Abstract

The purpose of this article is to critically review the available evidence pertaining to occupational, environmental, and individual factors that can affect the development of occupational asthma (OA). Increasing evidence suggests that exploration of the intrinsic characteristics of OA-causing agents and associated structure-activity relationships offers promising avenues for quantifying the sensitizing potential of agents that are introduced in the workplace. The intensity of exposure to sensitizing agents has been identified as the most important environmental risk factor for OA and should remain the cornerstone for primary prevention strategies. The role of other environmental co-factors (e.g., non-respiratory routes of exposure and concomitant exposure to cigarette smoke and other pollutants) remains to be further delineated. There is convincing evidence that atopy is an important individual risk factor for OA induced by high-molecular-weight agents. There is some evidence that genetic factors, such as leukocyte antigen class II alleles, are associated with an increased risk of OA; however, the role of genetic susceptibility factors is likely to be obscured by complex gene-environment interactions. OA, as well as asthma in general, is a complex disease that results from multiple interactions between environmental factors and host susceptibilities. Determining these interactions is a crucial step towards implementing optimal prevention policies.

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