夜班工作与肺癌风险:一项来自英国生物银行的前瞻性队列研究和中介分析。

IF 4.9 2区 医学 Q1 Medicine
Sleep Pub Date : 2025-08-14 DOI:10.1093/sleep/zsaf159
Xiangyuan Zheng, Yi Feng, Juan He, Xusen Zou, Jie Liang, Xinyi Wu, Zixun Wang, Xin Bi, Bo Cheng, Kexin Chen, Chengfu Xian, Xianzhe Fan, Xiaohong Xie, Jianxing He, Wenhua Liang
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引用次数: 0

摘要

研究目的:本研究利用英国生物银行278650名参与者的数据,调查夜班工作与肺癌风险之间的关系,同时探索潜在的生物介质和基因与环境的相互作用。方法:Cox比例风险模型评估当前夜班状态、一生持续时间和夜班频率与肺癌发病率之间的关系。中介分析检查了物理测量、生活习惯、血液免疫细胞参数和血浆蛋白作为潜在的中介途径。多基因风险评分评估遗传易感性相互作用。结果:在中位随访10.64年期间,共发现1524例肺癌病例。增加夜班工作类别与肺癌风险之间存在显著的剂量-反应关系(轮班但从不/很少夜班HR 1.18, 95% CI:1.00-1.39, p= 0.047;部分夜班HR 1.28, 95% CI: 1.06-1.55, p= 0.010;部分夜班HR 1.19, 95% CI: 0.90-1.57, p= 0.220;P表示趋势= 0.004)。吸烟在这一关联中起着重要的中介作用。中介分析还发现前列腺蛋白酶(PRSS8)、碱性磷酸酶(ALPP)和癌胚抗原相关细胞粘附分子5 (CEACAM5)是关键中介,它们共同解释了超过25%的总效应。结论:这项研究表明,夜班工作,特别是当与吸烟结合时,与肺癌风险增加有关。前列腺蛋白酶、碱性磷酸酶和癌胚抗原相关细胞黏附分子5等潜在介质的鉴定为其潜在的生物学机制提供了见解。未来的研究应该验证这些发现,并探索针对高危人群的有针对性的预防策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Night shift work and lung cancer risk: a prospective cohort study with mediator analysis from the UK Biobank.

Study objectives: This study investigated the association between night shift work and lung cancer risk using data from the UK Biobank cohort of 278 650 participants, while exploring potential biological mediators and gene-environment interactions.

Methods: Cox proportional hazards models assessed relationships between current night shift status, lifetime duration, and frequency of night shifts with lung cancer incidence. Mediation analyses examined physical measurements, lifestyle habits, blood immune cell parameters, and plasma proteins as potential mediating pathways. Polygenic risk scores evaluated genetic predisposition interactions.

Results: During a median follow-up of 10.64 years, 1524 incident lung cancer cases were identified. A significant dose-response relationship was observed between increasing categories of current night shift work and lung cancer risk (Shift but never/rarely night shifts HR 1.18, 95% CI = 1.00 to 1.39, p = .047; Some night shifts HR 1.28, 95% CI = 1.06 to 1.55, p = .010; Some night shifts HR 1.19, 95% CI = 0.90 to 1.57, p = .220; p for trend = .004). Smoking plays a significant mediating role in this association. Mediation analysis also identified prostasin (PRSS8), alkaline phosphatase (ALPP), and carcinoembryonic antigen-related cell adhesion molecule 5 (CEACAM5) as key mediators, collectively explaining over 25 per cent of the total effect.

Conclusions: This study suggests that night shift work, particularly when combined with smoking, is associated with an increased risk of lung cancer. The identification of potential mediators such as prostasin, ALPP and CEACAM5 provides insights into the underlying biological mechanisms. Future research should validate these findings and explore targeted prevention strategies for high-risk populations.

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来源期刊
Sleep
Sleep Medicine-Neurology (clinical)
CiteScore
8.70
自引率
10.70%
发文量
0
期刊介绍: SLEEP® publishes findings from studies conducted at any level of analysis, including: Genes Molecules Cells Physiology Neural systems and circuits Behavior and cognition Self-report SLEEP® publishes articles that use a wide variety of scientific approaches and address a broad range of topics. These may include, but are not limited to: Basic and neuroscience studies of sleep and circadian mechanisms In vitro and animal models of sleep, circadian rhythms, and human disorders Pre-clinical human investigations, including the measurement and manipulation of sleep and circadian rhythms Studies in clinical or population samples. These may address factors influencing sleep and circadian rhythms (e.g., development and aging, and social and environmental influences) and relationships between sleep, circadian rhythms, health, and disease Clinical trials, epidemiology studies, implementation, and dissemination research.
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