Purpose of review: Developments in the understanding of causes and natural history of occupational asthma may allow improved primary, secondary and tertiary preventive strategies for occupational asthma. This may also lead to improved understanding of preventable contributing factors to the development and severity of nonoccupational asthma.
Recent findings: Animal studies have demonstrated the opportunity to identify chemical sensitizers relevant to asthma. Studies of genetic markers in occupational asthma pose logistic difficulties, but preliminary studies suggest that glutathione S-transferase genotypes may predispose to development of occupational asthma induced by diisocyanates and these have also been implicated in nonoccupational asthma. Some occupational sensitizers/irritants are also found outside the workplace and may be relevant in nonoccupational asthma, for example cleaning agents, epoxy glues, hairdressing products. Accidental exposures to high concentrations of respiratory irritants have the potential to induce new asthma as well as aggravate underlying asthma in both occupational and nonoccupational settings.
Summary: Better understanding of the pathogenesis of occupational asthma is important for affected workers, and also has potential relevance for nonoccupational asthma.