Hunter Amanda L, Unosson Jon, Bosson Jenny A, Langrish Jeremy P, Pourazar Jamshid, Raftis Jennifer B, Miller Mark R, Lucking Andrew J, Boman Christoffer, Nyström Robin, Donaldson Kenneth, Flapan Andrew D, Shah Anoop S V, Pung Louis, Sadiktsis Ioannis, Masala Silvia, Westerholm Roger, Sandström Thomas, Blomberg Anders, Newby David E, Mills Nicholas L
BHF Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, UK.
Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden.
Part Fibre Toxicol. 2014 Dec 9;11:62. doi: 10.1186/s12989-014-0062-4.
Myocardial infarction is the leading cause of death in fire fighters and has been linked with exposure to air pollution and fire suppression duties. We therefore investigated the effects of wood smoke exposure on vascular vasomotor and fibrinolytic function, and thrombus formation in healthy fire fighters.
In a double-blind randomized cross-over study, 16 healthy male fire fighters were exposed to wood smoke (~1 mg/m³ particulate matter concentration) or filtered air for one hour during intermittent exercise. Arterial pressure and stiffness were measured before and immediately after exposure, and forearm blood flow was measured during intra-brachial infusion of endothelium-dependent and -independent vasodilators 4-6 hours after exposure. Thrombus formation was assessed using the ex vivo Badimon chamber at 2 hours, and platelet activation was measured using flow cytometry for up to 24 hours after the exposure.
Compared to filtered air, exposure to wood smoke increased blood carboxyhaemoglobin concentrations (1.3% versus 0.8%; P < 0.001), but had no effect on arterial pressure, augmentation index or pulse wave velocity (P > 0.05 for all). Whilst there was a dose-dependent increase in forearm blood flow with each vasodilator (P < 0.01 for all), there were no differences in blood flow responses to acetylcholine, sodium nitroprusside or verapamil between exposures (P > 0.05 for all). Following exposure to wood smoke, vasodilatation to bradykinin increased (P = 0.003), but there was no effect on bradykinin-induced tissue-plasminogen activator release, thrombus area or markers of platelet activation (P > 0.05 for all).
Wood smoke exposure does not impair vascular vasomotor or fibrinolytic function, or increase thrombus formation in fire fighters. Acute cardiovascular events following fire suppression may be precipitated by exposure to other air pollutants or through other mechanisms, such as strenuous physical exertion and dehydration.
心肌梗死是消防员死亡的主要原因,且与接触空气污染及灭火任务有关。因此,我们研究了木烟暴露对健康消防员血管舒缩功能、纤溶功能及血栓形成的影响。
在一项双盲随机交叉研究中,16名健康男性消防员在间歇运动期间暴露于木烟(颗粒物浓度约1毫克/立方米)或过滤空气中1小时。在暴露前和暴露后立即测量动脉压和硬度,并在暴露后4 - 6小时内进行肱动脉内输注内皮依赖性和非依赖性血管舒张剂期间测量前臂血流量。在暴露后2小时使用体外Badimon腔评估血栓形成,并在暴露后长达24小时使用流式细胞术测量血小板活化。
与过滤空气相比,木烟暴露增加了血液中碳氧血红蛋白浓度(1.3%对0.8%;P < 0.001),但对动脉压、增强指数或脉搏波速度无影响(所有P > 0.05)。虽然每种血管舒张剂使前臂血流量呈剂量依赖性增加(所有P < 0.01),但不同暴露之间对乙酰胆碱、硝普钠或维拉帕米的血流反应无差异(所有P > 0.05)。暴露于木烟后,对缓激肽的血管舒张作用增强(P = 0.003),但对缓激肽诱导的组织纤溶酶原激活物释放、血栓面积或血小板活化标志物无影响(所有P > 0.05)。
木烟暴露不会损害消防员的血管舒缩功能或纤溶功能,也不会增加血栓形成。灭火后的急性心血管事件可能是由接触其他空气污染物或通过其他机制引发的,如剧烈体力活动和脱水。