Abstract：
Epidemiological findings have determined the linkage of fine particulate matter (PM2.5) and the morbidity of hypertension. However, the mode of action and specific contribution of PM2.5 component in the blood pressure elevation remain unclear. Platelets are critical for vascular homeostasis and thrombosis, which may be involved in the increase of blood pressure. Among 240 high-PM2.5 exposed, 318 low-PM2.5 exposed workers in a coking plant and 210 workers in the oxygen plant and cold-rolling mill enrolled in present study, both internal and external exposure characteristics were obtained, and we performed linear regression, adaptive elastic net regression, quantile g-computation and mediation analyses to analyze the relationship between urine metabolites of polycyclic aromatic hydrocarbons (PAHs) and metals fractions with platelets indices and blood pressure indicators. We found that PM2.5 exposure leads to increased systolic blood pressure (SBP) and pulse pressure (PP). Specifically, for every 10 μg/m3 increase in PM2.5, there was a 0.09 mmHg rise in PP. Additionally, one IQR increase in urinary 1-hydroxypyrene (1.06 μmol/mol creatinine) was associated with a 3.43 % elevation in PP. Similarly, an IQR increment of urine cobalt (2.31 μmol/mol creatinine) was associated with a separate 1.77 % and 4.71 % elevation of SBP and PP. Notably, platelet-to-lymphocyte ratio (PLR) played a mediating role in the elevation of SBP and PP induced by cobalt. Our multi-pollutants results showed that PAHs and cobalt were deleterious contributors to the elevated blood pressure. These findings deepen our understanding of the cardiovascular effects associated with PM2.5 constituents, highlighting the importance of increased vigilance in monitoring and controlling the harmful components in PM2.5.
摘要：
流行病学发现已确定细颗粒物（PM2.5）与高血压发病率之间的联系。然而,PM2.5成分在血压升高中的作用方式和具体贡献尚不清楚。血小板对于血管稳态和血栓形成至关重要，这可能与血压升高有关。在暴露的240种高PM2.5中，参与本研究的焦化厂318名低PM2.5暴露工人和制氧厂和冷轧机210名工人，获得了内部和外部暴露特性，我们进行了线性回归，自适应弹性网络回归，分位数计算和调解分析，以分析多环芳烃（PAHs）的尿液代谢产物与血小板指数和血压指标的金属组分之间的关系。我们发现PM2.5暴露会导致收缩压（SBP）和脉压（PP）升高。具体来说,PM2.5每增加10μg/m3，PP增加0.09mmHg。此外,尿1-羟基芘（1.06μmol/mol肌酐）的IQR增加与PP升高3.43％相关。同样，尿钴的IQR增加(2.31μmol/mol肌酐)与SBP和PP分别升高1.77%和4.71%相关.值得注意的是,血小板与淋巴细胞比值（PLR）在钴引起的SBP和PP升高中起中介作用。我们的多污染物结果表明，多环芳烃和钴是导致血压升高的有害因素。这些发现加深了我们对与PM2.5成分相关的心血管效应的理解，强调在监测和控制PM2.5中有害成分方面提高警惕的重要性。
