Farraj Aimen K, Malik Fatiha, Haykal-Coates Najwa, Walsh Leon, Winsett Darrell, Terrell Dock, Thompson Leslie C, Cascio Wayne E, Hazari Mehdi S
a Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park , NC , USA.
Inhal Toxicol. 2016;28(4):170-9. doi: 10.3109/08958378.2016.1148088.
Within urban air sheds, specific ambient air pollutants typically peak at predictable times throughout the day. For example, in environments dominated by mobile sources, peak nitrogen dioxide (NO2) levels coincide with morning and afternoon rush hours, while peak levels of ozone (O3), occur in the afternoon.
Given that exposure to a single pollutant might sensitize the cardiopulmonary system to the effects of a subsequent exposure to a second pollutant, we hypothesized that a morning exposure to NO2 will exaggerate the cardiovascular effects of an afternoon O3 exposure in rats.
Rats were divided into four groups that were each exposed for 3 h in the morning (m) and 3 h in the afternoon (a) on the same day: (1) m-Air/a-Air, (2) m-Air/a-O3 (0.3 ppm), (3) m-NO2 (0.5 ppm)/a-Air and (4) m-NO2/a-O3. Implanted telemetry devices recorded blood pressure and electrocardiographic data. Sensitivity to the arrhythmogenic agent aconitine was measured in a separate cohort.
Only m-NO2/a-O3-exposed rats had significant changes in electrophysiological, mechanical and autonomic parameters. These included decreased heart rate and increased PR and QTc intervals and increased heart rate variability, suggesting increased parasympathetic tone. In addition, only m-NO2/a-O3 exposure decreased systolic and diastolic blood pressures and increased pulse pressure and QA interval, suggesting decreased cardiac contractility.
The findings indicate that initial exposure to NO2 sensitized rats to the cardiovascular effects of O3 and may provide insight into the epidemiological data linking adverse cardiovascular outcomes with exposures to low concentrations of O3.
在城市空气流域内，特定的环境空气污染物通常在一天中可预测的时间达到峰值。例如，在以移动源为主的环境中，二氧化氮（NO₂）的峰值水平与早晚高峰时段一致，而臭氧（O₃）的峰值水平出现在下午。
鉴于暴露于单一污染物可能会使心肺系统对随后暴露于第二种污染物的影响更加敏感，我们假设上午暴露于NO₂会夸大下午暴露于O₃对大鼠心血管系统的影响。
将大鼠分为四组，每组在同一天上午暴露3小时（m），下午暴露3小时（a）：（1）m-空气/a-空气，（2）m-空气/a-O₃（0.3 ppm），（3）m-NO₂（0.5 ppm）/a-空气，（4）m-NO₂/a-O₃。植入的遥测设备记录血压和心电图数据。在另一组中测量对致心律失常剂乌头碱的敏感性。
只有暴露于m-NO₂/a-O₃的大鼠在电生理、机械和自主神经参数方面有显著变化。这些变化包括心率降低、PR和QTc间期延长以及心率变异性增加，提示副交感神经张力增加。此外，只有m-NO₂/a-O₃暴露会降低收缩压和舒张压，增加脉压和QA间期，提示心脏收缩力下降。
研究结果表明，最初暴露于NO₂会使大鼠对O₃的心血管影响更加敏感，这可能为将不良心血管结局与低浓度O₃暴露联系起来的流行病学数据提供见解。
