Grantee Research Project Results
Effects of Traffic-Related Air Pollution Components on Asthma in the Young Mammalian Lung
EPA Grant Number: F5D40820Title: Effects of Traffic-Related Air Pollution Components on Asthma in the Young Mammalian Lung
Investigators: Vancza, Elizabeth M.
Institution: New York University
EPA Project Officer: Packard, Benjamin H
Project Period: September 1, 2005 through January 1, 2008
Project Amount: $105,340
RFA: STAR Graduate Fellowships (2005) RFA Text | Recipients Lists
Research Category: Academic Fellowships
Objective:
Asthma is a chronic lung disease whose prevalence is on the rise in the urban populations of our society, particularly in children. Although the specific mechanisms behind the cause of this complex respiratory disease remain unclear, mounting evidence suggests that some components of air pollution, such as diesel exhaust and other ambient urban particles, play a major role. In addition, mounting evidence has shown that asthma is largely allergic in nature with local and central components of the immune system strongly influencing its severity. The goal of this research is to investigate the effects of traffic-related air pollutants on the varying degrees of allergic asthma reactivity between children and adults using a mouse model.
Current evidence supports the idea that diesel exhaust particles (DEPs) worsen the respiratory symptoms in individuals with preexisting asthma or allergies. In addition, very few studies have examined the relative differences in susceptibility of young vs. old/adult lungs to inhaled pollutants. Therefore, we will expose normal and “asthmatic” adult or neonatal CD1 mice to relevant levels of DEPs, concentrated ambient particulate matter (CAPs) or filtered air and examine airway reactivity, lavageable inflammatory cell counts and cytokine profiles. “Asthmatic” mice will be generated through sensitization to inhaled cockroach antigen, an antigen relevant to urban communities where asthma rates are highest, and differences in the immune response to antigen challenge will also be recorded for young versus old mice. Since susceptible populations like asthmatics and children are biased towards a Th2 immune response, we expect to see an exacerbation of Th2 cytokine expression and lymphocyte numbers in mice exposed to DEPs with the most drastic response in neonates. Data from this research may provide insight into the mechanisms behind airway hypersensitivity induced by antigens and air pollutants found in urban areas and may contribute important information for the treatment and prevention of pediatric asthma, as well as strategies regarding diesel emission standards and risk assessment.