Department of Chemistry, SUNY College of Environmental Science and Forestry, 1 Forestry Drive, Syracuse, NY, 13210, USA.
Curriculum in Toxicology, University of North Carolina, Chapel Hill, NC, USA.
Environ Health. 2017 Nov 21;16(1):126. doi: 10.1186/s12940-017-0335-0.
Air pollution is a major risk factor for cardiovascular disease, of which ozone is a major contributor. Several studies have found associations between ozone and cardiovascular morbidity, but the results have been inconclusive. We investigated associations between ozone and changes across biological pathways associated with cardiovascular disease.
Using a panel study design, 13 participants with coronary artery disease were assessed for markers of systemic inflammation, heart rate variability and repolarization, lipids, blood pressure, and endothelial function. Daily measurements of ozone and particulate matter (PM) were obtained from central monitoring stations. Single (ozone) and two-pollutant (ozone and PM) models were used to assess percent changes in measurements per interquartile ranges of pollutants.
Per interquartile increase in ozone, changes in tissue plasminogen factor (6.6%, 95% confidence intervals (CI) = 0.4, 13.2), plasminogen activator inhibitor-1 (40.5%, 95% CI = 8.7, 81.6), neutrophils (8.7% 95% CI = 1.5, 16.4), monocytes (10.2%, 95% CI = 1.0, 20.1), interleukin-6 (15.9%, 95% CI = 3.6, 29.6), large-artery elasticity index (-19.5%, 95% CI = -34.0, -1.7), and the baseline diameter of the brachial artery (-2.5%, 95% CI = -5.0, 0.1) were observed. These associations were robust in the two-pollutant model.
We observed alterations across several pathways associated with cardiovascular disease in 13 coronary artery disease patients following ozone exposures, independent of PM. The results support the biological plausibility of ozone-induced cardiovascular effects. The effects were found at concentrations below the EPA National Ambient Air Quality Standards for both ozone and PM.
空气污染是心血管疾病的主要危险因素，其中臭氧是主要贡献者。一些研究发现臭氧与心血管发病率之间存在关联，但结果尚无定论。我们研究了臭氧与心血管疾病相关生物途径变化之间的关联。
使用面板研究设计，对 13 名患有冠状动脉疾病的患者进行了全身炎症标志物、心率变异性和复极、脂质、血压和内皮功能的评估。从中央监测站获得了臭氧和颗粒物（PM）的每日测量值。使用单（臭氧）和双污染物（臭氧和 PM）模型来评估每四分位间距污染物变化的百分比。
臭氧每增加一个四分位间距，组织纤溶酶原激活物因子（6.6%，95%置信区间[CI] = 0.4，13.2）、纤溶酶原激活物抑制剂-1（40.5%，95% CI = 8.7，81.6）、中性粒细胞（8.7%，95% CI = 1.5，16.4）、单核细胞（10.2%，95% CI = 1.0，20.1）、白细胞介素-6（15.9%，95% CI = 3.6，29.6）、大动脉弹性指数（-19.5%，95% CI = -34.0，-1.7）和肱动脉基线直径（-2.5%，95% CI = -5.0，0.1）。这些关联在双污染物模型中是稳健的。
我们在 13 名冠状动脉疾病患者中观察到臭氧暴露后与心血管疾病相关的几种途径发生了变化，而与 PM 无关。结果支持臭氧诱导心血管效应的生物学合理性。这些效应是在臭氧和 PM 的 EPA 国家空气质量标准以下的浓度下发现的。
