Personal Exposures and Acute Airway Response in Children

虽然环境空气污染已被认为是哮喘急性发作的危险因素，但对 流行病学研究的结果受到暴露的不确定性和精确的 气道反应的性质。这项拟议研究的总体目标是增进我们对以下问题的了解： 柴油机废气暴露对哮喘急性加重的影响， 结果测量。我们建议优化和测试一种新的微型“智能”个人采样系统， 尺寸和成分分类的颗粒物，并在个人研究中实施该系统 在CCCEH登记的儿童中暴露和急性气道反应。智能采样器将监测 30名9/10岁哮喘儿童和30名非哮喘儿童的DEP/BC（柴油机废气）个人暴露 颗粒物-黑碳）、多种元素和PM2.5，并将区分三种情况下发生的暴露 关键环境（在家里、在学校和其他/在运输途中）。对于每个孩子，我们将收集一个序列， 48-小时的个人样本，定时与2周平均家庭室内和室外测量相一致 在项目1中提出。我们将量化和比较家庭、学校和社区中DEP/BC的个人暴露， 其他/过境，并将分析个人DEP/BC暴露之间的关系，同时- 测量家庭室内/室外DEP/BC浓度。基于粒子元素组成，我们还 将分析个人PM2.5暴露受交通相关颗粒物排放影响的程度。在 在每个48小时监测期结束后，我们将测量呼气生物标志物（cys- 白三烯、NO、8-异前列烷）和腺苷，通过肺活量测定法测定的肺功能，和呼吸症状（即， 60个孩子中的每一个。统计分析和假设检验将：1）确定 家庭、学校和其他/运输中暴露环境对个人暴露的重要性，2） 个人DEP/BC暴露对呼出8-异前列烷、NO、pH、cys-白三烯和 腺苷，以及3）确定这些生物标志物的平均水平是否随儿童而变化， 哮喘状态和/或平均DEP/BC暴露。本文提出的目标和方法， 促进我们对DEP/BC急性气道效应的理解，并补充其他目的 项目

While ambient air pollution has been implicated as a risk factor for asthma exacerbations, interpretation of findings from epidemiologic studies has been hampered by uncertainties in exposures and in the precise nature of the airway responses. The overall goal of the proposed study is to advance our understanding of the influence of diesel exhaust exposures in acute asthma exacerbations by linking innovative exposure and outcome measures. We propose to optimize and test a new miniature "smart" personal sampling system for size- and composition-classified particulate matter, and to implement the system in a study of personal xposures and acute airway responses among children enrolled in CCCEH. The smart sampler will monitor personal exposures for 30 asthmatic and 30 non-asthmatic children ages 9/10 to DEP/BC (Diesel Exhaust Particulates-Black Carbon), multiple elements, and PM2.5 and will distinguish exposures occurring in three key environments (at home, at school and other/in-transit). For each child, we will collect a sequence of six 48-hour personal samples, timed to coincide with 2-week average home indoor and outdoor measurements proposed in project 1. We will quantify and compare personal exposures to DEP/BC at home, school, and other/transit, and will analyze the relationship between personal DEP/BC exposures and concurrently- measured home indoor/outdoor DEP/BC concentrations. Based on particle elemental composition, we also will analyze the extent to which personal PM2.5 exposures are driven by traffic-related particle emissions. At the completion of each 48-hour monitoring period, we will measure exhaled-breath biomarkers (cys- leukotrienes, NO, 8-isoprostane) and adenosine, lung function by spirometry, and respiratory symptoms (i.e., wheeze) for each of the 60 children. Statistical analyses and hypothesis testing will 1) determine the relative importance of home, school, and other/in-transit exposure environments for personal exposures, 2) test for acute effects of personal DEP/BC exposures on exhaled-breath 8-isoprostane, NO, pH, cys-leukotrienes and adenosine, and 3) determine whether average levels of these biomarkers vary across children as a function of asthma status and/or average DEP/BC exposure. The aims and methods proposed here will both advance our understanding of acute airway effects of DEP/BC and complement the aims of the other projects.