Department of Environmental and Occupational Health Sciences, School of Public Health, University of Washington, 4225 Roosevelt Way NE, Seattle, WA, 98105, USA; Department of Epidemiology, School of Public Health, University of Washington, 3980 15th Ave NE, Seattle, WA, 98195, USA.
Department of Pathology and Laboratory Medicine, Department of Biochemistry, Larner College of Medicine, University of Vermont, 360 S. Park Drive, Colchester, VT, 05446, USA.
Environ Pollut. 2021 Jun 15;279:116893. doi: 10.1016/j.envpol.2021.116893. Epub 2021 Mar 11.
To help understand the pathophysiologic mechanisms linking air pollutants and cardiovascular disease (CVD), we employed a repeated measures design to investigate the associations of four short-term air pollution exposures - particulate matter less than 2.5 μm in diameter (PM), nitrogen dioxide (NO), ozone (O) and sulfur dioxide (SO), with two blood markers involved in vascular effects of oxidative stress, soluble lectin-like oxidized LDL receptor-1 (sLOX-1) and nitrite, using data from the Multi-Ethnic Study of Atherosclerosis (MESA). Seven hundred and forty participants with plasma sLOX-1 and nitrite measurements at three exams between 2002 and 2007 were included. Daily PM, NO, O and SO zero to seven days prior to blood draw were estimated from central monitors in six MESA regions, pre-adjusted using site-specific splines of meteorology and temporal trends, and an indicator for day of the week. Unconstrained distributed lag generalized estimating equations were used to estimate net effects over eight days with adjustment for sociodemographic and behavioral factors. The results showed that higher short-term concentrations of PM, but not other pollutants, were associated with increased sLOX-1 analyzed both as a continuous outcome (percent change per interquartile increase: 16.36%, 95%CI: 0.1-35.26%) and dichotomized at the median (odds ratio per interquartile increase: 1.21, 95%CI: 1.01-1.44). The findings were not meaningfully changed after adjustment for additional covariates or in several sensitivity analyses. Pollutant concentrations were not associated with nitrite levels. This study extends earlier experimental findings of increased sLOX-1 levels following PM inhalation to a much larger population and at ambient concentrations. In light of its known mechanistic role in promoting vascular disease, sLOX-1 may be a suitable translational biomarker linking air pollutant exposures and cardiovascular outcomes.
为了帮助理解将空气污染物与心血管疾病(CVD)联系起来的病理生理机制,我们采用重复测量设计来研究四种短期空气污染物暴露-直径小于 2.5μm 的颗粒物(PM)、二氧化氮(NO)、臭氧(O)和二氧化硫(SO)与两种参与血管氧化应激的血液标志物之间的关联,这两种标志物是可溶性凝集素样氧化型 LDL 受体-1(sLOX-1)和亚硝酸盐,使用来自动脉粥样硬化多民族研究(MESA)的数据。纳入了 740 名在 2002 年至 2007 年期间三次检查中具有血浆 sLOX-1 和亚硝酸盐测量值的参与者。根据 MESA 六个地区的中央监测器,在采血前 0 至 7 天估计每日 PM、NO、O 和 SO,使用特定地点的气象和时间趋势样条进行预调整,并使用一周中的某天的指标进行调整。使用无约束分布滞后广义估计方程在调整社会人口统计学和行为因素的情况下,对 8 天的净效应进行估计。结果表明,较高的短期 PM 浓度与 sLOX-1 的增加有关,但其他污染物则没有,这两种分析都是作为连续结果(每四分位数增加的百分比变化:16.36%,95%CI:0.1-35.26%)和在中位数处二分(每四分位数增加的比值比:1.21,95%CI:1.01-1.44)。在调整其他协变量或进行几项敏感性分析后,这些发现并没有明显改变。污染物浓度与亚硝酸盐水平无关。这项研究将 PM 吸入后 sLOX-1 水平升高的早期实验发现扩展到了更大的人群和环境浓度。鉴于其在促进血管疾病方面的已知机制作用,sLOX-1 可能是将空气污染物暴露与心血管结局联系起来的合适转化生物标志物。