Ambient and Controlled Particle Exposures as Triggers for Acute ECG Changes.

D. Rich, A. Peters, A. Schneider, W. Zareba, S. Breitner, D. Oakes, Jelani Wiltshire, Cathleen Kane, M. Frampton, Regina Hampel, P. Hopke, J. Cyrys, M. Utell
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The aims of the cur- rent study were to investigate whether exposure to PM was associated with rapid changes (< 60 minutes or con- current hour up to a delay of 6 hours) in markers of car- diac rhythni or changes in total antioxidant capacity (a marker of protection against oxidative stress) and whether any PM effects on cardiac rhythm markers were modified by total antioxidant capacity, age, obesity, smoking, hypertension, exertion, prior myocardial infarction (MI), or medication.\n\n\nMETHODS\nWe obtained data from a completed study in Augsburg, Germany (a panel study in N= 109 subjects, including a group with type 2 diabetes or impaired glucose tolerance [IGT; also known as prediabetes]) and a group of other- wise healthy subjects with a potential genetic susceptibil- ity to detoxifying and inflammatory pathways (Hampel et al. 2012b), as well as three completed studies in Rochester, New York (the REHAB panel study of N= 76 postinfarction patients in a cardiac rehabilitation pro- gram [Rich et al. 2012b]; the UPDIABETES study of con- trolled exposure to ultrafine particles [UFPs, particles with an aerodynamic diameter < 100 nm] of N = 19 patients with type 2 diabetes [Stewart et al. 2010; Vora et al. 2014j; and the UPCON controlled-exposure study of concentrated UFP exposure in N = 20 young, healthy, life- time nonsmokers). Data included 5-minute and 1-hour values for HRV and repolarization parameters from elec- trocardiogram (ECG) recordings and total antioxidant capacity measured in stored blood samples. Ambient con- centrations of UFPs, accumulation-mode particles (AMP, particles with an aerodynamic diameter of 100-500 nm), fine PM (PM2.5, particles with an aerodynamic diameter 2.5 pm), and black carbon (BC) were also available. We first conducted factor analyses in each study to find subgroups of correlated ECG outcomes and to reduce the number of outcomes examined in our statistical models. We then restricted the statistical analyses to the factors and representative.outcomes that were common to all four studies, including total HRV (measured as the standard deviation of normal-to-normal [NN] beat intervals [SDNNj), parasympathetic modulation (measured as the root mean square of the successive differences [RMSSD between adjacent NN beat intervals), and T-wave morphol- ogy (measured as T-wave complexity). Next, we used addi- tive mixed models to estimate the change in each outcome associated with increased pollutant concentrations in the . concurrent and previous 6 hours and with 5-minute inter- vals up to the previous 60 minutes, accounting for the correlation of repeated outcome measures for each subject and adjusting for time trend, hour of the day, temperature, relative humidity, day of the week, month, and visit number. Because multiple comparisons were an issue in our. analyses, we used a discovery-and-replication approach to draw conclusions across studies for each research question.\n\n\nRESULTS\nIn the Augsburg study, interquartile range (IQR) increases in UFP concentrations lagged 2 to 5 hours were associated with 1%-3% decreases in SDNN (e.g., lagged 3 hours in the group with a genetic susceptibility: -2.26%; 95% confidence interval [CI], -3.98% to -0.53%). In the REHAB study, similarly, IQR increases in UFP concentra- tions in the previous 5 hours were associated with < 3% decreases in SDNN (e.g., lagged 1 hour: -2.69%; 95% CI, -5.13% to -0.26%). We also found decreases in SDNN associated with IQR increases in total particle count-(a surrogate for UFP) in the UPDIABETES study (lagged 1 hour: -13.22%; 95% CI, -24.11% to -2.33%) but not in the UPCON study. In the Augsburg study, IQR increases in PM2.5 concen- trations in the concurrent hour and lagged 1-5 hours, AMP concentrations lagged 1 and 3 hours, and BC con- centrations lagged 1-5 hours were associated with -1%-5% decreases in SDNN (e.g., PM2.5 lagged 2 hours in the group with diabetes or IGT: -4.59%; 95% CI, -7.44% to -1.75%). In the REHAB study, IQR increases in PM2.5 concentrations lagged 5 and 6 hours and AMP concentra- tions in the concurrent hour and lagged up to 5 hours were associated with 1%-2% decreases in SDNN (e.g., PM2.5 lagged 4 hours: -2.13%; 95% CI, -3.91% to -0.35%). In the Augsburg study, IQR increases in PM2.5 concen- trations in the concurrent hour and BC lagged 1 and 6 hours were associated with 3%-7% decreases in RMSSD (e.g., PM2.5 concurrent hour in the group with diabetes or IGT: -7.20%; 95% CI, -12.11% to -2.02%). In the REHAB study, similarly, increases in PM2.5 concen- trations lagged 4 to 6 hours-though not AMP or BC con- centrations at any lag hour-were associated with -2.5%-3.5% decreases in RMSSD (e.g., PM2.5 lagged 5 hours: -3.49%; 95% CI, -6.13% to -0.84%). We did not find consistent evidence of any pollutant effects on T-wave complexity in 1-hour recordings. For 5-minute record- ings, there was no consistent evidence of UFP effects on SDNN, RMSSD, or T-wave complexity at any 5-minute interval within 60 minutes. We further concluded that these replicated hourly effects of UFP and PM2.5 on short-term measures of SDNN and RMSSD generally did not differ between the groups in the studies (i.e., type 2 diabetes, pre-diabetes/IGT, post- infarction, and healthy subjects). Last, we found no con- sistent evidence of effects of any pollutant on total anti- oxidant capacity and no consistent evidence of modification of our PM2.5-outcome associations by any of the potential effect modifiers.\n\n\nONCLUSIONS\nIncreased UFP concentrations were associated with decreased SDNN in both of the panel studies and one of the two controlled-exposure studies. We also found that decreased SDNN was associated with both increased PM2.5 and AMP concentrations in the previous 6 hours in the panel studies and that decreased RMSSD was associ- ated with increased PM2.5 concentrations in the previous 6 hours in the panel studies. We therefore concluded that the research questions were replicated. Our findings suggest that both UFPs and PM2.5 are associated with autonomic dysfunction within hours of exposure, which may in part. explain the previously reported risk of acute cardiovascular events associated with increased PM in the previous few hours. Despite the heterogeneity of the study populations,and protocols, our findings provided consistent evidence for the induction of rapid pathophysiological responses by UFPs and PM2.5- The absence of consistent associations between UFPs, PM2.5, and these outcomes when examining shorter time intervals indicates that the 5- to 60-minute responses may be less pronounced than the responses occurring within hours. However, the findings from the 5-minute intervals may have been affected by the variety of proto- cols and conditions from study to study as well as by the potential effects of underlying diseases (e.g., healthy indi- viduals versus individuals with diabetes or a recent cor- onary artery. event), physical activity, circadian rhythms, stress, and/or medications.","PeriodicalId":21038,"journal":{"name":"Research report","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2014-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"11","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Research report","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1289/isee.2014.o-030","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 11

Abstract

INTRODUCTION Previous studies have examined changes in heart rate variability (HRV*) and repolarization associated with increased particulate matter (PM) concentrations on the same and previous few days. However, few studies have examined whether these health responses to PM occur within a few hours or even less. Moreover, it is not clear whether exposure of subjects to ambient or-controlled PM concentrations both lead to similar health effects or whether any of the subjects' individual characteristics modify any of their responses to PM. The aims of the cur- rent study were to investigate whether exposure to PM was associated with rapid changes (< 60 minutes or con- current hour up to a delay of 6 hours) in markers of car- diac rhythni or changes in total antioxidant capacity (a marker of protection against oxidative stress) and whether any PM effects on cardiac rhythm markers were modified by total antioxidant capacity, age, obesity, smoking, hypertension, exertion, prior myocardial infarction (MI), or medication. METHODS We obtained data from a completed study in Augsburg, Germany (a panel study in N= 109 subjects, including a group with type 2 diabetes or impaired glucose tolerance [IGT; also known as prediabetes]) and a group of other- wise healthy subjects with a potential genetic susceptibil- ity to detoxifying and inflammatory pathways (Hampel et al. 2012b), as well as three completed studies in Rochester, New York (the REHAB panel study of N= 76 postinfarction patients in a cardiac rehabilitation pro- gram [Rich et al. 2012b]; the UPDIABETES study of con- trolled exposure to ultrafine particles [UFPs, particles with an aerodynamic diameter < 100 nm] of N = 19 patients with type 2 diabetes [Stewart et al. 2010; Vora et al. 2014j; and the UPCON controlled-exposure study of concentrated UFP exposure in N = 20 young, healthy, life- time nonsmokers). Data included 5-minute and 1-hour values for HRV and repolarization parameters from elec- trocardiogram (ECG) recordings and total antioxidant capacity measured in stored blood samples. Ambient con- centrations of UFPs, accumulation-mode particles (AMP, particles with an aerodynamic diameter of 100-500 nm), fine PM (PM2.5, particles with an aerodynamic diameter 2.5 pm), and black carbon (BC) were also available. We first conducted factor analyses in each study to find subgroups of correlated ECG outcomes and to reduce the number of outcomes examined in our statistical models. We then restricted the statistical analyses to the factors and representative.outcomes that were common to all four studies, including total HRV (measured as the standard deviation of normal-to-normal [NN] beat intervals [SDNNj), parasympathetic modulation (measured as the root mean square of the successive differences [RMSSD between adjacent NN beat intervals), and T-wave morphol- ogy (measured as T-wave complexity). Next, we used addi- tive mixed models to estimate the change in each outcome associated with increased pollutant concentrations in the . concurrent and previous 6 hours and with 5-minute inter- vals up to the previous 60 minutes, accounting for the correlation of repeated outcome measures for each subject and adjusting for time trend, hour of the day, temperature, relative humidity, day of the week, month, and visit number. Because multiple comparisons were an issue in our. analyses, we used a discovery-and-replication approach to draw conclusions across studies for each research question. RESULTS In the Augsburg study, interquartile range (IQR) increases in UFP concentrations lagged 2 to 5 hours were associated with 1%-3% decreases in SDNN (e.g., lagged 3 hours in the group with a genetic susceptibility: -2.26%; 95% confidence interval [CI], -3.98% to -0.53%). In the REHAB study, similarly, IQR increases in UFP concentra- tions in the previous 5 hours were associated with < 3% decreases in SDNN (e.g., lagged 1 hour: -2.69%; 95% CI, -5.13% to -0.26%). We also found decreases in SDNN associated with IQR increases in total particle count-(a surrogate for UFP) in the UPDIABETES study (lagged 1 hour: -13.22%; 95% CI, -24.11% to -2.33%) but not in the UPCON study. In the Augsburg study, IQR increases in PM2.5 concen- trations in the concurrent hour and lagged 1-5 hours, AMP concentrations lagged 1 and 3 hours, and BC con- centrations lagged 1-5 hours were associated with -1%-5% decreases in SDNN (e.g., PM2.5 lagged 2 hours in the group with diabetes or IGT: -4.59%; 95% CI, -7.44% to -1.75%). In the REHAB study, IQR increases in PM2.5 concentrations lagged 5 and 6 hours and AMP concentra- tions in the concurrent hour and lagged up to 5 hours were associated with 1%-2% decreases in SDNN (e.g., PM2.5 lagged 4 hours: -2.13%; 95% CI, -3.91% to -0.35%). In the Augsburg study, IQR increases in PM2.5 concen- trations in the concurrent hour and BC lagged 1 and 6 hours were associated with 3%-7% decreases in RMSSD (e.g., PM2.5 concurrent hour in the group with diabetes or IGT: -7.20%; 95% CI, -12.11% to -2.02%). In the REHAB study, similarly, increases in PM2.5 concen- trations lagged 4 to 6 hours-though not AMP or BC con- centrations at any lag hour-were associated with -2.5%-3.5% decreases in RMSSD (e.g., PM2.5 lagged 5 hours: -3.49%; 95% CI, -6.13% to -0.84%). We did not find consistent evidence of any pollutant effects on T-wave complexity in 1-hour recordings. For 5-minute record- ings, there was no consistent evidence of UFP effects on SDNN, RMSSD, or T-wave complexity at any 5-minute interval within 60 minutes. We further concluded that these replicated hourly effects of UFP and PM2.5 on short-term measures of SDNN and RMSSD generally did not differ between the groups in the studies (i.e., type 2 diabetes, pre-diabetes/IGT, post- infarction, and healthy subjects). Last, we found no con- sistent evidence of effects of any pollutant on total anti- oxidant capacity and no consistent evidence of modification of our PM2.5-outcome associations by any of the potential effect modifiers. ONCLUSIONS Increased UFP concentrations were associated with decreased SDNN in both of the panel studies and one of the two controlled-exposure studies. We also found that decreased SDNN was associated with both increased PM2.5 and AMP concentrations in the previous 6 hours in the panel studies and that decreased RMSSD was associ- ated with increased PM2.5 concentrations in the previous 6 hours in the panel studies. We therefore concluded that the research questions were replicated. Our findings suggest that both UFPs and PM2.5 are associated with autonomic dysfunction within hours of exposure, which may in part. explain the previously reported risk of acute cardiovascular events associated with increased PM in the previous few hours. Despite the heterogeneity of the study populations,and protocols, our findings provided consistent evidence for the induction of rapid pathophysiological responses by UFPs and PM2.5- The absence of consistent associations between UFPs, PM2.5, and these outcomes when examining shorter time intervals indicates that the 5- to 60-minute responses may be less pronounced than the responses occurring within hours. However, the findings from the 5-minute intervals may have been affected by the variety of proto- cols and conditions from study to study as well as by the potential effects of underlying diseases (e.g., healthy indi- viduals versus individuals with diabetes or a recent cor- onary artery. event), physical activity, circadian rhythms, stress, and/or medications.
环境和受控颗粒暴露作为急性心电图改变的触发因素。
以前的研究已经检查了心率变异性(HRV*)和复极化在同一天和前几天与颗粒物(PM)浓度增加相关的变化。然而,很少有研究检查这些对PM的健康反应是否在几小时甚至更短的时间内发生。此外,尚不清楚受试者暴露于环境或受控的PM浓度是否会导致类似的健康影响,也不清楚受试者的任何个体特征是否会改变他们对PM的任何反应。本研究的目的是调查暴露于PM是否与心律标记物的快速变化(< 60分钟或同步一小时至延迟6小时)或总抗氧化能力(抗氧化应激的标志)的变化有关,以及PM对心律标记物的影响是否因总抗氧化能力、年龄、肥胖、吸烟、高血压、劳累、既往心肌梗死(MI)或药物治疗而改变。方法:我们从德国奥格斯堡的一项已完成的研究中获得数据(N= 109名受试者的小组研究,包括2型糖尿病或糖耐量受损组[IGT;也被称为前驱糖尿病])和一组对解毒和炎症途径具有潜在遗传易感性的健康受试者(Hampel et al. 2012b),以及在纽约州罗切斯特市完成的三项研究(心脏康复计划中N= 76例梗死后患者的康复小组研究[Rich et al. 2012b];UPDIABETES对N = 19例2型糖尿病患者的控制暴露于超细颗粒[ufp,空气动力学直径< 100 nm的颗粒]的研究[Stewart et al. 2010;Vora et al. 2014j;以及UPCON控制暴露研究(集中UFP暴露于N = 20名年轻、健康、终生不吸烟的人)。数据包括5分钟和1小时HRV值和心电图(ECG)记录的复极化参数,以及储存血液样本中测量的总抗氧化能力。ufp、累积模式粒子(AMP,空气动力学直径为100-500 nm的粒子)、细颗粒物(PM2.5,空气动力学直径为2.5 PM的粒子)和黑碳(BC)的环境浓度也可用。我们首先对每项研究进行因素分析,以找到相关心电图结果的亚组,并减少统计模型中检查的结果数量。然后,我们将统计分析限制在因素和代表性上。所有四项研究共有的结果,包括总HRV(以正常到正常[NN]心跳间隔[ssdnj]的标准偏差测量),副交感神经调节(以相邻NN心跳间隔之间连续差异的均方根测量[RMSSD])和t波形态(以t波复杂性测量)。接下来,我们使用加性混合模型来估计与大气中污染物浓度增加相关的每个结果的变化。同时和之前的6小时,间隔5分钟直到之前的60分钟,考虑到每个受试者重复结果测量的相关性,并根据时间趋势、每天的小时、温度、相对湿度、星期几、月份和就诊次数进行调整。因为多重比较是个问题。在分析中,我们使用了发现和复制的方法来得出每个研究问题的结论。结果在Augsburg研究中,UFP浓度滞后2 - 5小时的四分位数范围(IQR)增加与SDNN下降1%-3%相关(例如,遗传易感性组滞后3小时:-2.26%;95%置信区间[CI], -3.98%至-0.53%)。在康复研究中,同样,前5小时内UFP浓度的IQR增加与SDNN下降< 3%相关(例如,滞后1小时:-2.69%;95% CI, -5.13%至-0.26%)。我们还发现,在UPDIABETES研究中,sdn的减少与总颗粒计数(UFP的替代指标)的IQR增加相关(滞后1小时:-13.22%;95% CI, -24.11%至-2.33%),但在UPCON研究中没有。在Augsburg的研究中,PM2.5浓度在同期1小时和滞后1-5小时,AMP浓度滞后1和3小时,以及BC浓度滞后1-5小时的IQR增加与SDNN下降-1%-5%相关(例如,PM2.5在糖尿病或IGT组滞后2小时:-4.59%;95% CI, -7.44%至-1.75%)。在康复研究中,PM2.5浓度的IQR增加滞后5和6小时,AMP浓度在同期和滞后5小时内的增加与SDNN下降1%-2%相关(例如,PM2.5滞后4小时:-2.13%;95% CI, -3.91%至-0.35%)。在Augsburg的研究中,PM2.5浓度的IQR增加与RMSSD降低3%-7%相关(例如,糖尿病或IGT组的PM2.5同时小时:-7)。 20%;95% CI, -12.11%至-2.02%)。同样,在康复研究中,PM2.5浓度的增加-滞后4至6小时-尽管AMP或BC浓度不在任何滞后时间-与RMSSD下降2.5%-3.5%相关(例如PM2.5滞后5小时:-3.49%;95% CI, -6.13%至-0.84%)。在1小时的记录中,我们没有发现任何污染物对t波复杂性影响的一致证据。对于5分钟的记录,没有一致的证据表明UFP在60分钟内任何5分钟间隔对SDNN、RMSSD或t波复杂性有影响。我们进一步得出结论,UFP和PM2.5对SDNN和RMSSD短期测量的重复小时效应在研究组(即2型糖尿病、糖尿病前期/IGT、梗死后和健康受试者)之间通常没有差异。最后,我们没有发现任何污染物对总抗氧化能力的影响的一致证据,也没有发现任何潜在影响调节剂改变我们的pm2.5结局关联的一致证据。结论UFP浓度的升高与SDNN的降低相关,在两项小组研究和两项对照暴露研究中的一项中都是如此。我们还发现,在小组研究中,SDNN的降低与前6小时PM2.5和AMP浓度的增加有关,RMSSD的降低与前6小时PM2.5浓度的增加有关。因此,我们得出结论,研究问题是重复的。我们的研究结果表明,ufp和PM2.5在暴露数小时内都与自主神经功能障碍有关,这可能是部分原因。解释先前报道的与前几小时PM升高相关的急性心血管事件风险。尽管研究人群和研究方案存在异质性,但我们的研究结果为ufp和PM2.5诱导快速病理生理反应提供了一致的证据——在检测较短时间间隔时,ufp、PM2.5和这些结果之间缺乏一致的关联,这表明5至60分钟的反应可能不如数小时内发生的反应明显。然而,5分钟间隔的结果可能受到不同研究的方案和条件的影响,也可能受到潜在疾病的潜在影响(例如,健康个体与糖尿病患者或新近患冠心病的个体)。事件)、身体活动、昼夜节律、压力和/或药物。
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