J Korean Med Sci.  2021 Aug;36(30):e193. 10.3346/jkms.2021.36.e193.

Association between Parental Cotinineverified Smoking Status and Childhood Asthma: a Population-based Nationally Representative Analysis

Affiliations
  • 1Department of Pediatrics, Kosin University Gospel Hospital, Kosin University School of Medicine, Busan, Korea
  • 2Department of Internal Medicine, Kosin University Gospel Hospital, Kosin University School of Medicine, Busan, Korea

Abstract

Background
Environmental tobacco smoke exposure due to parents is a modifiable risk factor for childhood asthma, but many studies have evaluated parental smoking using selfreported data. Therefore, we aimed to analyze the relationship between parental cotinineverified smoking status and asthma in their children.
Methods
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.
Results
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 (P < 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.
Conclusion
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.

Keyword

Asthma; Child; Tobacco Smoke Pollution; Cotinine; Parents; Smoke

Figure

  • Fig. 1 Flow chart showing study population.KNHANES = Korean National Health and Nutrition Examination Survey.

  • Fig. 2 Correlation between paternal and maternal urinary cotinine levels. Maternal urinary cotinine levels were positively associated with paternal urinary cotinine levels (r = 0.19; 95% confidence interval, 0.17–0.23; P < 0.001)

  • Fig. 3 Trends of parental smoking status and incidence of childhood asthma by year. (A) The proportion of paternal non-smoker increased every year (Ptrend = 0.009). (B) The proportion of maternal active smoking abruptly increase in 2017 (Ptrend < 0.001). Asthma incidence showed no significant annual changes (P = 0.991).


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