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Pneumoconioses are still a common cause of chronic lung disease. In industrialized countries, improvements in working conditions and dust control measures have led to a decrease in the incidence of severe forms of silicosis, coal worker pneumoconiosis, and parenchymal asbestosis. However, the diversity of settings in which silica and asbestos are used fuels a continued input of cases, and the burden of cases related to remote exposures is still considerable. Overall, the clinical picture of the classic pneumoconioses and their complications has not changed substantially. However, their limits and links have expanded toward systemic and connective tissue disease, idiopathic pulmonary fibrosis, and antineutrophil cytoplasmic autoantibody-positive vasculitides. Immunologically mediated occupational lung diseases have emerged, such as berylliosis and hard-metal disease. Advances in imaging, mineralogic analysis of bronchoalveolar lavage fluid, and immunologic techniques have been instrumental in describing new patterns of disease and are helpful in litigious or difficult cases.

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