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终身不吸烟者中环境烟雾与慢性阻塞性肺疾病相关性的流行病学证据:一项系统综述

Epidemiological evidence relating environmental smoke to COPD in lifelong non-smokers: a systematic review.

作者信息

Lee Peter N, Forey Barbara A, Coombs Katharine J, Hamling Jan S, Thornton Alison J

机构信息

P.N. Lee Statistics and Computing Ltd, Sutton, Surrey, SM2 5DA, UK.

Independent Consultant in Statistics, Okehampton, Devon, EX20 1SG, UK.

出版信息

F1000Res. 2018 Feb 5;7:146. doi: 10.12688/f1000research.13887.3. eCollection 2018.

Abstract

Some evidence suggests environmental tobacco smoke (ETS) might cause chronic obstructive pulmonary disease (COPD). We reviewed available epidemiological data in never smokers. We identified epidemiological studies providing estimates of relative risk (RR) with 95% confidence interval (CI) for various ETS exposure indices. Confounder-adjusted RRs for COPD were extracted, or derived using standard methods. Meta-analyses were conducted for each exposure index, with tests for heterogeneity and publication bias. For the main index (spouse ever smoked or nearest equivalent), analyses investigated variation in RR by location, publication period, study type, sex, diagnosis, study size, confounder adjustment, never smoker definition, and exposure index definition. : Twenty-eight relevant studies were identified; nine European or Middle Eastern, nine Asian, eight American and two from multiple countries. Five were prospective, seven case-control and 16 cross-sectional. The COPD definition involved death or hospitalisation in seven studies, GOLD stage 1+ criteria in twelve, and other definitions in nine. For the main index, random-effects meta-analysis of 33 heterogeneous (p<0.001) estimates gave a RR of 1.20 (95%CI 1.08-1.34). Higher estimates for females (1.59,1.16-2.19, n=11) than males (1.29,0.94-1.76, n=7) or sexes combined (1.10,0.99-1.22, n=15 where sex-specific not available), and lower estimates for studies of 150+ cases (1.08,0.97-1.20, n=13) partly explained the heterogeneity. Estimates were higher for Asian studies (1.34,1.08-1.67, n=10), case-control studies (1.55,1.04-2.32, n=8), and COPD mortality or hospitalisation (1.40,1.12-1.74, n=11). Some increase was seen for severer COPD (1.29,1.10-1.52, n=7). Dose-response evidence was heterogeneous. Evidence for childhood (0.88,0.72-1.07, n=2) and workplace (1.12,0.77-1.64, n=4) exposure was limited, but an increase was seen for overall adulthood exposure (1.20,1.03-1.39, n=17). We discuss study weaknesses that may bias estimation of the association of COPD with ETS. : Although the evidence suggests ETS increases COPD, study weaknesses and absence of well-designed large studies precludes reliable inference of causality. More definitive evidence is required.

摘要

一些证据表明,环境烟草烟雾(ETS)可能导致慢性阻塞性肺疾病(COPD)。我们回顾了从不吸烟者中现有的流行病学数据。我们确定了提供各种ETS暴露指数相对风险(RR)估计值及95%置信区间(CI)的流行病学研究。提取或使用标准方法得出COPD的混杂因素调整RR。对每个暴露指数进行荟萃分析,并进行异质性检验和发表偏倚检验。对于主要指数(配偶曾吸烟或最接近的等效情况),分析研究了RR在地点、发表时间、研究类型、性别、诊断、研究规模、混杂因素调整、从不吸烟者定义和暴露指数定义方面的差异。共确定了28项相关研究;9项来自欧洲或中东,9项来自亚洲,8项来自美国,2项来自多个国家。5项为前瞻性研究,7项为病例对照研究,16项为横断面研究。COPD的定义在7项研究中涉及死亡或住院,12项研究采用GOLD 1+标准,9项研究采用其他定义。对于主要指数,对33个异质性(p<0.001)估计值进行随机效应荟萃分析,得出RR为1.20(95%CI 1.08 - 1.34)。女性的估计值(1.59,1.16 - 2.19,n = 11)高于男性(1.29,0.94 - 1.76,n = 7)或合并性别(1.10,0.99 - 1.22,n = 15,无性别特异性数据),而病例数超过150例的研究估计值较低(1.08,0.97 - 1.20,n = 13),这部分解释了异质性。亚洲研究(1.34,1.08 - 1.67,n = 10)、病例对照研究(1.55,1.04 - 2.32,n = 8)以及COPD死亡率或住院率(1.40,1.12 - 1.74,n = 11)的估计值较高。重度COPD也有一定程度的增加(1.29,1.10 - 1.52,n = 7)。剂量反应证据存在异质性。儿童期(0.88,0.72 - 1.07,n = 2)和工作场所暴露(1.12,0.77 - 1.64,n = 4)的证据有限,但成年期总体暴露有增加(1.20,1.03 - 1.39,n = 17)。我们讨论了可能使COPD与ETS关联估计产生偏倚的研究弱点。尽管有证据表明ETS会增加患COPD的风险,但研究弱点以及缺乏精心设计的大型研究妨碍了对因果关系的可靠推断。需要更确凿的证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9046/6953601/0b042f01a5ba/f1000research-7-24188-g0000.jpg

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