Cardiovascular effects of fine and ultrafine particles
Cardiovascular effects of fine and ultrafine particles
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DOI：
10.1089/jam.2005.18.1
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发表时间：
2005-03-01
期刊：
影响因子：
--
通讯作者：
Peters, A
中科院分区：
文献类型：
--
作者：
Schulz, H;Harder, V;Peters, A
过去几十年的流行病学研究提供了强有力的证据表明，环境颗粒物污染(PM)水平的升高与心血管和呼吸系统发病率和死亡率的增加有关。缺血性和/或心律失常心脏病的恶化与PM暴露有关。2003年11月，在GSF-国家环境与健康中心举办的讲习班上，汇编了过去5年的相关流行病学和毒物学数据，并讨论了可能的生物学途径。现有的临床和实验证据支持以下机制：(I)肺和/或全身炎症反应导致内皮功能障碍、促凝状态和促进动脉粥样硬化病变，(Ii)自主神经系统对肺部受体的直接反射和/或局部或系统炎症刺激的反应，以及(Iii)由于心肌缺血反应和/或心肌细胞离子通道功能改变而导致的心脏功能障碍。虽然越来越多针对这些问题的研究支持PM暴露与心血管效应相关的概念，但目前这些研究对所涉及的复杂生物学途径只提供了一个零散的、有时并不确定的图景。现有的数据与全身炎症反应的发生和自主神经心脏控制的改变是一致的，但关于内皮功能障碍、促凝血状态和PM相关的心肌功能障碍的证据尚不多见。因此，需要进一步的研究来证实我们目前对PM暴露和不良心血管后果之间的病理生理联系的理解。
Epidemiological studies of the past decades have provided a strong body of evidence that elevated levels of ambient particulate air pollution (PM) are associated with increased cardiovascular and respiratory morbidity and mortality. Exacerbations of ischemic and/or arrhythmic cardiac diseases have been linked to PM exposure. At a workshop held at the GSF-National Center for Environment and Health in November 2003, relevant epidemiological and toxicological data of the past 5 years were compiled and potential biological pathways discussed. Available clinical and experimental evidence lends support to the following mechanisms mediating cardiovascular effects of inhaled ambient particles: (i) pulmonary and/or systemic inflammatory responses inducing endothelial dysfunction, a pro-coagulatory state and promotion of atherosclerotic lesions, (ii) dysfunction of the autonomic nervous system in response to direct reflexes from receptors in the lungs and/or to local or systemic inflammatory stimuli, and (iii) cardiac malfunction due to ischemic responses in the myocardium and/or altered ion-channel functions in myocardial cells. While an increasing number of studies addressing these questions support the notion that PM exposure is associated with cardiovascular effects, these studies at present provide only a fragmentary and at times inconclusive picture of the complex biological pathways involved. The available data are consistent with the occurrence of a systemic inflammatory response and an alteration of autonomic cardiac control, but evidence on endothelial dysfunction, pro-coagulatory states, and PM-related myocardial malfunction is as yet scarce. Further studies are therefore needed to substantiate our current understanding of the pathophysiological links between PM exposure and adverse cardiovascular outcomes.