Lead poisoning and lead absorption

by Sir Thomas Morison Legge; Kenneth Weldon Goadby

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

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

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

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

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

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

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

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

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

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