The epidemiology, clinical manifestations and course, pathogenesis and prevention of silicosis were reviewed. Silicosis was defined as a fibrotic disease of the lungs produced by inhalation and deposition of dust containing silicon-dioxide (7631869). An acute form of silicosis occurred under conditions of intense exposure, but the chronic form which required several years to develop was more common. The chronic form of silicosis was characterized by nodular lesions more prominent in the upper lobes which often progressed to massive nodular fibrosis and was frequently associated with tuberculosis. Acute silicosis, which could appear after 1 to 3 years of very high exposure to silica, was characterized by interstitial fibrosis in the middle and lower lobes. Silicosis often progressed even in the absence of further silica exposure. The factors determining progression of silicosis were unclear. There was apparently an innate individual susceptibility to develop chronic silicosis, possibly genetically determined. A relationship between duration of silica exposure and the prevalence of silicosis was demonstrated. Occupational exposure to silica occurred in several large categories of industry in the United States, including: mining, manufacturing, construction, and agricultural. Accurate estimates of the incidence and prevalence of silicosis could not be made with the current state of knowledge. The pathogenesis, and gross and microscopic pathology of silicosis were summarized. Clinical signs and symptoms included: dry cough, dyspnea, and hypoxemia. In severe cases, progressive massive fibrosis culminated in pneumothorax and respiratory failure. Effects of pulmonary function were minimal until the disease was fairly far advanced. Radiographically, small discrete round opacities were usually observed in the upper lung fields, which increased in size and number as the disease progressed. The author concludes that airborne silica dust concentrations must be reduced to a minimum in order to prevent silicosis.