Rückerl Regina, Phipps Richard P, Schneider Alexandra, Frampton Mark, Cyrys Josef, Oberdörster Günther, Wichmann H Erich, Peters Annette
Institute of Epidemiology, GSF National Research Centre for Environment and Health, Neuherberg, Germany.
Part Fibre Toxicol. 2007 Jan 22;4:1. doi: 10.1186/1743-8977-4-1.
Epidemiological studies on health effects of air pollution have consistently shown adverse cardiovascular effects. Toxicological studies have provided evidence for thrombogenic effects of particles.A prospective panel study in a susceptible population was conducted in Erfurt, Germany, to study the effects of daily changes in ambient particles on various blood cells and soluble CD40ligand (sCD40L, also known as CD154), a marker for platelet activation that can cause increased coagulation and inflammation. Blood cells and plasma sCD40L levels were repeatedly measured in 57 male patients with coronary heart disease (CHD) during winter 2000/2001. Fixed effects linear regression models were applied, adjusting for trend, weekday and meteorological parameters.Hourly data on ultrafine particles (UFP, number concentration of particles from 0.01 to 0.1 microm), mass concentration of particles less than 10 and 2.5 microm in diameter (PM10, PM2.5), accumulation mode particle counts (AP, 0.1-1.0 microm), elemental and organic carbon, gaseous pollutants and meteorological data were collected at central monitoring sites.
An immediate increase in plasma sCD40L was found in association with UFP and AP (% change from geometric mean: 7.1; CI: [0.1, 14.5] and 6.9; CI: [0.5, 13.8], respectively). Platelet counts decreased in association with UFP showing an immediate, a three days delayed (lag 3) and a 5-day average response (% change from the mean: -1.8; CI: [-3.4,-0.2]; -2.4; CI: [-4.5,-0.3] and -2.2; CI: [-4.0,-0.3] respectively).
The increased plasma sCD40L levels support the hypothesis that higher levels of ambient air pollution lead to an inflammatory response in patients with CHD thus providing a possible explanation for the observed association between air pollution and cardiovascular morbidity and mortality in susceptible parts of the population.
关于空气污染对健康影响的流行病学研究一直表明其对心血管有不良影响。毒理学研究已为颗粒物的致血栓作用提供了证据。在德国埃尔福特对易感人群进行了一项前瞻性队列研究,以探讨环境颗粒物每日变化对各种血细胞和可溶性CD40配体(sCD40L,也称为CD154)的影响,sCD40L是血小板活化的标志物,可导致凝血和炎症增加。在2000/2001年冬季,对57名男性冠心病(CHD)患者的血细胞和血浆sCD40L水平进行了多次测量。应用固定效应线性回归模型,并对趋势、工作日和气象参数进行了调整。在中央监测点收集了超细颗粒物(UFP,粒径为0.01至0.1微米的颗粒物数量浓度)、直径小于10微米和2.5微米的颗粒物质量浓度(PM10、PM2.5)、积聚模态颗粒计数(AP,0.1至1.0微米)、元素碳和有机碳、气态污染物以及气象数据的每小时数据。
发现血浆sCD40L与UFP和AP立即增加相关(相对于几何平均值的变化百分比:分别为7.1;置信区间:[0.1, 14.5]和6.9;置信区间:[0.5, 13.8])。血小板计数与UFP相关下降,呈现立即、三天延迟(滞后3)和五天平均反应(相对于平均值的变化百分比:分别为-1.8;置信区间:[-3.4, -0.2];-2.4;置信区间:[-4.5, -0.3]和-2.2;置信区间:[-4.0, -0.3])。
血浆sCD40L水平升高支持以下假设,即更高水平的环境空气污染会导致冠心病患者出现炎症反应,从而为在易感人群中观察到的空气污染与心血管发病率和死亡率之间的关联提供了一种可能的解释。