Genetic Susceptibility for Occupational Asthma.

摘要

Diisocyanates are highly reactive chemicals that cause occupational asthma (OA) in 5-15% of exposed workers. Since new cases are not entirely preventable, there is a need to find markers of susceptibility to identify those worker groups at risk for OA, caused by diisocyanates (DA) to further guide risk assessment strategies. The clinical manifestations of DA are similar to those found in non-occupational asthma, including airway hyperresponsiveness, airway remodeling, as well as a unique ability to illicit isolated late phase responses, with infiltration of eosinophils, basophils, and/or neutrophils. Evidence suggesting immune mechanisms underlying DA susceptibility include a latency period of exposure preceding sensitization, and elicitation of asthmatic responses by sub]irritant levels of chemical. However, unlike OA induced by high molecular weight sensitizers, no sensitive and specific antibody markers of DA have yet been identified. Due to the inherent toxic nature of these chemicals, pathogenesis of DA is likely to be multifactorial in nature, involving innate and acquired immune mechanisms, oxidative stress, and impaired epithelial cell barrier function.