University of Rochester Medical Center, Rochester, NY, USA.
University of California at San Francisco, San Francisco, CA, USA.
Environ Res. 2022 Apr 1;205:112522. doi: 10.1016/j.envres.2021.112522. Epub 2021 Dec 15.
The cardiovascular effects of ozone exposure are unclear. Using measurements from the 87 participants in the Multicenter Ozone Study of oldEr Subjects (MOSES), we examined whether personal and ambient pollutant exposures before the controlled exposure sessions would be associated with adverse changes in pulmonary and cardiovascular function.
We used mixed effects linear regression to evaluate associations between increased personal exposures and ambient pollutant concentrations in the 96 h before the pre-exposure visit, and 1) biomarkers measured at pre-exposure, and 2) changes in biomarkers from pre-to post-exposure.
Decreases in pre-exposure forced expiratory volume in 1 s (FEV) were associated with interquartile-range increases in concentrations of particulate matter ≤2.5 μm (PM) 1 h before the pre-exposure visit (-0.022 L; 95% CI -0.037 to -0.006; p = 0.007), carbon monoxide (CO) in the prior 3 h (-0.046 L; 95% CI -0.076 to -0.016; p = 0.003), and nitrogen dioxide (NO) in the prior 72 h (-0.030 L; 95% CI -0.052 to -0.008; p = 0.007). From pre-to post-exposure, increases in FEV were marginally significantly associated with increases in personal ozone exposure (0.010 L; 95% CI 0.004 to 0.026; p = 0.010), and ambient PM and CO at all lag times. Ambient ozone concentrations in the prior 96 h were associated with both decreased pre-exposure high frequency (HF) heart rate variability (HRV) and increases in HF HRV from pre-to post-exposure.
We observed associations between increased ambient PM, NO, and CO levels and reduced pulmonary function, and increased ambient ozone concentrations and reduced HRV. Pulmonary function and HRV increased across the exposure sessions in association with these same pollutant increases, suggesting a "recovery" during the exposure sessions. These findings support an association between short term increases in ambient PM, NO, and CO and decreased pulmonary function, and increased ambient ozone and decreased HRV.
臭氧暴露对心血管的影响尚不清楚。本研究使用来自老年人多中心臭氧研究（MOSES）87 名参与者的测量数据，考察了在受控暴露前，个人和环境污染物暴露是否与肺和心血管功能的不良变化相关。
我们使用混合效应线性回归来评估暴露前 96 小时内个人暴露和环境污染物浓度的增加与 1）暴露前测量的生物标志物，以及 2）暴露前后生物标志物的变化之间的关系。
暴露前用力呼气量（FEV）的降低与暴露前访问前 1 小时 PM 1 小时内浓度的四分位距增加相关（-0.022 L；95%CI -0.037 至 -0.006；p = 0.007），前 3 小时一氧化碳（CO）浓度（-0.046 L；95%CI -0.076 至 -0.016；p = 0.003）和前 72 小时二氧化氮（NO）浓度（-0.030 L；95%CI -0.052 至 -0.008；p = 0.007）。从暴露前到暴露后，FEV 的增加与个人臭氧暴露的增加呈边缘显著相关（0.010 L；95%CI 0.004 至 0.026；p = 0.010），以及所有滞后时间的环境 PM 和 CO。暴露前 96 小时的环境臭氧浓度与降低的高频（HF）心率变异性（HRV）和从暴露前到暴露后的 HF HRV 增加有关。
我们观察到环境 PM、NO 和 CO 水平的升高与肺功能下降有关，环境臭氧浓度的升高与 HRV 下降有关。在暴露过程中，随着这些污染物浓度的增加，肺功能和 HRV 呈上升趋势，这表明在暴露过程中存在“恢复”。这些发现支持了短期环境 PM、NO 和 CO 增加与肺功能下降，以及环境臭氧增加和 HRV 下降之间的关联。
