The clinical, radiographic, pathological, and environmental features of a case of extensive aluminium fibrosis of the lungs are reported in a man of 49 years of age who had worked for 13½ years in the ball-mill room of an aluminium powder factory.
It is noteworthy that his symptoms were referable to the central nervous system, and that he died from terminal broncho-pneumonia following rapidly progressive encephalopathy, associated with epileptiform attacks. He had no presenting pulmonary symptoms, and ϰ-ray examination of the chest showed only slight abnormalities. Radiographic examination of the chests of 53 other workers in the same factory, and clinical examination with lung function tests of 23 of them revealed no other definite cases of aluminium fibrosis of the lung, nor any other cases with neurological signs and symptoms.
Estimations of the aluminium contents of the body tissues such as the lungs, brain, liver, and bone are also recorded. When compared with normal values, it was found that the lungs and brain contained about 20 times and the liver 122 times more than normal. As a contribution to the study of the aluminium content of normal tissues, and as a control series for the results given by Tipton, Cook, Steiner, Foland, McDaniel, and Fentress (1957), and Tipton, Cook, Foland, Rittner, Hardwick, and McDaniel (1958, 1959), the aluminium content of eight “normal” brains was estimated and in all cases it was found to be less than 0·6 μg. Al/g. wet weight.
The results of a survey of the dust concentrations in the factory are also given.
The use of aluminium compounds in the experimental production of epilepsy in primates is reviewed, and it is suggested that the neurological signs and symptoms with epileptiform convulsions which occurred in this case might have been related to aluminium intoxication. We hold the view, however, that the interstitial and nodular fibrosis found in the lungs was undoubtedly associated with the inhalation and retention of aluminium dust.