Kaufman Joel D, Adar Sara D, Barr R Graham, Budoff Matthew, Burke Gregory L, Curl Cynthia L, Daviglus Martha L, Diez Roux Ana V, Gassett Amanda J, Jacobs David R, Kronmal Richard, Larson Timothy V, Navas-Acien Ana, Olives Casey, Sampson Paul D, Sheppard Lianne, Siscovick David S, Stein James H, Szpiro Adam A, Watson Karol E
Department of Environmental and Occupational Health Sciences, University of Washington, Seattle, WA, USA; Department of Epidemiology, University of Washington, Seattle, WA, USA; Department of Medicine, University of Washington, Seattle, WA, USA.
Department of Epidemiology, University of Michigan, Ann Arbor, MI, USA.
Lancet. 2016 Aug 13;388(10045):696-704. doi: 10.1016/S0140-6736(16)00378-0. Epub 2016 May 24.
Long-term exposure to fine particulate matter less than 2.5 μm in diameter (PM2.5) and traffic-related air pollutant concentrations are associated with cardiovascular risk. The disease process underlying these associations remains uncertain. We aim to assess association between long-term exposure to ambient air pollution and progression of coronary artery calcium and common carotid artery intima-media thickness.
In this prospective 10-year cohort study, we repeatedly measured coronary artery calcium by CT in 6795 participants aged 45-84 years enrolled in the Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air) in six metropolitan areas in the USA. Repeated scans were done for nearly all participants between 2002 and 2005, for a subset of participants between 2005 and 2007, and for half of all participants between 2010 and 2012. Common carotid artery intima-media thickness was measured by ultrasound in all participants at baseline and in 2010-12 for 3459 participants. Residence-specific spatio-temporal pollution concentration models, incorporating community-specific measurements, agency monitoring data, and geographical predictors, estimated concentrations of PM2.5 and nitrogen oxides (NOX) between 1999 and 2012. The primary aim was to examine the association between both progression of coronary artery calcium and mean carotid artery intima-media thickness and long-term exposure to ambient air pollutant concentrations (PM2.5, NOX, and black carbon) between examinations and within the six metropolitan areas, adjusting for baseline age, sex, ethnicity, socioeconomic characteristics, cardiovascular risk factors, site, and CT scanner technology.
In this population, coronary calcium increased on average by 24 Agatston units per year (SD 58), and intima-media thickness by 12 μm per year (10), before adjusting for risk factors or air pollutant exposures. Participant-specific pollutant concentrations averaged over the years 2000-10 ranged from 9.2-22.6 μg PM2.5/m(3) and 7.2-139.2 parts per billion (ppb) NOX. For each 5 μg PM2.5/m(3) increase, coronary calcium progressed by 4.1 Agatston units per year (95% CI 1.4-6.8) and for each 40 ppb NOX coronary calcium progressed by 4.8 Agatston units per year (0.9-8.7). Pollutant exposures were not associated with intima-media thickness change. The estimate for the effect of a 5 μg/m(3) higher long-term exposure to PM2.5 in intima-media thickness was -0.9 μm per year (95% CI -3.0 to 1.3). For 40 ppb higher NOX, the estimate was 0.2 μm per year (-1.9 to 2.4).
Increased concentrations of PM2.5 and traffic-related air pollution within metropolitan areas, in ranges commonly encountered worldwide, are associated with progression in coronary calcification, consistent with acceleration of atherosclerosis. This study supports the case for global efforts of pollution reduction in prevention of cardiovascular diseases.
US Environmental Protection Agency and US National Institutes of Health.
长期暴露于直径小于2.5微米的细颗粒物(PM2.5)以及与交通相关的空气污染物浓度与心血管风险相关。这些关联背后的疾病过程仍不确定。我们旨在评估长期暴露于环境空气污染与冠状动脉钙化进展和颈总动脉内膜中层厚度之间的关联。
在这项为期10年的前瞻性队列研究中,我们对参加美国六个大都市地区动脉粥样硬化与空气污染多族裔研究(MESA Air)的6795名45 - 84岁参与者通过CT反复测量冠状动脉钙化情况。几乎所有参与者在2002年至2005年间进行了重复扫描,一部分参与者在2005年至2007年间进行了扫描,所有参与者的一半在2010年至2012年间进行了扫描。在基线时以及2010 - 2012年对3459名参与者通过超声测量颈总动脉内膜中层厚度。结合社区特定测量、机构监测数据和地理预测因素的特定居住地时空污染浓度模型,估算了1999年至2012年间PM2.5和氮氧化物(NOX)的浓度。主要目的是在六个大都市地区内,在两次检查之间,调整基线年龄、性别、种族、社会经济特征、心血管危险因素、地点和CT扫描仪技术,检验冠状动脉钙化进展和平均颈动脉内膜中层厚度与长期暴露于环境空气污染物浓度(PM2.5、NOX和黑碳)之间的关联。
在该人群中,在调整危险因素或空气污染物暴露之前,冠状动脉钙化平均每年增加24阿加斯顿单位(标准差58),内膜中层厚度平均每年增加12微米(10)。2000 - 2010年期间参与者特定的污染物浓度平均值范围为9.2 - 22.6微克PM2.5/立方米和7.2 - 139.2十亿分率(ppb)NOX。每增加5微克PM2.5/立方米,冠状动脉钙化每年进展4.1阿加斯顿单位(95%置信区间1.4 - 6.8),每增加40 ppb NOX,冠状动脉钙化每年进展4.8阿加斯顿单位(0.9 - 8.7)。污染物暴露与内膜中层厚度变化无关。长期暴露于比PM2.5高5微克/立方米时,对内膜中层厚度影响的估计值为每年 - 0.9微米(95%置信区间 - 3.0至1.3)。对于比NOX高40 ppb,估计值为每年0.2微米( - 1.9至2.4)。
大都市地区内PM2.5浓度增加以及与交通相关的空气污染,在全球普遍遇到的范围内,与冠状动脉钙化进展相关,这与动脉粥样硬化加速一致。本研究支持全球为预防心血管疾病而努力减少污染的理由。
美国环境保护局和美国国立卫生研究院。