The mechanisms responsible for pollutant-induced asthma are uncertain and the appropriate pharmacologic interventions are unknown. The report reviews recent data suggesting that indoor allergens, notably those derived from dust mite, cat, and cockroach, are critical factors in the etiology of asthma, and that individuals spend the vast majority of their time in an indoor environment, presumably exposed to these allergens. Outdoor pollutants are relevant as well, since such molecules as ozone and oxides of nitrogen and sulfur are also present indoors. It is possible that irritants and pollutants act synergistically with allergens. Ozone and sulfur dioxide, as mentioned above, are reported to worsen asthma and increase bronchial hyperreactivity.
Diesel exhaust particulates apparently enhance IgE antibody production to allergens.
Environmental tobacco exposure not only reduces pulmonary function, but also appears to enhance IgE antibody production to allergens. The physicochemical nature of particulates in the air also are said to regulate IgE antibody production, perhaps because size, charge, and other properties influence allergen binding and processing. However, the mechanisms by which these events occur have not been well characterized. Research Goals and Scope Areas of research that would be responsive to this Program Announcement should be focused on mechanistic studies, with both basic and preclinical investigation, involving animal models, cultured human cell models, and human patients. Defining the relationship between outdoor allergens and other environmental agents in the development and exacerbation of asthma.