This study will investigate the role of traffic-related pollution in childhood asthma and lung function. The work will capitalize on findings from the southern California Children's Health Study (CHS), a population-based prospective cohort study. The CHS includes children from southern California communities that vary in regional air quality. We have found clinically significant lung function deficits, increased incidence of asthma, and increased respiratory symptoms among those living in communities with high regional pollution, compared to lower-pollution communities. We have found increased rates of prevalent and incident asthma and decreased lung function growth associated with indicators of traffic that vary within communities. These within-community associations with traffic indicators have been independent of the effects of regional pollution. We have also identified children susceptible to respiratory effects of oxidant pollutants, based on history of asthma, specific candidate genes, sex, in utero tobacco smoke exposure, and early life deficits in airway flow rates. We propose to build on these results by investigating the relationship between airways disease and specific traffic-related pollutants likely to be causing these effects. We hypothesize that respiratory effects will be linked to variation in toxicologically relevant components of particulate matter. including transition metals and total and water soluble organic carbon, which will be measured in different size fractions (PM[0.25], PM[0.25-2.5] and PM[2.5-10]). We will examine (1) associations of these specific traffic-related pollutants and gaseous co-pollutants with well-characterized incident asthma and with lung function level and growth;and (2) modification of the effect of traffic-related pollutant effects on lung function growth by asthma and exhaled nitric oxide (eNO, a marker of airway inflammation). In addition, we will jointly model respiratory outcomes, including asthma, lung function, and other available respiratory health indicators including eNO, that may reflect vulnerability to effects of particulate air pollution. Longitudinal lung function will be measured in 1,900 children between approximately 11 and 15 years of age and new-onset asthma cases will be identified. Particulate and gaseous pollutants will be monitored at multiple locations within each of eight study communities that have large within-community gradients in traffic and between-community variation in regional air quality. Long-term average exposures will be estimated for each child, using state-of- the-art GIS methods and spatial modeling. This study will further our understanding of the childhood origins of obstructive lung disease and has important implications for development of interventions and regulatory policy, since traffic is a common exposure and asthma and chronic obstructive pulmonary disease are major public health problems.
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