National Health and Environmental Effects, Research Laboratory MD 58D, US EPA, Research Triangle Park, NC 27711, USA.
Circulation. 2012 Jul 3;126(1):104-11. doi: 10.1161/CIRCULATIONAHA.112.094359. Epub 2012 Jun 25.
Recent epidemiology studies have reported associations between short-term ozone exposure and mortality. Such studies have previously reported associations between airborne particulate matter pollution and mortality, and support for a causal relationship has come from controlled-exposure studies that describe pathophysiological mechanisms by which particulate matter could induce acute mortality. In contrast, for ozone, almost no controlled-human-exposure studies have tested whether ozone exposure can modulate the cardiovascular system.
Twenty-three young healthy individuals were exposed in a randomized crossover fashion to clean air and to 0.3-ppm ozone for 2 hours while intermittently exercising. Blood was obtained immediately before exposure, immediately afterward, and the next morning. Continuous Holter monitoring began immediately before exposure and continued for 24 hours. Lung function was performed immediately before and immediately after exposure, and bronchoalveolar lavage was performed 24 hours after exposure. Immediately after ozone exposure, we observed a 98.9% increase in interleukin-8, a 21.4% decrease in plasminogen activator inhibitor-1, a 51.3% decrease in the high-frequency component of heart rate variability, and a 1.2% increase in QT duration. Changes in interleukin-1B and plasminogen activator inhibitor-1 were apparent 24 hours after exposure. In agreement with previous studies, we also observed ozone-induced drops in lung function and an increase in pulmonary inflammation.
This controlled-human-exposure study shows that ozone can cause an increase in vascular markers of inflammation and changes in markers of fibrinolysis and markers that affect autonomic control of heart rate and repolarization. We believe that these findings provide biological plausibility for the epidemiology studies that associate ozone exposure with mortality.
URL: http://www.clinicaltrials.gov. Unique identifier: NCT01492517.
最近的流行病学研究报告了短期臭氧暴露与死亡率之间的关联。这些研究之前报告了空气中颗粒物污染与死亡率之间的关联，并支持了一项因果关系，该关系来自于描述颗粒物如何诱发急性死亡率的受控暴露研究。相比之下，对于臭氧，几乎没有受控人体暴露研究测试过臭氧暴露是否可以调节心血管系统。
23 名年轻健康个体以随机交叉方式暴露于清洁空气和 0.3ppm 臭氧中 2 小时，同时间歇性运动。血液在暴露前、暴露后立即和次日清晨采集。连续 Holter 监测在暴露前立即开始，并持续 24 小时。在暴露前和暴露后立即进行肺功能检查，在暴露后 24 小时进行支气管肺泡灌洗。臭氧暴露后立即观察到白细胞介素-8 增加 98.9%，纤溶酶原激活物抑制剂-1 减少 21.4%，心率变异性高频成分减少 51.3%，QT 间期增加 1.2%。白细胞介素-1B 和纤溶酶原激活物抑制剂-1 的变化在暴露后 24 小时明显。与之前的研究一致，我们还观察到臭氧引起的肺功能下降和肺部炎症增加。
这项受控人体暴露研究表明，臭氧可引起血管炎症标志物增加，纤溶标志物和影响心率和复极化自主控制的标志物变化。我们认为这些发现为将臭氧暴露与死亡率相关联的流行病学研究提供了生物学依据。
