Enhanced allergic sensitization in animals exposed to particulate air pollution

Epidemiological studies have round an association between elevated levels o f particulate matter (PM) air pollution and increased medication use and ho spital visits by asthmatics. While it is known that asthmatics are generall y more sensitive to airborne contaminants such as sulfur dioxide and tobacc o smoke, it is difficult to test which components of air pollution may also contribute to the induction of pulmonary allergy (sensitization) because o f the risk in creating disease. Recent studies in mice and rats, however, h ave demonstrated that pulmonary exposure to combustion particles such as di esel and residual oil ny ash (ROFA) can exacerbate immunological sensitizat ion tin the form of immunoglobulin E antibody and lymphocyte reactivity) to experimental and natural allergens. Subsequent allergen challenge in these animals results in a greater allergen-induced bronchoconstriction, elevate d numbers of eosinophils in the lung, and enhanced airway responsiveness to cholinergic agents compared to what occurs in similarly immunized animals pretreated with vehicle or "inert" particles. Although the mechanisms for t hese effects are not known, it has been demonstrated that the adjuvant effe cts of diesel and ROFA can be reproduced with hydrocarbons and soluble tran sition metals from diesel and ROFA, respectively. in addition, analysis of mediator expression and release over the sensitization phase has revealed t hat PM exposure can enhance production of Th2 cytokines such as interleukin -5 (IL-5) and the proinflammatory cytokine tumor necrosis factor-alpha (TNF -alpha). These experimental systems demonstrate the potential of particulat e air pollutants to enhance allergic sensitization and can be further used to elucidate the mechanism for these effects.