Pediatric Asthma, Particulate Air Pollution and NO2

描述(申请人提供)：空气的促炎作用 污染物及其修饰对变态反应性炎症的影响可能部分 解释哮喘患病率、发病率和死亡率的增加。代理 必须考虑具有重大急性影响的问题，同时要了解 易感人群的相关个人暴露。然而，它是 从流行病学研究中还不清楚这种联系的程度 哮喘结果和受监管的EPA标准空气污染物之间的关系，如 二氧化氮(NO2)是独立的或可归因于其他被监测的 标准污染物，如颗粒物(PM)质量，或空气有毒物质不 通常监测与燃烧有关的有机化合物等。我们建议 进行哮喘小组研究，每天重复测量发病率和 高空气污染地区儿童哮喘患者的污染物暴露 污染水平：洛杉矶东部的一个地区(机动车排放源) 和Riverside(顺风向烟雾感受器站点)。发病率将被衡量为 急性哮喘症状严重程度、肺功能和必要的哮喘药物 使用。具体目标包括检查日常哮喘的关系 发病率：(1)个人暴露于空气中PM的实时测量；(2) 个人暴露于PM10元素和PM10 24小时平均浓度 有机化合物(EC-OC)；(3)个人接触24小时平均NO2 与上述暴露同时收集；以及(4)NO2和PM暴露 与使用AIMS中的度量标准的共污染模型进行比较 一比三。独立和相互作用的污染物影响的优势将是 检查以测试个人PM暴露，包括EC-OC， 修改个人接触NO2对呼吸健康的影响，但 混淆了室外NO2，这是与交通相关的污染物的指示性气体。 将使用个人的嵌套样本开发个人暴露模型 预测两个研究地区的PM和NO2暴露的暴露。两块嵌板 将对32名哮喘患者进行为期两个月的随访，每个地点一人(总计3584人 人-天)。剂量学模型将使用个人和 以上暴露调整后的PM和NO2，以评估剂量估计是否提高 联想。长期目标是提高对独立人士的了解 以及颗粒物和气态空气污染物的综合不利影响 使用动态监测方法检查急性暴露和反应。

DESCRIPTION (provided by applicant): The pro-inflammatory role of air pollutants and their modifying influence on allergic inflammation may partly explain the increase in asthma prevalence, morbidity, and mortality. Agents that have major acute effects must be considered along with an understanding of the relevant personal exposures of susceptible individuals. However, it is unclear from the epidemiological research the extent to which associations between asthma outcomes and regulated EPA criteria air pollutants such as nitrogen dioxide (NO2)are independent or attributable to other monitored criteria pollutants such as particulate matter (PM) mass, or to air toxics not usually monitored such as combustion-related organic compounds. We propose to conduct an asthma panel study with daily repeated measurements of morbidity and pollutant exposures in 64 pediatric asthmatics living in areas with high air pollution levels: an area of East Los Angeles (vehicular emission source site) and Riverside (down-wind smog receptor site). Morbidity will be measured as acute asthma symptom severity, lung function, and as-needed asthma medication use. Specific Aims include examining the relationships of daily asthma morbidity to: (1) personal exposures to airborne PM measured in real-time; (2) personal exposures to 24-hr average concentrations of PM10 elemental and organic compounds (EC-OC); (3) personal exposures to 24-hr average NO2 collected concurrently with the above exposures; and (4) NO2 and PM exposures in single as compared with co-pollutant models using the metrics in aims one-three. Strengths of independent and interactive pollutant effects will be examined to test the hypothesis that personal PM exposures, including EC-OC, modifies the respiratory health effects of personal NO2 exposures, but confounds outdoor NO2, an indicator gas for traffic-related pollutants. Personal exposure models will be developed using a nested sample of personal exposures to predict PM and NO2 exposures for the two study regions. Two panels of 32 asthmatics will be followed for two months, one at each site (total 3,584 person-days). Dosimetric models will be developed using personal and exposure-adjusted PM and NO2 above to assess whether dose estimates enhance associations. Long-term goals are to improve knowledge about the independent and combined adverse effects of particulate and gaseous air pollutants by examining acute exposures and responses using ambulatory monitoring methods.