Traffic-related air pollutants and exhaled markers of airway inflammation and oxidative stress in New York City adolescents.
Traffic-related air pollutants and exhaled markers of airway inflammation and oxidative stress in New York City adolescents.
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DOI：
10.1016/j.envres.2012.10.012
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发表时间：
2013-02
影响因子：
8.3
通讯作者：
Kinney, Patrick L.
中科院分区：
文献类型：
--
作者：
Patel, Molini M.;Chillrud, Steven N.;Deepti, K. C.;Ross, James M.;Kinney, Patrick L.
暴露于环境柴油机废气颗粒与儿童呼吸道症状和哮喘加重有关;然而，短期暴露于环境柴油机废气颗粒与气道炎症有关的流行病学证据有限。我们对哮喘和非哮喘青少年进行了一项小组研究，以描述环境柴油废气颗粒暴露与呼吸道炎症和氧化应激的呼出生物标志物之间的关系。在四周内，每周两次收集来自纽约市两所学校的18名哮喘患者和18名非哮喘患者（年龄14-19岁）的呼出气冷凝物，并分别分析pH和8-异前列烷作为气道炎症和氧化应激的指标。学校外的空气中黑碳的浓度是一种柴油机尾气颗粒物的指标。在最近的中心监测点获得了二氧化氮、臭氧和细颗粒物的空气测量值。环境污染物和呼出的生物标志物之间的关系，其特征在于使用混合效应模型。在所有受试者中，1- 5天平均黑碳的增加与呼出气冷凝物pH值的降低相关，表明气道炎症增加，8-异前列烷的增加表明氧化应激增加。1- 5天平均二氧化氮的增加与8-异前列烷的增加有关。臭氧和细颗粒物与呼出的生物标志物不一致。哮喘患者和非哮喘患者之间的相关性没有差异。研究结果表明，短期暴露于交通相关的空气污染物可能会增加城市青年的气道炎症和/或氧化应激，并为交通相关的污染物暴露和呼吸道疾病之间的关联提供机械支持。
Exposures to ambient diesel exhaust particles have been associated with respiratory symptoms and asthma exacerbations in children; however, epidemiologic evidence linking short-term exposure to ambient diesel exhaust particles with airway inflammation is limited. We conducted a panel study with asthmatic and nonasthmatic adolescents to characterize associations between ambient diesel exhaust particle exposures and exhaled biological markers of airway inflammation and oxidative stress. Over four weeks, exhaled breath condensate was collected twice a week from 18 asthmatics and 18 nonasthmatics (ages 14–19 years) attending two New York City schools and analyzed for pH and 8-isoprostane as indicators of airway inflammation and oxidative stress, respectively. Air concentrations of black carbon, a diesel exhaust particle indicator, were measured outside schools. Air measurements of nitrogen dioxide, ozone, and fine particulate matter were obtained for the closest central monitoring sites. Relationships between ambient pollutants and exhaled biomarkers were characterized using mixed effects models. Among all subjects, increases in 1- to 5-day averages of black carbon were associated with decreases in exhaled breath condensate pH, indicating increased airway inflammation, and increases in 8-isoprostane, indicating increased oxidative stress. Increases in 1- to 5-day averages of nitrogen dioxide were associated with increases in 8-isoprostane. Ozone and fine particulate matter were inconsistently associated with exhaled biomarkers. Associations did not differ between asthmatics and nonasthmatics. The findings indicate that short-term exposure to traffic-related air pollutants may increase airway inflammation and/or oxidative stress in urban youth and provide mechanistic support for associations documented between traffic-related pollutant exposures and respiratory morbidity.
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影响因子：
5
作者：
Maciejczyk, PB;Offenberg, JH;Chen, LC
通讯作者：
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影响因子：
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作者：
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作者：
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发表时间：
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影响因子：
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作者：
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通讯作者：
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影响因子：
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作者：
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