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The initial early reaction of pulmonary tissue to inorganic dust inhalation is a ftbrosing macrophagic alveolitis. This initial pulmonary lesion can be detected by an enhanced gallium 67 pulmonary uptake and analyses of bronchoalveolar lavage. These two techniques can document not only the increased proliferation of macrophages, but also the activation of macrophages to produce excessive amounts of fibronectin and other factors of fibroblastic growth implicated in the pathogenesis of the pneumoconioses. Of equal clinical interest is the development of computed tomography, which has permitted better characterization of the early stages of fibrosis in the pneumoconioses. These refinements in disease recognition will contribute to the earlier detection of pneumoconioses before they become incapacitating. Newer therapeutic methods are also under investigation that could permit inactivation of either the dust itself or the pulmonary macrophage. The coupling of these new diagnostic and therapeutic developments will bring in a new era in occupational pulmonary medicine.