Occupational asthma-asthma induced by an agent inhaled at work-provides a valid model for the examination of the more general environmental causes of asthma. In many instances, definable populations exposed to a novel allergen in the workplace at concentrations that are relatively easily measured develop IgE-associated asthma and characteristic eosinophilic bronchitis. Carefully designed epidemiological studies suggest that the incidence of IgE antibody and asthma is highest in the first one to two years of exposure; and that the risk is directly related to the intensity of airborne allergen exposure. The relationship between exposure and outcome is modified both by concurrent cigarette smoking and by genotype, although the details of this latter interaction remain unclear. Symptoms, airway hyper-responsiveness and airway inflammation may persist for several years after avoidance of exposure to the initiating agent. If the relevance of the model is accepted then these insights require testing and further investigation, both within the field of occupational asthma and, by extension, in the wider field of asthma in the general environment.