Impact/Purpose:

This project focuses on environmental influences that act directly as allergens to induce asthma or agents that enhance either the induction or exacerbation of the disease via non-specific stimulation of immune or inflammatory responses. Its objectives are to identify and rank mold allergens that may be important in the induction of allergic asthma and assess the effect of air pollutant exposure on the induction and exacerbation phases of the disease.

The results from this research will greatly contribute to the understanding of environmental risk factors for asthma and will address several key EPA needs including species extrapolation and quantitative risk assessment, identification of susceptible sub-populations, aspects of children's health, as well as assessing the health effects of air pollutants (both indoor and ambient). This work will also contribute to the identification of biomarkers of both exposure and effect that will be subsequently used in the National Children's Study (NCS) .

Description:

The incidence of asthma has doubled in the last 20 years with the largest increase among children below the age of 15 years (CDC, 1998). This increase cannot be explained by changes in diagnostic categorization or by alterations in the gene pool, and suggests a strong association between environmental influences and the incidence of disease. About 75% of asthma is associated with allergy, and it appears that early in life, the immune system can be programmed to promote asthmatic responses to certain antigens. While some allergens have been studied extensively (e.g., dust mite and cockroach), almost none of the mold allergens have been characterized, despite their widespread distribution and potential importance in the induction and exacerbation of asthma. Epidemiologic and clinical studies have also demonstrated that asthmatic responses can be exacerbated by ambient combustion-related products and by domestic and occupational exposures to airborne chemicals (air toxics). Clinical and epidemiologic studies have also shown that children with asthma are especially sensitive to the respiratory effects of ambient combustion-related pollutants such as sulfur dioxide and ozone. This project will study environmental influences that act directly as allergens to induce asthma or as agents that enhance the induction or exacerbate the disease via non-specific stimulation of immune or inflammatory responses. We will use a mouse model to study the role of fungal antigens as initiators of allergic asthma, and we will develop laboratory-based assays that can predict the ability of various pollutants to enhance the induction or exacerbate the severity of allergic asthma in a dose-dependent manner.

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