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LEAD POISONING AND LEAD ABSORPTION

INTERNATIONAL MEDICAL MONOGRAPHS

General Editors {

Leonard Hill, M.B., F.R.S.
William Bulloch, M.D.

THE VOLUMES ALREADY PUBLISHED OR IN
PREPARATION ARE:

THE MECHANICAL FACTORS OF DIGESTION. By Walter B. Cannon, A.M., M.D., George Higginson Professor of Physiology, Harvard University. [Ready.

SYPHILIS: FROM THE MODERN STANDPOINT. By James Macintosh, M.D., Grocers’ Research Scholar; and Paul Fildes, M.D., B.C., Assistant Bacteriologist to the London Hospital. [Ready.

BLOOD-VESSEL SURGERY AND ITS APPLICATIONS. By Charles Claude Guthrie, M.D., Ph.D., Professor of Physiology and Pharmacology, University of Pittsburgh, etc. [Ready.

CAISSON SICKNESS AND THE PHYSIOLOGY OF WORK in Compressed Air. By Leonard Hill, M.B., F.R.S., Lecturer on Physiology, London Hospital. [Ready.

LEAD POISONING AND LEAD ABSORPTION. By Thomas Legge, M.D., D.P.H., H.M. Medical Inspector of Factories, etc.; and Kenneth W. Goadby, D.P.H., Pathologist and Lecturer on Bacteriology, National Dental Hospital.

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

SHOCK: The Pathological Physiology of Some Modes of Dying. By Yandell Henderson, Ph.D., Professor of Physiology, Yale University.

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

DIABETES. By J. J. MacLeod, Professor of Physiology, Western Reserve Medical College, Cleveland, U.S.A.

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LONDON: EDWARD ARNOLD

New York: Longmans, Green & Co.

INTERNATIONAL MEDICAL MONOGRAPHS

General Editors {

Leonard Hill, M.B., F.R.S.
William Bulloch, M.D.

LEAD POISONING AND
LEAD ABSORPTION

THE
SYMPTOMS, PATHOLOGY AND PREVENTION,
WITH SPECIAL REFERENCE TO THEIR

INDUSTRIAL ORIGIN AND AN ACCOUNT OF THE
PRINCIPAL PROCESSES INVOLVING RISK

BY
THOMAS M. LEGGE, M.D. Oxon., D.P.H. Cantab.
H.M. MEDICAL INSPECTOR OF FACTORIES; LECTURER ON FACTORY HYGIENE
UNIVERSITY OF MANCHESTER

AND
KENNETH W. GOADBY, M.R.C.S., D.P.H. Cantab.
PATHOLOGIST AND LECTURER ON BACTERIOLOGY, NATIONAL DENTAL HOSPITAL
APPOINTED SURGEON TO CERTAIN SMELTING AND WHITE
LEAD FACTORIES IN EAST LONDON

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

GENERAL EDITORS’ PREFACE

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

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

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

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

LEONARD HILL.
WILLIAM BULLOCH.

September, 1912.

AUTHORS’ PREFACE

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

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

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

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

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

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

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

September, 1912.

CONTENTS

LIST OF PLATES

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.

[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:

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—

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:

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.

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.

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

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

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

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

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

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

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

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

Age.

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

Sex.

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

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

Predisposing Causes of Lead Poisoning.

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

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

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

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

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

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

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

Malnutrition.

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

Anæmia.

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

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

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

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

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

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

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

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

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

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

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

REFERENCES.

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

[ [2] Oliver, Sir T.: Diseases of Occupation, p. 142.

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

[ [4] Meillère and Richer: Meillère’s Le Saturnisme. Paris, 1903.

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

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

[ [7] Dixon Mann: British Medical Journal, 1893.

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

[ [9] Oliver, Sir T.: British Medical Journal, May 13, 1911, p. 1096.

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

[11] Oliver, Sir T.: Diseases of Occupation, p. 139.

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

[13] Garrod: The Lancet, 1870.

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

[15] Hunter, William: Severest Anæmias.

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

CHAPTER IV
STATISTICS OF PLUMBISM[A]

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

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

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

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

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

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

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

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

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

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.”

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

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:

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.

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.

Table VI.—Encephalopathy.

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.

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).

[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.

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

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.