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Asbestosis is a pneumoconiosis that results from the inhalation of asbestos fibers. There is a body of evidence that implicates the alveolar macrophage in the pathogenesis of asbestosis because of its prominence in asbestos-related histologic lesions. Injury to the alveolar epithelium also may contribute to the pathogenesis of asbestosis. Evidence is presented to suggest that pulmonary fibrosis may result from the persistent release of inflammatory mediators (chemoattractants, lysosomal enzymes, toxic oxygen radicals, arachidonic acid metabolites, interleukins, and fibroblast growth factors) at sites of asbestos deposition. Histologic features of asbestosis can be detected within months after the initial contact with asbestos. In contrast, the stigmata of asbestos-related disease usually are not radiologically detectable, even by the most sensitive imaging techniques, until after a latency period of at least a decade, and often considerably longer. There is, therefore, a long diagnostic delay between the time when asbestosis is histologically detectable and when it is radiographically detectable.