Pediatric Asthma, Particulate Air Pollution and NO2

描述（由申请人提供）：空气的促炎作用 污染物及其对过敏性炎症的修饰作用可能部分 解释哮喘患病率、发病率和死亡率的增加。剂 必须沿着考虑具有重大急性影响的 易感个体的相关个人暴露。但据 从流行病学研究中还不清楚 哮喘的结果和受监管的EPA标准之间的空气污染物， 二氧化氮（NO2）是独立的或可归因于其他监测 标准污染物，如颗粒物（PM）质量，或空气中的有毒物质 通常被监测，例如与燃烧有关的有机化合物。我们建议 进行哮喘小组研究，每天重复测量发病率， 高空气污染地区64例儿童哮喘患者的污染物暴露 污染水平：东洛杉矶地区（车辆排放源站点） 和滨江（顺风烟雾接收点）。死亡率将被衡量为 急性哮喘症状严重程度、肺功能和按需哮喘药物 使用.具体目的包括检查日常哮喘的关系 发病率：（1）实时测量的空气中PM的个人暴露;（2） 个人暴露于24小时平均浓度的PM10元素和 有机化合物（EC-OC）;（3）个人暴露于24小时平均NO2 （4）NO2和PM暴露 与使用aims中指标的共污染物模型相比， 一比三独立和相互作用的污染物影响的强度将是 检查以检验个人PM暴露的假设，包括EC-OC， 改变个人NO2暴露对呼吸健康的影响， 混淆了室外NO2，一种与交通有关的污染物的指示气体。 个人暴露模型将使用一个嵌套的个人样本来开发。 暴露来预测两个研究区域的PM和NO2暴露。两个面板 的32名哮喘患者将被随访两个月，每个地点一名（总共3，584名 人日）。将使用个人和 确定调整后的PM和NO2，以评估剂量估计值是否增强 协会.长期目标是提高对独立的知识 以及颗粒和气体空气污染物的综合不利影响， 使用流动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.