Zhang Xian, Staimer Norbert, Gillen Daniel L, Tjoa Tomas, Schauer James J, Shafer Martin M, Hasheminassab Sina, Pakbin Payam, Vaziri Nosratola D, Sioutas Constantinos, Delfino Ralph J
Department of Epidemiology, School of Medicine, University of California, Irvine, CA, USA.
Department of Statistics, School of Information and Computer Sciences, University of California, Irvine, CA, USA.
Environ Res. 2016 Oct;150:306-319. doi: 10.1016/j.envres.2016.06.019. Epub 2016 Jun 21.
Exposure to air pollution has been associated with cardiorespiratory morbidity and mortality. However, the chemical constituents and pollution sources underlying these associations remain unclear.
We conducted a cohort panel study involving 97 elderly subjects living in the Los Angeles metropolitan area. Airway and circulating biomarkers of oxidative stress and inflammation were measured weekly over 12 weeks and included, exhaled breath condensate malondialdehyde (EBC MDA), fractional exhaled nitric oxide (FeNO), plasma oxidized low-density lipoprotein (oxLDL), and plasma interleukin-6 (IL-6). Exposures included 7-day personal nitrogen oxides (NOx), daily criteria-pollutant data, five-day average particulate matter (PM) measured in three size-fractions and characterized by chemical components including transition metals, and in vitro PM oxidative potential (dithiothreitol and macrophage reactive oxygen species). Associations between biomarkers and pollutants were assessed using linear mixed effects regression models.
We found significant positive associations of airway oxidative stress and inflammation with traffic-related air pollutants, ultrafine particles and transition metals. Positive but nonsignificant associations were observed with PM oxidative potential. The strongest associations were observed among PM variables in the ultrafine range (PM <0.18µm). It was estimated that an interquartile increase in 5-day average ultrafine polycyclic aromatic hydrocarbons was associated with a 6.3% (95% CI: 1.1%, 11.6%) increase in EBC MDA and 6.7% (95% CI: 3.4%, 10.2%) increase in FeNO. In addition, positive but nonsignificant associations were observed between oxLDL and traffic-related pollutants, ultrafine particles and transition metals while plasma IL-6 was positively associated with 1-day average traffic-related pollutants.
Our results suggest that exposure to pollutants with high oxidative potential (traffic-related pollutants, ultrafine particles, and transition metals) may lead to increased airway oxidative stress and inflammation in elderly adults. This observation was less clear with circulating biomarkers.
暴露于空气污染与心肺疾病的发病率和死亡率相关。然而，这些关联背后的化学成分和污染源仍不清楚。
我们开展了一项队列研究，涉及97名居住在洛杉矶大都市区的老年人。在12周内每周测量气道和循环系统中氧化应激和炎症的生物标志物，包括呼出气冷凝物丙二醛（EBC MDA）、呼出一氧化氮分数（FeNO）、血浆氧化型低密度脂蛋白（oxLDL）和血浆白细胞介素-6（IL-6）。暴露因素包括7天的个人氮氧化物（NOx）、每日标准污染物数据、按三个粒径分级测量并以包括过渡金属在内的化学成分表征的五日平均颗粒物（PM），以及体外PM氧化潜力（二硫苏糖醇和巨噬细胞活性氧）。使用线性混合效应回归模型评估生物标志物与污染物之间的关联。
我们发现气道氧化应激和炎症与交通相关空气污染物、超细颗粒物和过渡金属之间存在显著正相关。观察到与PM氧化潜力呈正相关但不显著。在超细范围（PM<0.18µm）的PM变量之间观察到最强的关联。据估计，五日平均超细多环芳烃的四分位数间距增加与EBC MDA增加6.3%（95%CI：1.1%，11.6%）和FeNO增加6.7%（95%CI：3.4%，10.2%）相关。此外，oxLDL与交通相关污染物、超细颗粒物和过渡金属之间观察到正相关但不显著，而血浆IL-6与一日平均交通相关污染物呈正相关。
我们的结果表明，暴露于具有高氧化潜力的污染物（交通相关污染物、超细颗粒物和过渡金属）可能导致老年人气道氧化应激和炎症增加。对于循环生物标志物，这种观察结果不太明显。
