Baja Emmanuel S, Schwartz Joel D, Wellenius Gregory A, Coull Brent A, Zanobetti Antonella, Vokonas Pantel S, Suh Helen H
Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts 02115 , USA.
Environ Health Perspect. 2010 Jun;118(6):840-6. doi: 10.1289/ehp.0901396. Epub 2010 Mar 1.
Acute exposure to ambient air pollution has been associated with acute changes in cardiac outcomes, often within hours of exposure.
We examined the effects of air pollutants on heart-rate-corrected QT interval (QTc), an electrocardiographic marker of ventricular repolarization, and whether these associations were modified by participant characteristics and genetic polymorphisms related to oxidative stress.
We studied repeated measurements of QTc on 580 men from the Veterans Affairs Normative Aging Study (NAS) using mixed-effects models with random intercepts. We fitted a quadratic constrained distributed lag model to estimate the cumulative effect on QTc of ambient air pollutants including fine particulate matter <or= 2.5 microm in aerodynamic diameter (PM2.5), ozone (O3), black carbon (BC), nitrogen dioxide (NO2), carbon monoxide (CO), and sulfur dioxide (SO2) concentrations during the 10 hr before the visit. We genotyped polymorphisms related to oxidative stress and analyzed pollution-susceptibility score interactions using the genetic susceptibility score (GSS) method.
Ambient traffic pollutant concentrations were related to longer QTc. An interquartile range (IQR) change in BC cumulative during the 10 hr before the visit was associated with increased QTc [1.89 msec change; 95% confidence interval (CI), -0.16 to 3.93]. We found a similar association with QTc for an IQR change in 1-hr BC that occurred 4 hr before the visit (2.54 msec change; 95% CI, 0.28-4.80). We found increased QTc for IQR changes in NO2 and CO, but the change was statistically insignificant. In contrast, we found no association between QTc and PM2.5, SO2, and O3. The association between QTc and BC was stronger among participants who were obese, who had diabetes, who were nonsmokers, or who had higher GSSs.
Traffic-related pollutants may increase QTc among persons with diabetes, persons who are obese, and nonsmoking elderly individuals; the number of genetic variants related to oxidative stress increases this effect.
急性暴露于环境空气污染与心脏结局的急性变化有关，通常在暴露后数小时内出现。
我们研究了空气污染物对心率校正QT间期（QTc）的影响，QTc是心室复极的心电图标志物，以及这些关联是否会因参与者特征和与氧化应激相关的基因多态性而改变。
我们使用具有随机截距的混合效应模型，对来自退伍军人事务部标准老化研究（NAS）的580名男性的QTc进行了重复测量。我们拟合了一个二次约束分布滞后模型，以估计在就诊前10小时内环境空气污染物（包括空气动力学直径≤2.5微米的细颗粒物（PM2.5）、臭氧（O3）、黑碳（BC）、二氧化氮（NO2）、一氧化碳（CO）和二氧化硫（SO2）浓度）对QTc的累积影响。我们对与氧化应激相关的多态性进行了基因分型，并使用遗传易感性评分（GSS）方法分析了污染易感性评分相互作用。
环境交通污染物浓度与更长的QTc相关。就诊前10小时内BC累积量的四分位间距（IQR）变化与QTc增加相关[变化1.89毫秒；95%置信区间（CI），-0.16至3.93]。我们发现，就诊前4小时出现的1小时BC的IQR变化与QTc也有类似关联（变化2.54毫秒；95%CI，0.28至4.80）。我们发现NO2和CO的IQR变化会使QTc增加，但该变化在统计学上不显著。相比之下，我们未发现QTc与PM2.5、SO2和O3之间存在关联。在肥胖、患有糖尿病、不吸烟或GSS较高的参与者中，QTc与BC之间的关联更强。
与交通相关的污染物可能会增加糖尿病患者、肥胖者和不吸烟老年人的QTc；与氧化应激相关的基因变异数量会增强这种影响。
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