Künzli Nino, Jerrett Michael, Mack Wendy J, Beckerman Bernardo, LaBree Laurie, Gilliland Frank, Thomas Duncan, Peters John, Hodis Howard N
Division of Environmental Health, Department of Preventive Medicine, Atherosclerosis Research Unit, Keck School of Medicine, University of Southern California, Los Angeles, California 90033-9013, USA.
Environ Health Perspect. 2005 Feb;113(2):201-6. doi: 10.1289/ehp.7523.
Associations have been found between long-term exposure to ambient air pollution and cardiovascular morbidity and mortality. The contribution of air pollution to atherosclerosis that underlies many cardiovascular diseases has not been investigated. Animal data suggest that ambient particulate matter (PM) may contribute to atherogenesis. We used data on 798 participants from two clinical trials to investigate the association between atherosclerosis and long-term exposure to ambient PM up to 2.5 microm in aerodynamic diameter (PM2.5). Baseline data included assessment of the carotid intima-media thickness (CIMT), a measure of subclinical atherosclerosis. We geocoded subjects' residential areas to assign annual mean concentrations of ambient PM2.5. Exposure values were assigned from a PM2.5 surface derived from a geostatistical model. Individually assigned annual mean PM2.5 concentrations ranged from 5.2 to 26.9 microg/m3 (mean, 20.3). For a cross-sectional exposure contrast of 10 microg/m3 PM2.5, CIMT increased by 5.9% (95% confidence interval, 1-11%). Adjustment for age reduced the coefficients, but further adjustment for covariates indicated robust estimates in the range of 3.9-4.3% (p-values, 0.05-0.1). Among older subjects (greater than or equal to 60 years of age), women, never smokers, and those reporting lipid-lowering treatment at baseline, the associations of PM2.5 and CIMT were larger with the strongest associations in women 60 years of age (15.7%, 5.7-26.6%). These results represent the first epidemiologic evidence of an association between atherosclerosis and ambient air pollution. Given the leading role of cardiovascular disease as a cause of death and the large populations exposed to ambient PM2.5, these findings may be important and need further confirmation.
长期暴露于环境空气污染与心血管疾病的发病率和死亡率之间已发现存在关联。空气污染对许多心血管疾病所基于的动脉粥样硬化的影响尚未得到研究。动物数据表明,环境颗粒物(PM)可能促成动脉粥样硬化的形成。我们利用来自两项临床试验的798名参与者的数据,研究动脉粥样硬化与长期暴露于空气动力学直径达2.5微米的环境细颗粒物(PM2.5)之间的关联。基线数据包括对颈动脉内膜中层厚度(CIMT)的评估,这是亚临床动脉粥样硬化的一项指标。我们对受试者的居住区域进行地理编码,以确定环境PM2.5的年均浓度。暴露值是根据从地理统计模型得出的PM2.5表面数据确定的。个体分配的年均PM2.5浓度范围为5.2至26.9微克/立方米(平均为20.3)。对于PM2.5浓度每立方米10微克的横断面暴露对比,CIMT增加了5.9%(95%置信区间为1%至11%)。年龄调整使系数降低,但进一步对协变量进行调整表明,估计值稳健,范围在3.9%至4.3%之间(p值为0.05至0.1)。在老年受试者(年龄大于或等于60岁)、女性、从不吸烟者以及那些在基线时报告接受降脂治疗的人群中,PM2.5与CIMT之间的关联更大,在60岁女性中关联最强(15.7%,5.7%至26.6%)。这些结果代表了动脉粥样硬化与环境空气污染之间存在关联的首个流行病学证据。鉴于心血管疾病作为死亡原因的主导作用以及大量人群暴露于环境PM2.5,这些发现可能具有重要意义,需要进一步证实。