Helmholtz Zentrum München, German Research Center for Environmental Health, Institute of Epidemiology, Munich, Germany.
Part Fibre Toxicol. 2009 Sep 26;6:25. doi: 10.1186/1743-8977-6-25.
Growing evidence indicates that ambient air pollution is associated with exacerbation of chronic diseases like chronic pulmonary disease. A prospective panel study was conducted to investigate short-term changes of blood markers of inflammation and coagulation in response to daily changes in air pollution in Erfurt, Germany. 12 clinical visits were scheduled and blood parameters were measured in 38 male patients with chronic pulmonary disease during winter 2001/2002. Additive mixed models with random patient intercept were applied, adjusting for trend, weekday, and meteorological parameters. Hourly data on ultrafine particles (UFP, 0.01-0.1 mum), accumulation mode particles (ACP, 0.1-1.0 mum), PM10 (particulate matter <10 mum in diameter), elemental (EC) and organic carbon (OC), gaseous pollutants (nitrogen monoxide [NO], nitrogen dioxide [NO2], carbon monoxide [CO], and sulphur dioxide [SO2]) were collected at a central monitoring site and meteorological data were received from an official network. For each person and visit the individual 24-hour average of pollutants immediately preceding the blood withdrawal (lag 0) up to day 5 (lag1-4) and 5-day running means were calculated.
Increased levels of fibrinogen were observed for an increase in one interquartile range of UFP, PM10, EC, OC, CO, and NO revealing the strongest effect for lag 3. E-selectin increased in association with ACP and PM10 with a delay of one day. The ACP effect was also seen with the 5-day-mean. The pattern found for D-dimer was inconsistent. Prothrombin fragment 1+2 decreased with lag 4 consistently for all particulate pollutants. Von Willebrand factor antigen (vWF) showed a consistent decrease in association with almost all air pollutants with all lags except for lag 0. No associations were found for C-reactive protein, soluble intercellular adhesion molecule 1, serum amyloid A and factor VII.
These results suggest that elevated concentrations of air pollution are associated with changes in some blood markers of inflammation and coagulation in patients with chronic pulmonary disease. The clinical implications of these findings need further investigation.
越来越多的证据表明，环境空气污染与慢性疾病（如慢性肺部疾病）的恶化有关。本研究开展了一项前瞻性面板研究，以调查德国埃尔福特空气污染每日变化对炎症和凝血血液标志物的短期影响。2001/2002 年冬季，38 名慢性肺部疾病男性患者接受了 12 次临床访视，并测量了血液参数。应用具有随机患者截距的加性混合模型，对趋势、周几和气象参数进行调整。在中央监测点收集了超细颗粒（UFP，0.01-0.1 µm）、积聚态颗粒（ACP，0.1-1.0 µm）、PM10（直径<10 µm 的颗粒物）、元素碳（EC）和有机碳（OC）、气态污染物（一氧化氮 [NO]、二氧化氮 [NO2]、一氧化碳 [CO]和二氧化硫 [SO2]）的每小时数据，并从官方网络接收气象数据。对于每个人和每次就诊，计算血液采集前（滞后 0）到第 5 天（滞后 1-4）的污染物 24 小时平均个体值（滞后 0-4）和 5 天移动平均值。
与 UFP、PM10、EC、OC、CO 和 NO 的一个四分位距增加相比，纤维蛋白原水平升高，表明 UFP 的滞后 3 期的影响最强。E-选择素的增加与 ACP 和 PM10 相关，滞后一天。ACP 的影响也出现在 5 天平均值中。D-二聚体的模式不一致。所有颗粒状污染物的滞后 4 期凝血酶原片段 1+2 一致下降。血管性血友病因子抗原（vWF）与几乎所有空气污染物均呈一致下降趋势，除滞后 0 外，所有滞后期均如此。C-反应蛋白、可溶性细胞间黏附分子 1、血清淀粉样蛋白 A 和因子 VII 均未发现关联。
这些结果表明，空气污染浓度升高与慢性肺部疾病患者某些炎症和凝血血液标志物的变化有关。这些发现的临床意义需要进一步研究。
