Frampton Mark W, Pietropaoli Anthony, Dentler Michael, Chalupa David, Little Erika L, Stewart Judith, Frasier Lauren, Oakes David, Wiltshire Jelani, Vora Rathin, Utell Mark J
Department of Environmental Medicine .
Inhal Toxicol. 2015 Feb;27(2):113-9. doi: 10.3109/08958378.2014.996272.
Exposure to ozone has acute respiratory effects, but few human clinical studies have evaluated cardiovascular effects.
We hypothesized that ozone exposure alters pulmonary and systemic vascular function, and cardiac function, with more pronounced effects in subjects with impaired antioxidant defense from deletion of the glutathione-S-transferase M1 gene (GSTM1 null).
Twenty-four young, healthy never-smoker subjects (12 GSTM1 null) inhaled filtered air, 100 ppb ozone and 200 ppb ozone for 3 h, with intermittent exercise, in a double-blind, randomized, crossover fashion. Exposures were separated by at least 2 weeks. Vital signs, spirometry, arterial and venous blood nitrite levels, impedance cardiography, peripheral arterial tonometry, estimation of pulmonary capillary blood volume (Vc), and blood microparticles and platelet activation were measured at baseline and during 4 h after each exposure.
Ozone inhalation decreased lung function immediately after exposure (mean ± standard error change in FEV1, air: -0.03 ± 0.04 L; 200 ppb ozone: -0.30 ± 0.07 L; p < 0.001). The immediate post-exposure increase in blood pressure, caused by the final 15-min exercise period, was blunted by 200 ppb ozone exposure (mean ± standard error change for air: 16.7 ± 2.6 mmHg; 100 ppb ozone: 14.5 ± 2.4 mmHg; 200 ppb ozone: 8.5 ± 2.5 mmHg; p = 0.02). We found no consistent effects of ozone on any other measure of cardiac or vascular function. All results were independent of the GSTM1 genotype.
We did not find convincing evidence for early acute adverse cardiovascular consequences of ozone exposure in young healthy adults. The ozone-associated blunting of the blood pressure response to exercise is of unclear clinical significance.
接触臭氧会产生急性呼吸效应，但很少有人类临床研究评估其对心血管的影响。
我们假设接触臭氧会改变肺和全身血管功能以及心脏功能，对于因谷胱甘肽-S-转移酶M1基因缺失（GSTM1基因缺失）而抗氧化防御受损的受试者，影响更为明显。
24名年轻、健康的从不吸烟者（12名GSTM1基因缺失者）以双盲、随机、交叉方式，在间歇性运动的情况下，吸入过滤空气、100 ppb臭氧和200 ppb臭氧3小时。暴露之间至少间隔2周。在基线以及每次暴露后4小时测量生命体征、肺活量测定、动脉和静脉血亚硝酸盐水平、阻抗心动图、外周动脉张力测量、肺毛细血管血容量（Vc）估计以及血液微粒和血小板活化情况。
吸入臭氧后，肺功能立即下降（第1秒用力呼气量的平均±标准误变化，空气：-0.03±0.04升；200 ppb臭氧：-0.30±0.07升；p<0.001）。最后15分钟运动期导致的暴露后立即血压升高，在200 ppb臭氧暴露时减弱（空气的平均±标准误变化：16.7±2.6 mmHg；100 ppb臭氧：14.5±2.4 mmHg；200 ppb臭氧：8.5±2.5 mmHg；p=0.02）。我们未发现臭氧对心脏或血管功能的任何其他测量指标有一致影响。所有结果均与GSTM1基因型无关。
我们未找到令人信服的证据表明年轻健康成年人接触臭氧会产生早期急性不良心血管后果。臭氧相关的运动血压反应减弱的临床意义尚不清楚。
