Lead poisoning and lead absorption

by Sir Thomas Morison Legge; Kenneth Weldon Goadby

REFERENCES.

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

[2] Goadby, K. W., and Goodbody: The Lancet, vol. ii., p. 988, 1909.

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

[4] Moore: Private communication.

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

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

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

CHAPTER VII
SYMPTOMATOLOGY AND DIAGNOSIS

Acute Poisoning.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Constipation.

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

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

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

The Pulse.

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

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

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

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

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

Lead Colic.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Chronic Colic.

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

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

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

The chief points associated with lead colic are—

1. The intermittent character.

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

3. The slowing of the pulse.

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

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

Headache.

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

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

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

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

The Burtonian Line.

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

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

There are two kinds of Burtonian line:

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

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

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

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

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

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

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

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

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

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

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

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