Association of Fine Particulate Matter Exposure With Bystander-Witnessed Out-of-Hospital Cardiac Arrest of Cardiac Origin in Japan
Association of Fine Particulate Matter Exposure With Bystander-Witnessed Out-of-Hospital Cardiac Arrest of Cardiac Origin in Japan
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DOI：
10.1001/jamanetworkopen.2020.3043
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发表时间：
2020-04-17
影响因子：
13.8
通讯作者：
Tsutsui, Hiroyuki
中科院分区：
文献类型：
--
作者：
Kojima, Sunao;Michikawa, Takehiro;Tsutsui, Hiroyuki
重要性院外心脏骤停（OHCAs）是一个主要的公共卫生问题，也是全球主要的死亡原因。暴露于环境空气污染与发病率和死亡率的增加有关，并已被公认为是全球疾病负担的主要贡献者。目的研究短期暴露于直径为2.5 μ m或更小的颗粒物之间的关系（PM2.5）和心源性OHCA的发生率以及初始心脏骤停节律的发展。设计，设置，该病例对照研究使用了2005年1月1日至2016年12月31日期间在全日本Utstein登记处登记的病例数据，该登记处是日本所有47个县的OHCA的前瞻性全国人口数据库。这些OHCA病例包括有旁观者见证的OHCA患者，以及紧急医疗服务响应者在医院转移前启动复苏的患者。研究分析采用病例交叉设计。应用特定地区的条件logistic回归模型估计比值比，并使用随机效应荟萃分析获得特定地区的汇总估计值。所有分析均于2019年5月7日至2020年1月23日进行。主要结局和指标主要结局是短期PM2. 5暴露与旁观者目击的心源性OHCA发生率的相关性。结果共有103189例OHCAs被纳入最终分析。在发生此类OHCA的患者中，平均（SD）年龄为75（15.5）岁，62795（60.9%）例为男性。在lag 0 -1（病例当天和前一天测量的PM2.5平均浓度的差异），PM2.5增加10 μ g/m3的百分比增加的点估计显示，在47个县中的大多数县，OHCA的发病率在统计学上显著较高，没有显著的异质性（I-2 = 20.1%; P = 0.12）。分层分析发现PM2.5暴露与OHCAs之间存在相关性（%增加，1.6; 95%CI，0.1%-3.1%）。初始可电击节律，如室颤或无脉性室性心动过速（%增加，0.6; 95% CI，-2.0%至3.2%），与PM2.5暴露无关。然而，最初的不可电击节律，如无脉电活动和心搏停止，与PM2.5暴露相关（增加%，1.4; 95%CI，0.1%-2.7%）。结论和相关性研究结果表明，PM2.5浓度增加与旁观者目击的心脏起源的OHCA相关，通常表现为不可电击节律。结果支持减少PM2.5暴露以预防心脏源性OHCAs的措施。
Importance Out-of-hospital cardiac arrests (OHCAs) are a major public health concern and a leading cause of death worldwide. Exposure to ambient air pollution is associated with increases in morbidity and mortality and has been recognized as a leading contributor to global disease burden.Objective To examine the association between short-term exposure to particulate matter with a diameter of 2.5 mu m or smaller (PM2.5) and the incidence of OHCAs of cardiac origin and with the development of initial cardiac arrest rhythm.Design, Setting, and Participants This case-control study used data from cases registered between January 1, 2005, and December 31, 2016, in the All-Japan Utstein Registry, a prospective, nationwide, population-based database for OHCAs across all 47 Japanese prefectures. These OHCA cases included patients who had bystander-witnessed OHCAs and for whom emergency medical services responders initiated resuscitation before hospital transfer. A case-crossover design was employed for the study analyses. A prefecture-specific, conditional logistic regression model to estimate odds ratios was applied, and a random-effects meta-analysis was used to obtain prefecture-specific pooled estimates. All analyses were performed from May 7, 2019, to January 23, 2020.Main Outcomes and Measures The main outcome was the association of short-term PM2.5 exposure with the incidence of bystander-witnessed OHCAs of cardiac origin. The differences in the distribution of initial cardiac arrest rhythm in OHCAs among those with exposure to PM2.5 were also examined.Results In total, 103 189 OHCAs witnessed by bystanders were included in the final analysis. Among the patients who experienced such OHCAs, the mean (SD) age was 75 (15.5) years, and 62 795 (60.9%) were men. Point estimates of the percentage increase for a 10-mu g/m(3) increase in PM2.5 at lag0-1 (difference in mean PM2.5 concentrations measured on the case day and 1 day before) demonstrated a statistically significantly higher incidence of OHCA across most of the 47 prefectures, without significant heterogeneity (I-2 = 20.1%; P = .12). A stratified analysis found an association between PM2.5 exposure and OHCAs (% increase, 1.6; 95% CI, 0.1%-3.1%). An initial shockable rhythm, such as ventricular fibrillation or pulseless ventricular tachycardia (% increase, 0.6; 95% CI, -2.0% to 3.2%), was not associated with PM2.5 exposure. However, an initial nonshockable rhythm, such as pulseless electrical activity and asystole, was associated with PM2.5 exposure (% increase, 1.4; 95% CI, 0.1%-2.7%).Conclusions and Relevance Findings from this study suggest that increased PM2.5 concentration is associated with bystander-witnessed OHCA of cardiac origin that commonly presents with nonshockable rhythm. The results support measures to reduce PM2.5 exposure to prevent OHCAs of cardiac origin.