Urban Air Pollution and Children's Respiratory Health

这项研究将调查交通污染对儿童哮喘和肺功能的影响。这项工作 将利用南加州儿童健康研究(CHS)的发现，CHS是一项基于人群的研究 前瞻性队列研究。社区卫生服务包括来自南加州社区的儿童，这些社区在 区域空气质量。我们已经发现了临床上显著的肺功能缺陷，哮喘的发生率增加， 以及居住在地区性高污染社区的人呼吸道症状增加， 与污染较低的社区相比。我们发现哮喘的患病率和发病率都有所增加 以及与社区内不同的交通指标相关的肺功能增长减少。这些 社区内与交通指标的关联一直独立于区域影响 污染。我们还确定了易受氧化性污染物呼吸影响的儿童，基于 哮喘史、特定候选基因、性别、宫内吸烟暴露和早期生活缺陷 呼吸道流率。我们建议在这些结果的基础上，通过研究航空公司之间的关系 疾病和与交通有关的特定污染物可能会造成这些影响。我们假设 呼吸影响将与颗粒物中与毒理相关的成分的变化有关。 包括过渡金属、总有机碳和水溶性有机碳，它们将在不同的 大小分数(PM[0.25]、PM[0.25-2.5]和PM[2.5-10])。我们将研究(1)这些特定流量相关的关联 具有明确特征的哮喘和肺功能的污染物和气态共污染物 水平和生长；以及(2)修改交通相关污染物对肺功能生长的影响 哮喘和呼出的一氧化氮(ENO，呼吸道炎症的标志)。此外，我们还将联合建模 呼吸结果，包括哮喘、肺功能和其他可用的呼吸健康指标 包括ENO在内，这可能反映了对颗粒性空气污染影响的脆弱性。纵向肺功能 将在约11至15岁和新发哮喘的1900名儿童中进行测量 将确定病例。颗粒物和气态污染物将在每个区域的多个地点进行监测 在八个研究社区中，社区内部和社区之间的流量梯度很大 区域空气质量的变化。将使用以下状态来估计每个儿童的长期平均暴露水平 先进的地理信息系统方法和空间建模。这项研究将加深我们对童年的理解 阻塞性肺疾病的起源，并对制定干预措施和 监管政策，由于交通是一种常见的暴露和哮喘和慢性阻塞性肺疾病 是主要的公共卫生问题。

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.