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自然发生的臭氧空气污染事件对肺部氧化应激和炎症的影响。

Effect of naturally occurring ozone air pollution episodes on pulmonary oxidative stress and inflammation.

作者信息

Pirozzi Cheryl, Sturrock Anne, Weng Hsin-Yi, Greene Tom, Scholand Mary Beth, Kanner Richard, Paine Robert

机构信息

Department of Internal Medicine, Division of Pulmonary and Critical Care Medicine, University of Utah, 26 North 1900 East, Salt Lake City, UT 84132, USA.

Department of Pediatrics, University of Utah, Salt Lake City, UT 84132, USA.

出版信息

Int J Environ Res Public Health. 2015 May 12;12(5):5061-75. doi: 10.3390/ijerph120505061.

DOI:10.3390/ijerph120505061
PMID:25985308
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4454954/
Abstract

This study aimed to determine if naturally occurring episodes of ozone air pollution in the Salt Lake Valley in Utah, USA, during the summer are associated with increased pulmonary inflammation and oxidative stress, increased respiratory symptoms, and decreased lung function in individuals with chronic obstructive pulmonary disease (COPD) compared to controls. We measured biomarkers (nitrite/nitrate (NOx), 8-isoprostane) in exhaled breath condensate (EBC), spirometry, and respiratory symptoms in 11 former smokers with moderate-to-severe COPD and nine former smokers without airflow obstruction during periods of low and high ozone air pollution. High ozone levels were associated with increased NOx in EBC in both COPD (8.7 (±8.5) vs. 28.6 (±17.6) μmol/L on clean air vs. pollution days, respectively, p < 0.01) and control participants (7.6 (±16.5) vs. 28.5 (±15.6) μmol/L on clean air vs. pollution days, respectively, p = 0.02). There was no difference in pollution effect between COPD and control groups, and no difference in EBC 8-isoprostane, pulmonary function, or respiratory symptoms between clean air and pollution days in either group. Former smokers both with and without airflow obstruction developed airway oxidative stress and inflammation in association with ozone air pollution episodes.

摘要

本研究旨在确定美国犹他州盐湖谷夏季自然发生的臭氧空气污染事件,与慢性阻塞性肺疾病(COPD)患者相比,是否会导致对照组个体肺部炎症和氧化应激增加、呼吸道症状增多以及肺功能下降。我们在臭氧空气污染水平较低和较高的时期,测量了11名中重度COPD既往吸烟者和9名无气流阻塞的既往吸烟者的呼出气冷凝物(EBC)中的生物标志物(亚硝酸盐/硝酸盐(NOx)、8-异前列腺素)、肺功能和呼吸道症状。高臭氧水平与COPD患者(清洁空气日与污染日的EBC中NOx分别为8.7(±8.5)与28.6(±17.6)μmol/L,p<0.01)和对照组参与者(清洁空气日与污染日的EBC中NOx分别为7.6(±16.5)与28.5(±15.6)μmol/L,p = 0.02)EBC中NOx增加有关。COPD组和对照组之间的污染效应没有差异,两组在清洁空气日和污染日的EBC 8-异前列腺素、肺功能或呼吸道症状方面也没有差异。有气流阻塞和无气流阻塞的既往吸烟者均会因臭氧空气污染事件而出现气道氧化应激和炎症。

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