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 me chanisms and pathophysiology of asthma in general. In an occupational setting the cause and onset of asthma may be easily iden tified, and the natural history may be examined in follow-up studies. The m echanisms involved in occupational asthma include genetic predisposition, i mmunologically mediated responses, as well as nonspecific airway inflammati on. In particular, high molecular weight (eg, grain dust, flour) and some l ow molecular weight sensitizers (eg, acid anhydrides and platinum halide sa lts) have been shown to induce occupational asthma through an immunoglobuli n 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 c ontained in western red cedar). The pathology of the airway mucosa of occup ational asthma is remarkably similar to the pathology of nonoccupational as thma, ie, characterized by infiltration and accumulation of eosinophils, ma st cells, and activated lymphocytes along with subepithelial fibrosis. In t his article, the most relevant mechanisms are discussed with particular ref erence to the similarities and discrepancies between occupational and nonoc cupational asthma.