Acute effects of fine particulate air pollution on ST segment height: a longitudinal study.
Acute effects of fine particulate air pollution on ST segment height: a longitudinal study.
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DOI：
10.1186/1476-069x-9-68
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发表时间：
2010-11-08
期刊：
影响因子：
--
通讯作者：
Liao D
中科院分区：
文献类型：
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作者：
He F;Shaffer ML;Rodriguez-Colon S;Bixler EO;Vgontzas AN;Williams RW;Wu R;Cascio WE;Liao D
颗粒空气污染与心脏病之间的关系机制尚未完全了解。空气污染引起的心肌缺血是其中一个潜在的重要机制。我们研究了急性效应和细颗粒物污染（PM2.5）对心肌缺血性损伤的时间过程，通过ST段高度评估106名健康非吸烟者的社区样本。使用高分辨率12导联霍尔特ECG系统获得24小时逐搏心电图（ECG）数据。在视觉上识别并去除所有伪影和心搏后，我们计算了10个导联（下导联II、III和aVF;前导联V3和V4;间隔导联V1和V2;外侧导联I、V5和V6）的心搏ST段高度。个人水平的24小时实时PM2.5浓度通过连续个人PM2.5监测仪获得。然后，我们以30分钟为基础计算了每位参与者在一天中相应时间的PM2.5平均暴露量。使用线性混合效应模型框架下的分布滞后模型来评估30分钟PM2.5和每个导联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分钟间隔。平均（SD）年龄为56（7.6）岁，其中41%为男性，74%为白色。平均（SD）PM2.5暴露量为14（22）μg/m3。所有下壁导联（II、III和aVF）和三分之二的外侧导联（I和V6）显示较高的PM2.5水平与较高的ST段高度之间存在显著相关性。大多数不良反应发生在PM2.5暴露后两小时内。Lag 0-4 PM2.5增加10 μg/m3对ST-I、II、III、aVF和ST-V6的累积效应的多变量调整回归系数β（95%CI）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均< 0.05。PM2.5浓度增加与下壁和外侧导联ST段高度立即增加相关，通常在两小时内。PM2.5的这种急性效应可能有助于增加健康个体局部心肌缺血性损伤的可能性。
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.