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个人每小时暴露于空气温度和污染与慢性阻塞性肺疾病静息心率的关联。

Associations of Personal Hourly Exposures to Air Temperature and Pollution with Resting Heart Rate in Chronic Obstructive Pulmonary Disease.

机构信息

Division of Pulmonary and Critical Care Medicine, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, United States.

Children's Environmental Health Initiative, University of Illinois Chicago, Chicago, Illinois 60607, United States.

出版信息

Environ Sci Technol. 2024 Oct 15;58(41):18145-18154. doi: 10.1021/acs.est.4c05432. Epub 2024 Oct 5.

Abstract

Previous studies linked higher daily ambient air temperature and pollution with increased cardiorespiratory morbidity, but immediate effects of personal, hourly exposures on resting heart rate remained unclear. We followed 30 older former smokers with chronic obstructive pulmonary disease (COPD) in Massachusetts for four nonconsecutive 30-day periods over 12 months, collecting 54,487 hourly observations of personal air temperature, fine particulate matter (PM), nitrogen dioxide (NO), ozone (O), and resting heart rate. We explored the single lag effects (0-71 h) and cumulative effects (0-5 h, the significant lag windows) of air temperature and pollution on resting heart rate using generalized additive mixed models with distributed lag nonlinear models. Single lag effects of higher air temperature and pollutants on higher resting heart rate were most pronounced at lag 0 to 5 h. Cumulative effects of higher air temperature, PM, O, and NO (each interquartile range increment) on higher resting heart rate at lag 0-5 h, show differences of (beats per minute [bpm], 95% CI) 1.46 (1.31-1.62), 0.35 (0.32-0.39), 2.32 (2.19-2.45), and 1.79 (1.66-1.92), respectively. In conclusion, higher personal hourly air temperature, PM, O, and NO exposures at lag 0-5 h are associated with higher resting heart rate in COPD patients.

摘要

先前的研究表明,较高的环境日平均温度和污染水平与心肺发病率的增加有关,但个人每小时暴露量对静息心率的即时影响仍不清楚。我们在马萨诸塞州对 30 名患有慢性阻塞性肺疾病(COPD)的老年前吸烟者进行了为期 12 个月的 4 次非连续 30 天的随访,收集了 54487 小时的个人空气温度、细颗粒物(PM)、二氧化氮(NO)、臭氧(O)和静息心率的每小时观察值。我们使用广义加性混合模型和分布式滞后非线性模型探索了空气温度和污染对静息心率的单一滞后效应(0-71 小时)和累积效应(0-5 小时,显著滞后窗口)。空气温度和污染物对静息心率的单一滞后效应在滞后 0 到 5 小时最为明显。在滞后 0-5 小时,空气温度、PM、O 和 NO(每四分位间距增量)的累积效应与静息心率升高相关,差异分别为(每分钟跳动数[bpm],95%置信区间)1.46(1.31-1.62)、0.35(0.32-0.39)、2.32(2.19-2.45)和 1.79(1.66-1.92)。总之,在滞后 0-5 小时内,较高的个人每小时空气温度、PM、O 和 NO 暴露与 COPD 患者的静息心率升高有关。

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