Department of Medicine, University of Washington, 4225 Roosevelt Way NE, Seattle, WA 98105, USA.
J Am Coll Cardiol. 2012 Nov 20;60(21):2158-66. doi: 10.1016/j.jacc.2012.08.973. Epub 2012 Oct 24.
This study evaluated the association of long- and short-term air pollutant exposures with flow-mediated dilation (FMD) and baseline arterial diameter (BAD) of the brachial artery using ultrasound in a large multicity cohort.
Exposures to ambient air pollution, especially long-term exposure to particulate matter <2.5 μm in aerodynamic diameter (PM(2.5)), are linked with cardiovascular mortality. Short-term exposure to PM(2.5) has been associated with decreased FMD and vasoconstriction, suggesting that adverse effects of PM(2.5) may involve endothelial dysfunction. However, long-term effects of PM(2.5) on endothelial dysfunction have not been investigated.
FMD and BAD were measured by brachial artery ultrasound at the initial examination of the Multi-Ethnic Study of Atherosclerosis. Long-term PM(2.5) concentrations were estimated for the year 2000 at each participant's residence (n = 3,040) using a spatio-temporal model informed by cohort-specific monitoring. Short-term PM(2.5) concentrations were based on daily central-site monitoring in each of the 6 cities.
An interquartile increase in long-term PM(2.5) concentration (3 μg/m(3)) was associated with a 0.3% decrease in FMD (95% confidence interval [CI] of difference: -0.6 to -0.03; p = 0.03), adjusting for demographic characteristics, traditional risk factors, sonographers, and 1/BAD. Women, nonsmokers, younger participants, and those with hypertension seemed to show a greater association of PM(2.5) with FMD. FMD was not significantly associated with short-term variation in PM(2.5) (-0.1% per 12 μg/m(3) daily increase [95% CI: -0.2 to 0.04] on the day before examination).
Long-term PM(2.5) exposure was significantly associated with decreased endothelial function according to brachial ultrasound results. These findings may elucidate an important pathway linking air pollution and cardiovascular mortality.
本研究采用超声技术,在一个大型多城市队列中评估长期和短期空气污染物暴露与肱动脉血流介导扩张(FMD)和肱动脉基础直径(BAD)之间的关系。
环境空气污染暴露,特别是空气动力学直径<2.5μm 的颗粒物(PM(2.5))的长期暴露与心血管死亡率相关。短期 PM(2.5)暴露与 FMD 降低和血管收缩有关,这表明 PM(2.5)的不良影响可能涉及内皮功能障碍。然而,尚未研究 PM(2.5)对内皮功能障碍的长期影响。
在动脉粥样硬化多民族研究的初始检查中,通过肱动脉超声测量 FMD 和 BAD。使用基于队列监测的时空模型,在每个参与者的住所(n=3040)估算 2000 年的长期 PM(2.5)浓度。短期 PM(2.5)浓度基于 6 个城市的每日中心监测。
长期 PM(2.5)浓度(3μg/m3)的四分位间距增加与 FMD 降低 0.3%(差异的 95%置信区间[CI]:-0.6 至-0.03;p=0.03)相关,调整了人口统计学特征、传统危险因素、超声技师和 1/BAD。女性、不吸烟者、年轻参与者和高血压患者似乎与 PM(2.5)与 FMD 之间的关联更大。FMD 与 PM(2.5)短期变化无显著相关性(检查前一天每日增加 12μg/m3 时,FMD 增加 0.1%[95%CI:-0.2 至 0.04])。
根据肱动脉超声结果,长期 PM(2.5)暴露与内皮功能下降显著相关。这些发现可能阐明了空气污染与心血管死亡率之间的一个重要联系途径。