| 曾芷青,温俏睿,孙点剑一,裴培,郭彧,杜怀东,陈君石,陈铮鸣,吕筠,李立明,余灿清,代表中国慢性病前瞻性研究项目协作组.中国10个地区成年人饮酒与慢性阻塞性肺疾病发病风险的观察与遗传流行病学研究[J].中华流行病学杂志,2026,47(4):595-602 |
| 中国10个地区成年人饮酒与慢性阻塞性肺疾病发病风险的观察与遗传流行病学研究 |
| Observational and genetic epidemiological study on the association of alcohol consumption and chronic obstructive pulmonary disease in adults in 10 areas of China |
| 收稿日期:2025-10-29 出版日期:2026-04-17 |
| DOI：10.3760/cma.j.cn112338-20251029-00770 |
| 中文关键词: 慢性阻塞性肺疾病 饮酒 队列研究 孟德尔随机化 |
| 英文关键词: Chronic obstructive pulmonary disease Alcohol consumption Cohort study Mendelian randomization |
| 基金项目:四大慢病重大专项（2023ZD0510101，2023ZD0510100）；国家自然科学基金（82192901，82192904，82192900，82388102）；英国Wellcome Trust（212946/Z/18/Z，202922/Z/16/Z，104085/Z/14/Z，088158/Z/09/Z）；中国香港Kadoorie Charitable基金 |
| 作者 | 单位 | E-mail | | 曾芷青 | 北京大学公共卫生学院流行病与卫生统计学系, 北京 100191 | | | 温俏睿 | 北京大学公共卫生学院流行病与卫生统计学系, 北京 100191 | | | 孙点剑一 | 北京大学公共卫生学院流行病与卫生统计学系, 北京 100191
北京大学公众健康与重大疫情防控战略研究中心, 北京 100191
重大疾病流行病学教育部重点实验室(北京大学), 北京 100191 | | | 裴培 | 北京大学公众健康与重大疫情防控战略研究中心, 北京 100191 | | | 郭彧 | 中国医学科学院阜外医院, 北京 100037 | | | 杜怀东 | 牛津大学临床与流行病学研究中心纳菲尔德人群健康系, 牛津OX3 7LF | | | 陈君石 | 国家食品安全风险评估中心, 北京 100022 | | | 陈铮鸣 | 牛津大学临床与流行病学研究中心纳菲尔德人群健康系, 牛津OX3 7LF | | | 吕筠 | 北京大学公共卫生学院流行病与卫生统计学系, 北京 100191
北京大学公众健康与重大疫情防控战略研究中心, 北京 100191
重大疾病流行病学教育部重点实验室(北京大学), 北京 100191
血管稳态与重构全国重点实验室, 北京 100191 | | | 李立明 | 北京大学公共卫生学院流行病与卫生统计学系, 北京 100191
北京大学公众健康与重大疫情防控战略研究中心, 北京 100191
重大疾病流行病学教育部重点实验室(北京大学), 北京 100191 | | | 余灿清 | 北京大学公共卫生学院流行病与卫生统计学系, 北京 100191
北京大学公众健康与重大疫情防控战略研究中心, 北京 100191
重大疾病流行病学教育部重点实验室(北京大学), 北京 100191 | yucanqing@pku.edu.cn | | 代表中国慢性病前瞻性研究项目协作组 | | |
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| 中文摘要: |
| 目的 评估中国10个地区成年人自报饮酒状况及基因预测的酒精摄入量与慢性阻塞性肺疾病（COPD）发病风险的关联。方法 利用中国慢性病前瞻性研究2004-2008年开展的基线调查数据，并通过长期随访确定COPD结局。观察性分析中剔除基线自报患有恶性肿瘤、冠心病、中风/小卒中发作、哮喘、肺结核或COPD的研究对象，最终纳入445 523例研究对象。在遗传分析中，采取相同的纳入排除标准，共纳入133 168例有完整基因分型数据的研究对象。饮酒信息通过基线问卷获取。按照ALDH2-rs671和ADH1B-rs1229984基因型组合及研究地区计算男性非戒酒者的平均纯酒精摄入量，并据此将所有研究对象分为6组（C1~C6）。采用Cox比例风险回归模型分析暴露因素与新发COPD结局风险间的关联。结果 观察性分析中，研究对象随访（11.8±2.1）年，共记录11 825例新发COPD事件。调整潜在的混杂因素后，男性中偶尔饮酒者及经常饮酒者COPD发病风险均有所降低，偶尔饮、经常饮<140.0、140.0~、280.0~和≥420.0 g/周的研究对象HR值（95%CI）分别为0.80（0.74~0.86）、0.75（0.68~0.83）、0.84（0.76~0.93）、0.86（0.76~0.97）和0.84（0.75~0.94），而戒酒与COPD发病风险无统计学关联；在女性中，与从不饮酒者相比，除经常饮酒70~ g/周与COPD发病风险无统计学关联外，其余各组发病风险均下降，已戒、偶尔饮、经常饮<70.0和≥140.0 g/周的研究对象HR值（95%CI）分别为0.81（0.68~0.96）、0.87（0.82~0.93）、0.78（0.62~0.99）和0.77（0.62~0.96）。遗传分析结果显示，与C1组研究对象相比，C2~C6组的男性COPD发病风险均无显著改变；在女性中，仅C4组COPD发病风险相较参照组有所降低（HR=0.79，95%CI：0.63~0.99）。结论 本研究结果不支持饮酒与COPD发病风险间的因果关联。 |
| 英文摘要: |
| Objective To investigate the associations between alcohol intake and risks of chronic obstructive pulmonary disease (COPD) using self-reported alcohol intake and genetically predicted mean alcohol intake in adults in 10 areas of China. Methods This study used baseline data collected in 2004-2008 from the China Kadoorie Biobank, and the COPD outcome was determined through long-term follow-up. After excluding participants with cancer, coronary heart disease, stroke or transient ischemic attack, asthma, tuberculosis, or COPD at baseline, 445 523 participants were included in the observational analysis. A total of 133 168 participants with complete genotyping data were included in the genetic analysis, after the same exclusion criteria were applied. Alcohol consumption patterns were obtained through a baseline questionnaire. The mean alcohol intake of male non-abstainers was calculated based on the combination of ALDH2-rs671 and ADH1B-rs1229984 genotypes and the study region, and all participants were divided into six groups (C1-C6) accordingly. Cox proportional hazards regression models were used to estimate the associations between exposure factors and risk of incident COPD. Results In the observational analysis, 11 825 incident cases of COPD were identified during an average follow-up period of (11.8±2.1) years. After adjusting for potential confounders, occasional and current drinking was associated with lower risk of incident COPD in males, with HRs (95%CIs) of 0.80 (0.74-0.86), 0.75 (0.68-0.83), 0.84 (0.76-0.93), 0.86 (0.76-0.97) and 0.84 (0.75-0.94) for occasional and current drinkers consuming pure alcohol <140.0, 140.0-, 280.0-, ≥420.0 g/week respectively, while there was no significant association between abstainers and risk of COPD. In females, compared with non-drinkers, the risk of COPD reduced in all groups except for current drinkers consuming pure alcohol 70.0-139.9 g/week, with HRs (95%CIs) of 0.81 (0.68-0.96), 0.87 (0.82-0.93), 0.78 (0.62-0.99) and 0.77 (0.62-0.96) for abstainers, occasional and current drinkers consuming pure alcohol <70.0, 70.0-, ≥140.0 g/week respectively. In the genetic analysis, the risk of COPD in the C2-C6 groups was similar to that of males in the C1 group. In females, only the C4 group had a lower COPD risk compared to the C1 group (HR=0.79, 95% CI: 0.63-0.99). Conclusion The study does not support a causal association between alcohol consumption and the risk of COPD. |
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