BACKGROUND & AIMS:
: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.
背景与目标:
: 暴露于环境柴油废气颗粒与儿童的呼吸道症状和哮喘发作有关; 然而,流行病学证据将短期暴露于环境柴油废气颗粒与气道炎症联系在一起是有限的。我们对哮喘和非哮喘青少年进行了一项小组研究,以表征周围柴油废气颗粒暴露与呼出的气道炎症和氧化应激生物标志物之间的关联。在四个星期内,每周两次从纽约市两所学校的18名哮喘患者和18名非哮喘患者 (年龄在14-19岁之间) 收集呼出气冷凝液,并分析pH和8-异前列腺素作为气道炎症和氧化应激的指标,分别。在学校外测量了柴油排气颗粒指示器黑碳的空气浓度。在最近的中央监测点获得了二氧化氮,臭氧和细颗粒物的空气测量值。使用混合效应模型表征了环境污染物与呼出生物标志物之间的关系。在所有受试者中,黑碳的1至5天平均值的增加与呼出气冷凝物pH的降低有关,这表明气道炎症增加,而8-异前列腺素的增加表明氧化应激增加。二氧化氮1至5天平均值的增加与8-异前列腺素的增加有关。臭氧和细颗粒物与呼出的生物标志物不一致。哮喘和非哮喘患者之间的关联没有差异。研究结果表明,短期暴露于与交通有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,并为记录与交通有关的污染物暴露与呼吸道发病率之间的关联提供机械支持。