Allergic Asthma and Rhinitis: Toxicological Considerations

Abstract

Immunotoxicity can manifest as an exaggerated immune response to a normally innocuous substance and lead to hypersensitivity or allergic reactions in the lung. Allergens are encountered environmentally or in the workplace and can be low‐ and high‐molecular‐weight substances. Allergic asthma and allergic rhinitis are examples of allergic reactions in the lung with immediate, late and chronic phases contributing to respiratory tract pathology. Mechanistically, allergic asthma and rhinitis reflect a combination of antibody and cell‐mediated immune reactions involving IgE antibody to allergen in the early stages and Th2 cell involvement as the disease progresses to late‐phase reactions and chronic allergic inflammation. Multiple cell types and mediators are involved in the inflammatory response in the lung. Mechanistic differences leading to the asthma/rhinitis phenotype have been noted with different allergens, primarily low‐molecular‐weight substances. Xenobiotics that are not allergens themselves may enhance the immune response to allergens or exacerbate pre‐existing asthma and airway hyper‐responsiveness. The complexity of the allergic response in terms of humoral and cell‐mediated immunity, as well as potential differences in mechanisms depending on the allergen, present a very challenging scenario for the toxicologist to predict the exposures that will result in allergic rhinitis or asthma.