Yuan N N, Xu H B, Liu S C, Wang Y, Wang T, Yi T C, Chen J, Zhang Y, Zhu Y T, Li L J, Li J P, Cao J J, Huang W
Department of Occupational and Environmental Health, Peking University School of Public Health, Beijing 100191, China.
Division of Cardiology, Peking University First Hospital, Beijing 100034, China.
Zhonghua Yu Fang Yi Xue Za Zhi. 2022 Jul 6;56(7):902-911. doi: 10.3760/cma.j.cn112150-20210924-00923.
To investigate the effects of exposure to ambient fine particulate matter-bound polycyclic aromatic hydrocarbons on blood coagulation in adults. A total of 73 adult volunteers were recruited in a cohort study and had four clinical visits from November 2014 to January 2016. Blood samples were obtained and used to measure biomarkers of blood thrombogenicity, including soluble CD40 Ligand (sCD40L), soluble P-selection (sCD62P) and Fibrinogen (FIB). White blood cell (WBC), 8-Hydroxy-2'-Deoxyguanosine (8-OHdG), matrix metalloproteinase-2 (MMP-2) and HDL cholesterol efflux capacity (HDL-CEC) were also determined. Daily concentrations of ambient fine particulate matter-bound polycyclic aromatic hydrocarbons (PAHs) were measured throughout the study period, and positive matrix factorization (PMF) approach was used to identity PAHs sources. Linear mixed-effect models including single-pollutant model, two-pollutant model and stratification analysis were constructed to estimate the effects of exposure to ambient fine particulate matter-bound PAHs on blood thrombogenicity in adults after adjusting for potential confounders. The mean age of participants was (23.3±5.4) years. During the study period, the median level of PM-bound PAHs was (55.29±74.99) ng/m. Six sources of PM-bound PAHs were identified by PMF, with traffic sources contributing more than 50%. The linear mixed-effect model showed that PAHs exposure had a significant effect on elevated blood thrombogenicity. Significant elevations in sCD40L, sCD62P and FIB associated with per increase (60.33 ng/m) in exposure to PAHs were 14.36% (95%:6.94%-22.28%), 9.33% (95%: 1.71%-17.51%) and 2.07% (95%:0.44%-2.07%) at prior 5 days, respectively. Blood thrombogenicity levels were significantly and positively correlated with source-specific PAHs, especially gasoline vehicle emissions, diesel vehicle emission and coal burning at prior 1 or 5 days. Stronger associations between PAHs and increased blood thrombogenicity were found in participants with high plaque vulnerability, reduced HDL function, and high levels of inflammation and oxidative stress. Acute exposure to ambient fine particulate matter-bound PAHs, especially PAHs from traffic sources may promote blood thrombogenicity in adults, and PAHs have stronger effects on participants with reduced vascular function and high levels of inflammation and oxidative stress.
为研究暴露于环境空气中与细颗粒物结合的多环芳烃对成年人血液凝固的影响。在一项队列研究中招募了73名成年志愿者，他们在2014年11月至2016年1月期间进行了4次临床访视。采集血样并用于测量血液血栓形成的生物标志物，包括可溶性CD40配体（sCD40L）、可溶性P选择素（sCD62P）和纤维蛋白原（FIB）。还测定了白细胞（WBC）、8-羟基-2'-脱氧鸟苷（8-OHdG）、基质金属蛋白酶-2（MMP-2）和高密度脂蛋白胆固醇流出能力（HDL-CEC）。在整个研究期间测量环境空气中与细颗粒物结合的多环芳烃（PAHs）的每日浓度，并采用正矩阵因子分解（PMF）方法确定PAHs的来源。构建包括单污染物模型、双污染物模型和分层分析的线性混合效应模型，以估计在调整潜在混杂因素后，暴露于环境空气中与细颗粒物结合的PAHs对成年人血液血栓形成的影响。参与者的平均年龄为（23.3±5.4）岁。在研究期间，与颗粒物结合的PAHs的中位数水平为（55.29±74.99）ng/m³。通过PMF确定了与颗粒物结合的PAHs的6个来源，其中交通源的贡献率超过50%。线性混合效应模型显示，PAHs暴露对血液血栓形成增加有显著影响。PAHs暴露每增加（60.33 ng/m³），前5天sCD40L、sCD62P和FIB的显著升高分别为14.36%（95%置信区间：6.94%-22.28%）、9.33%（95%置信区间：1.71%-17.51%）和2.07%（95%置信区间：0.44%-2.07%）。血液血栓形成水平与特定来源的PAHs显著正相关，尤其是前1天或5天的汽油车排放、柴油车排放和煤炭燃烧。在斑块易损性高、HDL功能降低以及炎症和氧化应激水平高的参与者中，发现PAHs与血液血栓形成增加之间的关联更强。急性暴露于环境空气中与细颗粒物结合的PAHs，尤其是来自交通源的PAHs，可能会促进成年人的血液血栓形成，并且PAHs对血管功能降低以及炎症和氧化应激水平高的参与者有更强的影响。
