Fine particulate matter air pollution, proximity to traffic, and aortic atherosclerosis.

Fine particulate matter air pollution, proximity to traffic, and aortic atherosclerosis.
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DOI:
10.1097/ede.0b013e31819644cc
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发表时间:
2009-03
期刊:
Epidemiology (Cambridge, Mass.)
影响因子:
--
通讯作者:
Kaufman JD
Kaufman JD
中科院分区:
其他
文献类型:
--
作者:
Allen RW;Criqui MH;Diez Roux AV;Allison M;Shea S;Detrano R;Sheppard L;Wong ND;Stukovsky KH;Kaufman JD

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动脉粥样硬化的起始和加速被假设为空气污染和心血管效应之间相关性的生理机制。尽管有毒理学证据,但流行病学数据有限。在这个横断面分析中,我们研究了暴露于细颗粒物(PM2.5)和住宅区靠近主要道路与腹主动脉钙化的关系,腹主动脉钙化是系统性动脉粥样硬化的敏感指标。在美国5个大城市的1147名参与多种族动脉粥样硬化研究(梅萨)的患者中,通过计算机断层扫描测量主动脉钙化。主动脉钙化的存在和数量分别使用相对风险回归和线性回归进行建模,并对潜在的混杂因素进行调整。我们观察到在PM2.5中使用10 μg/m3造影剂时主动脉钙化的风险略有升高(RR = 1.06; 95%置信区间= 0.96-1.16)。PM2.5相关的主动脉钙化风险在长期居住在PM2.5监测器附近的参与者(RR = 1.11; 1.00-1.24)和最近没有在外面工作的参与者(RR = 1.10; 1.00-1.22)中更强。PM2.5与主动脉钙化(Agatston评分)数量增加无关,也未观察到道路邻近效应。有迹象表明,降脂药物的使用对PM2.5的影响有所改变,在使用者中影响更大,在西班牙裔美国人中观察到的PM2.5相关性最一致。虽然我们在整个研究人群中没有发现有说服力的相关性,但在暴露错误分类较少的参与者中,相关性更强。这些发现支持了空气颗粒污染与系统性动脉粥样硬化之间关系的假设。
The initiation and acceleration of atherosclerosis is hypothesized as a physiologic mechanism underlying associations between air pollution and cardiovascular effects. Despite toxicologic evidence, epidemiologic data are limited. In this cross-sectional analysis we investigated exposure to fine particulate matter (PM2.5) and residential proximity to major roads in relation to abdominal aortic calcification a sensitive indicator of systemic atherosclerosis. Aortic calcification was measured by computed tomography among 1147 persons, in 5 U.S. metropolitan areas, enrolled in the Multi-Ethnic Study of Atherosclerosis (MESA). The presence and quantity of aortic calcification were modeled using relative risk regression and linear regression, respectively, with adjustment for potential confounders. We observed a slightly elevated risk of aortic calcification (RR = 1.06; 95% confidence interval = 0.96–1.16) with a 10-μg/m3 contrast in PM2.5. The PM2.5-associated risk of aortic calcification was stronger among participants with long-term residence near a PM2.5 monitor (RR = 1.11; 1.00–1.24) and among participants not recently employed outside the home (RR = 1.10; 1.00–1.22). PM2.5 was not associated with an increase in the quantity of aortic calcification (Agatston score) and no roadway proximity effects were noted. There was indication of PM2.5 effect modification by lipid-lowering medication use, with greater effects among users, and PM2.5 associations were observed most consistently among Hispanics. Although we did not find persuasive associations across our full study population, associations were stronger among participants with less exposure misclassification. These findings support the hypothesis of a relationship between particulate air pollution and systemic atherosclerosis.