Department of Public Health Sciences, Penn State University College of Medicine, A210, 600 Centerview Dr, Suite 2200, Hershey, PA 17033, USA.
Environ Health. 2010 Nov 8;9:68. doi: 10.1186/1476-069X-9-68.
The mechanisms for the relationship between particulate air pollution and cardiac disease are not fully understood. Air pollution-induced myocardial ischemia is one of the potentially important mechanisms.
We investigate the acute effects and the time course of fine particulate pollution (PM2.5) on myocardium ischemic injury as assessed by ST-segment height in a community-based sample of 106 healthy non-smokers. Twenty-four hour beat-to-beat electrocardiogram (ECG) data were obtained using a high resolution 12-lead Holter ECG system. After visually identifying and removing all the artifacts and arrhythmic beats, we calculated beat-to-beat ST-height from ten leads (inferior leads II, III, and aVF; anterior leads V3 and V4; septal leads V1 and V2; lateral leads I, V5, and V6,). Individual-level 24-hour real-time PM2.5 concentration was obtained by a continuous personal PM2.5 monitor. We then calculated, on a 30-minute basis, the corresponding time-of-the-day specific average exposure to PM2.5 for each participant. Distributed lag models under a linear mixed-effects models framework were used to assess the regression coefficients between 30-minute PM2.5 and ST-height measures from each lead; i.e., one lag indicates a 30-minute separation between the exposure and outcome.
The mean (SD) age was 56 (7.6) years, with 41% male and 74% white. The mean (SD) PM2.5 exposure was 14 (22) μg/m3. All inferior leads (II, III, and aVF) and two out of three lateral leads (I and V6), showed a significant association between higher PM2.5 levels and higher ST-height. Most of the adverse effects occurred within two hours after PM2.5 exposure. The multivariable adjusted regression coefficients β (95% CI) of the cumulative effect due to a 10 μg/m3 increase in Lag 0-4 PM2.5 on ST-I, II, III, aVF and ST-V6 were 0.29 (0.01-0.56) μV, 0.79 (0.20-1.39) μV, 0.52 (0.01-1.05) μV, 0.65 (0.11-1.19) μV, and 0.58 (0.07-1.09) μV, respectively, with all p < 0.05.
Increased PM2.5 concentration is associated with immediate increase in ST-segment height in inferior and lateral leads, generally within two hours. Such an acute effect of PM2.5 may contribute to increased potential for regional myocardial ischemic injury among healthy individuals.
颗粒物空气污染与心脏疾病之间的关系机制尚未完全阐明。空气污染引起的心肌缺血是潜在的重要机制之一。
我们在一个由 106 名健康不吸烟者组成的社区样本中，通过 ST 段高度来研究细颗粒物（PM2.5）对心肌缺血损伤的急性影响和时间过程。使用高分辨率 12 导联 Holter ECG 系统获得 24 小时逐拍心电图（ECG）数据。在视觉识别并去除所有伪影和心律失常后，我们从 10 个导联计算逐拍 ST 高度（下壁导联 II、III 和 aVF；前壁导联 V3 和 V4；间隔导联 V1 和 V2；侧壁导联 I、V5 和 V6）。通过连续个人 PM2.5 监测器获得个体水平的 24 小时实时 PM2.5 浓度。然后，我们以 30 分钟为基础，计算每个参与者相应的特定时间段内 PM2.5 的平均暴露量。在线性混合效应模型框架下使用分布滞后模型，评估 30 分钟 PM2.5 与来自每个导联的 ST 高度测量值之间的回归系数；即，一个滞后表示暴露和结果之间的 30 分钟分离。
平均（标准差）年龄为 56（7.6）岁，41%为男性，74%为白人。平均（标准差）PM2.5 暴露量为 14（22）μg/m3。所有下壁导联（II、III 和 aVF）和三个侧壁导联中的两个（I 和 V6）都显示出较高的 PM2.5 水平与较高的 ST 高度之间存在显著关联。大多数不良影响发生在 PM2.5 暴露后两小时内。由于 Lag 0-4 PM2.5 增加 10 μg/m3，ST-I、II、III、aVF 和 ST-V6 的累积效应的多变量调整后回归系数β（95%CI）分别为 0.29（0.01-0.56）μV、0.79（0.20-1.39）μV、0.52（0.01-1.05）μV、0.65（0.11-1.19）μV 和 0.58（0.07-1.09）μV，所有 p 值均<0.05。
PM2.5 浓度增加与下壁和侧壁导联 ST 段高度的即刻升高有关，通常在两小时内。PM2.5 的这种急性效应可能导致健康个体中区域性心肌缺血损伤的潜在增加。
