Department of Environmental and Occupational Health, University of Pittsburgh, Bridgeside Point I, Pittsburgh, PA 15219, USA.
Environ Health. 2013 Jan 18;12:7. doi: 10.1186/1476-069X-12-7.
While air pollution exposures have been linked to cardiovascular outcomes, the contribution from acute gas and particle traffic-related pollutants remains unclear. Using a panel study design with repeated measures, we examined associations between personal exposures to traffic-related air pollutants in Mexico City and changes in heart rate variability (HRV) in a population of researchers aged 22 to 56 years.
Participants were monitored for approximately 9.5 hours for eight days while operating a mobile laboratory van designed to characterize traffic pollutants while driving in traffic and "chasing" diesel buses. We examined the association between HRV parameters (standard deviation of normal-to-normal intervals (SDNN), power in high frequency (HF) and low frequency (LF), and the LF/HF ratio) and the 5-minute maximum (or average in the case of PM(2.5)) and 30-, 60-, and 90-minute moving averages of air pollutants (PM(2.5), O(3), CO, CO(2), NO(2), NO(x), and formaldehyde) using single- and two-pollutant linear mixed-effects models.
Short-term exposure to traffic-related emissions was associated with statistically significant acute changes in HRV. Gaseous pollutants - particularly ozone - were associated with reductions in time and frequency domain components (α = 0.05), while significant positive associations were observed between PM(2.5) and SDNN, HF, and LF. For ozone and formaldehyde, negative associations typically increased in magnitude and significance with increasing averaging periods. The associations for CO, CO(2), NO(2), and NO(x) were similar with statistically significant associations observed for SDNN, but not HF or LF. In contrast, PM(2.5) increased these HRV parameters.
Results revealed an association between traffic-related PM exposures and acute changes in HRV in a middle-aged population when PM exposures were relatively low (14 μg/m(3)) and demonstrate heterogeneity in the effects of different pollutants, with declines in HRV - especially HF - with ozone and formaldehyde exposures, and increases in HRV with PM(2.5) exposure. Given that exposure to traffic-related emissions is associated with increased risk of cardiovascular morbidity and mortality, understanding the mechanisms by which traffic-related emissions can cause cardiovascular disease has significant public health relevance.
虽然空气污染暴露与心血管疾病结果相关，但急性气体和颗粒交通相关污染物的贡献仍不清楚。我们采用重复测量的面板研究设计，检测了墨西哥城交通相关空气污染物个人暴露与 22 至 56 岁研究人员的心率变异性 (HRV) 变化之间的关联。
参与者在驾驶移动实验室车时大约 9.5 小时内，每天进行 8 天监测，旨在描绘交通污染物特征，同时“追逐”柴油公共汽车。我们检测了 HRV 参数（正常到正常间隔标准差 (SDNN)、高频 (HF) 和低频 (LF) 的功率，以及 LF/HF 比值）与 5 分钟最大（或 PM(2.5) 的平均）和 30 分钟、60 分钟和 90 分钟的空气污染物（PM(2.5)、O(3)、CO、CO(2)、NO(2)、NO(x) 和甲醛）移动平均值之间的关联，使用单污染物和双污染物线性混合效应模型。
短期接触交通相关排放物与 HRV 的急性变化有统计学显著关联。气态污染物 - 特别是臭氧 - 与时间和频率域成分的减少有关（α=0.05），而 PM(2.5)与 SDNN、HF 和 LF 之间观察到显著正相关。对于臭氧和甲醛，随着平均时间的增加，负相关的幅度和显著性通常增加。CO、CO(2)、NO(2)和 NO(x)的关联类似，SDNN 有统计学显著关联，但 HF 或 LF 没有。相反，PM(2.5)增加了这些 HRV 参数。
结果表明，当 PM 暴露相对较低（14 μg/m(3)）时，交通相关 PM 暴露与中年人群的 HRV 急性变化之间存在关联，并且不同污染物的影响存在异质性，臭氧和甲醛暴露导致 HRV 下降，尤其是 HF 下降，而 PM(2.5)暴露导致 HRV 增加。鉴于交通相关排放物与心血管发病率和死亡率增加相关，了解交通相关排放物如何导致心血管疾病的机制具有重要的公共卫生意义。
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