Mechanisms of occupational asthma.

BACKGROUND The pathogenesis and the pathologic alterations of occupational asthma are similar to those of nonoccupational asthma. Occupational asthma may therefore represent a useful model of "human asthma" to investigate mechanisms and pathophysiology of asthma in general. In an occupational setting the cause and onset of asthma may be easily identified, and the natural history may be examined in follow-up studies. The mechanisms involved in occupational asthma include genetic predisposition, immunologically mediated responses, as well as nonspecific airway inflammation. In particular, high molecular weight (eg, grain dust, flour) and some low molecular weight sensitizers (eg, acid anhydrides and platinum halide salts) have been shown to induce occupational asthma through an immunoglobulin E (IgE)-dependent mechanism, while cell-dependent immunologic mechanisms are likely to be more relevant for occupational asthma induced by other low molecular weight sensitizers (eg, toluene diisocyanate and plicatic acid contained in western red cedar). The pathology of the airway mucosa of occupational asthma is remarkably similar to the pathology of nonoccupational asthma, ie, characterized by infiltration and accumulation of eosinophils, mast cells, and activated lymphocytes along with subepithelial fibrosis. In this article, the most relevant mechanisms are discussed with particular reference to the similarities and discrepancies between occupational and nonoccupational asthma.