Combustion-derived nanoparticulate induces the adverse vascular effects of diesel exhaust inhalation.

Combustion-derived nanoparticulate induces the adverse vascular effects of diesel exhaust inhalation.
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DOI:
10.1093/eurheartj/ehr195
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发表时间:
2011-11
影响因子:
39.3
通讯作者:
Newby DE
Newby DE
中科院分区:
医学1区
文献类型:
--
作者:
Mills NL;Miller MR;Lucking AJ;Beveridge J;Flint L;Boere AJ;Fokkens PH;Boon NA;Sandstrom T;Blomberg A;Duffin R;Donaldson K;Hadoke PW;Cassee FR;Newby DE

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暴露于道路交通和空气污染可能是急性心肌梗死的触发因素,但导致这种影响的个别污染物尚未确定。我们评估了燃烧衍生的纳米颗粒在介导空气污染对心血管的不良影响中的作用。为了确定吸入柴油机废气成分的体内效应,在随机双盲交叉研究中,将16名健康志愿者暴露于(i)稀释的柴油机废气,(ii)纯碳纳米颗粒,(iii)过滤的柴油机废气,或(iv)过滤的空气。每次暴露后,在肱动脉内输注缓激肽、乙酰胆碱、硝普钠和维拉帕米期间测量前臂血流。与过滤空气相比,吸入柴油机废气使收缩压升高(145 ± 4 vs. 133 ± 3 mmHg,P< 0.05),并减弱缓激肽(P= 0.005)、乙酰胆碱(P= 0.008)和硝普钠(P< 0.001)对血管的舒张作用。暴露于纯碳纳米颗粒或过滤废气对内皮依赖性或非依赖性血管舒张没有影响。为了确定纳米颗粒的直接血管影响,通过钢丝肌造影术在体外评估了离体大鼠主动脉环(n= 6-9/组),并将其暴露于柴油机尾气颗粒、纯碳纳米颗粒和溶剂。与汽车相比,柴油机尾气颗粒(但不是纯碳纳米颗粒)减弱乙酰胆碱(P< 0.001)和硝普钠(P= 0.019)诱导的血管舒张。这些影响部分归因于颗粒的可溶性和不溶性组分。燃烧衍生的纳米颗粒似乎主要介导柴油机废气吸入的不良血管效应。这为测试旨在减少交通微粒排放的环境健康干预措施提供了依据。
Exposure to road traffic and air pollution may be a trigger of acute myocardial infarction, but the individual pollutants responsible for this effect have not been established. We assess the role of combustion-derived-nanoparticles in mediating the adverse cardiovascular effects of air pollution. To determine the in vivo effects of inhalation of diesel exhaust components, 16 healthy volunteers were exposed to (i) dilute diesel exhaust, (ii) pure carbon nanoparticulate, (iii) filtered diesel exhaust, or (iv) filtered air, in a randomized double blind cross-over study. Following each exposure, forearm blood flow was measured during intra-brachial bradykinin, acetylcholine, sodium nitroprusside, and verapamil infusions. Compared with filtered air, inhalation of diesel exhaust increased systolic blood pressure (145 ± 4 vs. 133 ± 3 mmHg, P< 0.05) and attenuated vasodilatation to bradykinin (P= 0.005), acetylcholine (P= 0.008), and sodium nitroprusside (P< 0.001). Exposure to pure carbon nanoparticulate or filtered exhaust had no effect on endothelium-dependent or -independent vasodilatation. To determine the direct vascular effects of nanoparticulate, isolated rat aortic rings (n= 6–9 per group) were assessed in vitro by wire myography and exposed to diesel exhaust particulate, pure carbon nanoparticulate and vehicle. Compared with vehicle, diesel exhaust particulate (but not pure carbon nanoparticulate) attenuated both acetylcholine (P< 0.001) and sodium-nitroprusside (P= 0.019)-induced vasorelaxation. These effects were partially attributable to both soluble and insoluble components of the particulate. Combustion-derived nanoparticulate appears to predominately mediate the adverse vascular effects of diesel exhaust inhalation. This provides a rationale for testing environmental health interventions targeted at reducing traffic-derived particulate emissions.
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