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首页> 外文期刊>Journal of exposure science & environmental epidemiology >Effects of ultrafine and fine particulate and gaseous air pollution on cardiac autonomic control in subjects with coronary artery disease: the ULTRA study.
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Effects of ultrafine and fine particulate and gaseous air pollution on cardiac autonomic control in subjects with coronary artery disease: the ULTRA study.

机译:超细,细颗粒物和气态空气污染对冠心病患者心脏自主控制的影响:ULTRA研究。

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摘要

Previous studies have shown an association between elevated concentrations of particulate air pollution and cardiovascular morbidity and mortality. Therefore, the association between daily variation of ultrafine and fine particulate air pollution and cardiac autonomic control measured as heart rate variability (HRV) was studied in a large multicenter study in Amsterdam, the Netherlands, Erfurt, Germany, and Helsinki, Finland. Elderly subjects (n=37 in Amsterdam, n=47 in both Erfurt and Helsinki) with stable coronary artery disease were followed for 6 months with biweekly clinical visits. During the visits, ambulatory electrocardiogram was recorded during a standardized protocol including a 5-min period of paced breathing. Time and frequency domain analyses of HRV were performed. A statistical model was built for each center separately. The mean 24-h particle number concentration (NC) (1,000/cm(3)) of ultrafine particles (diameter 0.01-0.1 microm) was 17.3 in Amsterdam, 21.1 in Erfurt, and 17.0 in Helsinki. The corresponding values for PM2.5 were 20.0, 23.1, and 12.7 microg/m(3). During paced breathing, ultrafine particles, NO(2), and CO were at lags of 0-2 days consistently and significantly associated with decreased low-to-high frequency ratio (LF/HF), a measure of sympathovagal balance. In a pooled analysis across the centers, LF/HF decreased by 13.5% (95% confidence interval: -20.1%, -7.0%) for each 10,000/cm(3) increase in the NC of ultrafine particles (2-day lag). PM2.5 was associated with reduced HF and increased LF/HF in Helsinki, whereas the opposite was true in Erfurt, and in Amsterdam, there were no clear associations between PM2.5 and HRV. The results suggest that the cardiovascular effects of ambient ultrafine and PM2.5 can differ from each other and that their effect may be modified by the characteristics of the exposed subjects and the sources of PM2.5.
机译:先前的研究表明,颗粒空气污染浓度升高与心血管疾病的发病率和死亡率之间存在关联。因此,在荷兰阿姆斯特丹,德国爱尔福特和芬兰赫尔辛基进行的一项大型多中心研究中,研究了超细微粒空气污染的每日变化与以心率变异性(HRV)衡量的心脏自主控制之间的关系。对患有稳定型冠状动脉疾病的老年受试者(阿姆斯特丹为37名,爱尔福特和赫尔辛基均为47名)进行了6个月的随访,每两周进行一次临床随访。在就诊期间,在包括5分钟的定速呼吸在内的标准化协议中记录了动态心电图。对HRV进行了时域和频域分析。分别为每个中心建立了统计模型。超细颗粒(直径0.01-0.1微米)的平均24小时颗粒数浓度(NC)(1,000 / cm(3))在阿姆斯特丹为17.3,在爱尔福特为21.1,在赫尔辛基为17.0。 PM2.5的相应值为20.0、23.1和12.7 microg / m(3)。在有节奏的呼吸过程中,超细颗粒,NO(2)和CO始终处于0-2天的滞后,并且与低频/高频比(LF / HF)的降低显着相关,LF / HF是一种交感神经平衡的指标。在各个中心的汇总分析中,超细颗粒的NC每增加10,000 / cm(3),LF / HF下降13.5%(95%置信区间:-20.1%,-7.0%)(3天) 。在赫尔辛基,PM2.5与HF降低和LF / HF升高有关,而在爱尔福特和阿姆斯特丹则相反,PM2.5与HRV之间没有明确的关联。结果表明,环境超微粉尘和PM2.5的心血管作用可能互不相同,并且暴露对象的特征和PM2.5的来源可能会改变它们的作用。

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