Black Carbon Exposure, DNA Methylation, Airway Inflammation in Pediatric Asthma

Exposure to traffic-related air pollution is associated with asthma exacerbations among children. Symptomatic adolescents tend to develop persistent disease. Despite increasing research on the associations between short-term exposure to black carbon (BC)/diesel and metal rich particulate matter and changes in DNA methylation, previous studies have lacked accurate assessment of personal exposure and consideration of the effects of early childhood exposure. Nor have they compared changes in DNA methylation that could lead to sustained effects on gene transcription with important clinical outcomes in children. Buccal mucosal cells may be used as a sentinel population representative of cells in the airways and accessed noninvasively.

This study tests the hypothesis that exposure to BC, nickel (Ni), and vanadium (V) is associated with changes in buccal DNA methylation of proinflammatory asthma genes (interleukin-4, interferon-gamma inducible nitric oxide synthases), and that such methylation changes are associated with greater airway inflammation and obstruction among urban adolescents in the CCCEH cohort. The aims are to a) Determine whether recent exposure to BC, Ni, V is associated with altered buccal DNA methylation of several asthma genes among children after controlling for multiple covariates including asthma, and b) Determine whether methylation of asthma genes is associated with greater airway inflammation (fractional exhaled nitric oxide, exhaled breath condensate pH) and airflow obstruction (both assessed twice; 5 days apart) among asthmatic children.

If the proposed aims are achieved, this study will allow for the identification of constituent pollutants that may drive clinically-relevant epigenetic events. A greater understanding of the role of ambient BC, nickel and vanadium in inner city asthma exacerbations will stimulate focused intervention to reduce disease among older children.

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