Susceptible workers exposed to coal mine and silica dust may develop a variety of pulmonary diseases. The prime example is classical pneumoconiosis, a nodular interstitial lung disease that, in severe cases, may lead to progressive massive fibrosis (PMF). Exposure to silica and coal mine dusts may also result in pulmonary scarring in a pattern that mimics idiopathic pulmonary fibrosis, and in chronic obstructive pulmonary disease (COPD), including emphysema and chronic bronchitis, that appears indistinguishable from obstructive lung disease caused by exposure to tobacco smoke. Coal mine and silica dust may therefore result in restrictive, obstructive, or mixed patterns of impairment on pulmonary function testing. Most physicians are aware of the nodular fibrosing pulmonary tissue reactions in response to retained dust, but they may not realize that these other reactions of the pulmonary parenchyma and airways to dust exist and can result in significant respiratory dysfunction in sensitive individuals. This article discusses current data on exposure to coal mine and silica dust in the United States, the epidemiology of the diseases caused by these exposures, and new concepts of causation and pathogenesis. We also review the patterns of pulmonary disease and impairment that may result.