The current argument about the carcinogenicity of inhaled silica is not clarified by reliance on morbidity and mortality experience divorced from or incompletely related to data on environmental exposure. Human evidence provides the ultimate basis for assessing such risks, and numerous studies of the effects of inhaling dusts rich or poor in silica content on the prevalence of pulmonary carcinoma have been performed on large series of cases from major mining areas of the world. When due allowance is made for substances inhaled concomitantly with exposure to silica and for personal pollution by cigarette smoking, the weight of evidence is against a carcinogenic role for uncombined silicon dioxide. Moreover, pneumoconiosis due to compact mineral particles does not appear to determine the onset of lung cancer. Cellular behaviour suggests reasons for the different responses to compact and fibrous particles acting alone.