Delfino Ralph J, Staimer Norbert, Tjoa Thomas, Arhami Mohammad, Polidori Andrea, Gillen Daniel L, Kleinman Michael T, Schauer James J, Sioutas Constantinos
Department of Epidemiology, School of Medicine, University of California-Irvine, Irvine, California 92617-7555, USA.
Environ Health Perspect. 2010 Jun;118(6):756-62. doi: 10.1289/ehp.0901407. Epub 2010 Feb 2.
Evidence is needed regarding the air pollutant components and their sources responsible for associations between particle mass concentrations and human cardiovascular outcomes. We previously found associations between circulating biomarkers of inflammation and mass concentrations of quasi-ultrafine particles <or= 0.25 microm in aerodynamic diameter (PM0.25) in a panel cohort study of 60 elderly subjects with coronary artery disease living in the Los Angeles Basin.
We reassessed biomarker associations with PM0.25 using new particle composition data.
Weekly biomarkers of inflammation were plasma interleukin-6 (IL-6) and soluble tumor necrosis factor-alpha receptor II (sTNF-RII) (n = 578). Exposures included indoor and outdoor community organic PM0.25 constituents [polycyclic aromatic hydrocarbons (PAHs), hopanes, n-alkanes, organic acids, water-soluble organic carbon, and transition metals]. We analyzed the relation between biomarkers and exposures with mixed-effects models adjusted for potential confounders.
Indoor and outdoor PAHs (low-, medium-, and high-molecular-weight PAHs), followed by hopanes (vehicle emissions tracer), were positively associated with biomarkers, but other organic components and transition metals were not. sTNF-RII increased by 135 pg/mL [95% confidence interval (CI), 45-225 pg/mL], and IL-6 increased by 0.27 pg/mL (95% CI, 0.10-0.44 pg/mL) per interquartile range increase of 0.56 ng/m3 outdoor total PAHs. Two-pollutant models of PM0.25 with PAHs showed that nominal associations of IL-6 and sTNF-RII with PM0.25 mass were completely confounded by PAHs. Vehicular emission sources estimated from chemical mass balance models were strongly correlated with PAHs (R = 0.71).
Traffic emission sources of organic chemicals represented by PAHs are associated with increased systemic inflammation and explain associations with quasi-ultrafine particle mass.
关于导致颗粒物质量浓度与人类心血管疾病结局之间关联的空气污染物成分及其来源，需要相关证据。在一项对居住于洛杉矶盆地的60名老年冠心病患者的队列研究中，我们先前发现炎症循环生物标志物与空气动力学直径≤0.25微米的准超细颗粒物（PM0.25）的质量浓度之间存在关联。
我们使用新的颗粒物成分数据重新评估生物标志物与PM0.25之间的关联。
炎症的每周生物标志物为血浆白细胞介素-6（IL-6）和可溶性肿瘤坏死因子-α受体II（sTNF-RII）（n = 578）。暴露因素包括室内和室外社区有机PM0.25成分[多环芳烃（PAHs）、藿烷、正构烷烃、有机酸、水溶性有机碳和过渡金属]。我们使用针对潜在混杂因素进行调整的混合效应模型分析了生物标志物与暴露因素之间的关系。
室内和室外PAHs（低、中、高分子量PAHs），其次是藿烷（车辆排放示踪剂），与生物标志物呈正相关，但其他有机成分和过渡金属则不然。室外总PAHs每增加一个四分位数间距（0.56 ng/m3），sTNF-RII增加135 pg/mL [95%置信区间（CI），45 - 225 pg/mL]，IL-6增加0.27 pg/mL（95%CI，0.10 - 0.44 pg/mL）。PM0.25与PAHs的双污染物模型显示，IL-6和sTNF-RII与PM0.25质量的名义关联完全被PAHs混淆。通过化学质量平衡模型估算的车辆排放源与PAHs高度相关（R = 0.71）。
以PAHs为代表的有机化学物质的交通排放源与全身炎症增加有关，并解释了与准超细颗粒物质量的关联。
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