  |       |    |      |      |     |     |      |     ||       |       |
  |       |    |      |      |     |     |      |     ||       |       |
  |       |    |      |      |     |     |China,|     ||       |       |
  |       |    |      |      |     |     |Furni-|     ||       |       |
  |       |    |      |      |     |     | ture |     ||       |       |
  |       |    |      |      |     | Jet |  and |     ||       |       |
  |       |    |      |      |     | and | Elec-|     ||       |       |
  |       |    |Earth-|      | Ma- |Rock-|trical|     ||       |Totals,|
  |       |Chi-| en-  |      |joli-| ing-| Fit- |Sani-||       | M. and|
  |       | na.|ware. |Tiles.| ca. | ham.|tings.|tary.||Totals.|   F.  |
  +-------+----+------+------+-----+-----+------+-----++-------+-------+
  |1904 M.| 536| 2,751|  557 | 100 | 216 |   44 | 190 ||4,394 }| 6,694 |
  |     F.| 238| 1,122|  562 | 110 |  71 |  158 |  39 ||2,300 }|       |
  |1907 M.| 625| 2,835|  474 |  96 | 171 |   66 | 237 ||4,504 }| 6,865 |
  |     F.| 302| 1,111|  487 | 170 |  70 |  179 |  42 ||2,361 }|       |
  +-------+----+------+------+-----+-----+------+-----++-------+-------+

NUMBER OF CASES OF LEAD POISONING.

  +----------+------+------+------+------+------+------+------+------+
  |          |      |Attack|      |Attack|      |Attack|      |Attack|
  |          |      | Rate |      | Rate |      | Rate |      | Rate |
  |          |      |  per |      |  per |      |  per |      |  per |
  |          |Cases.|1,000.|Cases.|1,000.|Cases.|1,000.|Cases.|1,000.|
  +----------+------+------+------+------+------+------+------+------+
  |1899    M.|  13  |  24  | 106  |  39  |   7  |  13  |   2  |  20  |
  |        F.|   8  |  34  |  83  |  74  |  21  |  37  |   4  |  36  |
  |1900    M.|  11  |  21  |  62  |  23  |  12  |  22  |   3  |  30  |
  |        F.|  10  |  42  |  67  |  60  |  15  |  27  |   2  |  18  |
  |1901    M.|   7  |  13  |  37  |  13  |   9  |  16  |  --  |  --  |
  |        F.|   2  |   8  |  28  |  25  |   7  |  12  |   2  |  18  |
  |1902[A] M.|   3  |   6  |  30  |  11  |   6  |  11  |  --  |  --  |
  |        F.|   2  |   8  |  33  |  29  |   5  |   9  |   2  |  18  |
  |1903    M.|   1  |   2  |  29  |  11  |   8  |  14  |   1  |  10  |
  |        F.|   6  |  25  |  32  |  29  |   9  |  16  |   6  |  55  |
  |1904[B] M.|   2  |   4  |  31  |  11  |   6  |  11  |  --  |  --  |
  |        F.|   1  |   4  |  41  |  37  |  19  |  34  |   1  |   9  |
  |1905    M.|   4  |   8  |  25  |   9  |   4  |   7  |  --  |  --  |
  |        F.|   3  |  13  |  23  |  20  |  14  |  25  |   4  |  36  |
  |1906    M.|   5  |   8  |  34  |  12  |   7  |  15  |  --  |  --  |
  |        F.|   2  |   7  |  41  |  37  |  10  |  21  |   3  |  18  |
  |1907    M.|   6  |  10  |  38  |  13  |   4  |   8  |  --  |  --  |
  |        F.|   7  |  23  |  33  |  30  |   6  |  12  |   1  |   6  |
  |1908    M.|   4  |   6  |  45  |  16  |   3  |   6  |  --  |  --  |
  |        F.|   1  |   3  |  42  |  38  |   8  |  16  |   1  |   6  |
  |1909    M.|   2  |   3  |  22  |   8  |   4  |   8  |  --  |  --  |
  |        F.|   1  |   3  |  17  |  15  |   7  |  14  |  --  |  --  |
  +----------+------+------+------+------+------+------+------+------+

  +----------+------+------+------+------+------+------+
  |          |      |Attack|      |Attack|      |Attack|
  |          |      | Rate |      | Rate |      | Rate |
  |          |      |  per |      |  per |      |  per |
  |          |Cases.|1,000.|Cases.|1,000.|Cases.|1,000.|
  +----------+------+------+------+------+------+------+
  |1899    M.|  --  |  --  |  --  |  --  |  --  |  --  |
  |        F.|  --  |  --  |   5  |  32  |  --  |  --  |
  |1900    M.|   5  |  23  |   1  |  23  |   1  |   5  |
  |        F.|  --  |  --  |  11  |  70  |  --  |  --  |
  |1901    M.|   3  |  14  |   1  |  23  |  --  |  --  |
  |        F.|   1  |  14  |   9  |  57  |  --  |  --  |
  |1902[A] M.|  --  |  --  |  --  |  --  |   1  |   5  |
  |        F.|   1  |  14  |   4  |  25  |  --  |  --  |
  |1903    M.|   3  |  14  |  --  |  --  |   1  |   5  |
  |        F.|  --  |  --  |   1  |   6  |  --  |  --  |
  |1904[B] M.|  --  |  --  |  --  |  --  |  --  |  --  |
  |        F.|   1  |  14  |   4  |  25  |  --  |  --  |
  |1905    M.|  --  |  --  |   2  |  45  |   1  |   5  |
  |        F.|   2  |  28  |   2  |  13  |  --  |  --  |
  |1906    M.|  --  |  --  |  --  |  --  |   1  |   4  |
  |        F.|  --  |  --  |   3  |  17  |   1  |  24  |
  |1907    M.|   1  |   6  |  --  |  --  |   3  |  13  |
  |        F.|  --  |  --  |   3  |  17  |   1  |  24  |
  |1908    M.|   1  |   6  |   1  |  15  |   2  |   8  |
  |        F.|  --  |  --  |   8  |  45  |   1  |  24  |
  |1909    M.|  --  |  --  |  --  |  --  |  --  |  --  |
  |        F.|   2  |  29  |   2  |  11  |   1  |  24  |
  +----------+------+------+------+------+------+------+

  +----------++------+------+------+------+
  |          ||      |Attack| Total|Attack|
  |          ||      | Rate |Cases,| Rate |
  |          || Total|  per | M. & |  per |
  |          ||Cases.|1,000.|  F.  |1,000.|
  +----------++------+------+------+------+
  |1899    M.|| 128  |  29} |  249 |  37  |
  |        F.|| 121  |  53} |      |      |
  |1900    M.||  95  |  22 }|  200 |  30  |
  |        F.|| 105  |  46 }|      |      |
  |1901    M.||  57  |  13} |  106 |  16  |
  |        F.||  49  |  21} |      |      |
  |1902[A] M.||  40  |   9 }|   87 |  13  |
  |        F.||  47  |  20 }|      |      |
  |1903    M.||  43  |  10} |   97 |  14  |
  |        F.||  54  |  23} |      |      |
  |1904[B] M.||  39  |   9 }|  106 |  16  |
  |        F.||  67  |  29 }|      |      |
  |1905    M.||  36  |   8} |   84 |  13  |
  |        F.||  48  |  21} |      |      |
  |1906    M.||  47  |  10 }|  107 |  16  |
  |        F.||  60  |  25 }|      |      |
  |1907    M.||  52  |  12} |  103 |  15  |
  |        F.||  51  |  22} |      |      |
  |1908    M.||  56  |  12 }|  117 |  17  |
  |        F.||  61  |  26 }|      |      |
  |1909    M.||  28  |   6} |   58 |   8  |
  |        F.||  30  |  13} |      |      |
  +----------++------+------+------+------+

  [A] Lord James’s Code--Rule 3 onwards--came into force.

  [B] Medical examination of men began.

The processes in so far as lead enters can best be divided into--(1)
Glaze; (2) decorative.

1. _Glaze Processes._--The charge of glaze is made by weighing
out and mixing carbonate of lead with the necessary silicates and
silico-borates in the lead house or mixing-room, where wet grinding
prepares the mixture for the dipping-tub. “Putters-up” hand the ware
to the dipper, from whom “takers-off” place it on boards for removal
to the drying still, or place it (in large works) directly on to the
shelf of an appliance known as a “mangle,” in which an endless chain
carries the ware through a heated chamber. Subsequently superfluous
glaze has to be removed from the base, rims, and not infrequently also
other parts of the articles. This ware cleaning is performed with a wet
sponge or flannel, either while the ware is still moist or by scraping,
the particles removed dropping into a vessel of water; or, if the glaze
is dry, over a grating provided with exhaust draught. The ware is next
removed by the glost-placer on boards, and each piece is separately
placed by him in the sagger (fireclay receptacle) and carried into an
oven to be fired.

2. _Decorative Processes._--Majolica painting is the application of a
coloured glaze rich in lead by means of a brush. Ground-laying consists
in dusting powdered enamel colour on to a pattern first printed on
glazed ware with an oily medium. Colour dusting differs from the same
only in detail.

Aerographing (colour blowing) is the blowing on to the ware, by means
of a jet of compressed air, coloured glaze, or enamel colour held
in suspension in oil or other liquid in a glaze kettle or aerograph
instrument.


_Dangers._--Apart from risk inseparable from, and increased by,
defective lighting, uneven floors of wood or brick, collection of
dust on benches and floors, and the risk entailed in the sweeping of
these even when watering is practised, and lack of care and attention
to detail on the part of the worker, the following special dangers
are incidental to the various processes: In dipping the glaze (except
in tiles, where the surface only is allowed to touch the liquid),
splashes on to the face and overalls of the dipper, “hander-up,” and
“taker-off” (dipper’s assistants), and “threader-up” (in the case
of china furniture), especially when, as with plates, there is much
shaking of the ware. These splashes dry, and the overalls may become
so coated with glaze that every movement, such as carrying boards or
leaning against the mangle, crumbles it off as dust into the air. As
the dipper shakes the ware, some of the drops are disseminated into
the atmosphere as a fine spray. In ware cleaning the work may have to
be done so rapidly that it is difficult always to observe proper care,
and the worker is tempted to withdraw the article from the range of the
exhaust. Sometimes a ware cleaner is seen blowing away with her mouth
dust lying on the ware.

Dipping-boards, unless freed from adherent glaze by washing after use,
create dust whenever ware is placed on, or removed from, them, when
they are handled and placed on or taken off the stillage bars, and when
they are stacked. Persons gathering at the mangle are exposed to dust
if there is any outward current of air from it. The glost-placer raises
a slight amount of dust as he takes the ware from the board and places
it in the sagger. The dangerous practice formerly almost universal of
rubbing the bottoms and rims of cups, etc., either together (without
use of an exhaust) or rubbing them on a piece of leather fixed round
the chest, is generally replaced by removal of the glaze on a moist
piece of flannel, but it is still possible to find men doing it in
outlying potteries. In majolica dipping and painting (apart from the
obvious risk of splashing and contamination of the hands), danger
arises mostly from scraping the edges and under surfaces of the tiles
on to which glaze, when applying the background, has overflowed. The
amount of glaze so removed is considerable, and if it is not all caught
in the trough of water, the floor becomes an added source of danger.

In all the _decorative processes_--ground-laying, aerographing,
colour-dusting, and grinding of colours for aerographing, etc., the
danger is one solely arising from dust.


_Prevention._--Meticulous attention to detail, not only in the
provision, but also in the maintenance, of the locally-applied exhaust
ventilation, alone can allay the danger in the processes to which
dust is incidental, such as ware cleaning, gathering at the mangle,
glost-placing, and the decorative processes. The Lead Committee
considered that, as there was no rapid method of testing the actual
degree of moisture, exhaust ventilation might be required in the case
of ware that was not cleaned within fifteen minutes of the application
of the glaze. Such a requirement would prevent the practice now
prevalent of painting as many as three dozen tiles, piling them one
on top of another, and then proceeding to the operation of scraping.
No danger attaches to removal of glaze with a damp sponge or flannel,
but means must always be at hand for washing and damping them. In the
dipping-house, (_a_) impervious floors should be provided, which could
be washed down so as to prevent the risks from sweeping, and from
glaze drying, and being raised as dust; (_b_) partial covering of the
dipping-tub to prevent splashing and spray; and (_c_) substitution
for the overalls at present worn by persons in the dipping-house,
glost-placers, millers and mixers of glaze, majolica paintresses, and
others, of overalls of some light waterproof material which could be
sponged, or of aprons of waterproof material worn in front of the
overalls. Dipping-tubs and walls and floors in close proximity to them
can with advantage be painted red. Dipping-boards should be washed with
clean water after every time of use. Automatic machines for washing and
scrubbing boards are in use in some factories.

To reduce risk or remove the danger of lead poisoning in this industry,
use of low solubility glazes or of leadless glazes are advocated. On
this point the Lead Committee say: “The effect of melting the lead
with silicious matter amounts to imprisoning it in such a manner as
to render it less liable to the action of the acids which it meets in
passing through the human body, and in consequence largely reduces the
likelihood of its absorption into the blood. If the frit is properly
compounded, all but a small fraction of the lead is rendered insoluble,
and glazes so made are spoken of as ‘low solubility glazes.’ The
finished glaze generally contains from 12 to 22 per cent., or more, of
lead oxide, but after the process of fritting with sufficient silicious
material only from 2 to 5 per cent. remains soluble.”[A]

  [A] Raw lead comprises red lead, white lead, and litharge. If
  introduced in this form as a constituent of glaze it is soluble in
  dilute acids. If, however, the raw lead is fluxed by heating with a
  part or the whole of the silica, it is converted into “fritted lead.”
  The solubility of the frit depends upon the relative proportions of
  material taken. Thorpe[23], as a result of numerous analyses of lead
  silicates (after determining their solubility as regards lead), both
  simple and complex, in use in the potteries and on the Continent,
  found that the quantity of lead dissolved had no necessary relation
  to the quantity of lead in the silicate. “Primarily and in the main
  the insolubility of the lead depends not upon any one oxide or group
  of oxides, but upon the maintenance of a certain proportion between
  the whole of the basic oxides on the one hand and the whole of the
  acidic oxides on the other. If the value of ratio bases/acids is
  higher than, or approximately equal to, two, the amount of the lead
  extracted is small, but if it fall much below two, the quantity of
  lead dissolved begins rapidly to increase.”

On the subject of the use of leadless glazes, the Committee conclude
that in all classes of pottery ware a great many articles can be
manufactured in a very high state of perfection, with reduction in
the cost of production of certain classes of common ware, such as
jampots and Persian painted ware; but that in certain other classes,
owing to the excessive number of “seconds,” their use would entail
increased cost or sacrifice of quality, so much so as to involve loss
of important markets; and, finally, that certain kinds of ware, in
consequence of difficulties relative to accuracy in reproducing old
patterns, colours, or methods of decoration, cannot at present be made
at all without use of lead.

In the case of manufacturers who are able to conform to the Thorpe test
of low solubility--_i.e._, glaze which yields to a dilute solution of
hydrochloric acid not more than 5 per cent. of its dry weight of a
soluble lead compound, calculated as lead monoxide (PbO)--important
relaxation of certain special rules are allowed, such as limitation
placed on the employment of females and young persons, and periodical
medical examination of the workers.

H. R. Rogers[24], one of H.M. Inspectors of Factories, Stoke-on-Trent,
has worked out a simple test to show approximately how much lead has
been used in the glaze of a piece of pottery. Thus, by treating glazes
with hydrofluoric acid for forty seconds, absorbing the liquid with
filter paper, precipitating the lead on the paper as the sulphate,
dissolving out the sulphate soluble in water, and then precipitating
the lead on the paper as sulphide, stains are produced varying, in
depth of colour, according to the proportion of lead in the glazes
concerned (see Plate IV.).

Briefly summarized, the recommendations of the Potteries Committee in
regard to the processes are--

_Manufacture of Glazes._--No handling of white or red lead without at
least 5 per cent. of added moisture, and no weighing out, etc., nor
employment in the room, to be allowed within thirty minutes of such
weighing out, etc., without the wearing of a respirator.

_Lawning_--_i.e._, straining glaze so as to remove insufficiently
ground material through a fine lawn sieve--to be done by an adult male
only, except where less than a quart of glaze is lawned.

_Dipping._--Impervious floors sloped towards a drain to be cleaned by
an adult male, after work has ceased, with a jet of water and a mop.
Walls adjacent to dipping-tubs to be tiled or painted with washable
paint, and cleaned daily. Dipping not to be done where artificial light
is necessary during hours of daylight.

_Threading-up and Thimble-picking_ to be done in a room sufficiently
separated from any place where scheduled processes are carried on.

_Drying Ware after Dipping._--The same requirement as to floors as in
dipping-house.

_Boards._--To be cleaned with clean water by an adult male after each
time that dipped ware has been placed on them and before subsequent
use. Boards for use in lead processes to be painted red at the ends.

_Mangles._--Ventilation to be so arranged as to maintain a flow of air
into the hot chamber from the workroom. Mangle shelves to be thoroughly
wet cleansed once a week.

_Ware Cleaning._--Local exhaust ventilation to be applied except when
the process is carried on entirely with use of wet materials (damp
sponges, etc.), or when done within fifteen minutes of application of
glaze. Troughs to be provided to collect glaze, and to be cleaned out
and supplied with fresh water at least once a week. The floors and
standard of lighting to be the same as for the dipping-house.

_Glost-placing._--Boards to be treated as already described. Floors
to be impervious. Women, young persons, and children to be excluded,
except that women to be allowed to place china furniture and electrical
fittings.

_Majolica Painting and Mottling._--A sponge and clean water to be
placed beside each paintress; special washing accommodation in the
painting-room or adjoining it; splashes to be removed immediately
by wet sponging. Work-benches and floors to be subject to the same
conditions as potters’ shops.

_Flow Material_--_i.e._, the substance usually containing much lead in
the form of powder and placed in the sagger to cause certain colours
applied to biscuit ware to run slightly--to be weighed out in front of
an exhaust draught and delivered to the glost-placer by an adult male.

PLATE IV

[Illustration: FIG. 1.--NO LEAD USED.]

[Illustration: FIG. 2.--FRITTED LEAD USED.

0·9 per cent. solubility.]

[Illustration: FIG. 3.--FRITTED LEAD USED.

   1·5 per cent. solubility.
  13·9 per cent. total lead.]

[Illustration: FIG. 4.--FRITTED LEAD USED.

  5·0 per cent. solubility.
  5·0 per cent. total lead.]

[Illustration: FIG. 5.--RAW LEAD USED.

  19·4 per cent. solubility.
  19·4 per cent. total lead.]

[Illustration: FIG. 6.--RAW LEAD USED.

  44·1 per cent. solubility.
  45·2 per cent. total lead.]

[Illustration: FIG. 7.--ROCKINGHAM (RAW LEAD) USED.

  50·9 per cent. solubility.
  50·9 per cent. total lead.]

Ground-laying, colour-dusting, and aerographing to be done under
locally applied exhaust ventilation. Proper receptacles to be
provided for cotton-wool used and waste cotton-wool to be burnt. No
short-sighted person to be employed to do either glaze or colour
blowing, unless wearing suitable glasses, and certificate to this
effect to be entered in the Health Register.


=Litho-Transfer Making[25].=--Transfers for the decoration of
earthenware and china are made in special factories, of which there
are seven, employing 257 persons. The patterns are impressed in the
ordinary chromo-lithographic fashion, but as the enamel colours,
containing high percentages of lead, are dusted either mechanically in
the machine, or by hand by means of a pad of cotton-wool, danger from
dust is great in the absence of maintenance of a negative pressure
inside the dusting machine and an efficient exhaust draught behind the
bench where the final dusting with flour, to remove the superfluous
colour, is done. In one factory, before a fresh colour was applied to
the adhesive pattern on the sheets, the machines had to be cleaned
as far as possible of the previous colour used. To do this it was
necessary for the attendant to enter a closed chamber at the back of
each machine, so as to supply the powder to the hoppers which feed the
rollers, or to clean them by means of a brush, sometimes as often as
every half-hour. The upward exhaust ventilation applied to the interior
of the machine tended to draw the dust created in brushing past the
worker’s face, and led to severe incidence of poisoning. The remedy
suggested by Pendock[26] was to dispense altogether with the need for
entering the chamber, to maintain a slight negative pressure inside the
machine by downward exhaust, and to remove the dust by means of a small
vacuum cleaning plant.

At the same factory the flouring bench was in the same room as the
machines, and the locally applied exhaust drew its air-supply from the
general atmosphere of the room. Apart from faulty arrangement of the
exhaust ducts leading to effects of too local a character, dust was
drawn from other parts of the room, including the machines, so much
so as to necessitate frequent cleaning of the glass hoods. Poisoning
among those employed in flouring occurred. To remedy this, an air-grid
with curved inlets at intervals of 2 inches apart, leading into a trunk
in connection with a fan, was placed along the back of the bench and
under the top of the glass hood. In order, however, that its action
should not interfere unduly with the general ventilation of the room,
but be, in large measure, independent of this, a somewhat similar grid,
introducing air from the street outside, was fitted along the front
of the bench. The whole arrangement was operated by one suction fan.
Ten cases occurred in this factory in the year before this arrangement
was carried out. In the three years since, three cases only have been
reported. In the ten years 1900-1909, 48 cases were reported among 257
persons employed.


=Vitreous Enamelling[27].=--Surfaces, such as sheet iron for
advertisement signs, cast iron for baths and gas stoves, copper
for copper letters and tablets, brass for jewellery, and glass for
lettering and decoration, are treated with glaze or enamel colours,
which, either in the mode of application or subsequent treatment before
final vitrefaction, give rise to dust.

In the manufacture of advertisement signs, glaze is swilled on to the
sheet of iron. After drying, it is fired or vitrified, and upon this
surface as many other coats of glaze are applied as may be wanted. As
soon as the colour is dry, lettering is effected by brushing away the
dried (but not fired) glaze exposed through stencils.


_Dangers and Prevention._--Exhaust ventilation for the removal of
the dust is essential, but it is, unfortunately, unable to draw the
dust away when brushing is done at a distance of more than about 18
inches from the exhaust opening. And some of the plates required are
very large. No exhaust-pipe has yet been invented which will follow
the hand of the worker without impeding movement. In consequence of
severe incidence of poisoning, mainly on young women who do the work
of brushing, when the process was first introduced with enamel glazes
containing from 15 to 75 per cent. of lead, manufacturers quickly
turned their attention to use of enamels free from lead. For this class
of work they appear to have been entirely successful, and now lead
poisoning is almost a thing of the past. Thus, of 122 samples examined
in 1910 from factories claiming exemption from the regulations by
reason of the use of enamels containing less than 1 per cent. of lead,
excess was found in three only[28].


=Porcelain Enamelling.=--The cast-iron bath or stove is heated to
redness in a muffle furnace. On withdrawal from the furnace it is
placed by the helpers on a table capable of being turned in every
direction. Enamel powder is then dusted on to the heated metallic
surface through a sieve attached to a long wooden handle, held by the
duster, who protects himself from the intense heat by a mask and an
asbestos cloth covering.

[Illustration: FIG. 12.--The first glaze is sprayed on with an
aerograph. The portion of the stove to be glazed is shown on supports
on the sliding table, which is half out of the cabinet. When the
casting is fully in the cabinet, the end piece and the centre piece
close the cabinet sides, and, fitting on a felt beading, make an
air-tight joint. The spray, shown in front of the cabinet, is worked
through the holes in the glass front. Exhaust is provided at the top.]


_Dangers and Prevention._--The heated column of air carries up much
of the powdered glaze as it is unevenly distributed by jolting the
handle of the receptacle, and in the absence of very efficient exhaust
ventilation this dust will, as the current of air strikes the roof and
cools, fall down again. The hood placed over the bath must have steep
sides and be brought down as low as is possible without interfering
with work, and the duct leading to the fan must be unusually wide, so
as to be able to cope with the up-rush of heated air. If the sides
of the hood be shallow, not only will the dust fail to be removed,
but the hood itself may become so hot as noticeably to increase the
discomfort from heat to which the men are exposed during the three or
four minutes, five or six times an hour, that the dusting operation
lasts. A method has been patented by M. Dormoy of Sougland[29], Aisne,
France, for carrying out automatically in a closed chamber the process
of dusting on to small red-hot castings, such as are required in the
manufacture of stoves. It is not applicable for baths.

Occasionally, in the case of small castings, again, the enamel is
sprayed on by means of an aerograph. For this excessively dangerous
process we have seen simple and ingenious devices for carrying it on
quite safely in a space under negative pressure, and covered in except
for the necessary openings through which to work the spray (see Figs.
12, 13, 14).[A]

  [A] The cabinets have been patented by Messrs. Wilsons and
  Mathiesons, Ltd., Leeds, by whom they are made and supplied. Since
  using them there has been no trace of illness among the persons
  employed.

[Illustration: FIG. 13.--After firing the casting is lifted out for
treatment with dry glaze, which is sprinkled on with a sifter shown on
the table. The turntable enables the operator to manipulate the red-hot
casting more easily.]

White enamel powders free from lead are used entirely by some firms,
but the black and coloured enamels on stove grates contain lead. A frit
analyzed in the Government Laboratory was found to contain 26·66 per
cent. of lead oxide. The fact that all the lead used is in the form of
a silicate, even although the silicate is readily soluble in dilute
acid, tends, we believe, to cause incidence of poisoning to be less
than might have been expected from the amount of dust often present in
the air, and attacks, when they occur, to be less severe, as a rule,
than they would be were raw carbonate of lead alone used. For the
arduous work entailed the men are specially selected. Despite their
exposure to lead dust, the majority continue to work for many years
without marked signs of lead absorption. The management should provide
a suitable room for the men to cool themselves in the intervals of
dusting.

[Illustration: FIG. 14.--The cabinet is shown when dry dusting is being
done. The casting is worked by tongs through a slot in the side of the
cabinet (not seen), while the worker dusts the casting with his arms
through the two front holes. He can see his work through the square
pane of glass. (Photographs kindly made by Mr. F. W. Hunt, Leeds.)]


=Manufacture of Electric Accumulators[30].=--Electric accumulators
are secondary batteries which serve for the storage of electricity,
in order to allow of a current when desired. A primary battery is
one in which the materials become exhausted by chemical action, and,
unless a portion or the whole of the materials is renewed, fails to
supply electricity. The secondary battery becomes exhausted in the
same way, but the chemical contents are of such a nature that it is
merely necessary to pass a current of electricity through the battery
(charging) in order to recharge them. In the accumulator battery the
positive element is peroxide of lead, and the negative element spongy
lead. The elements--several positive connected together and several
negative--are placed in dilute sulphuric acid contained in vessels of
glass.

The form of accumulator in almost universal use now is the pasted
plate, but it varies greatly in size, according to the use for which
it is required. It may be either large, to act as an equalizer or
reservoir of current in electric-lighting installations, or quite small
for ignition purposes in motor-cars. The litharge smeared on to one
plate becomes converted into the positive element, peroxide of lead,
during what is called the “forming process” (passage of the electric
current through the dilute sulphuric acid solution in which it is
placed), and red lead smeared on to the other becomes spongy lead to
form the negative.

The industry gives employment to about 1,200 persons. Plates are first
cast in moulds from a bath containing molten lead or of lead with
admixture of antimony. Irregularities in the plates so cast are removed
by a saw or knife (trimming), and sometimes filed or brushed with a
wire brush. The interstices in the plates are next filled in by means
of a spatula with paste of litharge or red lead, as the case may be,
which has been previously mixed either by hand at the bench or in a
special mechanical mixing machine. After drying, the plates are removed
to the formation room to be charged. To allow of the passage of the
current, positive elements are connected together, and negative also,
by means of a soldering iron or, more frequently, of an oxy-hydrogen
blowpipe flame. After formation is complete the plates have to be
built into batteries, or “assembled.” Tailpieces, technically known as
“lugs,” have to be connected with each plate, effected usually by the
oxy-hydrogen blowpipe flame. Finally, a connecting bar of lead is cast
on or burnt on to the lugs.


_Dangers and Prevention._--In casting, danger is mainly from dust in
depositing the skimmings, and from fume also when old accumulator
plates are melted down. For these reasons exhaust ventilation over the
melting pots should be provided, embracing also (by branch ducts if
necessary) the receptacles into which the lead ashes are thrown. In
mixing and pasting, the danger is from dust of oxides of lead to be
controlled (see Fig. 6) by--(1) Exhaust ventilation by branch ducts
protecting (_a_) the barrel from which the material is scooped, (_b_)
the mechanical mixer into which the weighed quantity of oxide is
discharged, (_c_) the bench at which the mixing by hand is done; (2)
dampness of benches and floor to prevent raising of dust either by
manipulation of the (often) heavy plates or trampling into powder the
paste which may fall on the ground.

In assembling or putting together of the formed plates, and in earlier
stages of the manufacture also, filing or use of a wire brush causes
production of metallic lead dust and of the oxides when the brush
touches them--a danger only to be met by exhaust ventilation. How far
the poisoning to which the lead burners engaged in assembling plates
is attributable to lead fume, produced by the high temperature of the
blowpipe flame, and how far to handling (with inevitable dislodgment of
dust) has not been satisfactorily settled. Incidence of poisoning on
this class of worker in the past has been marked.

Generally there is need for impervious floors, solidly built, so as
to prevent vibration and the raising of dust from passage of trolleys
conveying the heavy plates. Gloves are frequently provided, more to
protect the hands from contact with the sulphuric acid used in making
the paste and jagged edges of the plates than as a preventive of lead
absorption.

In the 10 years 1900-1909 incidence, according to precise occupation,
has been--Casting, 33; pasting, 114; lead burning, 69; and assembling
the plates, etc., 69.


=Glass-Cutting[31].=--Red lead enters largely into the mixture of raw
materials for the manufacture of glass. Flint glass, for instance,
contains 43 per cent. of lead. The raw materials (white sand, red
lead, and generally saltpetre) require to be very carefully mixed, and
a few cases of poisoning have been reported from the dust raised in
sieving. One man works the sieve, resting on two runners across the
bin, while another shovels the mixture into the sieve. The operation is
not a continuous one, and respirators have principally been relied on
to protect the workers. It should be possible to carry out the mixing
operations in a dust-tight closed apparatus.

Poisoning from lead fumes generated in a glass furnace is unknown. Lead
poisoning used to be common in the process of polishing cut glass on a
brush by means of “putty powder” (oxide of tin, 29 per cent.; and oxide
of lead, 71 per cent.), mixed with water to the consistency of a paste.
The brush was made to revolve at high speed, with dissemination of
the putty powder as a fine spray into the atmosphere of the workroom.
Although rouge and oxide of iron have replaced putty powder to some
extent--especially for the polishing of the bevelled edges of plate
glass--no substitute can at present be found to give the final lustre
and brilliancy required in the case of cut glass and in certain kinds
of high-class work, such as polishing lenses.

Locally applied exhaust ventilation has robbed the process of its
dangers. Pyramidal-shaped hoods enclose the spindle and putty box and
brush before which the workman sits. The draught of the fan prevents
escape of spray. The lad who feeds the brush with putty powder stands
at the side, and in our experience his cap and clothes are now free
from signs of splashing. Formerly the polishing was done by each man
at his own berth, thus endangering the health of all working in the
vicinity, as the custom of the trade is that the same man carries
through the work both of cutting and polishing. Polishing occupies only
about a fifth of a man’s time, and it has now, owing to the position of
the fan, to be carried out in one particular part of the room.

  Dr. D’Arcy Ellis[32], Certifying Surgeon for the Stourbridge
  district, has described the processes as formerly carried out:

  “The mixture of lead and tin is heated over a bright fire in a
  shallow iron pan. As it melts, the top scum which forms is skimmed
  off, dried, pounded to a powder in an iron mortar, and afterwards
  sieved. The person who does this work always suffers more or less.
  He usually protects himself by wearing a respirator--there is a good
  draught at the flue, and the sieve is enclosed in a box--but there
  is always a certain amount of dust. This putty-powder is used on the
  wooden wheel, and is dabbed on the wheel as it revolves. All good
  bold work can be polished in this way, and there is not much risk
  to the workman, as the speed at which the wheel revolves causes the
  mixture to cling and not fly about. This process does not answer
  for any fine work, so it is contended; and to enable this kind of
  work to be properly polished brushes made of bristles are used. They
  are mounted on an iron spindle, and are usually about 6 inches to 7
  inches in diameter, with a face of 1 inch to 1¹⁄₂ inches broad. They
  are driven at a speed of about 2,000 revolutions a minute. The putty
  powder is applied to these brushes (which are of various sizes) in
  the same way as to the wooden wheel--that is, by dabbing it on. For
  smaller work, such as tumblers and wine-glasses, the workman applies
  the putty mixture himself, holding the glass against the brush with
  his right hand, and using his left underneath to apply the mixture.
  Where, however, larger work has to be done in which the workman
  cannot manage with one hand, the service of a boy is called in, who
  does what is called the ‘feeding up.’ This boy stands partly in front
  and partly at the side of the brush, and applies the mixture with one
  hand with the wisp of straw. In this position the boy gets splashed
  with the putty mixture which flies off the brush, and it is generally
  believed by the workmen to be the most dangerous occupation. At
  one time--not very long ago--all the various processes of the work
  were done indiscriminately in the workshop, and consequently the
  men were frequently found working in a perfect haze of fine dust,
  which had been thrown off from the brushes. There was no attempt
  made to separate and detach the less injurious part of the work,
  such as the roughing and cutting, from the general workshop, the
  lead polishing only occupying about one-fifth of the workmen’s time.
  After the glass has been polished by the putty it is taken away to
  another department, where girls are employed as ‘wipers out.’ They
  take the glass with the dried putty upon it, dip it into a basin of
  water, and then wipe it dry. Some of these girls have been known
  to suffer from lead poisoning.... Drop-wrist was frequently to be
  seen--in fact, there was hardly a workshop in the district in which
  cases of wrist-drop could not be found. They were all anæmic, and the
  albuminuric and prematurely aged were frequently met with.”

In this small industry in the past the poisoning must have been
considerable. In 1898 nineteen cases were reported. Reference to the
table on p. 47 shows that the number now is greatly reduced. Those
reported are generally cases which have ended fatally from the sequelæ
of lead poisoning contracted many years previously.

Stained-glass painting--a form of vitreous enamelling--very rarely
gives rise to poisoning, as no dust is generated (see vitreous
enamelling for use of aerograph in glass-painting).


=Paints and Colours[33].=--Most of the cases have occurred in the
manufacture of white-lead paint, although manufacture of chromate of
lead and of Brunswick greens (barytes with which Prussian blue and
chrome yellows are mixed) account for several. The following table
shows the precise occupation of persons affected, the number of cases
distributed according to precise occupation, and the proportion of
these to the total in 225 cases which were closely examined:

  +------------------------------------+------------+--------------+
  |                                    |  Number of |              |
  |                                    |    Cases   | Proportion of|
  |        Precise Occupation          |   in each  |Cases to Total|
  |        of Person affected.         |Subdivision.| (per Cent.). |
  +------------------------------------+------------+--------------+
  |Mixing and grinding (mainly of white|    144     |     64·0     |
  |lead)                               |            |              |
  |Packing (mainly of red lead)        |     19     |      8·4     |
  |Sieving                             |      2     |      0·9     |
  |Manufacture of chrome yellow        |     22     |      9·8     |
  |Colour house and filters            |     16     |      7·2     |
  |Painting and stencilling            |      6     |      2·7     |
  |Other processes                     |     16     |      7·0     |
  +------------------------------------+------------+--------------+

Knowing the conditions of work, we can confidently assert that the
poison must have entered the system in the form of dust in at least
90·0 per cent. of the cases, and in the remainder the possibility of
dust having been the cause is not excluded.

In a small factory the cask of white lead is broken and the material
scooped out into a pail. Scales are at hand, and when the amount of
lead removed weighs half a hundredweight the contents of the pail are
discharged either into a cylindrical pug-mill or into the pan of an
edge-runner to be mixed with oil. In large factories the dry white lead
is generally shovelled directly from the cask down openings or shoots
in the floor to the grinding mills below.


_Dangers and Prevention._--Dust arises in unheading the casks from the
displacement of air following the scooping or shovelling out of the
lead, in filling the pails, and in discharging the lead into the mill.
All points should, and can, be adequately protected by locally applied
exhaust ventilation at each one of the points enumerated. A telescopic
arrangement of the branch duct in connection with the barrel enables
dust generated in scooping out to be removed as the contents of the
barrel get lower and lower (see Fig. 15).

[Illustration: FIG. 15.[A]]

  [A] FIG. 15 shows the arrangement for preventing dust at every point
  where it is produced in a factory where dry colours are ground,
  sifted, and packed on a large scale. On the upper floor, the chamber
  is shown in which the contents of a cask are tipped down a shoot
  leading in the one case to the burr stone mill on the left, and
  in the other into the Blackstone sifters. Exhaust is arranged at
  two levels to catch the dust arising from the displacement of air.
  After grinding in the closed-in burr stone mill, a hood and duct
  is arranged over the point where the material is discharged into
  the barrel. Similarly, the casing of the two Blackstone sifters is
  connected with the exhaust fan, and also the cover of the barrel into
  which the ground material falls. Inside the edge-runner (the door
  of which is shown open) a negative pressure is maintained, and one
  branch duct controls the dust in the scooping out of the material
  from the barrel, while another is connected to the cover of the
  receptacle into which the ground material is discharged.

  Tapering of the ducts, tangential entry of branches, fan-box, and
  collecting filters, are all shown. In the factory in question there
  are four edge-runners, three burr stone mills, and two Blackstone
  sifters. Altogether exhaust ventilation is applied at twenty-five
  points. (Drawing kindly supplied by the Sturtevant Engineering
  Company, Limited, London.)

The lighter shades of yellow chrome are made by a cold precipitation
process, or (as is usual for the deeper shades of chrome, orange,
and red) by boiling the ingredients--lead acetate, pulp white lead,
bichromate of potash and soda, and sulphate of soda--while barytes is
added as the colour is being made. Danger in the first method does not
arise (or only in minor degree when steam is injected to bring about
more speedy solution) until drying and grinding (in edge-runners),
sieving, and packing, are effected. The dust, when inhaled, is quickly
absorbed, and in all these dry processes danger, in the absence of
very carefully thought out exhaust ventilation, is great. In processes
involving ebullition, danger is present in the steam which carries
up with it chromate of lead in fine particulate state. Vats and
vessels, therefore, in which the boiling is effected require partial
hooding over and connection of the hood with an efficient exhaust. In
subsequent wet processes of pressing the cakes of chromate of lead, the
hands, arms, and overalls become thickly coated with pigment. Danger
from chrome greens is practically limited to the dust created in dry
grinding, usually effected in large edge-runners.

  For references, see end of Chapter XVII.




CHAPTER XVII

DESCRIPTION OF PROCESSES--_Continued_


=Coach-Painting[34].=--Lead poisoning is peculiarly prevalent in this
industry, and no corresponding reduction in the number reported can be
observed from year to year (see the table on p. 47), or in the many
industries grouped under the heading, “Paint used in Other Industries,”
such as is noted for lead industries taken as a whole.

Of the 697 cases included in returns during the ten years 1900-1909,
352 were reported from railway carriage and waggon works, 299 from
ordinary carriage works and wheelwrights’ shops, and 46 (separate
tabulation was only commenced in 1905) in motor-car works. In the year
1903 inquiry was made in 603 factories and workshops, including all
classes of coach and carriage building, railway carriage and engine
works, and agricultural implement works. Information was asked (among
other things) as to--(1) The number of persons employed in painting
with lead paints; (2) description of the method adopted for smoothing
the coats of paint; and (3) the substitutes tried for white-lead
paint. Persons employed numbered 9,608. In 52 factories and workshops
smoothing of the coats of paint was not practised, while in the
remaining 551 it was affirmed that a wet method alone (pumicestone
and water) was used in 178, a dry method alone (sandpaper) in 39, and
both wet and dry methods at some stage or other of the work in 334.
Substitutes were mentioned as having been tried in 94 instances, but
this was almost exclusively for filling and jointing, and not for the
first or priming coat.

The figure 178 (wet method alone) is probably much too high, because,
while it is true that pumicestone and water alone are used for the
flat surfaces of the body--the bulk of the work--dry sandpapering of
the first two priming coats and of the final finishing coats (when
of white, cream, or yellow colour), of the under parts of carriages,
iron chassis of motor-cars, and of curved surfaces, such as the spokes
of wheels, is almost universal. The reason for thus treating the
priming coat dry is that a wet process would raise the grain of the
wood. The 52 factories in which it was stated that no smoothing was
done were nearly all premises for the repair or manufacture of railway
trucks, requiring no special finish, and the 39 factories in which
only sandpaper was said to be used in smoothing were premises in which
rough, cheap, or common vehicles, such as carts, were made. Use of
sandpaper is quicker and less expensive than use of pumicestone, and
water and wet methods cannot be used very well on iron surfaces.

In ordinary coach and carriage painting, after the sandpapering of
the first two priming coats, six or seven coats of “filling” (usually
ground slate mixed with gold size and turpentine) are applied, and
each coat is rubbed down wet. Joints and interstices of woodwork and
irregularities in iron surfaces are generally filled in with a stopping
or paste of white lead, in the smoothing of which sandpaper is used.

In the manufacture of motor-cars, the terne (lead) coated sheets which
form the body, after preliminary preparation, receive two coats of a
lead paint. These are either lightly sandpapered or “flatted” with
pumice and water. Three coats of non-poisonous filling follow, and are
flatted with pumice or German brick and water. The body then passes to
a skilled workman, who applies the final coats of colour. For facing
mouldings and for corners throughout all stages of the processes, dry
sandpaper takes the place of pumice and water. All stopping on the
chassis, the first lead coat on the bonnet, and all coats of paint on
the wheels, are sandpapered dry. Sometimes a third of a man’s time may
be taken up in sandpapering alone.


_Dangers and Prevention._--Grave risk of inhaling lead dust is present
(see the table on p. 47) when sandpaper is used, often at a point just
above the mouth and nostrils. Rubbing down the wheels is perhaps the
most dangerous work, and for this exhaust ventilation can be applied
locally. Inventive genius has yet to be directed to some modification
of the vacuum-cleaning apparatus, so that an exhaust can be attached to
the back of the worker’s hand or in connection with a frame in which
the sandpaper is held. In the process of wet rubbing, the abraded
coats drip on to the floor, and when dry may rise as dust into the
atmosphere.

Precisely similar operations, or only modified in detail, have
accounted for heavy incidence of lead poisoning in the painting of
perambulators, of safes, of bicycles, of bedsteads, of gas-meters,
the “metallic” enamelling of baths (in which also chipping off of
the old paint not infrequently occasions an attack), in engineering
and machine-making works, in cabinet and furniture making, in French
polishing, in the making of artists’ canvases, etc. Several cases are
reported among railway employees engaged in the painting of bridges,
girders, and signal-posts. A method for the removal of the dust given
off in these processes has not yet been arranged. Chipping off of old
paint can be effectually replaced by solvent solutions, in the use of
which, as they are very inflammable, precautions against naked lights
are necessary.

In the making of better-class measuring tapes, the tape, after passage
through the white-lead mixture and drying, is made to travel through
a machine to remove roughnesses, and subsequently through the fingers
of the worker, protected by leather. Dust arises in both the last
operations, and requires to be removed by exhaust ventilation. Similar
means of prevention are necessary wherever paint is applied, as in
photo-engraving, and colouring artificial flowers by means of an
aerograph instrument.

Owing to the limited extent to which exhaust ventilation is possible,
reliance must be placed on substitution of wet processes for dry
wherever possible. Cleanliness of floors requires special attention.
Although in all painting operations dust is the most potent cause of
poisoning, we would assign to contamination of the hands and the eating
of food with unwashed hands a more prominent place as a cause than in
any of the other processes involving use of lead or lead colours. In
a post-mortem on a sign-painter employed only a few days, made three
weeks after his cessation of employment on account of an attack of
encephalopathy, paint was found thickly adherent under the nails.

Substitution of colours containing no lead suggests itself as a
simple remedy, but the progress in this direction made so far in the
industries mentioned is limited. Several important firms manufacturing
motor-cars use no lead colours at all; more than one important railway
company (the outside of the carriages of which has no white colour)
and a few makers of perambulators do the same. It is difficult to
obtain knowledge how far leadless are replacing lead colours. In the
manufacture of cornice poles (in which small industry several severe
attacks were reported) the suggestion of a factory inspector to employ
lithopone was adopted, with entire success. A patent graphite has been
substituted for orange lead, with which wooden patterns to form the
moulds of articles to be subsequently cast in metal are frequently
painted.


=House-Painting[35].=--The work of house-painting and plumbing outside
a workshop does not come under the Factory and Workshop Act, 1901,
except to a limited extent under Section 105 in buildings in course
of erection; and even in that case the requirement of notification of
lead poisoning imposed by Section 73 does not apply. If, however, a
house-painter is employed for part of his time in mixing paints in a
workshop belonging to a builder, then the question may legitimately be
raised as to whether plumbism may not have been due in some measure to
such workshop conditions. Despite the limited extent to which the Act
applies to lead poisoning of house-painters and plumbers, seeing that
it is industrial in origin many practitioners notify cases, with the
result that the number every year exceeds considerably that from any
other lead industry in the country. Thus, the number notified in the
ten years 1900-1909 was 1,973, including 383 deaths. The proportion
of deaths to persons notified is much higher than for lead industries
generally (19·4 per cent., as compared with 4·0 per cent.). If the
proportion of cases to deaths were the same in house-painting as in
other industries (and it is a fair assumption to make), the number of
cases would be 9,418.

When investigation is made into the reported cases, the pre-dominance
of the severer symptoms--paralysis, brain symptoms, and chronic
plumbism--is brought out. Causation of poisoning, in order of
importance, appears to be: (1) Dust from sandpapering one surface of
paint before applying another; (2) dust from mixing dry white lead
with oil; (3) dust arising from paint that has dried on overalls; (4)
contamination of food with unwashed hands; and (5) fumes from burning
off old paint.


=Use of Leadless Paints.=--Opinion still differs as to the feasibility
of substituting zinc sulphide or zinc oxide (or a combination of the
two) for white lead in paints, in spite of elaborate investigation of
the point by commissions of inquiry appointed notably by the French,
Austrian, and Dutch Governments. There is, however, general consensus
of opinion that for the painting of internal surfaces of houses and
of all surfaces which are not exposed to the weather zinc paints have
the advantage (apart from their non-poisonous quality) over white-lead
paint of not changing colour. The technique for applying zinc oxide
paint differs much from that for applying white lead. Being much less
dense, it requires to be ground with a greater proportion of oil, and
the vehicles and driers necessary for the thinning of the stiff paste
are different from those ordinarily used for thinning and mixing white
lead. Coats of zinc oxide should be applied as thin as possible, and
hence there is the drawback that where three coats of white lead will
suffice, four coats of zinc oxide may be necessary unless the paint
is skilfully applied. The best method of applying zinc oxide paint
with the brush has to be learnt in order to get the best effect. The
ordinary house-painter, therefore, accustomed to the use of lead paint,
cannot expect to obtain the same result from zinc paint treated in the
same way. And zinc oxides differ in value as pigments according to the
methods of production. That obtained by direct roasting of the ore
(franklinite and zincite) is superior to that prepared by the indirect
method of oxidation of spelter.

Zinc sulphide enters into the composition of many white paints mixed
with zinc oxide, barytes, and often lead sulphate. Its defect in
colour is thus concealed, and it adds to the mixture the important
property known to the painter as “body.” Under a variety of names,
such as “Orr’s enamel white,” “patent zinc white,” and “lithopone,”
such mixtures have a large sale, and for many purposes can act as a
substitute for white-lead paint.

Extensive inquiries have been made in recent years in Continental
countries into the effect of use of white-lead paint in producing
plumbism, the processes employed, and the possibility of
substitutes--in Austria, from 1904 to 1907; in Germany, in 1905;
in Holland, from 1903 to 1909; in France, from 1901 to 1909; in
Switzerland, in 1904; and in Belgium, from 1904 to 1909. In 1902
the French Government, by a decree applying to house-painting,
prohibited (1) use of white lead except when ready mixed with oil; (2)
direct handling of white lead; (3) dry-rubbing or sand-papering of
painted surfaces; and required (4) provision of the usual means for
cleanliness, including overalls. This decree in 1904 was extended to
all kinds of painting with use of white lead. Finally, in 1909, a law,
to take effect from 1914, was passed prohibiting the use of white lead
in paint altogether.

In Belgium, following on regulations issued under royal decree in 1905,
in which, among other things, quarterly periodical medical examination
of house-painters was required, the law dated August 20, 1909, came
into force, prohibiting the sale, transport, and use, of white lead in
the form of powder, lumps, or small pieces, and requiring, if intended
for the purpose of painting, the white lead to be mixed ready ground in
oil. Dry-rubbing and sandpapering are also prohibited.

In the German Empire the work of house-painting is controlled by
regulations dated June 27, 1905, of which the following are the main
provisions: (1) Prohibition of actual contact with white lead in
grinding and mixing, and adequate protection from the dust so created;
(2) mechanical incorporation of the white lead with the oil or varnish,
and prevention of the escape of dust into the workroom; (3) preliminary
moistening prior to scraping, chipping off, or rubbing down, dry oil
colours; (4) and (5) provision of overalls and washing accommodation,
including soap, nailbrushes, and towels (in erection of new buildings
the workmen must be able to wash in a place free from frost); (7)
instruction of the workman by the employer as to the risk attaching
to the work by supplying him with a copy of the regulations and
cautionary notice. Further, where painting operations are carried on
in factories or workshops as subsidiary to other processes, there must
be (8) provision of washing accommodation in a special room capable of
being heated, and of a place in which to keep clothing; (9) periodical
medical examination at half-yearly periods; and (10) prohibition of
smoking and consumption of alcohol in the workrooms.

The Austrian Regulations, dated April 15, 1909, follow the German
Code closely, but differ in that they (1) prohibit the use of white
lead paint for the interior surfaces of houses or of any surfaces
not exposed to the weather; (2) affixing of a notice on the can or
cask that it contains lead; and (3) periodical medical examination at
quarterly instead of half-yearly periods.

At the present time committees appointed by the Home Office are
inquiring into the coach-painting and house-painting industries in this
country.

The results of careful and detailed experiments made by the White Lead
Commission appointed by the Dutch Government, which inquired into the
subject, are summarized as follows:

  I. Zinc-white paints are much better able to withstand the action of
  sulphuretted hydrogen gas than white-lead paints.

  II. Zinc-white paints do not withstand the action of sulphurous acid
  in the atmosphere as well as white-lead paints.

  As this gas is present in coal-smoke of locomotives, steamers, tall
  chimneys, etc., zinc-white paint much exposed to such smoke--for
  instance, in railway-stations, etc.--will soon become corroded, and
  cannot then replace white lead.

  III. Zinc-white paints applied on zinc, Portland cement, or iron (the
  latter having previously been provided with first coats of red oxide
  of lead or iron), are able to withstand the action of the open air
  for a space of five years quite as well as white-lead paints, and can
  entirely replace the latter, provided they are not exposed to the
  action of vapours containing sulphurous acid.

  IV. In the interior of buildings zinc-white paints, applied on wood,
  iron, zinc, Portland cement, and plaster, are as good as white-lead
  paints; and can entirely replace the latter, provided they are not
  exposed much to vapours containing sulphurous acid or to much damp.

  V. Zinc-white paints applied on wood, if not exposed much to the
  action of sulphurous acid gas, will in many cases last during
  five years in the open air as well as white-lead paints, and can
  replace the latter with good results. But in all places where water
  accumulates, as on window-sills, the lower side of cornice-work,
  etc., they will, even after three or four years, deteriorate to such
  a degree that repainting will become necessary for the preservation
  of the wood; in this respect, therefore, they are inferior to
  white-lead paints.

  VI. Zinc-white paints, such as the White Lead Commission have used
  successfully, cover at least equally as well as the white-lead paints
  customary in this country.

  The zinc-white putty used by the White Lead Commission is quite as
  serviceable as ordinary white-lead putty.

  VII. Painting with zinc-white paint, such as the Commission used on
  new woodwork in the open air, does not cost more than painting with
  the white-lead paints customary for that purpose.

  VIII. Painting on existing paintwork, so-called “repainting,” in the
  open air, with zinc-white paints such as the White Lead Commission
  used, costs more than the white-lead paints hitherto in use, inasmuch
  as the preparation of the wood painted with zinc-white paints
  involves greater expense in rendering it fit for the repainting than
  in the case of wood painted with white lead in rendering it fit for
  further painting with white lead.

  In the case of painted wood which is exposed to the open air, the
  possibility is, moreover, not excluded that, where such wood is in
  an unfavourable condition of humidity (see under § V.), it may have
  to be repainted sooner than if it had been painted with white-lead
  paints.

  In these circumstances the cost of maintenance of wood painted with
  zinc-white paint, and exposed to the open air, is further increased
  as compared with wood painted with white-lead paint.

  IX. Lithopone paints cannot replace white-lead paints in the open
  air; they have proved to be quite unfit in this respect.

  X. For paintwork above water, first coats of oxide of iron have,
  during five years, proved to be quite as good and serviceable as
  first coats of red oxide of lead.

  For coats of paint under water, oxide of iron cannot be used.

  Coats of oxide of iron paint are cheaper than coats of red oxide of
  lead paint.

  When oxide of iron is used for the first coat, much more technical
  skill is required for the painting of the covering coats than is the
  case when red oxide of lead is used for the first coat.


=Shipbuilding[36].=--Cases arising in shipbuilding are due not so
much to mixing the paints or red-lead paste as to the dust produced
in sandpapering the coats of white paint applied in cabins, etc., in
chipping and scraping off old red-lead paint, often in confined spaces
such as double bottoms, tanks, bilges, etc. Splashing from injecting
red lead between plates, fumes from burning off old paint, and fumes
from paint while using it in confined spaces, are mentioned in reports.
Several attacks have occurred to persons engaged in inserting red-hot
rivets into holes containing yarn soaked in red lead and oil. Lead
fumes, it is suggested, are given off. The number of cases included
under this heading each year has been--

  1900     32
  1901     28
  1902     15
  1903     24
  1904     48
  1905     32
  1906     26
  1907     22
  1908     15
  1909     27
  1910     21

The figures illustrate the difficulty of obtaining a reduction in
the attacks when the cause is to be found in conditions not amenable
to control by exhaust ventilation. The possibility of effecting some
reduction by such precautions as can be adopted is suggested by the
diminution (from 110 to 60) in the number of cases in the Government
dockyards in the six years 1905-1910 and 1899-1904 respectively, as
compared with the increase (from 67 to 87) in all other shipbuilding
yards.

In the Government dockyards, among other precautions, men employed on
red-leading appear before the medical officer periodically, and no man
is allowed to do the work for more than two days a week. Further, oxide
of iron paint is to be used in the double bottoms, wing passages, and
other confined spaces on board ships. All men employed as painters are
allowed five minutes out of their working time for washing.


=Other Industries.=--The industries and processes which are gathered
together under this head will be seen from the following distribution:

          Industries.                       Cases (Ten Years:
                                                1900-1909).
   (1) Iron drums and kegs                           47
   (2) Harness furniture                             23
   (3) Tempering springs                             13
   (4) Other contact with molten lead               103
   (5) Metal sorting                                 13
   (6) Handling lead and dust from metallic lead    122
   (7) Shot-making                                   14
   (8) Glass-making                                  13
   (9) India-rubber                                  23
  (10) Yarn-dyeing                                   28
  (11) Copper letters and opal signs                 28
  (12) Other lead compounds                         196
  (13) Miscellaneous                                 36
                                                    ---
                      Total                         659

(1) and (2) have been described under tinning of metals, as the
processes are similar, and in the year 1909 they were included along
with tinning of hollow-ware under the same code of regulations.

Tempering of steel buffer springs (3)[37], carried on in Sheffield,
gives rise to poisoning from fumes of molten metal into which the
springs are immersed, and from dust of skimmings, unless there is
efficient hooding and exhaust. A sample of dust collected from a
lampshade over a melting-pot was found in the Government laboratory
to contain 48·1 of metallic lead, or 51·8 per cent. of lead monoxide.
In testing the springs under a hydraulic press, and subsequent
straightening by hammering on an anvil, the thin coating of lead on
the surface scales off, and may be inhaled.

Other contact with molten metal (4) includes operations which do not
differ from several already described, in which danger is incurred from
either fumes and dust in skimming the dross or subsequent handling,
such as manufacture of solder, coating cables, filling copper cylinders
with molten lead for the purpose of bending them, and subsequently
re-immersing them in the bath to melt out the lead, tinning of nails,
making lead patterns for fenders (in which there may be danger, also,
from use of a wire brush to get rid of adhering sand), etc.

Handling lead and dust from metallic lead (5) includes operations such
as die-stamping, stamping tickets and other articles on a leaden slab
(where the danger is akin to, though probably less in degree than in
file-cutting), examining bullets, manufacture of metallic capsules,
lining boxes with sheet lead, lead glazing (where the danger is
essentially that of plumbing work), etc.

It includes also a number of cases which were reported previous
to 1905 in the markers of testing ranges at a small-arms factory.
Duckering[38], who investigated these cases, found that the bullets
were stopped by dry sand in boxes 8 feet long. On entering the sand
the bullets became disintegrated, so that, after being in use for some
time, the sand contained a large amount of lead, and had to be removed.
In doing this the box was turned over, and the sand deposited on the
floor immediately behind the targets. The lead was then separated by
sifting by hand, and the sand used over again. In these operations much
floating dust was produced, which was inhaled by the markers, who stood
in an open trench immediately in front of and below the targets.


=Metallic Capsules.=--Some cases have occurred from the manufacture
of capsules for bottles. The capsule consists of a lead leaf rolled
between two leaves of tin. Cases arising in the early processes of
casting and rolling do not differ from those described as due to
contact with molten metal and handling of lead. The most difficult to
deal with are those which occur in the final process of cleaning and
colouring. Before colouring with varnish paint, the capsule is placed
on a rapidly revolving lathe, and the hand of the worker, carrying a
cloth containing whitening, is placed lightly on the capsule. A slight
amount of dust is inevitably raised, and this dust, collected from the
bench, was found to contain from 11·5 to 25·6 per cent. of lead; while
dust which had settled on a beam 9 feet from the floor contained 9·3
per cent. Of thirty-one workers employed in cleaning and colouring,
fifteen showed evidence of lead absorption in a blue line on the gums,
and in one there was considerable weakness of the left wrist. Similar
experience of lead poisoning in this industry has been noted in German
and Austrian factories.

Periodical medical examination at quarterly intervals has been
instituted in the principal factory, with good results, as it enables
those who show early signs of lead absorption to be transferred to
other processes. Exhaust ventilation has been tried, but, except at the
few lathes where cleaning alone is done, without complete success, in
view of the nature of the work.


=Shot-making.=--Cases in shot-making arise from the dust given off when
sifting the shot into different sizes--an operation which should be
carried on in sieves entirely closed in and under negative pressure.
Dust collected from the glass casing over a sifting machine contained
60·3 per cent. of metallic lead. The sample was free from arsenic.


=Heading of Yarn dyed with Chromate of Lead.=--Cotton yarn is dyed (10)
on a considerable scale with chromate of lead, chiefly for Oriental
markets; and it is the orange chrome--that most heavily weighted with
lead--which is most in demand there. The orange chrome colour is
obtained by dipping hanks of yarn into solution of lime, and then into
acetate of lead. The process is repeated a second time, after which
the chromate is formed by dipping in bichromate of soda, and finally
boiling in lime-water[39].

In production of yellow chrome colour, the yarn is treated only once
in a bath of lead acetate. Other colours made are lemon chrome and (by
addition of an indigo bath) chrome green.

The early processes of dyeing rarely give rise to poisoning, but the
strong solution of bichromate of soda readily causes characteristic
ulceration of the skin--“chrome holes.” Danger arises from dust in
the process of heading or “noddling,” as it is sometimes called, of
the dried yarn over posts. The hanks of yarn are tugged and shaken by
women as a rule, and in the case of orange chrome very considerable
quantities of dust are liberated. We have been told that a hank of this
kind of yarn does not commend itself to an Oriental buyer unless, when
shaken, dust is visible.

The industry was certified as dangerous in 1895, in view of serious
illness and death in Glasgow and Manchester, and special rules were
made to apply, not only to the heading operations, but also to the
winding, reeling, and weaving, of the dyed yarn--processes in which
cases of poisoning are very rare.

Detailed inquiry was made in 1906 in eleven factories where yarn was
dyed on a considerable scale by means of chromate of lead--in eight
mainly for export to India, and in three for the home market. Yarn dyed
for the home market gives off less dust when headed, as the material
undergoes additional washing in water and in dilute acid; and it is
also sometimes passed through a sizing of starch, which fixes the
chromate of lead to the yarn more securely.

Proof of the greater danger from orange chrome is found in the fact
that Dupré was able to wash 1 pound of dust (0·29 per cent.) from 345
pounds of heavy orange yarn, and only 1 pound (0·03 per cent.) could be
washed from 3,300 pounds of light yellow or green yarn.

In none of the factories were the workers engaged solely on the
dangerous yellow and orange chrome-dyed yarn. In some the work may
last an hour or two every day, in others for an hour or two every day
in alternate weeks, or for one week in every three or four weeks, and
perhaps in a dozen factories the work may not be done more frequently
than half a day a month, or even one in three months.

Particular attention was paid to the nature of the exhaust ventilation
at the “heading” posts, as this is the most important point in the
protection of the workers. It was provided in eight out of the nine
principal yarn-dyeing factories. The exception was one where the work
was said to be solely for the home market. In one a 2 foot 6 inch
Blackman fan was placed in the wall without connection of the “heading”
posts with it by means of ducts and hoods. In four, hoods and ducts
of wood, square in section, with right-angle bends, had been locally
applied to the posts. In other four, hoods and ducts were of metal,
circular in section. The velocities in feet per minute (obtained with
a Davis self-timing anemometer) were taken at the opening into the
branch duct behind or under the post. The value of anemometric tests in
detecting blockages or interference in the ducts is evident from the
table on p. 300.

  +----+-----+---------+-----+--------------+----+---------+----+
  |    |     |         |     |              |    |         |    |
  | (1)| (2) |   (3)   | (5) |     (6)      | (7)|   (8)   |(10)|
  |    |     |         |     |              |    |         |    |
  +----+-----+---------+-----+--------------+----+---------+----+
  |Fan.|Fan. |Fan. Fan.| Fan.|Fan. Fan. Fan.|Fan.|Fan. Fan.|Fan.|
  | 240| 820 | 330  Nil|1,200| 420  450  210| 780| 570  700| 850|
  | 450|     | 450   20|     | 420  510  210|    | 570  700|    |
  |    |     |         |     |              |    |         |    |
  | 480| 270 | 450  270|  780| 360  420  390| 660| 540  490| 850|
  | 480|(750)| 420  270|     | 360  420  430| 540| 570  570|    |
  |    |     |         |     |              |    |         |    |
  | 480| 330 | Nil  250|     | 270  120  420| 510| 540  530|    |
  | 450|(440)| Nil  300|     | 300  120  490|    | 540  540|    |
  |    |     |         |     |              |    |         |    |
  | 324| 320 | 300  180|     | 350  480  450| 300| 300  450|    |
  | 280|(420)| 250  150|     | 290  480  420|    | 300  450|    |
  |    |     |         |     |              |    |         |    |
  |  25|     | 130  350|     | 430  390  510|    |      420|    |
  |  25|     | 220  180|     | 420  360  460|    |      400|    |
  |    |     |         |     |              |    |         |    |
  |    |     | 360  300|     | 240       420|    |         |    |
  |    |     | 240  280|     | 450       480|    |         |    |
  |    |     |         |     |              |    |         |    |
  |    |     | Nil  210|     | 390          |    |         |    |
  |    |     | Nil  210|     | 390          |    |         |    |
  |    |     |         |     |              |    |         |    |
  |    |     |      Nil|     |              |    |         |    |
  |    |     |      Nil|     |              |    |         |    |
  +----+-----+---------+-----+--------------+----+---------+----+

(1) The draught here was obtained from the main chimney-shaft. The
small velocities at the end post, it was subsequently found, arose from
the fact that the double heading post was connected by means of a very
small duct to the end of the large duct which served the other posts.

(2) Wooden duct connected up with fan. The area of the openings into
the duct could be enlarged or diminished by means of a shutter. The
figures in brackets were those obtained when the shutter was fully
opened.

(3) In this factory originally a 2 foot 6 inch fan was simply placed
in the wall. Subsequently they were boxed in and ducts of wood brought
within a foot of the noddling bar. Four of the branch ducts were found
to be blocked.

(5) Wooden ducts and hoods behind bar both close to the fan.

(6) Circular metal ducts with curved angles, and placed about 8 to 10
inches behind post; all connected up with a 4 foot 6 inch fan. The
small velocities (120 feet) at two posts was due to loose connection of
the branch ducts allowing air to be drawn in at the foot.

(7) Metal duct distant about 2¹⁄₂ feet from the post, and situated
immediately below and not behind the bar. Dust was prevented from
rising above the post by a glass screen, the projection of which also
prevented the worker from coming too near to, or getting his head over,
the post.

(8) Metal ducts, 9¹⁄₂ inches in diameter. Evidence of ill-health was
greatest here, notwithstanding good draught, because the branch ducts
were not brought close enough to the point where “heading” was done,
but were distant 15 inches from the centre of the post, and “noddling”
was done at a distance of 2 feet from the duct, one man standing
between the draught and the bar.

(10) Draught arranged as in (7), below the bar, without protection of
the worker by a glass screen.

Regulations now apply to the industry. So clear is it that
locally-applied exhaust ventilation is of paramount importance in
prevention of poisoning, that, however intermittent the operation
of “heading,” exemption from this requirement cannot be permitted.
Determination periodically by the occupier of the speed of the draught
at each exhaust opening should prevent blockage of ducts.

The regulations do not apply to the winding of, and weaving with,
yarn dyed with chromate of lead. Rarely in the spinning and weaving
factories of Blackburn does the amount of the particular yarn in
question constitute as much as 5 per cent. of the total quantity of
_coloured_ yarn used. Section 74, 1901, is sufficient to meet the
isolated cases where injury to health arises. The habit of biting
chrome-dyed thread has given rise to lead poisoning. Nor do the
regulations apply to treatment of calico or cloth into which lead may
enter. Such poisoning as may occur must be practically confined to
persons employed in the paint-mixing house.


=Manufacture of India-rubber.=[9]--Litharge, massicot, red lead, and
sulphide of lead, are generally mixed with rubber. Litharge is regarded
not only as a valuable filler for rubber, but has the faculty of
hastening vulcanization. All dry-heat goods depend upon it where a dark
or black effect is wanted.

Every year a few cases are reported in the process of mixing the
batches in the weighing room of the rubber factory, or more frequently
at the hot calender rolls, where the batch of dry powder containing
the lead compound is gradually distributed by hand on to the rubber
so as to effect an intimate mixture. The heated air over the rollers
causes dust to rise. According to the purpose for which the rubber is
wanted, the quantity of litharge in the batch varies. In one factory of
fourteen men employed at the calender rolls, ten showed a blue line,
five were markedly anæmic, one had weakness of the wrists, and two
weakness of grasp[40]. Only one case has been reported since exhaust
ventilation was applied locally over each calender roll. In a rubber
tyre factory five cases followed one another in quick succession,
all in persons employed on the rolls. There should be no hesitation
in requiring exhaust ventilation wherever employment in mixing the
batches or at the rolls is constant. In general, however, the work in
weighing out is intermittent, and reliance is placed on the wearing of
a respirator.

No attempt has been made to enumerate all the industries and processes
in which lead poisoning may arise. The task would become wearisome, as
they are so numerous. Nor is it necessary to give details of all that
are known, as it is doubtful whether there can be any different in
nature or requiring different treatment from the many which have been
described.


REFERENCES.

  [1] Special Report on Dangerous or Injurious Processes in the
  Smelting of Materials containing Lead, and in the Manufacture of Red
  and Orange Litharge and Flaked Litharge, by E. L. Collis, M.B. Cd.
  5152. 1910. Wyman and Sons, Ltd. Price 6d.

  [2] Annual Report of the Chief Inspector of Factories for 1901, p.
  213.

  [3] _Ibid._, p. 242.

  [4] _Ibid._ for 1906, p. 272.

  [5] H. O. HOFMAN: Metallurgy of Lead. 1906.

  [6] Annual Report of the Chief Inspector of Factories for 1900, p.
  438.

  [7] _Ibid._ for 1910, p. 154.

  [8] Special Report above, p. 15.

  [9] LAYET: Quoted by Oliver in Dangerous Trades, p. 288.

  [10] DIXON MANN: Forensic Medicine and Toxicology, p. 477.

  [11] SOMMERFELD: Bekämpfung der Bleigefahr, p. 220.

  [12] SOMMERFELD: Quoted by Silberstein below, p. 257.

  [13] SILBERSTEIN: Die Krankheiten der Buchdrucker, in Weyl’s Handbuch
  der Arbeiterkrankheiten, p. 257. Gustav Fischer, Jena, 1908.

  [14] TATHAM: Decennial Supplement to Sixty-fifth Annual Report of the
  Registrar-General. Cd. 2619.

  [15] Third Interim Report of the Departmental Committee on Certain
  Miscellaneous Dangerous Trades. C. 9073. 1898.

  Report on the Draft Regulations for File-Cutting by Hand, by Chester
  Jones. Cd. 1658. 1903.

  [16] Annual Report of the Chief Inspector of Factories for 1904, p.
  125.

  [17] _Ibid._ for 1906, p. 273.

  [18] Special Report on Dangerous or Injurious Processes in the
  Coating of Metal with Lead or a Mixture of Lead and Tin, by Miss A.
  M. Anderson, H.M. Principal Lady Inspector of Factories, and T. M.
  Legge, M.D., H.M. Medical Inspector of Factories; together with a
  Report on an Experimental Investigation into the Conditions of Work
  in Tinning Workshops, and Appendices, by G. Elmhirst Duckering, one
  of H.M. Inspectors of Factories. Cd. 3793. London: Wyman and Sons,
  1907.

  Annual Report of the Chief Inspector of Factories for 1902, pp.
  296-318.

  Report on Draft Regulations on the Tinning of Metal Articles, by E.
  T. H. Lawes.

  The Cause of Lead Poisoning in the Tinning of Metals, by G. E.
  Duckering.

  [19] The Health of Brass Workers, by T. M. Legge. Annual Report of
  the Chief Inspector of Factories for 1905, pp. 388-397.

  [20] _Ibid._ for 1898, pp. 119-123; and many references in later
  Annual Reports.

  [21] The Bischof Process for the Manufacture of White Lead, by
  Professor Sir William Ramsay, K.C.B., D.Sc. 1906.

  [22] Report of the Departmental Committee on the Use of Lead, and
  the Danger or Injury to Health arising from Dust and Other Causes in
  the Manufacture of Earthenware and China: vol. i., Report; vol. ii.,
  Appendices. Cd. 5277-8. 1910.

  Lead Compounds in Pottery: Report to H.M. Principal Secretary of
  State for the Home Department on the Employment of Compounds of
  Lead in the Manufacture of Pottery; their Influence upon the Health
  of the Workpeople; with Suggestions as to the Means which might be
  adopted to Counteract their Evil Effects, by Professor T. E. Thorpe,
  LL.D., F.R.S., Principal of the Government Laboratory; and Professor
  Thomas Oliver, M.D., F.R.C.P., Physician to the Royal Infirmary,
  Newcastle-on-Tyne. London: Eyre and Spottiswoode, February, 1899.
  Price 5¹⁄₂d.

  [23] Work of the Government Laboratory on the Question of the
  Employment of Lead Compounds in Pottery, by Professor T. E. Thorpe.
  Cd. 679. 1901.

  [24] H. R. Rogers: Report of a Series of Experiments for Determining
  the Amount of Lead in the Glaze of Finished Ware, based on the Method
  described by Sir Henry Cunynghame, K.C.B., in his evidence before the
  Departmental Committee on the Use of Lead (see 22, above).

  [25] See 22, above, pp. 93, 94.

  [26] C. R. PENDOCK: Unpublished Report.

  [27] Special Report on Dangerous and Injurious Processes in the
  Enamelling and Tinning of Metals, by Miss A. M. Anderson and T. M.
  Legge, in Annual Report of the Chief Inspector of Factories for 1902,
  pp. 296-318.

  [28] Annual Report of the Chief Inspector of Factories for 1910, p.
  154.

  [29] Zeitschrift für Gewerbehygiene, Unfall Verhütung und
  Arbeiter-Wohlfahrtseinrichtungen, January, 1902.

  [30] Annual Report of the Chief Inspector of Factories for 1901, pp.
  221-229.

  Die in electrischen Akkumulatoren Fabriken beobachteten
  Gesundheitsschädigungen. Arbeiten aus dem Kaiserlichen
  Gesundheitsamte, by Dr. Wutzdorff. 1898.

  [31] Third Interim Report of the Departmental Committee appointed to
  inquire into and report upon Certain Miscellaneous Dangerous Trades,
  pp. 16-19. C. 9073. 1898.

  [32] D’ARCY ELLIS: Brit. Med. Journ., vol. ii., pp. 406-408, 1901.

  [33] Report on the Manufacture of Paints and Colours containing Lead,
  as affecting the Health of the Operatives employed, by T. M. Legge,
  M.D. Cd. 2466. 1905.

  Painters’ Colours, Oils, and Varnishes, by G. H. Hunt, Griffin, p.
  357. 1901.

  [34] Annual Report of the Chief Inspector of Factories for 1905, pp.
  366-368, and references in other Annual Reports.

  [35] Report of the Departmental Committee appointed to inquire into
  the Dangers attendant on Building Operations, Appendix IX., pp.
  184-187. Cd. 3848. 1907.

  Painters’ Colours, Oils, and Varnishes, by G. H. Hunt, Griffin. 1901.

  [36] Annual Report of the Chief Inspector of Factories for 1910, pp.
  175-176.

  [37] _Ibid._ for 1906, pp. 272, 273.

  [38] Annual Report of the Chief Inspector of Factories for 1905, pp.
  368, 369.

  [39] Dangerous Trades Committee’s Final Report, C. 9509, pp. 26-30.

  ALEX. SCOTT: Minutes of Evidence of Various Lead Industries
  Committee, 1894, C. 7239-1, pp. 105-108.

  J. S. CLAYTON: Industrial Lead Poisoning among Yarn Workers. Brit.
  Med. Journ., vol. i., p. 310, 1906.

  [40] Annual Report of the Chief Inspector of Factories for 1901, p.
  231.




INDEX


  Abortion caused by lead, 35

  Absorption of lead: cutaneous, 25; from lung, 23; gastric, 19;
  intestinal, 21, 22; in liver, 24; mechanism of, 20; prevention of,
  from stomach, 23

  Accumulators. See Electric accumulators

  Acetate of lead, poisoning by, 94

  Acetic acid, solvent action of, on lead oxide, 15

  Acid lemonade, 185

  Acidity, gastric contents, 15

  Action of lead: on gold and silver, 3; on water, 3

  Acute encephalopathy, 54, 95

  Acute lead poisoning, 110, 111

  Acute nephritis, 60, 131

  Aerographing, 272, 280

  Ætiology of lead poisoning, 7

  Age as affecting lead poisoning, 35, 239

  Akremnin soap, 238

  Albuminate of lead, preparation of, 17

  Albuminuria, 128

  Albuminuric retinitis, 160

  Alcohol: as predisposing cause, 37, 64; gastritis and plumbism, 64;
  in experimental poisoning, 85; similar effect to lead on kidney, 131

  Alteration in blood-corpuscles in lead anæmia, 133

  Alternation of employment, 34, 251

  Amaurosis, 70, 160

  Amblyopia, 76

  Amenorrhœa, 36

  Anæmia, 39, 112, 132, 136, 227; treatment of, 190

  Anemometers, 219

  Antibrachial paralysis, 144, 148

  Antimony, effect of, on lead fume, 199

  Appointed surgeon, 112, 221

  Aran-Duchenne paralysis, 149

  Armit, nickel poisoning, 11

  Arsenic: Cloetta’s experiments, 24; excretion of, in fæces, 24

  Arterio-sclerosis, 116

  Arthralgia, 50, 161

  Arthritis, 40

  Artificial gastric juice, action of, 17

  Atrophic nerve changes, 69

  Attack rate from lead poisoning (table), 55

  Autopsy, points to be noted in, 162


  Bacup epidemic, 4

  Basophile granules, 77, 133, 135, 179

  Baths, 238

  Blood: action of lead salts on, 2; in lead poisoning, 70, 78, 134,
  179; pressure, 116, 180; vessels, 68, 70, 75

  Blue line, 122, 123, 128, 226; experimental production of, 41, 124;
  from diachylon, 13

  Brachial paralysis, 148

  Brain, analysis of, 96

  Brass, presence of lead in, 263

  Brassworkers and plumbism, 51, 263

  Breathing experiments, 81

  Bright’s disease and lead poisoning, 60

  Burtonian line. See Blue line


  Carbon in lung, 11

  Card system, use of, 186

  Central nervous system, 69, 157; treatment, 196

  Cerebral symptoms, 51, 157

  Certifying surgeons, reports of, 45, 221

  Chandelier fitters, poisoning among, 264

  Channels of lead absorption, 8

  Chemical analysis of brain, 95

  Chemical characters of lead salts, 4

  Chemical diagnosis, 166

  Chemical examination of organs, 163

  Chemistry of lead, 2

  Choroidal atrophy, 161

  Chromate of lead in yarn-dyeing, 298

  Chrome colours, 287

  Chronic colic, 119

  Circulatory system, 75, 137

  Cirrhosis of kidney, 74

  Coach-painting, 288; dust in atmosphere breathed, 205; leadless
  paints, 290; reported cases from, 289; sandpapering in, 289

  Colic, 116, 117, 118, 119, 188, 190; differential diagnosis, 188;
  treatment of, 187

  Colloidal lead, 5

  Colon, palpation of, 126

  Colours, 285

  Comparative mortality, 59

  Conjunctiva in lead anæmia, 132

  Constipation, 115

  Copper extraction, plumbism in, 246

  Cutaneous absorption, 25


  Death certificates in plumbism, 57

  Degeneration of blood vessels, 68

  Determination of lead in urine, 169

  Diachylon, 13

  Diagnosis: from chemical analysis, 166; of lead colic, 120, 188

  Diarrhœa, 115

  Differential count in lead anæmia, 134, 137, 180

  Digestion experiments, 16, 17

  Drink for lead-workers, 186

  Drugs in lead colic, 189

  Duration of employment and plumbism, 52

  Dust, lead: amount of, in air breathed, 199, 207; chief cause of
  plumbism, 10; “laying,” difficulties of, 11; rate of settling, 7;
  respirators for, 207

  Dysmenorrhœa, 36


  Earthenware: and china, 270; attack rate, 56; decorative processes,
  272; dust in atmosphere, 204, 206; glaze processes, 272; leadless
  glaze, 274; low solubility glaze, 274; Potteries Committee on,
  recommendations of, 275; reported cases in (table), 271

  Electric accumulators, 281; reported plumbism in, 283; ventilation
  in, 216

  Electrical reactions, 151, 153, 154

  Electrical treatment, 194

  Electro-chemical tests, 168

  Electrolytic estimation of lead, 174; reactions, 5

  Enamelling (vitreous), 278; aerographing in, 280; use of leadless
  colours in, 278

  Encephalitis, case of chronic, 71

  Encephalopathy, 54, 68, 71, 157

  Estimation of lead: in digestion, difficulties of, 18; in urine, 169,
  170, 175

  Excretion: of arsenic, 24; of lead salts, 32, 127, 128

  Excretory system, 72

  Exhaust ventilation. See Ventilation

  Experimental lead poisoning: pathology of, 81; post-mortem findings,
  91; symptoms, 69, 89, 103

  Experimental arsenic poisoning, 24

  Experimental results, summary, 104

  Eye changes, 76, 150, 158


  Facial nerve, paralysis of, 195

  Fæces: examination for lead in, 182; lead in, 32, 64

  Family susceptibility, 30

  Fans. See Ventilation

  Faradism for paralysis, 195

  File-cutting, 256; atrophy of muscles in, 52, 257; reported cases in,
  258

  File-hardening, 258; lead fume from, 200, 201; use of fused metallic
  salts for, 258

  Forms of paralysis, 54, 142

  Fritted lead: action of water on, 89; poisoning, 34, 97; solubility
  test, 14

  Fume (lead) in atmosphere breathed, 198, 207


  Gastric absorption, 19, 21, 22

  Gastric digestion, artificial, 17

  Gastric juice, action on lead salts, 15, 16

  Gastritis in plumbism, 65

  Gastro-intestinal absorption, 12, 13, 64

  Generalized paralysis, 151

  Glass-cutting, 283

  Glaze, 272; leadless, 274; low solubility, 274

  Gout, 38


  Hæmatoporphyrin, 180, 182

  Hæmoglobin, 113, 132

  Hæmorrhages in plumbism, 76

  Hæmostatic action of lead salts, 2

  Hair lotions, poisoning from, 13

  Harness furniture, tinning of, 259

  Headache, 120

  Health Register, 228

  Heart, 139, 193

  Heart symptoms, 193

  Heat, exhaust by, 208

  Histological examination of lead tissues, 163, 176

  Histology: of experimental poisoning, 92; of nervous system, 67

  House-painting, 291; regulations for, 293; reported plumbism in, 291

  Hunter, John, “dry bellyache” from rum, 1

  Hyperæsthesia, 161


  Immunity, 27, 29, 113

  Incipient symptoms, 112, 222

  India-rubber, manufacture of, 301

  Inhalation experiments (table), 101

  Inoculation experiments, 83, 88, 99

  Instruction of worker, 240

  Interstitial nephritis, 130

  Intestinal absorption, 22, 94

  Intestinal staining, 21, 94, 125

  Iodine in plumbism, 192

  Ionization in paralysis, 195

  Iron drums, tinning of, 260

  Italians and lead poisoning, 30


  Kidney: changes, 73, 74, 129; excretion of lead by, 128; interstitial
  hæmorrhages, 130


  Lactic acid, solvent action of, 15

  Large intestine and lead absorption, 21

  Lavatories, 235, 238

  Lead: compounds, 7; fume and dust in atmosphere, 198-207; in urine,
  129, 167; melting-point, 2, 199

  Lead bed in file-cutting, 257

  Lead burning, 262; in electric accumulators, 283

  Lead chloride in tinning, 200

  Lead dust: minimal toxic dose, 31, 207; rate of settling, 7; size of
  particles, 12

  Lead fume in tinning, 202

  Lead oxide, danger from skimming, 200

  Lead piping, 251

  Lead poisoning: acute, 110; mortality, 57; entry of poison, 8

  Lead silicate, 34

  Lead smelting: and silver refining, 242; analysis of fumes in, 246;
  cupellation process, 246; Huntingdon-Heberlein process, 243; in blast
  furnace, 243; Parkes’s process, 244; Pattinson process, 245; reported
  plumbism, 248

  Leadless glaze, 274

  Leadless paints, 291

  Lead salts: action on blood, 2; action of gastric juice on, 16, 17

  Lemonade, sulphuric acid, 185

  Letterpress printing. See Printing

  Litharge, manufacture of, 250

  Lithopone, 291, 292

  Litho-transfers, 277

  Liver, absorption by, 24

  Loss of fat in plumbism, 112

  Lumbago, 115, 192

  Lung: absorption by, 98; phagocytic absorption of lead, 23


  Meal-rooms, requirements of, 234

  Mechanism of lead absorption, 20

  Medical examination, periodical, 115, 221-229

  Medical Health Register, 228

  Medical practitioners and notification, 44

  Melting-point of lead, 2, 199

  Menorrhagia, 36

  Mental symptoms, 114, 121, 158

  Metallic capsules, 297

  Metallic taste, 127

  Micro-chemical tests, 167

  Molten lead, contact with, 297

  Mortality figures, 59

  Motor-cars. See Coach-painting

  Muscles paralyzed in experimental poisoning, 144

  Muscular system, affections of, 114-161


  Nephritis, 192

  Nervous symptoms, 66, 67, 140; treatment, 193

  Neuritis, peripheral, 66, 67

  Nickel carbonyl poisoning via lung, 11

  Normal lead, 33

  Notification of plumbism, 44


  Œdema of brain, 159

  Olive oil in colic, 189

  Ophthalmoscopic examination, 160

  Oral sepsis, 38

  Orange chrome, 299

  Organic mixtures, lead in, 173

  Organic compounds of lead, 5

  Organs of generation, effect on, 36

  Overalls and head coverings, 230

  Oxides of lead, 3, 249


  Painters and lead poisoning, 107. See also House-painting

  Paints: and colours, manufacture of, 285; leadless, 29, 291

  Pancreatic digestion, action of, 17

  Paralysis: in animals, 14; electrical reactions in, 181; forms of,
  64, 66, 142; general, 151; in file-cutters, 152; insidious onset of,
  114; of special sense organs, 150; prognosis of, 197; statistics of,
  53

  Parotitis, 127

  Pathology of lead poisoning, 62

  “Pentarcomb” exhaust, 217, 254

  Peptonate of lead, 18

  Peptone, solvent action of, 19

  Perambulators, painting of, 290

  Perihepatitis, 264

  Peripheral neuritis, 266

  Peritonitis, saturnine, 65

  Peroneal paralysis, 149

  Phagocytosis of lead particles, 20

  Phthisis: in printing, 256; not a sequela, 60

  Physiology of digestion, 16

  Plumbing, 261

  Plumbism, reported cases (1900-1909), 46, 47

  Plumbo-solvency of water, 4

  Porcelain enamelling, 278

  Post-mortem signs, 91, 161

  Potassium iodide, action of, 32, 191

  Pottery. See Earthenware

  Predisposing causes, 36, 42

  Presaturnine state, 184

  Preventive measures: age of employment, 239; baths, 238; cloakroom,
  231; exhaust ventilation, 207; floors, 240; food, 86; head coverings,
  231; instruction of worker, 240; meal-room, 234; overalls, 230;
  periodical examination, 221; separation of processes, 239; washing
  accommodation, 235

  Printing: compositors’ work, 255; linotype machine, 200, 211, 217,
  253; reported cases from, 252; stereo-casting, 254; type-casting, 252

  Prodromal symptoms: of colic, 118; of paralysis, 141

  Prognosis in lead poisoning, 197

  Progressive spinal muscular atrophy, 68

  Pulse-rate, alteration of, 76, 115, 118

  Purgatives in lead colic, 188

  Putty powder, 283

  Pyorrhœa alveolaris as predisposing cause, 40, 124


  Qualitative tests, 166

  Quantitative estimation of lead, 170


  Reactions of degeneration, 152

  Red lead: manufacture of, 249; reported attacks in, 249

  Relative toxic dose of lead compounds, 105

  Repairs in factory as cause of plumbism, 10

  Respirators, inefficiency of, 217

  Respiratory absorption, 9

  Rheumatic pains, 121, 161, 192


  Safes, painting of, 290

  Salivary glands and excretion of lead, 125

  “Selective” action of lead on nerves, 147

  Sequelæ of lead poisoning, 57, 60

  Sex as affecting susceptibility, 35

  Sheet lead, 241

  Shipbuilding, 295; reported plumbism, 295

  Shot-making, 298

  Silicates of lead, 34

  Silver refining. See Lead smelting

  Size of particles of lead compounds, 12, 34

  Skin, colour of, 132

  Smelting of lead. See Lead smelting

  Solar plexus, 65

  Soldering, 261

  Solubility: of lead salts, 5, 15, 16, 17; test for fritted lead, 14

  Solvent action of peptone, 19

  Spastic paraplegia, 68

  Spiegeleisen, poisoning in manufacture of, 246

  Spring tempering, fume from, 201, 296

  Stained-glass painting, 285

  Statistics of plumbism, 44, 45

  Susceptibility, 27


  Tape measures, painting of, 290

  Tea lead, 251

  Temperature in lead poisoning, 118

  Tempering files, 200

  Terne plates, 260

  Tests for lead, 167

  Tetramethyl diphenyl test, 169

  Thorpe test, 275

  Tiles. See Earthenware

  Tinning: of hollow-ware, 259; of harness furniture, 259; of
  irondrums, 260; dust in, 203; lead chloride fume in, 202-203;
  repeated attacks in, 261

  Tolerance of lead, 28, 113

  Toxic dose: of lead acetate, 110; of lead carbonate, 110; of lead
  dust, 31, 207; of fritted lead dust, 88, 97; of white-lead dust, 85

  Treatment of acute lead poisoning, 111, 184

  Tremor, 142, 156

  Turpentine poisoning, experimental, 108

  Type metal, 202


  Urine: acidity, 181; chemical examination of, 180; determination of
  lead in, 167; lead in, 32, 73, 169; phosphates, 181


  Vaso-motor changes, 65, 76, 140

  Ventilation (exhaust), 207-220; by fans, 210; by heat, 208; composing
  boxes, 255; essential points, 208; in earthenware, 273; in electric
  accumulators, 216, 282; in enamelling, 278; in glass-cutting, 284;
  in india-rubber, 302; in lead smelting, 245; in litharge, 251; in
  paints, 215, 286; in printing foundry, 254; in red lead, 250; in
  spelter, 249; in tinning, 259; in vacuum cleaning, 218; in white
  lead, 214, 268; in yarn-heading, 300; smoke-test, 218

  Volatility of lead, 2


  Washing accommodation, 235

  Wasting in lead poisoning, 113, 115, 145

  Water, action on lead, 3, 4

  White lead: Brimsdown process, 269; casual labour in, 269; cause of
  dangers in, 266; chamber process, 268; diminution in reported cases,
  270; Dutch process, 265; precipitation process, 269; ventilation in,
  214

  Works’ medicines, 185

  Wrist-drop. See Paralysis


  Yarn-dyeing with chromate of lead, 298


  Zinc: action on kidney, 130; paints, 292, 294


BILLING AND SONS, LTD., PRINTERS, GUILDFORD




  Transcriber’s Notes


  The text used in this document is the one used in the source
  document, except as mentioned below. In particular, non-English words
  and phrases and titles and author names of references, and summations
  and other calculations in tables have not been corrected, unless
  mentioned below. Table numbering (or the lack thereof) has not been
  standardised.

  Depending on the hard- and software used to read this text and their
  settings, not all elements may display as intended.

  Page 1, 6: Stockhusen is probably an error for Stockhausen.

  Page 38, the reference to Goadby[13] points to a publication by
  Garrod.

  Page 52: hyperthenar eminence may be an error for hypothenar eminence.

  Page 64, ... se recontrant d’une manière diffuse ...: possibly an
  error for ... se rencontrant d’une manière diffuse ....

  Page 70, bottom row of Table IX: possibly the first column should
  read Average age at death.

  Page 220, Literature reference [5]: there is no footnote marker in
  the text.


  Changes made

  Tables and illustrations have been moved out of text paragraphs. Some
  of the tables have been re-arranged or split for legibility; ditto
  marks and the word Ditto have in several places been replaced with
  the dittoed text.

  Some obvious minor typographical and punctuation errors have been
  corrected silently.

  Page 3: ... mascicot and litharge ... changed to ... massicot and
  litharge ....

  Page 47, Table III bottom part: value for 1911 in the row Other
  industries changed from 8 to 88⁴ (based on the totals given).

  Page 61, Footnote [2]: Dr. John Tathan changed to Dr. John Tatham.

  Page 75: Pfleuger changed to Pflueger.

  Page 76: Seiffert changed to Seifert.

  Page 79, references [16] and [27]: Bleilähnung changed to
  Bleilähmung; reference [49]: les Maladies du Pois et Reins changed to
  les Maladies du Foie et des Reins.

  Page 88: eutetic entangling changed to eutectic entangling.

  Page 137: The footnote under second table
  (Furniture-Makers--Sand-Paperers) has been copied to under the first
  table (on Lead Sulphate Workers) for clarity.

  Page 151: _Electrical Reactions._ changed to =Electrical
  Reactions.=

  Page 169: magnese changed to manganese.

  Page 220: Leclere de Pulligny changed to Leclerc de Pulligny.