Air Pollution Exposures and Circulating Biomarkers of Effect in a Susceptible Population: Clues to Potential Causal Component Mixtures and Mechanisms
Air Pollution Exposures and Circulating Biomarkers of Effect in a Susceptible Population: Clues to Potential Causal Component Mixtures and Mechanisms
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DOI：
10.1289/ehp.0800194
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发表时间：
2009-08-01
影响因子：
10.4
通讯作者：
Sioutas, Constantinos
中科院分区：
文献类型：
--
作者：
Delfino, Ralph J.;Staimer, Norbert;Sioutas, Constantinos
背景技术背景：氧化应激和炎症机制已被提出来解释环境空气污染与心血管疾病发病率和死亡率的关系。实验证据表明，有机成分和超细颗粒（UFP）是important.METHODS：我们进行了一项小组研究的60名老年人患有冠状动脉疾病生活在退休社区内的洛杉矶，加州，空气盆地。每周一次的炎症生物标志物包括血浆白细胞介素-6、肿瘤坏死因子-α可溶性受体II（sTNF-RII）、可溶性血小板选择素（sP-选择素）和C-反应蛋白（CRP）。红细胞抗氧化活性的生物标志物包括谷胱甘肽过氧化物酶-1和超氧化物歧化酶。暴露量包括户外家庭每日颗粒物质量[空气动力学直径< 0.25、0.25-2.5和2.5-10 μ m的颗粒物（PM0.25，PM0.25-2.5，PM2.5-10）]，以及每小时元素碳和黑碳（EC-BC），估算的一级和二级有机碳（OCpri，SOC）、颗粒数（PN）、一氧化碳（CO）和氮氧化物-二氧化氮（NOx-NO2）。我们分析了生物标志物暴露与混合效应模型调整的潜在confers.RESULTS：主要燃烧标志物（EC-BC，OCpri，CO，NOx-NO2），但不SOC，与炎症生物标志物呈正相关，与红细胞抗氧化酶呈负相关（n = 578）。PN和PM0.25与生物标志物的相关性比PM0.25-2.5更强。所有暴露的协会在较冷的时期，只有OCpri，PN和NOx较高。我们发现他汀类药物（sTNF-RII，CRP）和氯吡格雷的使用（sP-selectin）较弱的关联。结论：与空气污染相关的空气污染物与全身炎症增加，血小板活化增加，红细胞抗氧化酶活性降低，这可能是部分落后于空气污染相关的全身炎症增加。关联的颗粒大小，OC分数，和季节性的差异表明UFP携带的组件是重要的。
BACKGROUND: Mechanisms involving oxidative stress and inflammation have been proposed to explain associations of ambient air pollution with cardiovascular morbidity and mortality. Experimental evidence suggests that organic components and ultrafine particles (UFP) are important.METHODS: We conducted a panel study of 60 elderly subjects with coronary artery disease living in retirement communities within the Los Angeles, California, air basin. Weekly biomarkers of inflammation included plasma interleukin-6, tumor necrosis factor-alpha soluble receptor II (sTNF-RII), soluble platelet selectin (sP-selectin), and C-reactive protein (CRP). Biomarkers of erythrocyte antioxidant activity included glutathione peroxidase-1 and superoxide dismutase. Exposures included outdoor home daily particle mass [particulate matter < 0.25, 0.25-2.5, and 2.5-10 mu m in aerodynamic diameter (PM0.25, PM0.25-2.5, PM2.5-10)], and hourly elemental and black carbon (EC-BC), estimated primary and secondary organic carbon (OCpri, SOC), particle number (PN), carbon monoxide (CO), and nitrogen oxides-nitrogen dioxide (NOx-NO2). We analyzed the relation of biomarkers to exposures with mixed effects models adjusted for potential confounders.RESULTS: Primary combustion markers (EC-BC, OCpri, CO, NOx-NO2), but not SOC, were positively associated with inflammatory biomarkers and inversely associated with erythrocyte antioxidant enzymes (n = 578). PN and PM0.25 were more strongly associated with biomarkers than PM0.25-2.5. Associations for all exposures were stronger during cooler periods when only OCpri, PN, and NOx were higher. We found weaker associations with statin (sTNF-RII, CRP) and clopidogrel use (sP-selectin).CONCLUSIONS: Traffic-related air pollutants are associated with increased systemic inflammation, increased platelet activation, and decreased erythrocyte antioxidant enzyme activity, which may be partly behind air pollutant-related increases in systemic inflammation. Differences in association by particle size, OC fraction, and seasonal period suggest components carried by UFP are important.