Coal mining, emphysema, and compensation revisited.

Seaton, in his editorial, relied mainly on three publications to support his thesis that coal mining may lead to disabling impairment in the absence of progressive massive fibrosis and cigarette smoking.2It is well established that the category of simple coal workers' pneumoconiosis is linearly related to the coal content of the lungs.5 6 In this context Ruckley et al have shown that the extent of emphysema found at postmortem increases with the amount of coal present in the lung and also with lifetime dust exposure.4 If this is so, and there seems little doubt that it is, then increasing category of simple coal workers' pneumoconiosis and its associated emphysema should be associated with a significant decrease in the forced expiratory volume in one second (FEV1). Thus it should follow that the more dust present in the lungs, the more emphysema, and the worse the lung function. This is not the case, there being no difference in lung function in those with and without simple coal workers' pneumoconiosis.7 8 Further evidence in support of the hypothesis is said to come from an examination of the lungs of a group of 95 non-smoking miners, which showed a clear inverse relation between the extent of the emphysema and the FEV1.' The evidence for this statement is said to be contained in a technical report,4 which was not available to us at the time Gee and I questioned the validity of certain conclusions in Seaton's editorial.9 The report has since become available to us, but nowhere in the report is there any evidence to support the claim that there is an inverse relation between emphysema and the FEV, in non-smoking miners. Of the lungs obtained from the 95 non-smoking miners only 40 (42%) showed the presence of emphysema, centriacinar, panacinar or both. In this connection, the study showed that panacinar emphysema was entirely unrelated to dust exposure.4 Of the 40 subjects whose lungs showed emphysema, only 33 (35%) had centriacinar emphysema, of whom 23 also had progressive massive fibrosis, an acknowledged cause of centriacinar emphysema. This left only 10 subjects whose lungs showed centriacinar emphysema in the absence of progressive massive fibrosis. Of these 10, eight had fibrotic nodulessimple coal workers' pneumoconiosis-whereas the other two did not. The authors concluded that because there were only two non-smoking subjects who had emphysema in the absence of coal workers' pneumoconiosis, no conclusions could be drawn as to the effect of dust in the induction of emphysema in those