We thank the correspondents for their interest in our work. As our study was not intended to address the role of immunology potentially contributing to thrombosis related to diesel exhaust (DE) and we did not include allergen exposure, we did not reference the suggested literature. With this opportunity, however, we note that the literature to date is sparse with regards to direct laboratory investigation of a role for allergens in DE-mediated thrombosis. Other explanations for such phenomena, perhaps equally likely to those proposed, include particle-related epithelial damage (either facilitating or taking advantage of predisposed access of allergen to sub-epithelial dendritic—and other—cells (CitationKnight, 2002) or allergen-related oxidative stress (CitationDworski et al., 1999) that (independent of formal hypersensitivity but coincident with DE-related oxidative stress (CitationLi et al., 2002) may augment thrombosis. Work in our laboratories and those of others will explore these possibilities.
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- Knight D. (2002). Increased permeability of asthmatic epithelial cells to pollutants. Does this mean that they are intrinsically abnormal? Clin Exp Allergy 32(9):1263–1265.
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