主动吸烟和被动吸烟在慢性阻塞性肺病和全身炎症中的作用:中国一项为期 12 年的前瞻性研究

IF 3.8 4区 医学 Q1 PUBLIC, ENVIRONMENTAL & OCCUPATIONAL HEALTH
Lu Chen, Haijuan Xiong, Qiaorui Wen, Jun Lv, Dianjianyi Sun, Pei Pei, Ling Yang, Yiping Chen, Huaidong Du, Lihui Li, Xiaoming Yang, Daniel Avery, Junshi Chen, Zhengming Chen, Liming Li, Canqing Yu
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引用次数: 0

摘要

背景:关于慢性阻塞性肺病(COPD)的全身慢性炎症(SCI)的原因和影响,目前尚无共识。关于二手烟(SHS)对慢性阻塞性肺病的影响,结论也不一致:对中国嘉道理生物库队列进行了从 2004-08 年基线调查至 2018 年 12 月 31 日的随访。在最终分析所选的445523名参与者中,分别进行了Cox回归和线性回归,以估计烟草暴露与慢性阻塞性肺疾病风险和对数转化炎症因子基线水平的危险比(HRs)和95%置信区间(CIs)[βs (95% CIs)]:对参与者进行了中位数为 12.1 年的随访,共记录了 11,825 例慢性阻塞性肺病事件。与非吸烟者相比,经常吸烟者患慢性阻塞性肺病的风险要高于非每周接触 SHS 的人。开始吸烟的年龄越小、每日吸烟量越大、吸入烟雾越深,患慢性阻塞性肺病的风险就越高,并且与血浆高敏C反应蛋白(hs-CRP,均为Ptrend趋势结论)水平的升高相关:烟草烟雾暴露量的增加与慢性阻塞性肺病发病前SCI水平的升高有关,然后增加了慢性阻塞性肺病的易感性。建议吸烟者尽早戒烟,这是降低慢性阻塞性肺病风险的实用方法。鉴于慢性阻塞性肺病和接触 SHS 的发病率都很高,与接触 SHS 相关的风险值得关注。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Role of Active and Passive Smoking in Chronic Obstructive Pulmonary Disease and Systemic Inflammation: A 12-year Prospective Study in China.

Background: There is no consensus on the cause and effect of systemic chronic inflammation (SCI) regarding chronic obstructive pulmonary disease (COPD). The impact of second-hand smoke (SHS) on COPD has reached inconsistent conclusions.

Methods: The China Kadoorie Biobank cohort was followed up from the 2004-08 baseline survey to 31 December 2018. Among the selected 445,523 participants in the final analysis, Cox and linear regressions were performed to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) of tobacco exposure with COPD risk and baseline levels of log-transformed inflammatory factors [βs (95% CIs)], respectively.

Results: Participants were followed up for a median of 12.1 years and 11,825 incident COPD events were documented. Ever-smokers were associated with a higher risk of COPD than non-smokers with non-weekly SHS exposure. A younger age to start smoking, a greater amount of daily tobacco consumption, and deeper inhalation were associated with increased risk of COPD and correlated with elevated levels of plasma high-sensitivity C-reactive protein (hs-CRP, all Ptrend < 0.001) even two years before COPD onset. Among former smokers, COPD risk declined with longer smoking cessation (Ptrend < 0.001) and those quitting smoking for over ten years presented no difference in COPD risk and hs-CRP level from non-smokers [HR (95% CI) = 1.05 (0.89, 1.25), β (95% CI) = 0.17 (- 0.09, 0.43)]. Among non-smokers, weekly SHS exposure was associated with a slightly higher COPD risk [HR (95% CI) = 1.06 (1.01, 1.12)].

Conclusions: Incremental exposure to tobacco smoke was related to elevated SCI level before COPD onset, then an increase in COPD susceptibility. Quitting smoking as early as possible is suggested as a practical approach to reducing COPD risk in smokers. Given the high prevalence of both COPD and SHS exposure, the risk associated with SHS exposure deserves attention.

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来源期刊
CiteScore
10.70
自引率
1.40%
发文量
57
审稿时长
19 weeks
期刊介绍: The Journal of Epidemiology and Global Health is an esteemed international publication, offering a platform for peer-reviewed articles that drive advancements in global epidemiology and international health. Our mission is to shape global health policy by showcasing cutting-edge scholarship and innovative strategies.
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