Miller Mark R, Shaw Catherine A, Langrish Jeremy P
BHF/University Centre for Cardiovascular Science, University of Edinburgh, Queens Medical Research Institute, 47 Little France Crescent, Edinburgh, Scotland, UK.
Future Cardiol. 2012 Jul;8(4):577-602. doi: 10.2217/fca.12.43.
Air pollution, especially airborne particulate matter (PM), is associated with an increase in both morbidity and mortality from cardiovascular disease, although the underlying mechanisms remain incompletely established. The one consistent observation that links the pulmonary and cardiovascular effects of inhaled PM is oxidative stress. This article examines the evidence for the role of oxidative stress in the cardiovascular effects of air pollution, beginning with observations from epidemiological and controlled exposure studies and then exploring potential mechanistic pathways involving free radical generation from PM itself, to effects of PM on cell cultures, isolated organs, healthy animals and animal models of disease. Particular emphasis is placed on the vascular and atherosclerotic effects of urban air pollution and diesel exhaust emissions as rich sources of environmental ultrafine particles.
空气污染，尤其是空气中的颗粒物（PM），与心血管疾病的发病率和死亡率增加有关，尽管其潜在机制尚未完全明确。将吸入性PM的肺部效应与心血管效应联系起来的一个一致观察结果是氧化应激。本文探讨了氧化应激在空气污染心血管效应中作用的证据，首先是来自流行病学和对照暴露研究的观察结果，然后探讨了潜在的机制途径，包括PM本身产生自由基的过程，以及PM对细胞培养、离体器官、健康动物和疾病动物模型的影响。特别强调了城市空气污染和柴油废气排放作为环境超细颗粒丰富来源所产生的血管和动脉粥样硬化效应。
