Arpa Medeni, Şen Bayram, Kazancıoğlu Leyla, Kılıç Hülya
Department of Medical Biochemistry, Faculty of Medicine, Recep Tayyip Erdogan University, Rize, Turkey.
Laboratory of Medical Biochemistry, Recep Tayyip Erdogan University Training and Research Hospital, Rize, Turkey.
Sci Rep. 2025 Aug 28;15(1):31696. doi: 10.1038/s41598-025-17768-7.
Coronavirus Disease 2019 (COVID-19), caused by SARS-CoV-2, has posed a significant global public health challenge, with long-term sequelae such as post-COVID-19 syndrome continuing to burden health systems. Tobacco use, a major preventable cause of morbidity and mortality, impairs the immune response and exacerbates respiratory diseases, including COVID-19. Passive smoking, an important but often overlooked public health problem, exposes non-smokers to harmful health risks and may contribute to worse outcomes in respiratory disease. This study aims to investigate the relationship between smoking exposure, including passive smoking, and the severity of COVID-19 using urinary cotinine levels to provide objective insights into a critical public health issue. This prospective observational study was conducted over six months in 2021 in the ICU of a tertiary care hospital. Forty-two patients were divided into four groups based on smoking and COVID-19 status: non-smoker/non-COVID-19, smoker/non-COVID-19, non-smoker/COVID-19, and smoker/COVID-19. COVID-19 diagnosis was confirmed by RT-PCR and/or imaging. Data collected included demographic information, clinical scores [APACHE II, mSOFA, GCS], respiratory function [stPaO2/FiO2 ratio], arterial blood gas parameters and routine laboratory findings. Urinary cotinine levels were measured by ELISA and normalised to spot urine creatinine levels to ensure accuracy. Urine cotinine levels were highest in the smoker/COVID-19 group and significantly higher than in the smoker/non-COVID-19 and non-smoker/COVID-19 groups (p = 0.010 and p = 0.002, respectively). Surprisingly, non-smoker/non-COVID-19 patients also had elevated cotinine levels, suggesting exposure to passive smoking. The stPaO2/FiO2 ratio was significantly lower in smoker/COVID-19 patients (p < 0.001), indicating impaired lung function. This study highlights the detrimental effects of smoking exposure, including passive smoking, on the severity of COVID-19. Elevated cotinine levels in non-smokers/non-COVID-19 patients emphasize the widespread public health impact of passive smoking and highlight the need for stronger policies and interventions to minimize tobacco exposure. Addressing both active and passive smoking is critical to improving public health outcomes and reducing the burden of respiratory diseases such as COVID-19. Further research is essential to validate these findings and to inform evidence-based public health strategies.
2019冠状病毒病（COVID-19）由严重急性呼吸综合征冠状病毒2（SARS-CoV-2）引起，对全球公共卫生构成了重大挑战，其长期后遗症如新冠后综合征继续给卫生系统带来负担。吸烟是发病率和死亡率的一个主要可预防原因，会损害免疫反应并加重包括COVID-19在内的呼吸道疾病。被动吸烟是一个重要但常被忽视的公共卫生问题，使不吸烟者面临有害健康风险，并可能导致呼吸道疾病出现更差的结果。本研究旨在利用尿可替宁水平调查吸烟暴露（包括被动吸烟）与COVID-19严重程度之间的关系，以便为一个关键的公共卫生问题提供客观见解。这项前瞻性观察性研究于2021年在一家三级护理医院的重症监护病房进行了六个月。42名患者根据吸烟和COVID-19状况分为四组：非吸烟者/非COVID-19组、吸烟者/非COVID-19组、非吸烟者/COVID-19组和吸烟者/COVID-19组。COVID-19诊断通过逆转录聚合酶链反应（RT-PCR）和/或影像学检查确认。收集的数据包括人口统计学信息、临床评分[急性生理与慢性健康状况评分系统II（APACHE II）、改良序贯器官衰竭评估（mSOFA）、格拉斯哥昏迷量表（GCS）]、呼吸功能[静态动脉血氧分压/吸入氧分数值（stPaO2/FiO2）比值]、动脉血气参数和常规实验室检查结果。尿可替宁水平通过酶联免疫吸附测定（ELISA）测量，并根据随机尿肌酐水平进行标准化以确保准确性。吸烟者/COVID-19组的尿可替宁水平最高，且显著高于吸烟者/非COVID-19组和非吸烟者/COVID-19组（分别为p = 0.010和p = 0.002）。令人惊讶的是，非吸烟者/非COVID-19患者的可替宁水平也有所升高，表明存在被动吸烟暴露。吸烟者/COVID-19患者的stPaO2/FiO2比值显著更低（p < 0.001），表明肺功能受损。本研究强调了吸烟暴露（包括被动吸烟）对COVID-19严重程度的有害影响。非吸烟者/非COVID-19患者中可替宁水平升高强调了被动吸烟对公共卫生的广泛影响，并突出了需要更强有力的政策和干预措施以尽量减少烟草暴露。解决主动吸烟和被动吸烟问题对于改善公共卫生结果和减轻诸如COVID-19等呼吸道疾病的负担至关重要。进一步的研究对于验证这些发现并为基于证据的公共卫生策略提供信息至关重要。
