Wauters Aurélien, Esmaeilzadeh Fatemeh, Bladt Sandrine, Beukinga Ingrid, Wijns Walter, van de Borne Philippe, Pradier Olivier, Argacha Jean-François
Aurélien Wauters, Department of Cardiology, Erasme Hospital, 808 Lennik Street, 1070 Brussels, Belgium, Tel.: +32 2 555 39 07, Fax: +32 2 555 67 13, E-mail:
Thromb Haemost. 2015 Jan;113(1):118-24. doi: 10.1160/TH14-03-0251. Epub 2014 Oct 9.
Exposure to diesel exhaust is an important cardiovascular risk factor and may promote atherothrombotic events. Some data suggest that polluted air exposure could affect haemostasis through platelet activation. The aim of the study was to investigate the effects of acute exposure to diesel exhaust on platelet activation and platelet function. We tested the hypothesis in a randomised, crossover study in 25 healthy men exposed to ambient and polluted air; 11 of the subjects also performed exercise during exposure sessions. Platelet activation was evaluated by surface expression of CD62P (P-selectin) and CD63 (dense granule glycoprotein) using flow cytometry of labelled platelets. Platelet function was measured using the PFA-100 platelet function analyser and by Multiplate whole blood impedance platelet aggregometry. Acute diesel exhaust exposure had no effect on platelet activation at rest, but exercise in polluted air increased the collagen-induced expression of CD62P and CD63 (both p< 0.05). The increase in the expression of CD62P and CD63 was related to the total amount of PM2.5 inhaled during the exercise sessions (r=+0.58 and +0.60, respectively, both p< 0.05). Platelet aggregation was not impaired after polluted air exposure at rest or during exercise. In conclusion, in healthy subjects, diesel exhaust exposure induces platelet activation as illustrated by a dose-response increase in the release of CD62P and CD63. This platelet priming effect could be a contributor to the triggering of atherothrombotic events related to air pollution exposure.
接触柴油废气是一个重要的心血管危险因素，可能会促进动脉粥样血栓形成事件。一些数据表明，接触污染空气可能通过血小板激活影响止血功能。本研究的目的是调查急性接触柴油废气对血小板激活和血小板功能的影响。我们在一项随机交叉研究中检验了这一假设，该研究纳入了25名暴露于环境空气和污染空气中的健康男性；其中11名受试者在暴露期间还进行了运动。通过对标记血小板进行流式细胞术检测CD62P（P-选择素）和CD63（致密颗粒糖蛋白）的表面表达来评估血小板激活。使用PFA-100血小板功能分析仪和Multiplate全血阻抗血小板聚集测定法测量血小板功能。急性接触柴油废气对静息状态下的血小板激活没有影响，但在污染空气中运动可增加胶原蛋白诱导的CD62P和CD63表达（均p<0.05）。CD62P和CD63表达的增加与运动期间吸入的PM2.5总量有关（分别为r=+0.58和+0.60，均p<0.05）。在静息状态或运动期间接触污染空气后，血小板聚集并未受损。总之，在健康受试者中，接触柴油废气会诱导血小板激活，如CD62P和CD63释放的剂量反应性增加所示。这种血小板预激效应可能是与空气污染暴露相关的动脉粥样血栓形成事件触发的一个因素。
