Effects of Stress and Traffic Pollutants on Childhood Asthma in an Urban Community

Higher levels of exposure to air pollutants and stress may contribute to asthma disparities in urban communities. Recent epidemiological evidence suggests that psychosocial stress may modify the effects of traffic-related air pollution on asthma. We will test a model in which chronic stress modifies the effects of acute exposures to traffic-related air pollutants by blunting the normally protective roles of the hypothalamic-pituitary-adrenal (HPA) and/or sympathetic-adrenal-medullary (SAM) axes in acute asthma exacerbation. We propose to test these hypotheses: 1) Exposure to the traffic pollution markers nitrogen dioxide (NO2) and black carbon (BC) will be inversely correlated with lung function (FEV1) and positively correlated with fraction exhaled nitric oxide (FENO), a marker of pulmonary inflammation. 2) Individual levels of chronic and episodic stress, assessed by interview, will modify the correlations between air pollutant levels and FEV1 and FENO. 3) The degree to which HPA and SAM responses are blunted will be correlated with the level of chronic and episodic stress obtained from the stress interviews. 4) The degree to which HPA and SAM responses are blunted will have a stronger modifying effect than the interview variables on the relationships between air pollution and asthma exacerbation.