Peretz Alon, Kaufman Joel D, Trenga Carol A, Allen Jason, Carlsten Chris, Aulet Mary R, Adar Sara D, Sullivan Jeffrey H
Department of Environmental and Occupational Health Sciences, University of Washington Occupational and Environmental Program, 4225 Roosevelt Way NE, Suite #302, Box 354695, Seattle, WA 98195, USA.
Environ Res. 2008 Jun;107(2):178-84. doi: 10.1016/j.envres.2008.01.012. Epub 2008 Mar 10.
Particulate matter (PM) air pollution is associated with alterations in cardiac conductance and sudden cardiac death in epidemiological studies. Traffic-related air pollutants, including diesel exhaust (DE) may be at least partly responsible for these effects. In this experimental study we assessed whether short-term exposure to DE would result in alterations in heart rate variability (HRV), a non-invasive measure of autonomic control of the heart.
In a double-blind, crossover, controlled-exposure study, 16 adult volunteers were exposed (at rest) in randomized order to filtered air (FA) and two levels of diluted DE (100 or 200 microg/m(3) of fine particulate matter) in 2-h sessions. Before, and at four time points after each exposure we assessed HRV. HRV parameters assessed included both time domain statistics (standard deviation of N-N intervals (SDNN), and the square root of the mean of the sum of squared differences between successive N-N intervals (RMSSD)) and frequency domain statistics (high-frequency (HF) power, low-frequency (LF) power, and the LF/HF ratio).
We observed an effect at 3-h after initiation of DE inhalation on the frequency domain statistics of HRV. DE at 200 microg/m(3) elicited an increase in HF power compared to FA (Delta=0.33; 95% CI: 0.01-0.7) and a decrease in LF/HF ratio (Delta=-0.74; 95% CI: -1.2 to -0.2). The effect of DE on HF power was not consistent among study participants. There was no DE effect on time domain statistics and no significant DE effect on HRV in later time points.
We did not observe a consistent DE effect on the autonomic control of the heart in a controlled-exposure experiment in young participants. Efforts are warranted to understand discrepancies between epidemiological and experimental studies of air pollution's impact on HRV.
在流行病学研究中，颗粒物（PM）空气污染与心脏传导改变及心源性猝死相关。包括柴油尾气（DE）在内的与交通相关的空气污染物可能至少部分导致了这些影响。在本实验研究中，我们评估了短期暴露于DE是否会导致心率变异性（HRV）改变，HRV是一种对心脏自主控制的非侵入性测量方法。
在一项双盲、交叉、对照暴露研究中，16名成年志愿者在静息状态下以随机顺序在2小时的时间段内暴露于过滤空气（FA）以及两种浓度的稀释DE（细颗粒物浓度分别为100或200微克/立方米）。在每次暴露前及暴露后的四个时间点，我们评估HRV。评估的HRV参数包括时域统计量（N-N间期标准差（SDNN）以及连续N-N间期平方差总和均值的平方根（RMSSD））和频域统计量（高频（HF）功率、低频（LF）功率以及LF/HF比值）。
我们观察到在开始吸入DE后3小时，HRV的频域统计量出现了效应。与FA相比，200微克/立方米的DE使HF功率增加（差值=0.33；95%置信区间：0.01 - 0.7），LF/HF比值降低（差值=-0.74；95%置信区间：-1.2至-0.2）。DE对HF功率的影响在研究参与者中并不一致。在时域统计量上没有DE效应，在后续时间点对HRV也没有显著的DE效应。
在针对年轻参与者进行的对照暴露实验中，我们未观察到DE对心脏自主控制有一致的效应。有必要努力去理解空气污染对HRV的流行病学研究和实验研究之间的差异。
