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

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Title: 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

Author: Sir Thomas Morison Legge
Kenneth Weldon Goadby

Release date: December 3, 2023 [eBook #72301]

Language: English

Original publication: London: Edward Arnold, 1912

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LEAD POISONING AND LEAD ABSORPTION

INTERNATIONAL MEDICAL MONOGRAPHS
General Editors { LW
eonard Hill, M.B., F.R.S.
illiam Bulloch, M.D.

THE VOLUMES ALREADY PUBLISHED OR IN
P R E PA R A T I O N A R E :
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 Reserve Medical College, Cleveland, U.S.A.
A Descriptive Circular of the Series will be sent free on
application to the Publishers:
L O N D O N : E D WA R D A R N O L D
New York: Longmans, Green & Co.

INTERNATIONAL MEDICAL MONOGRAPHS
General Editors { LW
eonard Hill, M.B., F.R.S.
illiam 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
E D WA R D A R N O L D
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
Number
of Total Cases Cases Cases of
Exami- Cases of in Dusty in Other Suspen- Cases of Cases of
Year nations Poisoning Processes Processes sion Anæmia Tremor Blue 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 c.c. White lead, 10 grms. 3 days at 37° C. 0·1471 grm.
0·1 per cent. HCl

(b) 1·0 per cent. peptone
- 100 c.c. Metallic lead, 4 grms. „ 0·0330 „
0·1 per cent. HCl
(c) 0·1 per cent. HCl, 100 c.c. White lead, 10 grms. 0·0983 „
(d) 0·1 per cent. HCl, 100 c.c. Metallic lead, 4 grms. 0·0194 „
(e) 0·3 per cent. Na2CO3 Metallic lead, 4 grms. None
(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
[A]
STATISTICS OF PLUMBISM
[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 Cases.
Total
Industry. 1900-09. 1909. 1908. 1907. 1906. 1905. 1904. 1903. 1902. 1901. 1900.
(1) (2) (3) (4) (5) (6) (7) (8) (9) (10) (11) (12)
Lead poisoning 6,762275 55330 64632 57826 63233 59223 59726 61419 62914 86334 1,05838
1. Smelting of
metals 41218 665 702 282 381 241 331 372 28 543 341
2. Brass works 754 5 6 91 11 51 101 15 5 61 3
3. Sheet lead and
lead piping 1093 92 14 6 7 9 7 11 12 17 171
4. Plumbing and
soldering 21712 28 27 202 164 242 213 26 231 23 9
5. Printing 20017 211 302 263 162 194 15 132 19 231 182
6. File-cutting 21119 8 92 10 15 12 204 242 271 467 403
7. Tinning and
enamelling 1382 21 10 25 181 141 10 14 11 10 5
8. White lead 1,29531 322 793 71 1087 901 1162 1092 1431 1897 3586
9. Red lead 108 10 12 7 6 10 11 6 13 14 19
10. China and
earthenware 1,06557 585 11712 1038 1074 843 1064 973 874 1065 2008
10a. Litho-transfers 48 1 2 10 5 5 3 3 2 7 10
11. Glass cutting
and
polishing 489 42 31 4 41 3 — 4 82 113 7
12. Enamelling
iron plates 521 3 7 6 4 2 3 4 31 9 11
13. Electric
accumulators 2856 272 251 21 26 271 33 28 161 491 33
14. Paints and
colours 4227 392 25 351 37 571 321 391 46 56 561
15. Coach-building 69741 956 703 703 857 563 494 745 631 654 705
16. Ship-building 26910 271 15 221 261 322 48 241 151 281 322
17. Paint used in
other
industries 45218 42 471 492 373 492 273 461 441 61 505
18. Other
industries 65920 572 785 562 662 701 533 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 37 2 251
Printing 32 2 334

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 366 212
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. Number of Attack.
Third,
No. Occupation. Total. Severe. Moderate. Slight. First. Second. Chron
(1) (2) (3) (4) (5) (6) (7) (8) (9)
M. F. M. F. M. F. M. F. M. F. M. F. M.
1 Smelting of
metals:
Cases 411 — 104 — 105 — 197 — 276 — 65 — 64
Per cent. 100 — 25·3 — 25·6 — 47·9 — 67·2 — 16·8 — 15·6
2 Brass works:
Cases 70 4 26 2 20 1 22 1 40 3 11 1 17
Per cent. 100 — 37·1 — 28·6 — 31·5 — 57·1 — 15·7 — 24·3
3 Sheet lead and
lead piping:
Cases 102 4 25 1 29 1 47 2 72 3 17 — 11
Per cent. 100 — 24·5 — 28·4 — 46·1 — 70·6 — 16·7 — 10·8
4 Plumbing and
soldering:
Cases 186 30 65 6 49 6 65 16 114 22 30 1 32
Per cent. 100 100 34·9 20·0 26·3 20·0 34·9 53·3 61·3 73·3 16·1 3·3 17·2 1
5 Printing:
Cases 190 6 55 — 43 1 82 5 118 6 29 — 33
Per cent. 100 — 28·9 — 22·6 — 43·2 — 62·1 — 15·3 — 17·4
6 File-cutting:
Cases 174 34 85 8 34 5 48 21 49 24 39 4 78
Per cent. 100 100 48·9 23·5 19·5 14·7 27·6 61·8 28·2 70·6 22·4 11·8 44·8 1
7 Tinning and
enamelling of
hollow-ware:
Cases 84 53 26 13 27 16 31 24 50 31 18 16 15

Per cent. 100 100 31·0 24·5 32·1 30·2 36·9 45·3 59·5 58·5 21·4 30·2 17·9 1
8 White lead:
Cases 1,167 76 317 27 235 11 593 33 961 56 108 9 49
Per cent. 100 100 27·2 35·5 20·1 14·5 50·8 43·4 82·4 73·7 9·3 11·8 4·2
9 Red lead:
Cases 108 — 30 — 31 — 45 — 90 — 8 — 8
Per cent. 100 — 27·8 — 28·7 — 41·7 — 83·3 — 7·4 — 7·4
10 China and
earthenware:
Cases 490 572 102 86 158 181 216 286 297 469 91 65 87
Per cent. 100 100 20·8 15·0 32·2 31·6 44·1 50·0 60·6 82·0 18·6 11·4 17·7
10a Litho-
transferers:
Cases 20 28 2 5 2 8 15 15 17 27 2 — —
Per cent. 100 100 10·0 17·9 10·0 28·6 75·0 53·6 85·0 96·4 10·0 — —
11 Glass cutting
and
polishing:
Cases 47 — 20 — 11 — 16 — 21 — 9 — 17
Per cent. 100 — 42·5 — 23·4 — 34·0 — 44·7 — 19·1 — 36·2
12 Enamelling of
iron plates:
Cases 38 14 6 6 19 4 13 3 31 11 7 2 —
Per cent. 100 100 15·8 42·9 50·0 28·6 34·2 21·4 81·6 78·6 18·4 14·3 —
13 Electric
accumulators:
Cases 281 — 58 — 70 — 151 — 222 — 40 — 13
Per cent. 100 — 20·6 — 24·9 — 53·7 — 79·0 — 14·2 — 4·6
14 Paint and colour
works:
Cases 397 21 111 2 104 4 176 15 290 16 61 3 39
Per cent. 100 100 27·9 9·5 26·2 19·0 44·4 71·5 73·1 76·2 15·4 14·3 9·8
15 Coach-making:
Cases 678 3 176 — 187 2 293 1 405 2 127 — 114
Per cent. 100 — 26·0 — 27·6 — 43·2 — 59·8 — 18·7 — 16·8
16 Ship-building:
Cases 261 — 93 — 51 — 108 — 181 — 41 — 24
Per cent. 100 — 35·6 — 19·5 — 41·4 — 69·0 — 15·7 — 9·2
17 Paints used in
other
industries:
Cases 405 42 127 11 97 7 174 22 238 36 83 4 71
Per cent. 100 100 31·4 26·2 23·9 16·7 43·0 52·4 58·8 85·7 20·5 9·5 17·5
18 Other
industries:
Cases 528 114 160 37 117 22 230 52 329 93 85 14 86
Per cent. 100 100 30·3 32·5 22·2 19·3 43·6 45·6 62·3 81·6 16·1 12·3 16·3
Total cases 5,637 1,001 1,588 204 1,389 269 2,522 496 3,800 799 871 119 758
„ per cent. 100 100 28·2 20·4 24·7 26·9 44·7 49·5 67·4 79·8 15·5 11·9 13·4

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:
Age Duration of
Distribution. Employment.
Under Over Under Over
Industry. 30. 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.

Form of Paralysis. 1910. 1911.
Paralysis. Weakness Total. Paralysis. Weakness Total.
of Arms of Arms

or Loss or Loss
of Power. of Power.
(1) (2) (3) (4) (5) (6) (7)
complete — — — 2 — 2
Arms and legs -
partial 4 6 10 1 4 5

complete — — — — — —
Legs -
partial 4 4 8 — 6 6

complete 15 — 15 27 — 27
Both forearms -
partial 19 30 49 20 44 64

complete 8 — 8 5 — 5
Right forearm -
partial 6 4 10 4 7 11

complete 3 — 3 2 — 2
Left 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)

complete 12 2 2 1 2 1 4
Arms and legs -
partial 62 13 7 9 13 9 11

complete 3 — — 1 — 1 1
Legs -
partial 25 5 7 1 3 5 4

complete 162 29 33 29 28 24 19
Both forearms -
partial 334 59 70 56 56 43 50

complete 39 11 6 7 4 8 3
Right forearm -
partial 62 9 17 14 11 5 6

complete 14 2 2 4 1 3 2
Left forearm -
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 Number of Attack
Exami- Persons Reported Rate per
Industry. nations. 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).
Processes. Persons Attack-Rate per
employed Cases Reported: Thousand employed:
in 1907. Average per Year. Average per Year.

1907- 1903- 1899- 1907- 1903- 1899-
1910. 1906. 1902. 1910.[A] 1906.[B] 1902.[C]
In dipping-house:
M. 786 17 18 26 22 23 34
Dippers -
F. 150 6 4 7 40 30 68

M. 463 3 3 7 7 7 15
Dippers’ assistants -
F. 397 13 18 17 33 46 45

M. 115 1 2 3 9 20 30
Ware-cleaners -
F. 461 15 18 30 33 41 65

M. 1,346 21 23 36 15 17 27
Total -
F. 1,008 34 40 54 34 42 58

M. 2,291 16 12 33 7 5 14
Glost-placers -
F. 120 1 1 1 8 10 14

M. 28 — — — — — —
Majolica-painters -
F. 358 6 8 10 13 14 20

M. 58 1 — 1 17 — 17
Ground-layers -
F. 157 1 1 4 6 5 13

M. 14 — — — — — —
Colour and litho dusters -
F. 143 — 1 4 — 7 33

Enamel colour and glaze M. 51 — — 1 — — 36
-
blowers F. 288 3 3 2 10 14 12

Colour-makers and millers and M. 371 5 5 6 13 13 17
-
mixers of glaze or colour F. 55 1 1 1 18 48 114

Other persons in contact with M. 327 2 1 2 6 5 11
-
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.

Pneumonia,
Bronchitis,
Heart
Failure,
Cerebral Colic,
Encepha- Bright’s Hæmor- Lead Hernia, and
Industry. lopathy. Disease. rhage. Paralysis. Poisoning. Phthisis. Aneurism. Total.
(1) (2) (3) (4) (5) (6) (7) (8) (9)
Smelting of metals 1 6 — 3 5 1 1 17
Brass works — 3 — 1 1 — 1 6
Sheet lead and lead
piping — 1 — — 1 — 1 3
Plumbing and
soldering 2 3 — 1 2 1 2 11
Printing 3 3 — 2 5 1 3 17
File-cutting 1 11 2 2 2 1 — 19
Tinning and
enamelling — 1 — — 1 — — 2
White lead 13 2 2 4 2 1 3 27
China and
earthenware 8 24 14 3 6 2 — 57
Glass-cutting 1 6 — — 1 — 1 9
Electric
accumulators 2 1 — 1 — — 2 6
Paints and colours 4 1 — — 2 1 3 11
Coach-making 1 8 5 6 10 3 4 37
Ship-building 1 4 1 — 1 1 — 8
Paints used in other
industries — 3 1 4 6 1 2 17
Other industries 1 2 1 — 11 — 2 17
Total 38 79 26 27 56 13 25 264
Average at death 32 43 47 43 44 38 40 —

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

Causes of Death.
Diseases Diseases Diseases Other
Diseases of the of the of the Diseases
of the Circu- Respi- Diges- of the
All Alco- Phthi- Nervous latory ratory tive Bright’s Urinary
Occupation. Causes. holism. Gout. sis. System. System. System. System. Disease. System.

(1) (2) (3) (4) (5) (6) (7) (8) (9) (10) (11)
All males 1,000 16 2 186 105 145 174 57 35 17
Printer 994 8 3 300 111 125 131 55 42 15
File-maker 1,700 14 — 387 225 198 325 78 134 26
Copper-
worker 1,090 7 3 162 104 139 357 45 24 21
Lead-
worker 1,408 38 — 165 134 222 309 14 160 —
Coach-
maker 824 4 4 129 113 129 150 46 39 14
Earthenware 1,493 8 — 285 131 219 473 57 33 20
Glass 1,260 7 4 283 131 177 268 54 58 16
Painter and
plumber 1,114 13 8 213 133 105 168 31 74 20

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
[A]
PATHOLOGY—Continued
[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.
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

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.

Fig. 2.—Intestinal Ulceration in
Turpentine Poisoning. (Stained
Eosin and Hæmatoxylin.) × 250.

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

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.

Fig. 2.—Lung of Animal exposed to
Turpentine Vapour. (Stained
Hæmatoxylin and Eosin.) × 250.

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

Fig. 1.—Kidney of Animal poisoned
with White Lead (Inhalation),
showing Microscopical
Hæmorrhages. (Stained
Hæmatoxylin and Eosin.) × 250.

Fig. 2.—Kidney of Man dying of
Chronic Lead Poisoning. (Stained
Hæmatoxylin and Eosin.) × 250.

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.

Date of
No. of Total Compound used Number of First
Animal. Weight. and Quantity. Inoculations. Symptoms. Duration. Result. W
Kgs.
16 3·200 0·91 grm. lead 3 Forty-fifth day 47 days Died
acetate: (1) 0·16; encephalopathy
(2) 0·5; (3) 0·25
25 3·350 Fritted lead: (1) 0·6; 2 Twenty-sixth day 26 days Killed
(2) 2·0 = 2·6 grms. slight paralysis
of left hind-
limb
28 3·050 2 grms. white lead 1 Fourth day 23 days Died W
aborted
a
31 3·450 0·35 grm. white lead — No symptoms 1 year Recovered
32 2·900 0·3 grm. frit 1 Eleventh day stiff 28 days Paralysis;
joint; stepping died
not normal

33 3·150 0·16 grm. PbO as 1 Fifteenth day 22 days Paralysis;
acetate paralysis killed
35 3·750 2·0 grms. water- 1 Ninth day aborted 1 year Recovered,
washed frit but thin
40 3·050 1·0 grm. unwashed 1 Forty-seventh day 58 days Died
frit some muscular
weakness
41 3·000 1·0 grm. acetic acid 1 No symptoms 5 months Recovered
and water-washed
frit
42 2·800 1·0 grm. water- 1 No symptoms 4 months Recovered
washed frit
43 2·900 Lead nitrate in water: — Thirtieth day 5 months Died
0·01 grm. per diem encephalopathy

TABLE XII.—FEEDING EXPERIMENTS.

Total
Duration
No. of Compound of Other First Appearance of of
Animal. Weight. Pb used. Substance. Poisoning Symptoms. Experiment. Result.
Kgs.
2 2·750 0·5 to 0·1 None Vomited fifth day; no 2 months Recovered
grm. flue other symptoms
dust (55
per cent.
PbO) from
blast-
furnace
flue
9a 3·500 0·5 grm. dry None Vomited fifth day; no 2 months —
white lead other symptoms
11a 3·850 0·8 grm. None None 8 months —
3·900 After 8 50 c.c. 1 month 2 months Died
months alcohol (encephalopath
given (port
alcohol wine)
12 3·800 0·8 grm. dry 50 c.c. 1 month slight 38 days Died
white lead port paralysis (encephalopath
wine
13 3·400 0·8 grm. dry None None 18 months Recovered
white lead

14 3·650 0·4 grm. low- None None 8 months Given port wine
solubility
frit
3·730 0·4 grm. low- 50 c.c. 6 months 1 year Died cerebral
solubility port encephalopathy symptoms
frit and wine
alcohol
23 4·100 1 grm. high- None None 1 year No symptoms
solubility
glaze
4·600 Given lead None None 5 months No symptoms
nitrate, except loss of
0·01 to 0·1 weight
grm.
24 2·900 1 grm. high- None None 6 months Recovered
solubility
glaze
46 2·150 0·1 grm. lead None 4 months 4 months Died cerebral
nitrate in opisthotonus symptoms
water
47 2·100 0·1 grm. lead None None 4 months Recovered[A]
nitrate in
milk
49 2·500 2 grs. acetate None None 3 months Recovered[A]
in keratin
pill
15 2·950 Control no None None 1 year No symptoms due
lead to confinement
in cage

[A] Increased in weight.

TABLE XIII.—INHALATION EXPERIMENTS.

Compound of Lead in Dust and
No. of Average Quantity in Air Number of Day of Duration
Animal. Weight. during Experiment. Method. Inhalations. First Symptoms. of Series
Kgs.
1 3·000 0·007 to 0·01 grm. flue dust A 11 of 1 13 days (4 2 month
from blast-furnace flue hour inhalations)

2 3·580 0·007 to 0·01 grm. litharge A 12 15 days (5 2 month
dust inhalations)

4 4·100 0·001 to 0·007 grm. white lead A 12 37 days (12 2 month
dust inhalations)

6 5·200 0·001 to 0·007 grm. white lead A 12 12 days (4 2 month
(alcohol: 50 c.c. port wine inhalations)
daily in milk)
7 3·000 0·001 to 0·007 grm. white A 11 30 days (9 2 month
lead; no alcohol inhalations)
10 4·500 0·0001 to 0·001 grm. white B 40 of 20 120 days (30 144 days
lead minutes inhalations)
11 3·750 0·0001 to 0·001 grm. white B 40 of 20 120 days (30 144 days
lead minutes inhalations)
21 3·900 0·001 to 0·09 grm. low- B 14 of 1 42 days (14 42 days
solubility glaze hour inhalations)
22 3·900 0·001 to 0·09 grm. low- B 26 60 80 days
solubility glaze
30 3·500 0·001 to 0·09 grm. low- B 14 45 45 days
solubility glaze

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. Work. Notes
Per
Cent.
1 60 3,460,000 7,000 0·7 63 20 6 3 8 0 + - + - + Paint mill 5 years
2 45 1,707,000 9,000 1·4 46 38 8 1 7 0 + + + + + Paint mill 10 year
3 55 2,620,000 20,000 1·0 58 32 4 2 4 0 + - + - + Paint mill 7 years
4 60 1,334,000 10,000 3·0 55 35 8 0 5 0 + - + + + Packer white 5 years
lead
5 54 3,210,000 8,000 0·9 52 41 4 2 1 0 + + + - + Grinder 6 years
6 60 1,347,000 10,000 3·0 59 32 3 2 3 1 + + + + + White lead 8 years
7 65 3,760,000 9,000 0·9 Press and 8 years
stoves
8 65 2,200,000 10,000 0·7 + + Zinc 20 year
distillation doub
still wris
drop
year

9 50 3,860,000 8,000 0·6 - + + White lead 10 year
beds
10 60 3,420,000 9,000 1·0 76 16 13 3 0 0 + + 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 + + - - + +

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. Faradism. Remarks.
M.A. M.A.
R. Deltoid K.C.C. 8 A.C.C. 8 Good Evidently extensor
(anterior communis digitorum
portion) on right side is
L. Deltoid K.C.C. 6 A.C.C. 9 Good completely
(anterior degenerated. First
portion) interosseous on right
side show reactions
R. Deltoid K.C.C. 6 A.C.C. 9 Good of degeneration. On
(posterior left side extensor
portion) communis digitorum
L. Deltoid Good shows normal but
(posterior feeble contractions
portion)
R. Supinator K.C.C. 6 A.C.C. 10 Reaction Good
longus brisk
L. Supinator K.C.C. 5 A.C.C. 6 Reaction Good
longus brisk
R. Extensor No reactions either A.C.C. or K.C.C.[15] No
communis reaction
digitorum
L. Extensor K.C.C. 8 A.C.C. 12 Brisk, but Feeble
communis feeble reaction
digitorum
R. Extensor K.C.C. none A.C.C. 13 Brisk Good
primi at
internodii 13
pollicis
L. Extensor K.C.C. 6 A.C.C. 12 Reaction Good (but
primi brisk less

internodii than
pollicis right)
R. Extensor K.C.C. 8 A.C.C. 8 Brisk Good
carpi ulnaris Contraction
L. Extensor K.C.C. 8 A.C.C. 12 Brisk Good
carpi ulnaris Contraction
R. First K.C.C. 8 A.C.C. 6 Contraction No
interosseous slow reaction
L. First K.C.C. 6 A.C.C. 6 Brisk Good
interosseous contraction
R. Second K.C.C. 8 A.C.C. 10 Brisk Slight
interosseous Contraction reaction
L. Second K.C.C. 6 A.C.C. 8 Brisk Good
interosseous Contraction
R. Third K.C.C. 9 A.C.C. 6 Brisk Slight
interosseous Contraction reaction
L. Third K.C.C. 6 A.C.C. 8 Brisk Slight
interosseous Contraction reaction
R. Fourth K.C.C. 8 A.C.C. 6 Brisk Slight
interosseous Contraction reaction
L. Fourth K.C.C. 10 A.C.C. 9 Brisk Good
interosseous Contraction

ELECTRICAL REACTIONS IN LEAD PARALYSIS. (CASE 2.)

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

Occupation. Estimated Time Approximate Percentage Remarks.
Present in (in Hours) Quantities of Lead
10 Cubic Metres during which of Lead (Pb) in Dust.
of Air Inhalation expressed
(Milligrammes). took place. in Milligrammes
inhaled by

Worker
Total Lead per Day.
Dust. (Pb).
(1) (2) (3) (4) (5) (6) (7)
Tinner using — 37·79 5¹⁄₂ 10·70 — The whole
open bath inhaled in the
form of vapour
of lead or
similar
compound.
Tinner using — 6·36 5¹⁄₂ 1·80 — The whole
bath inhaled in the
covered by form of vapour
hood, and of lead or
having similar
fumes compound.
exhausted
by draught
of furnace
Wiping off — 124·31 5¹⁄₂ 35·20 — 14·1
(tinning) milligrammes
of metallic lead
inhaled as lead
chloride, and
21·1
milligrammes
as metallic lead
adhering to
floating fibres
of tow.
Earthenware 38 1·80 7¹⁄₂ 0·69 (average of 8·30 Dipping boards
dipping 4 expts.) not used.
(pottery)
Earthenware 84 6·27 7¹⁄₂ 2·40 (single 7·42 Very dirty dipping
dipping expt.) boards used.
(pottery) Work very
rapid, and
much shaking
of ware after
dipping.
China 36 2·12 7³⁄₄ 0·83 (average of 5·43 China glaze
dipping 4 expts.) usually
(pottery) contains about
two-thirds as
much lead as
that of
earthenware.

Rockingham 44 2·26 7¹⁄₂ 0·86 (single 14·37 Dirty dipping
ware expt.) boards in use.
dipping Glaze contains
(pottery) three times as
much lead as
ordinary
earthenware
glaze, but the
ware is not
shaken after
dipping.
Earthenware 47 2·29 7¹⁄₂ 0·88 (average of 5·90 Cleaning done in
cleaning 7 expts.) or at front of
(pottery) exhaust hood.
China ware 123 13·34 6 4·08 (single 10·85 Very defective
cleaning expt.) exhaust; hood
(pottery) so arranged that
cleaning had to
be done
outside. Glaze
contains about
two-thirds as
much lead as
that for
earthenware.
Earthenware 25 2·19 8 0·92 (average of 8·58 Filter placed at
drying 3 expts.) breathing level
(pottery) in centre of
drying stillage.
Earthenware 34 2·08 8³⁄₄ 0·93 (average of 6·58
glost 3 expts.)
placing
(pottery)
China glost 30 1·08 9 0·50 (single 3·64 Boards used were
placing expt.) fairly dirty.
(pottery)
China glost 21 0·32 9¹⁄₂ 0·16 (single 1·50 One man only
placing expt.) working.
(pottery)
Majolica- 61 9·11 7¹⁄₂ 3·48 (single 15·00 Tiles cleaned,
painting of expt.) while still
tiles damp, with
(pottery) knife. Much
dry waste glaze
on wooden
floor, and much
traffic. Several

cases of lead
poisoning in
this room.
206 53·70 — — 26·10 Passenger fish
truck after one
Sand- coat of lead
papering colour.
and
- ​ 241 116·10 — — 48·10 Railway coach
dusting
railway after one coat
coaches of lead colour
on filled and
faced surface.

453 83·10 — — 18·30 After two coats of
quick-drying
Sand- white lead
papering paint.
-​
coach 1343 1025·60 — — 76·40 Old cream-
wheels painted wheel
before
repainting.
Sand- 600 278·30 — — 46·40 Door of motor
papering body after one
motor-car coat of lead
body colour and
quick-drying
sand-paper
stopping.
Urgent work.
88 38·70 — — 44·00 Wooden motor
wheels after
two coats of
lead colour and
Sand- sand-papering
papering between.
-​
motor-car Exhaust not
wheels running.
35 4·70 — — 13·30 Same point, but
with exhaust
running.