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首页> 外文期刊>American Journal of Physiology >Exposure to medium and high ambient levels of ozone causes adverse systemic inflammatory and cardiac autonomic effects
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Exposure to medium and high ambient levels of ozone causes adverse systemic inflammatory and cardiac autonomic effects

机译：暴露于含量的含量和高环境水平导致不良全身炎症和心脏自主效应

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摘要

Epidemiological evidence suggests that exposure to ozone increases cardiovascular morbidity. However, the specific biological mechanisms mediating ozone-associated cardiovascular effects are unknown. To determine whether short-term exposure to ambient levels of ozone causes changes in biomarkers of cardiovascular disease including heart rate variability (HRV), systemic inflammation, and coagulability, 26 subjects were exposed to 0, 100, and 200 ppb ozone in random order for 4 h with intermittent exercise. HRV was measured and blood samples were obtained immediately before (0 h), immediately after (4 h), and 20 h after (24 h) each exposure. Bronchoscopy with bron-choalveolar lavage (BAL) was performed 20 h after exposure. Regression modeling was used to examine dose-response trends between the endpoints and ozone exposure. Inhalation of ozone induced dose-dependent adverse changes in the frequency domains of HRV across exposures consistent with increased sympathetic tone [increase of (parameter estimate ± SE) 0.4 ± 0.2 and 0.3 ± 0.1 in low- to high-frequency domain HRV ratio per 100 ppb increase in ozone at 4 h and 24 h, respectively (P = 0.02 and P = 0.01)] and a dose-dependent increase in serum C-reactive protein (CRP) across exposures at 24 h [increase of 0.61 ± 0.24 mg/1 in CRP per 100 ppb increase in ozone (P = 0.01)]. Changes in HRV and CRP did not correlate with ozone-induced local lung inflammatory responses (BAL granulocytes, IL-6, or IL-8), but changes in HRV and CRP were associated with each other after adjustment for age and ozone level. Inhalation of ozone causes adverse systemic inflammatory and cardiac autonomic effects that may contribute to the cardiovascular mortality associated with short-term exposure.
机译：流行病学证据表明，暴露于臭氧增加心血管发病率。然而，介导臭氧相关心血管效应的特定生物机制是未知的。为了确定臭氧环境水平的短期暴露是否会导致心血管疾病的生物标志物的变化，包括心率变异性（HRV），全身炎症和凝固性，以0,100和200ppb臭氧暴露于0,100和200ppb臭氧4小时间歇性运动。测量HRV并立即在（0h）之前立即获得血液样品，在（4小时）之后（4小时），每次暴露后20小时暴露后20小时进行带支气管镜（BAL）的支气管镜检查。回归建模用于检查端点和臭氧暴露之间的剂量 - 反应趋势。吸入臭氧诱导的剂量依赖性不利变化，其横跨曝光的HRV频率域，这一致于升高的交感神经音调[（参数估计±SE）的增加0.4±0.2和0.3±0.1，低于每100的高频域HRV比率PPB分别在4小时和24小时的臭氧增加（p = 0.02和p = 0.01）]和血清C-反应蛋白（CRP）的剂量依赖性增加，在24小时的曝光中[增加0.61±0.24 mg / 1在每100ppb每100 ppb中增加臭氧（p = 0.01）]。 HRV和CRP的变化与臭氧诱导的局部肺炎症反应（BAL粒细胞，IL-6或IL-8）不相关，但在调整年龄和臭氧水平后，HRV和CRP的变化彼此相关。吸入臭氧导致有助于与短期暴露相关的心血管死亡率的不良全身炎症和心脏自主主义效应。

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