Occupational and Environmental Medicine, Unit of Lung Toxicology, Katholique Universiteit Leuven, Leuven, Belgium.
Environ Health Perspect. 2010 Feb;118(2):191-6. doi: 10.1289/ehp.0900942.
Population studies suggest that persons with diabetes are more sensitive to the effects of particulate matter (PM) air pollution. However, the biological mechanisms of a possible prothrombotic effect underlying this enhanced susceptibility remain largely unknown.
We hypothesized that exposure to PM causes prothrombotic changes in persons with diabetes, possibly via systemic inflammation.
Our study included 137 nonsmoking adults with diabetes who were outpatients at the University Hospital Leuven. Recent exposure (2 hr before examination) to ambient PM was measured at the entrance of the hospital. Individual chronic exposure to PM was assessed by measuring the area occupied by carbon in airway macrophages obtained by sputum induction. Platelet function was measured ex vivo with the PFA-100 platelet function analyzer, which simulates a damaged blood vessel; we analyzed the function of platelets in primary hemostasis under high shear conditions. Total and differential blood leukocytes were counted.
Independent of antiplatelet medication, an interquartile range (IQR) increase of 39.2 microg/m3 in PM10 (PM with aerodynamic diameter <or= 10 microm) concentration measured 2 hr before the clinical examination (recent exposure) was associated with a decrease of 21.1 sec [95% confidence interval (CI), 35.3 to 6.8] in the PFA-100 closure time (i.e., increased platelet activation) and an increase in blood leukocytes of 512 per microliter of blood (95% CI, 45.2979). Each area increase of 0.25 microm2 (IQR) in carbon load of airway macrophages (chronic exposure) was associated with an increase of 687 leukocytes per microliter of blood (95% CI, 2241,150).
A relevant increase in recent PM exposure was associated with a change in platelet function toward a greater prothrombotic tendency. The magnitude of the change was about two-thirds (in the opposite direction) of the average effect of antiplatelet medication. Diabetic patients showed evidence of proinflammatory response to both recent and chronic exposure to PM air pollution.
人群研究表明,糖尿病患者对颗粒物(PM)空气污染的影响更为敏感。然而,这种易感性增强的潜在促血栓形成效应的生物学机制在很大程度上仍不清楚。
我们假设 PM 暴露会导致糖尿病患者发生促血栓形成变化,可能是通过全身炎症。
我们的研究包括 137 名在鲁汶大学医院就诊的非吸烟糖尿病成年患者。在医院入口处测量最近(检查前 2 小时)暴露于环境 PM 的情况。通过测量诱导痰中气道巨噬细胞中碳所占的面积来评估个体慢性 PM 暴露。使用 PFA-100 血小板功能分析仪体外测量血小板功能,该分析仪模拟受损血管;我们分析了在高剪切条件下血小板在原发性止血中的功能。计数全血和白细胞分类。
无论是否使用抗血小板药物,与临床检查前 2 小时(最近暴露)测量的 PM10(空气动力学直径≤10μm 的 PM)浓度的中位数(IQR)增加 39.2μg/m3 相关联的是 PFA-100 闭合时间(即血小板激活增加)减少 21.1 秒[95%置信区间(CI),35.3 至 6.8],以及血液白细胞增加 512 个/μl(95%CI,45.2979)。气道巨噬细胞碳负荷(慢性暴露)每增加 0.25μm2(IQR),血液白细胞增加 687 个/μl(95%CI,2241,150)。
最近 PM 暴露的显著增加与血小板功能向更大的促血栓形成倾向的变化有关。变化的幅度大约是抗血小板药物平均作用的三分之二(方向相反)。糖尿病患者对 PM 空气污染的近期和慢性暴露均表现出促炎反应的证据。