[Occupational dust exposure and chronic obstructive bronchopulmonary disease. Etiopathogenic approach to the problem of compensation in the mining environment].

In order to support the hypothesis of a causal relationship between exposure to respirable coal mine dusts and chronic obstructive pulmonary disease (COPD), investigations were performed to assess the biological disorders affecting the distal air spaces in coal workers with pneumoconiosis. Broncho alveolar lavage studies demonstrated a continual influx of mononuclear phagocytes loaded with mineral particles, associated with neutrophils in small number, in smokers as well as in non smokers. The alveolar macrophages were in activated state, spontaneously releasing various mediators, particularly interleukin I, Tumor necrosis factor alpha and superoxide anion. So, they appeared as responsible both for a chronic inflammation of the distal airways and for a protease-antiprotease imbalance leading to pulmonary emphysema, partly due to an oxidative inactivation of alpha 1 antiprotease inhibitor. In spite of additive effect of tobacco smoke, as shown by longitudinal studies of lung function in coal miners, it is now reasonable to consider the evidence of association between coal mine exposure and COPD to be sufficiently strong to infer causality, and to justify compensation for COPD in coal miners with or without radiological evidence of pneumoconiosis.