Effect of smoking on prostate cancer: Results from the National Health and Nutrition Examination Survey 2003-2018 and Mendelian randomization analyses.

IF 2.2 4区医学 Q2 PUBLIC, ENVIRONMENTAL & OCCUPATIONAL HEALTH

Tobacco Induced Diseases Pub Date : 2024-06-04 eCollection Date: 2024-01-01 DOI:10.18332/tid/189199

Hairong He, Liang Liang, Tao Tian, Xiaoyu Zhang, Jun Lyu

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引用次数: 0

Abstract

Introduction: The controversial relationship between smoking and prostate cancer (PCa) risk prompted us to conduct a cross-sectional study using the National Health and Nutrition Examination Survey (NHANES) database and apply Mendelian randomization (MR) analyses in order to clarify the possible causal effect of smoking on PCa risk.

Methods: Using univariate and multivariate logistic regression methods, a secondary analysis of the pooled 2003-2018 NHANES dataset was performed to explore the association between smoking and PCa risk. Propensity-score matching was used to reduce selection bias. Then, we conducted subsequent MR analysis study to investigate the potential causal effect of smoking on PCa risk, with genetic variants of four exposure factors including the lifetime smoking index, light smoking, smoking initiation, and the amount of smoking per day obtained from genome-wide association studies, and PCa summary statistics obtained from three database populations. Inverse-variance weighting was the primary analytical method, and weighted median and MR-Egger regression were used for sensitivity analyses. The MR results for the three PCa databases were combined using meta-analysis.

Results: The study included 16073 NHANES subjects, comprising 554 with PCa and 15519 without PCa. Logistic regression before and after matching did not reveal any significant association. Meta-analysis of the MR results also did not support an association of PCa risk with lifetime smoking index (OR=0.95; 95% CI: 0.83-1.09), light smoking (OR=1.00; 95% CI: 0.95-1.06), smoking initiation (OR=0.99, 95% CI=0.99-1.00), or the amount of smoking per day (OR=1.00; 95% CI: 0.99-1.00) and PCa risk.

Conclusions: There was no evidence for an association between smoking and the risk of PCa. Further studies are needed to determine if there are any associations of other forms of smoking with the risk of PCa at different stages.

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吸烟对前列腺癌的影响：2003-2018年全国健康与营养调查的结果以及孟德尔随机分析。

导言：吸烟与前列腺癌（PCa）风险之间的关系存在争议，这促使我们利用美国国家健康与营养调查（NHANES）数据库开展一项横断面研究，并应用孟德尔随机化（MR）分析，以明确吸烟对PCa风险可能产生的因果效应：采用单变量和多变量逻辑回归方法，对2003-2018年NHANES数据集进行二次分析，探讨吸烟与PCa风险之间的关联。为减少选择偏倚，我们采用了倾向分数匹配法。然后，我们利用从全基因组关联研究中获得的终生吸烟指数、轻度吸烟、开始吸烟和每天吸烟量等四个暴露因素的遗传变异，以及从三个数据库人群中获得的 PCa 概要统计数据，开展了后续的 MR 分析研究，以探讨吸烟对 PCa 风险的潜在因果效应。反方差加权法是主要的分析方法，加权中位数和MR-Egger回归法用于敏感性分析。使用荟萃分析法合并了三个 PCa 数据库的 MR 结果：研究纳入了 16073 名 NHANES 受试者，其中 554 人患有 PCa，15519 人未患 PCa。配对前后的逻辑回归均未发现任何明显的关联。对MR结果进行的元分析也不支持PCa风险与终生吸烟指数（OR=0.95；95% CI：0.83-1.09）、轻度吸烟（OR=1.00；95% CI：0.95-1.06）、开始吸烟（OR=0.99，95% CI=0.99-1.00）或每天吸烟量（OR=1.00；95% CI：0.99-1.00）有关：没有证据表明吸烟与 PCa 风险之间存在关联。结论：没有证据表明吸烟与 PCa 风险之间存在关联，需要进一步研究以确定其他形式的吸烟是否与不同阶段的 PCa 风险存在关联。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Tobacco Induced Diseases SUBSTANCE ABUSE-PUBLIC, ENVIRONMENTAL & OCCUPATIONAL HEALTH

CiteScore

5.30

自引率

5.40%

发文量

审稿时长

12 weeks

期刊介绍： Tobacco Induced Diseases encompasses all aspects of research related to the prevention and control of tobacco use at a global level. Preventing diseases attributable to tobacco is only one aspect of the journal, whose overall scope is to provide a forum for the publication of research articles that can contribute to reducing the burden of tobacco induced diseases globally. To address this epidemic we believe that there must be an avenue for the publication of research/policy activities on tobacco control initiatives that may be very important at a regional and national level. This approach provides a very important "hands on" service to the tobacco control community at a global scale - as common problems have common solutions. Hence, we see ourselves as "connectors" within this global community. The journal hence encourages the submission of articles from all medical, biological and psychosocial disciplines, ranging from medical and dental clinicians, through health professionals to basic biomedical and clinical scientists.