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Effect of wood smoke exposure on vascular function and thrombus formation in healthy fire fighters.
Particle and Fibre Toxicology ( IF 10 ) Pub Date : 2014-12-09 , DOI: 10.1186/s12989-014-0062-4
Amanda L Hunter 1 , Jon Unosson 2 , Jenny A Bosson 2 , Jeremy P Langrish 1 , Jamshid Pourazar 2 , Jennifer B Raftis 3 , Mark R Miller 1 , Andrew J Lucking 1 , Christoffer Boman 4 , Robin Nyström 4 , Kenneth Donaldson 3 , Andrew D Flapan 5 , Anoop S V Shah 1 , Louis Pung 1 , Ioannis Sadiktsis 6 , Silvia Masala 6 , Roger Westerholm 6 , Thomas Sandström 2 , Anders Blomberg 2 , David E Newby 1 , Nicholas L Mills 1
Affiliation  

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. ClinicalTrials.gov Identifier: NCT01495325 .

中文翻译:

木烟暴露对健康消防员血管功能和血栓形成的影响。

心肌梗塞是消防员死亡的主要原因,并且与暴露于空气污染和灭火任务有关。因此,我们研究了木烟暴露对健康消防员血管舒缩和纤溶功能以及血栓形成的影响。在一项双盲随机交叉研究中,16 名健康男性消防员在间歇性运动期间暴露于木烟(约 1 mg/m3 颗粒物浓度)或过滤空气中一小时。在暴露前和暴露后立即测量动脉压力和硬度,并在暴露后 4-6 小时臂内输注内皮依赖性和非依赖性血管扩张剂期间测量前臂血流。在 2 小时使用离体 Badimon 室评估血栓形成,在暴露后长达 24 小时内,使用流式细胞仪测量血小板活化。与过滤空气相比,暴露于木烟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没有影响(P > 0.05)。虽然每种血管扩张剂的前臂血流量呈剂量依赖性增加(所有 P < 0.01),但暴露之间对乙酰胆碱、硝普钠或维拉帕米的血流量反应没有差异(所有 P > 0.05)。暴露于木烟后,缓激肽的血管舒张作用增加(P = 0.003),但对缓激肽诱导的组织纤溶酶原激活剂释放、血栓面积或血小板活化标志物没有影响(P > 0.05)。木材烟雾暴露不会损害血管舒缩或纤溶功能,或增加消防员的血栓形成。灭火后的急性心血管事件可能因暴露于其他空气污染物或通过其他机制(例如剧烈的体力消耗和脱水)而诱发。ClinicalTrials.gov 标识符:NCT01495325。
更新日期:2014-12-09
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