The increase in morbidity and mortality attributable to chronic obstructive pulmonary disease (COPD) has focused attention on environmental and host factors causally associated with the clinical entities included under the rubric of this term with a view to early preventive intervention. Despite the biologic plausibility of inhaled agents being causally implicated, only the role of tobacco smoke has been accepted beyond doubt. However, evidence implicating occupational exposures has accumulated, in particular over the last 2 yr, from: (1) community-based studies (in which larger study populations provide greater power than the usually smaller workforce based studies); (2) longitudinal studies of lung function (which enhance the signal of interest, namely the effects of the occupational exposures, and diminish the noise due to between-individual differences); (3) pathology studies (in which the outcome of interest is the quantitative measurement of emphysema), and (4) cohort mortality studies of all or specific causes of death. This evidence, reviewed here according to accepted criteria for establishing causality, leaves little doubt that occupational exposure to dust and/or to dust and fumes may be causally implicated in the genesis of COPD. As with tobacco exposure, both bronchitis (mucus hypersecretion) and airflow limitation are recognized as causally related to exposure, but not necessarily to each other. As with tobacco exposure, though effects are in general dose related to exposure, there is evidence for individual susceptibility. As with tobacco exposure, a possible host factor is the reactivity of airways to inhaled materials.(ABSTRACT TRUNCATED AT 250 WORDS)