Urban Air Pollution and Children's Respiratory Health

本研究将探讨交通相关污染在儿童哮喘和肺功能中的作用。工作 将利用南部加州儿童健康研究（CHS）的发现， 前瞻性队列研究。CHS包括来自南部加州社区的儿童，这些社区的儿童在 区域空气质量。我们发现临床上显著的肺功能缺陷，哮喘发病率增加， 以及生活在高区域污染社区的人呼吸道症状增加， 与低污染社区相比。我们发现哮喘的流行率和发病率增加 以及与社区内不同的交通指标相关的肺功能增长下降。这些 与交通指标的社区内协会一直独立于区域的影响， 污染我们还发现儿童易受氧化污染物的呼吸影响， 哮喘病史、特定候选基因、性别、子宫内烟草烟雾暴露和 气道流速我们建议通过调查气道之间的关系来建立这些结果 疾病和与交通有关的特定污染物可能造成这些影响。我们假设 呼吸影响将与颗粒物中毒理学相关成分的变化有关。 包括过渡金属和总的和水溶性有机碳，这将在不同的测量 粒径组分（PM[0.25]、PM[0.25-2.5]和PM[2.5-10]）。我们将研究（1）这些特定的交通相关的协会 污染物和气态共污染物与特征明确的哮喘发作和肺功能 水平和生长;（2）交通相关污染物对肺功能生长影响的修正 哮喘和呼出的一氧化氮（eNO，气道炎症的标志物）。此外，我们还将联合 呼吸结局，包括哮喘、肺功能和其他可用的呼吸健康指标 包括eNO，这可能反映了对颗粒空气污染影响的脆弱性。纵向肺功能 将在1，900名11至15岁的新发哮喘儿童中进行测量 案件将被发现。颗粒和气体污染物将在每个区域内的多个地点进行监测。 八个研究社区，有大的社区内梯度的交通和社区之间 区域空气质量的变化。将使用以下状态估计每个儿童的长期平均暴露量： 最先进的GIS方法和空间建模。这项研究将进一步加深我们对童年的理解 阻塞性肺疾病的起源，并对干预措施的发展具有重要意义， 监管政策，因为交通是一种常见的暴露和哮喘和慢性阻塞性肺病 是重大的公共卫生问题。

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.