Allen Ryan W, Criqui Michael H, Diez Roux Ana V, Allison Matthew, Shea Steven, Detrano Robert, Sheppard Lianne, Wong Nathan D, Stukovsky Karen Hinckley, Kaufman Joel D
Faculty of Health Sciences, Simon Fraser University, Burnaby, BC, Canada.
Epidemiology. 2009 Mar;20(2):254-64. doi: 10.1097/EDE.0b013e31819644cc.
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 US metropolitan areas, enrolled in the Multi-Ethnic Study of Atherosclerosis. 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 microg/m 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.
动脉粥样硬化的起始和加速被假定为空气污染与心血管效应之间关联的生理机制。尽管有毒理学证据,但流行病学数据有限。
在这项横断面分析中,我们调查了细颗粒物(PM2.5)暴露及居住地与主要道路的距离与腹主动脉钙化(全身动脉粥样硬化的敏感指标)之间的关系。在参与动脉粥样硬化多民族研究的美国5个大都市地区的1147人中,通过计算机断层扫描测量主动脉钙化情况。分别使用相对风险回归和线性回归对主动脉钙化的存在情况和数量进行建模,并对潜在混杂因素进行校正。
我们观察到,PM2.5每增加10微克/立方米,主动脉钙化风险略有升高(相对风险=1.06;95%置信区间=0.96 - 1.16)。在长期居住在PM2.5监测器附近的参与者中(相对风险=1.11;1.00 - 1.24)以及近期未外出工作的参与者中(相对风险=1.10;1.00 - 1.22),与PM2.5相关的主动脉钙化风险更强。PM2.5与主动脉钙化数量(阿加斯顿评分)增加无关,未观察到道路距离的影响。有迹象表明,降脂药物使用可改变PM2.5的效应,使用者的效应更大,且在西班牙裔人群中最一致地观察到了PM2.5的关联。
尽管在整个研究人群中我们未发现有说服力的关联,但在暴露错误分类较少的参与者中关联更强。这些发现支持了颗粒空气污染与全身动脉粥样硬化之间存在关系的假设。