[1] Annual Reports of the Chief Inspector of Factories since 1898, especially for 1909, p. 19.
[2] Supplement to the Sixty-fifth Annual Report of the Registrar-General on the Mortality in Certain Occupations in the Three Years 1900, 1901, 1902, by Dr. John Tatham, pp. cxix-cxxii, Cd. 2619.
CHAPTER V
PATHOLOGY
The pathology of lead poisoning has formed the subject of scientific inquiry from the time that the association of certain pathological symptoms was definitely correlated with poisoning by means of the metal or its salts.
Acute poisoning, due to accidental swallowing of large doses of lead salts or to use of lead salts criminally, generally produces a train of symptoms different from those met with in chronic industrial poisoning. But it is difficult to understand why so many writers upon the subject of lead poisoning should have attempted to draw a hard-and-fast line between the pathological symptoms in acute and chronic poisoning. This is especially the case when the after-history of cases of acute poisoning is traced, for in a large number of instances a case of acute poisoning drifts on into a subacute, and finally a chronic, stage. All the symptoms of paralysis, encephalopathy, and even kidney degeneration, have been described in persons who were first of all the subjects of acute poisoning.
The direct effect of a lead salt, such as the acetate, upon the mucous membrane of the stomach, is a caustic one, and the attention of observers seems to have been focussed on what is really a secondary effect of the lead salt, and not one intrinsically associated with actual poisoning by the metal itself.
A good deal of experimental work has also been performed in one way or another—mainly by feeding with, or inoculation of, considerable quantities of soluble lead salts—but, with one or two notable exceptions, such experiments have not carried the knowledge of the true pathology of lead poisoning very much farther. The statement is not uncommonly made that no definite correlation exists between the symptoms observed in animals and those observed in man, the reason being that the massive doses given to animals cannot be similar to, nor can they produce results comparable with, the slow intoxication taking place in man; although the after-history of the majority of cases of acute poisoning shows that the symptoms suffered are generally identical with the severer symptoms seen in cases of chronic poisoning of industrial origin. One of the chief reasons explaining this remarkable point of view arises from the fact that the tissues which come into the hands of the pathologist for post-mortem and histological examination are as a rule derived from cases of chronic poisoning, cases in which the acute symptoms have drifted into the subacute or chronic stage, when any minute changes existing in the initial stages of the poisoning have long since disappeared, or their significance has been so far obscured by secondary changes that the primary lesions are lost sight of.
A critical examination of the very large amount of literature published on lead poisoning negatives the idea that acute and chronic poisoning differ fundamentally in their pathology, and observers are found describing identical pathological lesions resulting from acute or chronic industrial poisoning. It is impossible to review the whole of the existing literature. Kobert[1], in summing up the general effect of lead upon the animal body, makes the following general statement: “Lead affects especially the striped and unstriped muscles, the epithelium of the excretory glands, the neuroglia of the central nervous system, and is essentially a protoplasmic poison.”
We base our knowledge on definite experiments, so arranged that the method of exposure was in every way similar to that in lead industries. The only point of difference that can be urged against them is one of degree; but as the train of symptoms produced was in every way comparable with those suffered by man, this objection cannot be sustained. The fact that the symptoms develop in a shorter time than they do in industrial processes is merely a function of the intensity of the poisoning.
An attempt will be made first to summarize the literature on the pathology of lead poisoning, and, as such literature covers an immense amount of ground, to group the pathological findings of various observers, as far as possible, under four main headings—namely: