Department of Pediatrics, Kosin University Gospel Hospital, Kosin University School of Medicine, Busan, Korea.
Department of Internal Medicine, Kosin University Gospel Hospital, Kosin University School of Medicine, Busan, Korea.
J Korean Med Sci. 2021 Aug 2;36(30):e193. doi: 10.3346/jkms.2021.36.e193.
Environmental tobacco smoke exposure due to parents is a modifiable risk factor for childhood asthma, but many studies have evaluated parental smoking using self-reported data. Therefore, we aimed to analyze the relationship between parental cotinine-verified smoking status and asthma in their children.
This population-based cross-sectional study used data from the Korean National Health and Nutrition Examination Survey from 2014 to 2017. Participants aged 0 to 18 years with complete self-reported physician-diagnosed childhood asthma and measurement of their parental urinary cotinine levels were included. Parental urinary cotinine-verified smoking status was defined using both urinary cotinine levels and self-report, as active, passive, and non-smoker. Sample weights were applied to all statistical analyses because of a complex, multistage and clustered survey design. Logistic regression model was used to analyze the relationship between childhood asthma and parental smoking.
A total of 5,264 subjects aged < 19 years were included. The prevalence of asthma was 3.4%. The proportions of paternal and maternal urinary cotinine-verified active smokers during the study period were 50.4% and 16.9%, respectively. When parental urinary cotinine level increased, the proportion of parental low household income was increased ( < 0.001). There was no significant association between the parental urinary cotinine-verified smoking group and childhood asthma group. However, the adjusted odds ratios of childhood asthma in the middle and highest tertile of paternal urinary cotinine levels compared with those in lowest tertile were 1.95 (95% confidence interval [CI], 0.98-3.89) and 2.34 (95% CI, 1.21-4.54), respectively.
There seems to be a dose-related association between paternal urinary cotinine levels and the risk of childhood asthma. Because of the high rate of paternal smoking, further studies are needed to develop a targeted strategy to reduce parental smoking for childhood asthma.
父母接触环境烟草烟雾是儿童哮喘的一个可改变的危险因素，但许多研究都是使用自我报告的数据来评估父母吸烟情况。因此，我们旨在分析父母可验证的尿 cotinine 吸烟状况与子女哮喘之间的关系。
这项基于人群的横断面研究使用了 2014 年至 2017 年韩国国家健康和营养检查调查的数据。研究对象为年龄在 0 至 18 岁之间，有完整的自我报告的经医生诊断的儿童哮喘病史，且测量了父母尿 cotinine 水平的人群。通过父母的尿 cotinine 水平和自我报告，将父母的尿 cotinine 验证的吸烟状况定义为主动吸烟、被动吸烟和非吸烟者。由于调查设计复杂、多阶段且呈聚类分布，因此对所有统计分析都应用了样本权重。采用 logistic 回归模型分析儿童哮喘与父母吸烟之间的关系。
共有 5264 名年龄<19 岁的受试者被纳入研究。哮喘的患病率为 3.4%。在研究期间，父亲和母亲的尿 cotinine 验证的主动吸烟者比例分别为 50.4%和 16.9%。随着父母尿 cotinine 水平的升高，父母低家庭收入的比例也随之增加（<0.001）。父母尿 cotinine 验证的吸烟组与儿童哮喘组之间没有显著关联。然而，与最低 tertile 相比，父亲尿 cotinine 水平处于中 tertile 和最高 tertile 的儿童哮喘的调整后比值比分别为 1.95（95%置信区间[CI]，0.98-3.89）和 2.34（95% CI，1.21-4.54）。
似乎存在父亲尿 cotinine 水平与儿童哮喘风险之间的剂量相关关系。由于父亲吸烟率较高，需要进一步研究制定针对父母吸烟的策略，以降低儿童哮喘的风险。
