Department of Public Health Sciences, University of Rochester Medical Center, Rochester, NY, United States of America; Department of Medicine, University of Rochester Medical Center, Rochester, NY, United States of America; Department of Environmental Medicine, University of Rochester Medical Center, Rochester, NY, United States of America.
Department of Medicine, University of California at San Francisco, San Francisco, CA, United States of America; Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley, CA, United States of America.
Environ Int. 2018 Oct;119:193-202. doi: 10.1016/j.envint.2018.06.014. Epub 2018 Jul 4.
To date, there have been relatively few studies of acute cardiovascular responses to controlled ozone inhalation, although a number of observational studies have reported significant positive associations between both ambient ozone levels and acute cardiovascular events and long-term ozone exposure and cardiovascular mortality.
We hypothesized that short-term controlled exposure to low levels of ozone in filtered air would induce autonomic imbalance, repolarization abnormalities, arrhythmia, and vascular dysfunction.
This randomized crossover study of 87 healthy volunteers 55-70 years of age was conducted at three sites using a common protocol, from June 2012 to April 2015. Subjects were exposed for 3 h in random order to 0 ppb (filtered air), 70 ppb ozone, and 120 ppb ozone, alternating 15 min of moderate exercise with 15 min of rest. A suite of cardiovascular endpoints was measured the day before, the day of, and up to 22 h after each exposure. Mixed effect linear and logit models evaluated the impact of exposure to ozone on pre-specified primary and secondary outcomes. Site and time were included in the models.
We found no significant effects of ozone exposure on any of the primary or secondary measures of autonomic function, repolarization, ST segment change, arrhythmia, or vascular function (systolic blood pressure and flow-mediated dilation).
In this multicenter study of older healthy women and men, there was no convincing evidence for acute effects of 3-h, relatively low-level ozone exposures on cardiovascular function. However, we cannot exclude the possibility of effects with higher ozone concentrations, more prolonged exposure, or in subjects with underlying cardiovascular disease. Further, we cannot exclude the possibility that exposure to ambient ozone and other pollutants in the days before the experimental exposures obscured or blunted cardiovascular biomarker response to the controlled ozone exposures.
迄今为止，关于受控臭氧吸入对急性心血管反应的研究相对较少，尽管一些观察性研究报告称，环境臭氧水平与急性心血管事件之间以及长期臭氧暴露与心血管死亡率之间存在显著的正相关关系。
我们假设，短期受控吸入过滤空气中的低水平臭氧会引起自主神经失衡、复极异常、心律失常和血管功能障碍。
这是一项在三个地点进行的、共有方案的、随机交叉研究，共纳入 87 名 55-70 岁的健康志愿者，研究时间为 2012 年 6 月至 2015 年 4 月。受试者以随机顺序分别暴露于 0 ppb（过滤空气）、70 ppb 臭氧和 120 ppb 臭氧 3 小时，每 15 分钟进行一次中度运动，随后休息 15 分钟。在每次暴露之前、当天和之后 22 小时，测量了一系列心血管终点。混合效应线性和逻辑回归模型评估了臭氧暴露对预先指定的主要和次要结局的影响。模型中包括了地点和时间。
我们未发现臭氧暴露对自主功能、复极、ST 段变化、心律失常或血管功能（收缩压和血流介导的扩张）的任何主要或次要指标有显著影响。
在这项对老年健康女性和男性的多中心研究中，没有令人信服的证据表明 3 小时相对低水平的臭氧暴露对心血管功能有急性影响。然而，我们不能排除在更高臭氧浓度、更长时间暴露或在有潜在心血管疾病的受试者中出现影响的可能性。此外，我们不能排除在实验暴露前几天暴露于环境臭氧和其他污染物可能会掩盖或削弱对受控臭氧暴露的心血管生物标志物反应的可能性。
