Potential role of ultrafine particles in associations between airborne particle mass and cardiovascular health.
Potential role of ultrafine particles in associations between airborne particle mass and cardiovascular health.
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超铁颗粒在空气颗粒质量与心血管健康之间关联中的潜在作用。
DOI：
10.1289/ehp.7938
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发表时间：
2005-08
影响因子：
10.4
通讯作者：
Malik S
中科院分区：
文献类型：
--
作者：
Delfino RJ;Sioutas C;Malik S
大量的流行病学时间序列研究表明，心血管住院和死亡率与室外空气污染，特别是直径为PM2.5或≤10μm的颗粒物(PM)的质量浓度之间的关系基本一致。重复测量的小组研究支持了时间序列结果，表明PM与心脏缺血和心律失常、血压升高、心率变异性降低以及炎症和血栓形成的循环标志物增加的风险有关。推动PM关联的因果成分仍有待确定。使用污染气体和颗粒物特征的流行病学数据，如颗粒物数量、浓度和元素碳，间接证明了化石燃料燃烧的产物是重要的。超细颗粒<；0.1μm(UFP)控制着颗粒数量、浓度和表面积，因此能够携带大量吸附或浓缩的有毒空气污染物。化石燃料燃烧产生的UFP中的氧化还原活性成分很可能会到达心血管靶点。高UFP暴露可通过氧化应激对活性氧物种的反应导致全身炎症，从而促进动脉粥样硬化的进展，并引发从血压升高到心肌梗死的急性心血管反应。流行病学研究的下一步是更清楚地确定与其来源有关的推定PM偶然成分和大小分数。为了推进这一点，我们在一篇配套的文章中讨论(.环境卫生展望113：947-955)超低密度脂蛋白暴露评估的必要性和方法。
Numerous epidemiologic time-series studies have shown generally consistent associations of cardiovascular hospital admissions and mortality with outdoor air pollution, particularly mass concentrations of particulate matter (PM) ≤2.5 or ≤10 μm in diameter (PM2.5, PM10). Panel studies with repeated measures have supported the time-series results showing associations between PM and risk of cardiac ischemia and arrhythmias, increased blood pressure, decreased heart rate variability, and increased circulating markers of inflammation and thrombosis. The causal components driving the PM associations remain to be identified. Epidemiologic data using pollutant gases and particle characteristics such as particle number concentration and elemental carbon have provided indirect evidence that products of fossil fuel combustion are important. Ultrafine particles < 0.1 μm (UFPs) dominate particle number concentrations and surface area and are therefore capable of carrying large concentrations of adsorbed or condensed toxic air pollutants. It is likely that redox-active components in UFPs from fossil fuel combustion reach cardiovascular target sites. High UFP exposures may lead to systemic inflammation through oxidative stress responses to reactive oxygen species and thereby promote the progression of atherosclerosis and precipitate acute cardiovascular responses ranging from increased blood pressure to myocardial infarction. The next steps in epidemiologic research are to identify more clearly the putative PM casual components and size fractions linked to their sources. To advance this, we discuss in a companion article (. Environ Health Perspect 113:947–955) the need for and methods of UFP exposure assessment.
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影响因子：
14.2
作者：
DiazSanchez, D;Tsien, A;Saxon, A
通讯作者：
Saxon, A
影响因子：
105.7
作者：
Danesh, J;Whincup, P;Pepys, MB
通讯作者：
Pepys, MB
DOI：
10.1097/00005373-199206000-00003
发表时间：
1992-06-01
影响因子：
--
作者：
DEMEULES, JE;PIGULA, FA;GAMELLI, RL
通讯作者：
GAMELLI, RL
人类受试者的个人暴露于亚微米颗粒和心率变异性。
影响因子：
10.4
作者：
Chan, Chang-Chuan;Chuang, Kai-Jen;Shiao, Guang-Ming;Lin, Lian-Yu
通讯作者：
Lin, Lian-Yu
影响因子：
5.4
作者：
D'Ippoliti, D;Forastiere, F;Perucci, CA
通讯作者：
Perucci, CA