Pope C Arden, Hansen Matthew L, Long Russell W, Nielsen Karen R, Eatough Norman L, Wilson William E, Eatough Delbert J
Department of Economics, Brigham Young University, Provo, UT 84602, USA.
Environ Health Perspect. 2004 Mar;112(3):339-45. doi: 10.1289/ehp.6588.
Epidemiologic studies report associations between particulate air pollution and cardiopulmonary morbidity and mortality. Although the underlying pathophysiologic mechanisms remain unclear, it has been hypothesized that altered autonomic function and pulmonary/systemic inflammation may play a role. In this study we explored the effects of air pollution on autonomic function measured by changes in heart rate variability (HRV) and blood markers of inflammation in a panel of 88 elderly subjects from three communities along the Wasatch Front in Utah. Subjects participated in multiple sessions of 24-hr ambulatory electrocardiographic monitoring and blood tests. Regression analysis was used to evaluate associations between fine particulate matter [aerodynamic diameter less than or equal to 2.5 microm (PM2.5)] and HRV, C-reactive protein (CRP), blood cell counts, and whole blood viscosity. A 100- microg/m3 increase in PM2.5 was associated with approximately a 35 (SE = 8)-msec decline in standard deviation of all normal R-R intervals (SDNN, a measure of overall HRV); a 42 (SE = 11)-msec decline in square root of the mean of the squared differences between adjacent normal R-R intervals (r-MSSD, an estimate of short-term components of HRV); and a 0.81 (SE = 0.17)-mg/dL increase in CRP. The PM2.5-HRV associations were reasonably consistent and statistically robust, but the CRP association dropped to 0.19 (SE = 0.10) after excluding the most influential subject. PM2.5 was not significantly associated with white or red blood cell counts, platelets, or whole-blood viscosity. Most short-term variability in temporal deviations of HRV and CRP was not explained by PM2.5; however, the small statistically significant associations that were observed suggest that exposure to PM2.5 may be one of multiple factors that influence HRV and CRP.
流行病学研究报告了空气中颗粒物污染与心肺疾病发病率及死亡率之间的关联。尽管潜在的病理生理机制仍不清楚，但据推测自主神经功能改变和肺/全身炎症可能起了作用。在本研究中，我们对犹他州瓦萨奇山前三个社区的88名老年受试者进行了研究，探讨空气污染对通过心率变异性（HRV）变化测量的自主神经功能以及炎症血液标志物的影响。受试者参与了多次24小时动态心电图监测和血液检测。采用回归分析评估细颗粒物[空气动力学直径小于或等于2.5微米（PM2.5）]与HRV、C反应蛋白（CRP）、血细胞计数和全血粘度之间的关联。PM2.5每增加100微克/立方米，所有正常R-R间期标准差（SDNN，一种总体HRV测量指标）大约下降35（标准误 = 8）毫秒；相邻正常R-R间期平方差均值的平方根（r-MSSD，HRV短期成分的估计值）下降42（标准误 = 11）毫秒；CRP升高0.81（标准误 = 0.17）毫克/分升。PM2.5与HRV的关联相当一致且在统计学上具有稳健性，但排除最具影响力的受试者后，CRP的关联降至0.19（标准误 = 0.10）。PM2.5与白细胞、红细胞计数、血小板或全血粘度无显著关联。HRV和CRP时间偏差的大多数短期变异性不能由PM2.5解释；然而，观察到的小的统计学显著关联表明，暴露于PM2.5可能是影响HRV和CRP的多种因素之一。
