Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina 27711, USA.
Environ Health Perspect. 2012 Mar;120(3):348-54. doi: 10.1289/ehp.1104244. Epub 2011 Dec 2.
Ozone (O₃) is a well-documented respiratory oxidant, but increasing epidemiological evidence points to extrapulmonary effects, including positive associations between ambient O₃ concentrations and cardiovascular morbidity and mortality.
With preliminary reports linking O₃ exposure with changes in heart rate (HR), we investigated the hypothesis that a single inhalation exposure to O₃ will cause concentration-dependent autonomic modulation of cardiac function in rats.
Rats implanted with telemeters to monitor HR and cardiac electrophysiology [electrocardiography (ECG)] were exposed once by whole-body inhalation for 4 hr to 0.2 or 0.8 ppm O₃ or filtered air. A separate cohort was tested for vulnerability to aconitine-induced arrhythmia 24 hr after exposure.
Exposure to 0.8 ppm O₃ caused bradycardia, PR prolongation, ST depression, and substantial increases in atrial premature beats, sinoatrial block, and atrioventricular block, accompanied by concurrent increases in several HR variability parameters that were suggestive of increased parasympathetic tone. Low-O₃ exposure failed to elicit any overt changes in autonomic tone, heart rhythm, or ECG. However, both 0.2 and 0.8 ppm O₃ increased sensitivity to aconitine-induced arrhythmia formation, suggesting a latent O₃-induced alteration in myocardial excitability.
O₃ exposure causes several alterations in cardiac electrophysiology that are likely mediated by modulation of autonomic input to the heart. Moreover, exposure to low O₃ concentrations may cause subclinical effects that manifest only when triggered by a stressor, suggesting that the adverse health effects of ambient levels of air pollutants may be insidious and potentially underestimated.
臭氧（O₃）是一种有充分文献记录的呼吸道氧化剂，但越来越多的流行病学证据表明其具有肺外效应，包括环境臭氧浓度与心血管发病率和死亡率之间存在正相关关系。
有初步报告将臭氧暴露与心率（HR）变化联系起来，我们假设单次吸入臭氧会导致大鼠心脏功能的自主调节呈浓度依赖性。
植入遥测仪以监测 HR 和心脏电生理学[心电图（ECG）]的大鼠通过全身吸入暴露于 0.2 或 0.8 ppm 的臭氧或过滤空气 4 小时。在暴露后 24 小时，另一组大鼠接受乌头碱诱导的心律失常易感性测试。
暴露于 0.8 ppm 的臭氧会导致心动过缓、PR 延长、ST 压低以及房性早搏、窦房结阻滞和房室传导阻滞显著增加，同时 HR 变异性参数也显著增加，提示副交感神经张力增加。低臭氧暴露未能引起自主神经张力、心率或 ECG 的任何明显变化。然而，0.2 和 0.8 ppm 的臭氧均增加了乌头碱诱导的心律失常形成的敏感性，表明臭氧诱导的心肌兴奋性改变是潜在的。
臭氧暴露会导致心脏电生理学的几种改变，这些改变可能是通过对心脏自主输入的调节介导的。此外，暴露于低臭氧浓度可能会引起亚临床效应，只有在受到应激源触发时才会表现出来，这表明环境空气污染物的不良健康影响可能是隐匿的，且可能被低估。
