Liao Duanping, Duan Yinkang, Whitsel Eric A, Zheng Zhi-jie, Heiss Gerardo, Chinchilli Vernon M, Lin Hung-Mo
Department of Health Evaluation Sciences, Pennsylvania State University College of Medicine, Hershey, PA 17033, USA.
Am J Epidemiol. 2004 Apr 15;159(8):768-77. doi: 10.1093/aje/kwh109.
An association between air pollution and increased cardiovascular disease (CVD) mortality has been reported, but underlying mechanisms are unknown. The authors examined short-term associations between ambient pollutants (particulate matter less than 10 microm in aerodynamic diameter (PM10), ozone, carbon monoxide, nitrogen dioxide, and sulfur dioxide) and cardiac autonomic control using data from the fourth cohort examination (1996-1998) of the population-based Atherosclerosis Risk in Communities Study. For each participant, the authors calculated PM10 and gaseous pollutant exposures as 24-hour averages and ozone exposure as an 8-hour average 1 day prior to the randomly allocated examination date. They calculated 5-minute heart rate variability indices and used logarithmically transformed data on high-frequency (0.15-0.40 Hz) and low-frequency (0.04-0.15 Hz) power, standard deviation of normal R-R intervals, and mean heart rate. Linear regression was used to adjust for CVD risk factors and demographic, socioeconomic, and meteorologic variables. Regression coefficients for a one-standard-deviation increase in PM10 (11.5 microg/m3) were -0.06 ms2 (standard error (SE), 0.018), -1.03 ms (SE, 0.31), and 0.32 beats/minute (SE, 0.158) for log-transformed high-frequency power, standard deviation of normal R-R intervals, and heart rate, respectively. Similar results were found for gaseous pollutants. These cross-sectional findings suggest that higher ambient pollutant concentrations are associated with lower cardiac autonomic control, especially among persons with existing CVD, and highlight a putative mechanism through which air pollution is associated with CVD.
空气污染与心血管疾病（CVD）死亡率增加之间的关联已有报道，但潜在机制尚不清楚。作者利用社区动脉粥样硬化风险研究中基于人群的第四队列检查（1996 - 1998年）的数据，研究了环境污染物（空气动力学直径小于10微米的颗粒物（PM10）、臭氧、一氧化碳、二氧化氮和二氧化硫）与心脏自主神经控制之间的短期关联。对于每位参与者，作者将PM10和气态污染物暴露计算为随机分配的检查日期前1天的24小时平均值，将臭氧暴露计算为8小时平均值。他们计算了5分钟心率变异性指数，并使用了高频（0.15 - 0.40赫兹）和低频（0.04 - 0.15赫兹）功率、正常R - R间期标准差和平均心率的对数转换数据。采用线性回归对心血管疾病风险因素以及人口统计学、社会经济和气象变量进行调整。PM10增加一个标准差（11.5微克/立方米）时，对数转换后的高频功率、正常R - R间期标准差和心率的回归系数分别为-0.06毫秒²（标准误（SE），0.018）、-1.03毫秒（SE，0.31）和0.32次/分钟（SE，0.158）。气态污染物也有类似结果。这些横断面研究结果表明，较高的环境污染物浓度与较低的心脏自主神经控制相关，尤其是在已有心血管疾病的人群中，并突出了空气污染与心血管疾病相关的一种假定机制。
