Impaired vascular function after exposure to diesel exhaust generated at urban transient running conditions.
Impaired vascular function after exposure to diesel exhaust generated at urban transient running conditions.
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DOI：
10.1186/1743-8977-7-19
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发表时间：
2010-07-23
影响因子：
10
通讯作者：
Blomberg A
中科院分区：
文献类型：
--
作者：
Barath S;Mills NL;Lundbäck M;Törnqvist H;Lucking AJ;Langrish JP;Söderberg S;Boman C;Westerholm R;Löndahl J;Donaldson K;Mudway IS;Sandström T;Newby DE;Blomberg A
包括柴油机废气在内的交通排放物与呼吸道和心血管疾病发病率和死亡率的增加有关。受控的人体接触研究表明，吸入柴油发动机在怠速状态下产生的废气后，血管功能受损。评估暴露于模拟环境“真实世界”暴露的城市循环运行条件下产生的柴油废气对血管和纤维蛋白溶解的影响。在一项随机双盲交叉研究中，18名健康男性志愿者在间歇性运动期间暴露于柴油废气（约250 μg/m3）或过滤空气1小时。柴油机废气是在标准化欧洲瞬态循环的城市部分产生的。暴露后6小时，在动脉内输注激动剂的静脉闭塞体积描记术期间评估血管扩张和纤溶功能。内皮依赖性（乙酰胆碱和缓激肽）和内皮非依赖性（硝普钠和维拉帕米）血管扩张剂均以剂量依赖性方式增加前臂血流量。柴油机尾气暴露可使乙酰胆碱（P < 0.001）、缓激肽（P < 0.05）、硝普钠（P < 0.05）和维拉帕米（P < 0.001）的舒张作用减弱。此外，柴油机尾气暴露后，缓激肽输注过程中组织型纤溶酶原激活物的净释放量明显减少（P < 0.05）。暴露于瞬态运行条件下产生的柴油机废气作为城市空气污染的相关模型，以与暴露于怠速时产生的柴油机废气类似的方式损害血管功能和内源性纤维蛋白溶解。这表明，柴油机废气吸入不良血管效应发生在不同的运行条件下，不同的废气成分和浓度以及物理化学颗粒特性。重要的是，在ETC条件下暴露于柴油机废气也与钙通道依赖性血管功能受损的新发现相关。这意味着某些心血管终点似乎与一般柴油机排气特性相关，而新的钙通量相关效应可能与ETC条件下更特异的排气特性相关，例如较高含量的柴油机烟灰颗粒沿着其吸附的有机化合物。
Traffic emissions including diesel engine exhaust are associated with increased respiratory and cardiovascular morbidity and mortality. Controlled human exposure studies have demonstrated impaired vascular function after inhalation of exhaust generated by a diesel engine under idling conditions. To assess the vascular and fibrinolytic effects of exposure to diesel exhaust generated during urban-cycle running conditions that mimic ambient 'real-world' exposures. In a randomised double-blind crossover study, eighteen healthy male volunteers were exposed to diesel exhaust (approximately 250 μg/m3) or filtered air for one hour during intermittent exercise. Diesel exhaust was generated during the urban part of the standardized European Transient Cycle. Six hours post-exposure, vascular vasomotor and fibrinolytic function was assessed during venous occlusion plethysmography with intra-arterial agonist infusions. Forearm blood flow increased in a dose-dependent manner with both endothelial-dependent (acetylcholine and bradykinin) and endothelial-independent (sodium nitroprusside and verapamil) vasodilators. Diesel exhaust exposure attenuated the vasodilatation to acetylcholine (P < 0.001), bradykinin (P < 0.05), sodium nitroprusside (P < 0.05) and verapamil (P < 0.001). In addition, the net release of tissue plasminogen activator during bradykinin infusion was impaired following diesel exhaust exposure (P < 0.05). Exposure to diesel exhaust generated under transient running conditions, as a relevant model of urban air pollution, impairs vasomotor function and endogenous fibrinolysis in a similar way as exposure to diesel exhaust generated at idling. This indicates that adverse vascular effects of diesel exhaust inhalation occur over different running conditions with varying exhaust composition and concentrations as well as physicochemical particle properties. Importantly, exposure to diesel exhaust under ETC conditions was also associated with a novel finding of impaired of calcium channel-dependent vasomotor function. This implies that certain cardiovascular endpoints seem to be related to general diesel exhaust properties, whereas the novel calcium flux-related effect may be associated with exhaust properties more specific for the ETC condition, for example a higher content of diesel soot particles along with their adsorbed organic compounds.
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DOI：
10.1056/nejmsa0805646
发表时间：
2009-01-22
期刊：
The New England journal of medicine
影响因子：
--
作者：
Pope CA 3rd;Ezzati M;Dockery DW
通讯作者：
Dockery DW
影响因子：
37.8
作者：
Newby, DE;Wright, RA;Webb, DJ
通讯作者：
Webb, DJ
影响因子：
6
作者：
Boman, C;Nordin, A;Pettersson, E
通讯作者：
Pettersson, E
影响因子：
2.1
作者：
Langrish, Jeremy P.;Lundback, Magnus;Blomberg, Anders
通讯作者：
Blomberg, Anders
影响因子：
4.5
作者：
Kittelson, DB
通讯作者：
Kittelson, DB