Department of Preventive Medicine, Yonsei University College of Medicine, Seoul, Korea.
Department of Occupational and Environmental Health, Yonsei University Graduate School, Seoul, Korea.
Yonsei Med J. 2024 Dec;65(12):752-760. doi: 10.3349/ymj.2023.0488.
Smoking is causally related to alcohol use disorder. Although polycyclic aromatic hydrocarbons (PAHs) are major neurotoxic pollutants in tobacco smoke, evidence is lacking on the role of PAHs in the relationship between smoking and alcohol use disorder. This study investigated the types of PAHs associated with smoking and whether exposure to those PAHs mediated the effect of smoking on alcohol use disorder.
A total of 968 male firefighters were analyzed. Smoking history and cumulative pack-years were obtained using self-reported questionnaires. Alcohol use disorder was defined using the Alcohol Use Disorder Identification Test. PAH exposure was assessed by urinary metabolites. Regression analyses were performed between exposure (smoking), outcome (alcohol use disorder), and mediator (PAH metabolites) variables. A mediation analysis was performed to test the indirect effect of PAH metabolites on the association between smoking and alcohol use disorder. All analyses were repeated for 770 participants who were followed up after 2 years, while alcohol use disorder was redefined from follow-up data ensuring the temporal sequence of the variables.
Both 2-naphthol [β=0.78, 95% confidence interval (CI): 0.59-0.98] and 2-hydroxyfluorene (β=0.69, 95% CI: 0.56-0.82) were associated with smoking history. Furthermore, 2-naphthol and 2-hydroxyfluorene mediated the associations of smoking history (proportion mediated: 14.2%, 23.6% respectively) or cumulative pack-years (proportion mediated: 14.4%, 25.4% respectively) with alcohol use disorder. The results were consistent in longitudinal settings.
Exposure to PAHs mediated the association between tobacco smoking and alcohol use disorder. PAH exposure from tobacco may increase the risk of addictive disorders.
吸烟与酒精使用障碍存在因果关系。尽管多环芳烃（PAHs）是烟草烟雾中的主要神经毒性污染物，但缺乏有关 PAHs 在吸烟与酒精使用障碍之间关系中的作用的证据。本研究调查了与吸烟相关的 PAH 类型，以及这些 PAHs 暴露是否介导了吸烟对酒精使用障碍的影响。
共分析了 968 名男性消防员。使用自我报告问卷获得吸烟史和累计吸烟包年数。使用酒精使用障碍识别测试定义酒精使用障碍。通过尿液代谢物评估 PAH 暴露。在暴露（吸烟）、结局（酒精使用障碍）和中介（PAH 代谢物）变量之间进行回归分析。进行中介分析以测试 PAH 代谢物对吸烟与酒精使用障碍之间关联的间接影响。所有分析均针对 770 名在 2 年后进行随访的参与者重复进行，同时根据变量的时间顺序从随访数据中重新定义酒精使用障碍。
2-萘酚[β=0.78，95%置信区间（CI）：0.59-0.98]和 2-羟基芴[β=0.69，95%CI：0.56-0.82]与吸烟史相关。此外，2-萘酚和 2-羟基芴介导了吸烟史（中介比例：14.2%，14.4%）或累计吸烟包年数（中介比例：23.6%，25.4%）与酒精使用障碍之间的关联。在纵向研究中结果一致。
PAH 暴露中介了吸烟与酒精使用障碍之间的关联。来自烟草的 PAH 暴露可能会增加成瘾障碍的风险。
