Department of Occupational and Environmental Health Sciences, Peking University School of Public Health, Beijing, China.
Institute of Reproductive & Child Health, Peking University School of Public Health, Beijing, China.
Sci Total Environ. 2016 Aug 1;560-561:141-9. doi: 10.1016/j.scitotenv.2016.03.228. Epub 2016 Apr 18.
Exposure to ambient air pollution has been associated with endothelial dysfunction as reflected by short-term alterations in circulating biomarkers, but the chemical constituents and pollution sources behind the association has been unclear.
We investigated the associations between various ambient air pollutants including gases and 31 chemical constituents and seven sources of fine particles (PM2.5) and biomarkers of endothelial function, including endothelin-1 (ET-1), E-selectin, soluble intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1), based on 462 repeated measurements in a panel of 40 college students who were followed for three study periods before and after relocating from a suburban area to an urban area in Beijing, China in 2010-2011. Air pollution data were obtained from central air-monitoring stations. Linear mixed-effects models were used to estimate the changes in biomarkers associated with exposures.
Total PM2.5 mass showed few appreciable associations with examined biomarkers. However, several PM2.5 constituents and related sources showed significant associations with examined biomarkers. PM2.5 from dust/soil and several crustal and transition metals, including strontium, iron, titanium, cobalt and magnesium, were significantly associated with increases in ET-1 at 1-day average; manganese and potassium were significantly associated with increases in ICAM-1 at 2-day average; and PM2.5 from industry and metal cadmium were significantly associated with decreases in VCAM-1 at 1-day average. In addition, carbon monoxide was significantly associated with increasing ICAM-1 at 1-day and 2-day averages, whereas nitric oxide was significantly associated with decreasing ICAM-1 at 1-day and 3-day averages.
Our results suggest that certain PM2.5 metal constituents were more closely associated with circulating biomarkers of endothelial function than PM2.5, and therefore highlight the research necessity to examine pollution chemical constituents in future studies.
暴露于环境空气中的污染物与短期循环生物标志物的变化所反映的内皮功能障碍有关，但关联背后的化学物质成分和污染来源尚不清楚。
我们研究了 2010-2011 年期间 40 名大学生从郊区搬至北京市区前后三个研究阶段中，各种环境空气污染物（包括气体和 31 种化学物质成分）与细颗粒物（PM2.5）的 7 个污染源和内皮功能生物标志物（包括内皮素-1（ET-1）、E-选择素、可溶性细胞间黏附分子 1（ICAM-1）和血管细胞黏附分子 1（VCAM-1））之间的关联。空气污染数据来自中心空气监测站。线性混合效应模型用于估计与暴露相关的生物标志物变化。
总 PM2.5 质量与所检查的生物标志物之间几乎没有明显关联。然而，PM2.5 的几种成分和相关来源与所检查的生物标志物显著相关。尘土/土壤和几种地壳和过渡金属（包括锶、铁、钛、钴和镁）产生的 PM2.5 与 ET-1 的 1 天平均水平升高显著相关；锰和钾与 2 天平均水平 ICAM-1 的升高显著相关；工业和金属镉产生的 PM2.5 与 1 天平均 VCAM-1 的降低显著相关。此外，一氧化碳与 1 天和 2 天平均 ICAM-1 的升高显著相关，而一氧化氮与 1 天和 3 天平均 ICAM-1 的降低显著相关。
我们的结果表明，某些 PM2.5 金属成分与循环内皮功能生物标志物的关联比 PM2.5 更密切，因此强调了在未来研究中检查污染化学物质成分的必要性。
