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§ 778. Statistics of Lead-Poisoning.—In the ten years, 1883 to 1892, no less than 1043 persons died from the effects of lead; of these, 3 only were suicidal, the remaining 1040 were mainly from the manufacture of white lead or from the use of lead in the arts or from the accidental contamination of food or drink.

The following table shows in what manner the 1040 were distributed as to age and sex:—

DEATHS FROM LEAD-POISONING IN ENGLAND AND WALES DURING THE TEN YEARS 1883-1892.

Ages,	0-1	1-5	5-15	15-25	25-65	65 and above	Total
Males,	...	4	14	44	733	36	831
Females,	3	5	...	68	129	4	209
Total,	3	9	14	112	862	40	1040

§ 779. Lead as a Poison.—All the compounds of lead are said to be poisonous; but this statement cannot be regarded as entirely correct, for the sulphocyanide has been proved by experiment not to be so,[823] and the sulphide is also probably inactive. In the treatment of cases of lead-poisoning, the flowers of sulphur given internally appear to be successful.[824]

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Lead-poisoning, either in its obscure form (producing uric acid in the blood, and, as a consequence, indigestion and other evils), or in the acute form (as lead colic and various nervous affections), is most frequent among those who are habitually exposed to the influence of the metal in its different preparations, viz., workers of lead, house-painters, artists, gilders, workers of arsenic, workers of gold, calico-printers, colourists, type-founders, type-setters, shot-founders, potters, faience makers, braziers, and many others.[825] In white-lead factories so large a number of the employés suffer from poisoning that it has excited more than once the attention of the Government.[826]

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Lead, again, has been found by the analyst in most of the ordinary foods, such as flour, bread, beer, cider, wines, spirits, tea, vinegar, sugar, confectionery, &c., as well as in numerous drugs, especially those manufactured by the aid of sulphuric acid (the latter nearly always containing lead), and those salts or chemical products which (like citric and tartaric acids) are crystallised in leaden pans. Hence it follows that in almost everything eaten or drunk the analyst, as a matter of routine, tests for lead. The channels through which it may enter into the system are, however, so perfectly familiar to practical chemists, that a few unusual instances of lead-poisoning only need be quoted here.

A cabman suffered from lead colic, traced to his taking the first glass of beer every morning at a certain public-house; the beer standing in the pipes all night, as proved by analysis, was strongly impregnated with lead.[827]

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The employment of red lead for repairing the joints of steam pipes has before now caused poisonous symptoms from volatilisation of lead.[828] The use of old painted wood in a baker’s oven, and subsequent adherence of the oxide of lead to the outside of the loaves, has caused the illness of sixty-six people.[829]

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Seven persons became affected with lead-poisoning through horse-hair coloured with lead.[830]

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The manufacture of American overland cloth creates a white-lead dust, which has caused serious symptoms among the workmen (Dr. G. Johnson). The cleaning of pewter pots,[831] the handling of vulcanised rubber,[832] the wrapping up of various foods in tinfoil,[833] and the fingering of lead counters covered with brine by fishmongers, have all caused accidents in men.

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The lead in glass, though in the form of an insoluble silicate, is said to have been dissolved by vinegar and other acid fluids to a dangerous extent. This, however, is hardly well established.[834]

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§ 780. Effects of Lead Compounds on Animals.—Orfila and the older school of toxicologists made a number of experiments on the action of sugar of lead and other compounds, but they are of little value for elucidating the physiological or toxic action of lead, because they were, for the most part, made under unnatural conditions, the gullet being ligatured to avoid expulsion of the salt by vomiting. Harnack, in order to avoid the local and corrosive effects of sugar of lead, used an organic compound, viz., plumbic triethyl acetate, which has no local action. Frogs exhibited symptoms after subcutaneous doses of from 2 to 3 mgrms., rabbits after 40 mgrms.; there was increased peristaltic action of the intestines, with spasmodic contraction rising to colic, very often diarrhœa, and death followed through heart paralysis. Dogs given the ethyl compound exhibited nervous symptoms like chorea. Gusserno[835] has also made experiments on animals as to the effects of lead, using lead phosphate, and giving from 1·2 grm. to a rabbit and a dog daily. Rosenstein[836] and Heubel[837] used small doses of acetate, the latter giving dogs daily from ·2 to ·5 grm. The results arrived at by Gusserno were, mainly, that the animals became emaciated, shivered, and had some paralysis of the hinder extremities; while Rosenstein observed towards the end epileptiform convulsions, and Heubel alone saw, in a few of his cases, colic. A considerable number of cattle have been poisoned from time to time with lead, and one instance of this fell under my own observation. A pasture had been manured with refuse from a plumber’s yard, and pieces of paint were in this way strewn about the field in every direction; a herd of fifteen young cattle were placed in the field, and in two or three days they all, without exception, began rapidly to lose condition, and to show peculiar symptoms—diarrhœa, loss of appetite; in two, blindness, the retina presenting an appearance not unlike that seen in Bright’s disease; in three, a sort of delirium. Four died, and showed on post-mortem examination granular conditions of the kidneys, which was the most striking change observable. In the fatal cases, paralysis of the hind extremities, coma, and convulsions preceded death. In another case[838] seven cows and a bull died from eating lead paint; the symptoms were loss of appetite, obstinate constipation, suspension of rumination, dry muffle, quick breathing, and coma. In other cases a marked symptom has been paralysis. Cattle[839] have also several times been poisoned from eating grass which has been splashed by the spray from bullets, as in pastures in the vicinity of rifle butts; here we must allow that the intestinal juices have dissolved the metal, and transformed it into compounds capable of being taken into the system.

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§ 781. Effects of Lead Compounds on Man—Acute Poisoning.—Acute poisoning by preparations of lead is not common, and, when it does occur, is seldom fatal. With regard to the common acetate, it would seem that a large single dose is less likely to destroy life than smaller quantities given in divided doses for a considerable period. The symptoms produced by a considerable dose of sugar of lead usually commence within a few minutes; there is immediately a metallic taste, with burning, and a sensation of great dryness in the mouth and throat; vomiting, which occurs usually within fifteen minutes, is in very rare cases delayed from one to two hours. The retching and vomiting are very obstinate, and continue for a long time; the matters thrown up are sometimes streaked with blood; there is pain in the abdomen of a colicky character—a pain relieved by pressure. The bowels are, as a rule, constipated, but occasionally relaxed. The stools at a later date are black from the presence of lead sulphide. The urine, as a rule, is diminished. The breath has a foul odour, and the tongue is coated; the skin is dry, and the pulse small and frequent. The full development of the toxic action is completed by the appearance of various nervous phenomena—headache, shooting pains in the limbs, cramps in the legs, and local numbness. All the symptoms enumerated are not present in each case; the most constant are the vomiting and the colic. If the sufferer is to die, death occurs about the second or third day. If the patient recovers, convalescence may be much retarded, as shown in the case of two girls,[840] who had each swallowed an ounce of lead acetate by mistake, and who suffered even after the lapse of a year from pain and tenderness in the stomach and sickness.

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There are “mass-poisonings” by acetate of lead on record, which afford considerable insight into the varying action of this salt on different individuals. A case (e.g.) occurred at Stourbridge in 1840,[841] in which no less than 500 people were poisoned by thirty pounds of lead acetate being accidentally mixed with eighty sacks of flour at a miller’s. The symptoms commenced after a few days; constriction of the throat, cramping and twisting pains round the umbilicus, rigidity of the abdominal muscles, dragging pains at the loins, cramps and paralysis of the lower extremities. There was obstinate constipation; the urine was scanty and of a deep red colour, and the secretions were generally arrested; the pulse was slow and feeble; the countenance depressed, often livid; and the gums showed the usual blue line. The temperature of the skin was low. In only a few cases was there sickness, and in these it soon ceased. It is curious that not one of the 500 cases proved fatal, although some of the victims were extremely ill, and their condition alarming. It was specially observed that, after apparent convalescence, the symptoms, without any obvious cause, suddenly returned, and this even in a more aggravated form. Remittance of this kind is of medico-legal import; it might, for example, be wrongly inferred that a fresh dose had been taken. In the 500 cases there were no inflammatory symptoms; complete recovery took some time. On examining the bread the poison was found so unequally distributed that no idea could be formed as to the actual amount taken.

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There is also recorded[842] an outbreak of lead-poisoning among 150 men of the 7th Infantry at Tione, in the Southern Tyrol. One case proved fatal, forty-five required treatment in hospital. The symptoms were pallor, a blue line in the gums, metallic taste in the mouth, a peculiar odour of the breath, a loaded tongue with a bluish tint, obstinate constipation with loss of appetite whilst all complained, in addition, of dragging of the limbs and of the muscles of the chest, and difficulty of breathing. In the severer cases there were tetanic spasms, muscular tremors, and anæsthesia of the fingers and toes. The pulse and temperature were normal, save in a few cases in which there were fever and sweats at night. In none was there colic, but the constipation was obstinate. In two of the worst cases there was strangury. Acute cases occur occasionally from poisoning by the carbonate of lead. Dr. Snow recorded an instance (in 1844) of a child who had eaten a piece as big as a marble, ground up with oil. For three days the child suffered from pain in the abdomen and vomiting, and died ninety hours after taking the poison. In another case, in which a young man took from 19 to 20 grms. of lead carbonate in mistake for chalk as a remedy for heartburn, the symptoms of vomiting, pain in the stomach, &c., commenced after a few hours; but, under treatment with magnesic sulphate, he recovered.

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The chromate of lead is still more poisonous (see Art. “Chromium”).

§ 782. Chronic Poisoning by Lead.—Chronic poisoning by lead—often caused by strange and unsuspected channels, more frequently an incident, nay, almost a necessity, of certain trades, and occasionally induced by a cunning criminal for the purpose of simulating natural disease—is of great toxicological and hygienic importance. In the white-lead trade it is, as might be expected, most frequently witnessed; but also in all occupations which involve the daily use of lead in almost any shape. The chief signs of chronic poisoning are those of general ill-health; the digestion is disturbed, the appetite lessened, the bowels obstinately confined, the skin assumes a peculiar yellowish hue, and sometimes the sufferer is jaundiced. The gums show a black line from two to three lines in breadth, which microscopical examination and chemical tests alike show to be composed of sulphide of lead; occasionally the teeth turn black.[843] The pulse is slow, and all secretions are diminished. Pregnant women have a tendency to abort. There are also special symptoms, one of the most prominent of which is often lead colic.

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In 142 cases of lead-poisoning, treated between 1852 and 1862 at the Jacob’s Hospital, Leipzig, forty-four patients (or about 31 per cent.) suffered from colic. Arthralgia—that is, pains in the joints—is also very common; it seldom occurs alone, but in combination with other symptoms. Thus, in seventy-five cases of lead-arthralgia treated at Jacob’s Hospital, in only seven were pain in the joints without other complications, fifty-six being accompanied by colic, five by paralysis, and seven by other affections of the nervous system. The total percentage of cases of lead-poisoning, in which arthralgia occurs, varies from 32 to 57 per cent.

Paralysis, in some form or other, Tanqueril[844] found in 5 to 8 per cent. of the cases, and noticed that it occurred as early as the third day after working in lead. The muscles affected are usually those of the upper extremity, then the legs, and still more rarely the muscles of the trunk. It is only exceptionally that the paralysis extends over an entire limb; it more usually affects a muscular group, or even a single muscle. Its common seat is the extensors of the hand and fingers; hence the expression “dropped-wrist,” for the hands droop, and occasionally the triceps and the deltoid are affected. The paralysis is usually symmetrical on both sides. Although the extensors are affected most, the flexors nearly always participate, and a careful investigation will show that they are weakened. If the paralysis continues, there is a wasting and degeneration of the muscle, but this is seen in paralysis from any cause. The muscular affection may cause deformities in the hands, shoulders, &c. Anæsthesia of portions of the skin is generally present in a greater or less degree. A complete analgesia affecting the whole body has been noticed to such an extent that there was absolute insensibility to burns or punctures; but it is usually confined to the right half of the body, and is especially intense in the right hand and wrist.

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§ 783. The older writers recognised the toxic effect of lead on the nervous system. Thus Dioscorides speaks of delirium produced by lead, Aretaeus of epilepsy, and Paul of Ægina refers to it as a factor of epilepsy and convulsions. But in 1830, Tanqueril first definitely described the production of a mental disease, which he called “lead encephalopathy.” This he divided into four forms—(1) a delirious form; (2) a comatose; (3) a convulsive; and (4) a combined form, comprising the delirious, convulsive, and comatose. Dr. Henry Rayner,[845] and a few other English alienists, have directed their attention to this question; and, according to Dr. Rayner’s researches, the number of male patients admitted into Hanwell Asylum, engaged in trades such as plumbing, painting, and the like, is larger in proportion to the number admitted from other trades than it should be, compared with the proportion of the various trades in the county of Middlesex, as ascertained from the census. Putting aside coarse lead-poisoning, which may occasionally produce acute mania, the insanity produced by prolonged minute lead intoxications possesses some peculiar features. It develops slowly, and in nearly all cases there are illusions of the senses, of hearing, taste, or smell, and especially of sight. Thus, in one of Dr. Rayner’s cases the patient saw round him “wind-bags blown out to look like men,” apparitions which made remarks to him, and generally worried him. Besides this form, there is also another which closely resembles general paralysis, and, in the absence of the history, might be mistaken for it.

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§ 784. The degenerative influence on the organ of sight is shown in six of Dr. Robertson’s patients, whose insanity was ascribed to lead—four of the six were either totally or partially blind.

The amaurosis has been known to come on suddenly, and after a very brief exposure to lead, e.g., a man, thirty-four years of age, after working for three days in a white-lead factory, was seized with intense ciliary neuralgia, had pains in his limbs and symptoms of lead-poisoning, and the right eye became amaurotic.[846] This form of impairment or loss of vision is different from the Retinitis albuminurica,[847] which may also be produced as a secondary effect of the poison; the kidneys in such cases being profoundly affected. The kind of diseased kidney produced by lead is the granular contracted kidney.

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Eulenberg speaks of the sexual functions being weakened, leading to more or less impotence.

Lewy,[848] in 1186 patients suffering from lead-poisoning, has found caries or necrosis in twenty-two cases, or about 1·8 per cent.; fifteen were carious affections of the upper jaw, four of the fore-arm, two of the thigh, and one of the rib and sternum. Epilepsy and epileptiform convulsions occur in a few cases; it is very possible that the epilepsy may be a result of the uræmic poisoning induced by diseased kidneys.

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Five cases of fatal poisoning occurred between 1884-6 among the employés of a certain white-lead factory in the east of London. The cases presented the following common characters. They were all adult women, aged from 18 to 33, and they had worked at the factory for short periods, from three to twelve months. They all exhibited mild symptoms of plumbism, such as a blue line round the gums, and more or less ill-defined indisposition; paralyses were absent. They were all in their usual state of health within a few hours or days preceding death. Death was unexpected, mostly sudden. In four cases it was preceded by epileptic fits and coma; but in the fifth case no convulsions were noted, although they may have occurred in the night.

The author[849] had an opportunity of investigating by chemical means the distribution of lead in the fourth and fifth cases in the liver, kidney, and brain.

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In the fourth case, from 402 grms. of liver 24·26 mgrms. of lead sulphate were separated. The right kidney (weighing 81 grms.) yielded 5·42 mgrms. of lead sulphate. The brain was dehydrated with alcohol, and then treated with ether, hot alcohol, and chloroform until an albuminoid residue remained; lead was extracted from each of these portions, viz., the alcohol used for dehydration, the ethereal and chloroform extracts, and the albuminoid residue, as follows:—

	Mgrms. of Lead Sulphate.
Soluble in cold alcohol,	1·11
Soluble in ether and chloroform and hot alcohol,	25·47
Albuminoid residue,	7·76
	34·34

In the fifth case, the brain was examined more in detail, and the lead present estimated in the following solutions and substances:—

1. Alcohol used for dehydration. This may be called “the watery extract,” for, after the brain has remained in strong alcohol for some weeks, the result is that the alcohol contains much water and substances extracted with water.

2. White matter—(a) from cerebrum; (b) from cerebellum.

3. Kephalin—(a) from cerebrum; (b) from cerebellum.

4. Ether extract, kephalin-free—(a) from cerebrum; (b) from cerebellum.

5. Substances soluble in cold alcohol—(a) from cerebrum; (b) from cerebellum.

6. The albuminoid residue—(a) from cerebrum; (b) from cerebellum.

The general results were as follows:—

	Cerebrum, 460·8 grms. Mgrms. of PbSO4.	Cerebellum, 156·2 grms. Mgrms. of PbSO4
White matter freed from kephalin by ether,	0·0	5·0
Kephalin,	1·5	6·0
Ether extract, kephalin-free,	0·0	0·0
Substances soluble in cold alcohol,	0·0	0·0
Albuminoid residue,	40·0	6·0
	41·5	17·0

The aqueous extract contained 1·5 mgrm. of lead sulphate. In neither of the cases did the pathologist ascertain the total weight of the brain, but, presuming that the weight was an average weight, and that the lead in the remainder of the brain was similarly distributed, the amount of lead calculated as sulphate would amount to 117 mgrms. From these results it appears to the author probable that lead forms a substitution compound with some of the organic brain matters. This view would explain the absence of changes apparent to the eye found in so many of the fatal cases of lead encephalopathy.

§ 785. Lead taken for a long time causes the blood to be impregnated with uric acid. In 136 cases of undoubted gout, 18 per cent. of the patients were found to follow lead occupations, and presented signs of lead impregnation.[850]

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Ellenberger and Hofmeister[851] found that, with chronic poisoning of sheep with lead, excretion of hippuric acid ceased, and the output of uric acid was diminished. This may be explained by the formation of glycocol being arrested.

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§ 786. There are some facts on record which would seem to countenance the belief that disease, primarily caused by an inorganic body like lead, may be transmitted. M. Paul (e.g.) has related the history of the offspring (thirty-two in number) of seven men, who were suffering from lead-poisoning—eleven were prematurely born and one still-born; of the remaining twenty, eight died in the first year, four in the second, and five in the third year, so that of the whole thirty-two, only three survived three years.

The influence of the poison on pregnant women is, indeed, very deleterious. M. Paul noted that in four women who were habitually exposed to the influence of lead, and had fifteen pregnancies, ten terminated by abortion, two by premature confinement, three went the full term, but one of the three children was born dead, a second only lived twenty-four hours; so that, out of the whole fifteen, one only lived fully. In another observation of M. Paul’s, five women had two natural confinements before being exposed to lead. After exposure, the history of the thirty-six pregnancies of these women is as follows:—there were twenty-six abortions (from two to five months), one premature confinement, two infants born dead, and five born alive, four of whom died in the first year.

Chronic poisoning may be nearly always accounted for by the inhaling of lead dust, or by the actual swallowing of some form of lead; but, if we are to accept the fact narrated by the late Dr. Taylor, viz., that he himself had an attack of lead colic from sitting in a room for a few hours daily, in which there was a large canvas covered with white lead and drying oil, and one or two other similar cases,[852] we must allow that there is some subtle volatile organic compound of lead evolved. In the present state of our knowledge, it seems more reasonable to account for such cases by the suggestion that lead has entered the system by an unsuspected channel.

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In 1882, a very interesting case occurred at Keighley, in which a mechanic, aged 42, died from the supposed effects of lead-poisoning, induced from drinking the town water, which was proved by Mr. Allen to contain about ³⁄₅ of a grain of lead per gallon. For six months he had been out of health, and a week before his death he suffered from colic, vomiting, constipation, and a blue line round the gums, and occasional epileptiform seizures. After death the kidneys were found granular, and the heart somewhat enlarged. The viscera were submitted to Mr. Allen for analysis; no lead was found in the heart or brain, a slight, non-estimable trace in the kidneys, and about a grain was separated from the liver and spleen. Dr. Tidy, who was called in as an expert, gave a very guarded opinion, rather against the theory of direct lead-poisoning; and the verdict returned by the jury was to the effect that the deceased died from granular kidney, accelerated by lead-poisoning. Murder by the administration of doses of sugar of lead is rare, but such a case has occurred.

At the Central Criminal Court, in December 1882, Louisa Jane Taylor was indicted for poisoning Mary Ann Tregillis at Plumstead, and convicted. From the evidence it appeared that the prisoner, who was thirty-six years of age, came to reside with Mr. and Mrs. Tregillis, an aged couple of eighty-five and eighty-one years respectively. The prisoner was proved to have purchased at different times an ounce and half an ounce of sugar of lead, and to have added a white powder to the medicine of Mrs. Tregillis. The illness of the latter extended from about August 23 to October 23—a period of two months. It is difficult to say when the first dose could have been given, but it was probably some time between August 13 and 23, while the administration, without doubt, ceased on or before October 6, for on that date different nursing arrangements were made. The symptoms observed were nausea, vomiting, pain in the pit of the stomach, burning in the throat, very dark teeth, a blue line round the gums, and slight jaundice. There was great muscular weakness, with trembling of the hands, and a week before death there was paralysis of the right side.

Lead was discovered in most of the viscera, which were in great part normal, but the kidneys were wasted, and the mucous membrane blackened. The actual quantity of lead recovered by analysis was small, viz., 16·2 mgrms. (¹⁄₄ grain) from the liver; from 8 ounces of brain, 3·2 mgrms. (¹⁄₂₀ grain); from half of the stomach, 16·2 mgrms. (¹⁄₄ grain); and from the spleen, the kidneys, and the lungs, small quantities. It is, therefore, probable that, if the whole body had been operated upon, the yield would have been more than ·15 grm. (a little over 2 grains); but then, it must be remembered that the deceased lived, at least, seventeen days after the last dose.

§ 787. Post-mortem Appearances.—In acute cases of poisoning by the acetate, there may sometimes be found a slight inflammatory appearance of the mucous membrane of the stomach and intestines. Orfila considered that streaks of white points adherent to the mucous membrane were pathognomonic; but there have been several cases in which only negative or doubtful signs of inflammatory or other action have presented themselves. A general contraction of the intestines has often been noticed, and is of considerable significance when present; so also is a grey-black mucous membrane caused by deposited lead sulphide. Loen found in dogs and guinea-pigs, poisoned by lead, local inflammation areas in the lungs, liver, and kidneys; but in no case fatty degeneration of the epithelial cells of the liver, kidneys, or intestines. As a rule, no unabsorbed poison will be found in the stomach; the case related by Christison, in which a person died on the third day after taking at a single dose some large quantity of acetate of lead; and at the autopsy a fluid was obtained from the stomach, which had a sweet metallic taste, on evaporation smelt of acetic acid, and from which metallic lead was obtained—is so very extraordinary in every respect, that its entire accuracy is to be questioned. In death from chronic lead-poisoning, there is but little that can be called diagnostic; a granular condition of the kidneys, and all the pathological changes dependent on such a condition, are most frequently seen. If the patient has suffered from colic, a constriction of portions of the intestine has been noticed; also, in cases in which there has been long-standing paralysis of groups of muscles, these muscles are wasted, and possibly degenerated. In instances, again, in which lead has induced gout, the pathological changes dependent upon gout will be prominent. The blue line around the gums, and sometimes a coloration by sulphide of lead of portions of the intestines, may help a proper interpretation of the appearances seen after death; but all who have given any attention to the subject will agree that, simply from pathological evidence, it is impossible to diagnose chronic lead-poisoning.

§ 788. Physiological Action of Lead.—The action of lead is still obscure, but it is considered to have an effect mainly on the nervous centres. The paralysed muscles respond to the direct current, but not to the induced, leading to the suspicion that the intramuscular terminations of the nerves are paralysed, but that the muscular substance itself is unattacked. On the other hand, the restriction of the action to groups of muscles supports the theory of central action.

The lead colic is due to a true spasmodic constriction of the bowel, the exciting cause of which lies in the walls of the bowel itself; the relief given by pressure is explained by the pressure causing an anæmia of the intestinal walls, and thus lessening their sensibility. The slowing of the pulse produced by small doses is explained as due to a stimulation of the inhibitory nerves; and, lastly, many nervous phenomena, such as epilepsy, &c., are in part due to imperfect elimination of the urinary excreta, causing similar conditions to those observed in uræmia.

§ 789. Elimination of Lead.—When a large dose of acetate or carbonate is taken, part is transformed into more or less insoluble compounds—some organic, others inorganic; so that a great portion is not absorbed into the body at all, but passes into the intestines, where, meeting with hydric sulphide, part is changed into sulphide, colouring the alvine evacuations black. Some of the lead which is absorbed is excreted by the kidneys, but the search often yields only traces. Thudichum[853] states that in fourteen cases of lead-poisoning, in two only was obtained a weighable quantity from a day’s urine; in the remaining twelve lead was detected, but only by the brownish colour produced in an acid solution of the ash by hydric sulphide.

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