Particulate matter and atherosclerosis: role of particle size, composition and oxidative stress.

Particulate matter and atherosclerosis: role of particle size, composition and oxidative stress.
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DOI:
10.1186/1743-8977-6-24
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发表时间:
2009-09-18
影响因子:
10
通讯作者:
Nel AE
Nel AE
中科院分区:
医学1区
文献类型:
--
作者:
Araujo JA;Nel AE

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空气污染与严重的不良健康影响有关,导致发病率和死亡率增加。累积的流行病学和实验数据表明,暴露在空气污染物中会导致心血管缺血事件增加和动脉粥样硬化加剧。这些关联似乎与空气颗粒物(PM)成分的相关性要强得多,在城市地区,较小的颗粒物可能更具致病性,因为它们更容易引发全身促氧化和促炎效应。关于环境颗粒物的毒理学以及导致不良心血管健康影响的致病机制,仍有许多未知之处。预计更好地了解这些影响将产生重大影响,并可能导致制定和实施新的监管政策。事实上,我们已经发现超细颗粒(<0.18μm)增强早期动脉粥样硬化,部分原因是它们在氧化还原循环化学物质中的高含量,以及它们在促进组织氧化应激方面与已知的致动脉粥样硬化介质协同作用的能力。这些变化发生的同时,有证据表明,通过电泳敏感的转录因子P45-NFE2相关的转录因子2(Nrf2),2期酶的表达增加。暴露在超细颗粒中还会导致血浆高密度脂蛋白抗炎功能的改变,这可能表明全身前动脉粥样硬化的作用。本文综述了支持颗粒物与动脉粥样硬化相关的流行病学、临床和实验动物证据。它还讨论了可能的致病机制,可能在小颗粒表现出更大毒性中起重要作用的物理化学变量,与基因和其他致动脉粥样硬化因素的相互作用,以及在未来机制研究设计中需要考虑的重要因素。广泛的流行病学证据支持空气污染与有害健康影响之间的联系。越来越多的人认识到,这种影响导致发病率和死亡率增加,主要是由于心血管疾病的恶化,主要是那些具有缺血性特征的疾病。事实上,除了经典的危险因素,如血脂、吸烟、高血压、衰老、性别、家族史、缺乏运动和饮食外,最近的数据表明空气污染是动脉粥样硬化的一个重要的额外危险因素。这是美国心脏协会广泛审查和共识声明的主题。本文综述了支持该疾病的流行病学和动物数据、可能的致病机制和未来展望。
Air Pollution has been associated with significant adverse health effects leading to increased morbidity and mortality. Cumulative epidemiological and experimental data have shown that exposure to air pollutants lead to increased cardiovascular ischemic events and enhanced atherosclerosis. It appears that these associations are much stronger with the air particulate matter (PM) component and that in urban areas, the smaller particles could be more pathogenic, as a result of their greater propensity to induce systemic prooxidant and proinflammatory effects. Much is still unknown about the toxicology of ambient particulates as well as the pathogenic mechanisms responsible for the induction of adverse cardiovascular health effects. It is expected that better understanding of these effects will have large implications and may lead to the formulation and implementation of new regulatory policies. Indeed, we have found that ultrafine particles (<0.18 μm) enhance early atherosclerosis, partly due to their high content in redox cycling chemicals and their ability to synergize with known proatherogenic mediators in the promotion of tissue oxidative stress. These changes take place in parallel with increased evidence of phase 2 enzymes expression, via the electrophile-sensitive transcription factor, p45-NFE2 related transcription factor 2 (Nrf2). Exposure to ultrafine particles also results in alterations of the plasma HDL anti-inflammatory function that could be indicative of systemic proatherogenic effects. This article reviews the epidemiological, clinical and experimental animal evidence that support the association of particulate matter with atherogenesis. It also discusses the possible pathogenic mechanisms involved, the physicochemical variables that may be of importance in the greater toxicity exhibited by a small particle size, interaction with genes and other proatherogenic factors as well as important elements to consider in the design of future mechanistic studies. Extensive epidemiological evidence supports the association of air pollution with adverse health effects. It is increasingly being recognized that such effects lead to enhanced morbidity and mortality, mostly due to exacerbation of cardiovascular diseases and predominantly those of ischemic character. Indeed, in addition to the classical risk factors such as serum lipids, smoking, hypertension, aging, gender, family history, physical inactivity and diet, recent data have implicated air pollution as an important additional risk factor for atherosclerosis. This has been the subject of extensive reviews and a consensus statement from the American Heart Association. This article reviews the supporting epidemiological and animal data, possible pathogenic mechanisms and future perspectives.
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发表时间: 2003-09-01
期刊: EPIDEMIOLOGY
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