Most studies on the association between parents’ smoking status and SHS exposure biomarkers have focused on adolescents in terms of smoking probability or on children with certain diseases. In this study of school-age children in Korea, at least one out of two children was living with a parent who smoked, and the NNAL and cotinine concentrations were higher in children whose parents were smokers. Further analysis confirmed that the higher the number of cigarettes smoked by both parents, the higher the degree of SHS exposure in children. To the best of our knowledge, no previous study in Asia has evaluated both NNAL and cotinine levels in school-age children to determine the extent of SHS exposure.
Our results are similar to those of previous studies [19,21]. While adolescents tend to spend more time outside the home, school-age children spend a lot of time at home and stay close to their parents, suggesting that living with parents who smoke can be a strong predictor of increased exposure to substances included in cigarettes. The highest NNAL and cotinine concentrations were observed in children when both parents smoked. These results were similar to those of previous studies [22,23]. Additionally, although a direct correlation is difficult, compared to when both the parents were non-smokers, the children’s NNAL and cotinine concentrations were higher when only the mother smoked than when only the father smoked. Compared to children of non-smokers, children whose mothers alone smoked or whose both parents were smokers were 2–13 times more likely to be exposed to SHS at home [24]. However, a recent study showed that SHS exposure among adolescents is associated with paternal smoking [17]. In fact, in East Asian countries influenced by Confucianism, the smoking rate in men is higher than that in women. Thus, smoking abstinence by paternal figures is often chosen as the first strategy to reduce children’s exposure to indirect smoking [19,25]. However, for school-age children, time spent with the mother tends to be more than two-fold longer than the time spent with the father. Therefore, smoking abstinence in mothers should also be considered [26]. Consistent with the results of previous research [24,27,28], we found that the higher the number of cigarettes smoked, the higher the children’s NNAL and cotinine concentrations, regardless of the child’s age. This could be because as the number of cigarettes smoked by the parents increased, the amount of harmful substances adhering to their clothes and skin also rose, indirectly exposing the children.
In the subgroup analysis, the association trend was significant according to sex (male and female), BMI (underweight, normal weight, and overweight), household income (Q1, Q2, Q3, and Q4), and parents’ education level (middle school or lower and college or higher). NNAL concentrations were highest in children with normal BMI, followed by in underweight and overweight children. However, cotinine concentrations were highest in underweight children, followed by in children with normal BMI and in overweight children. This is assumed to be due to the amount of nicotine consumed through food, which influenced the urinary concentration of cotinine; in contrast, NNAL is produced mainly through smoking [29]. NNAL and cotinine concentrations were both highest in children from the low-income group. People from this group have less awareness regarding the risks of exposure to SHS; thus, these children may be more vulnerable [30]. The children of parents with a higher level of education had lower NNAL and cotinine concentrations. This supports the premise that education level has a greater influence on SHS exposure than income, and individuals with higher education levels are less likely to smoke and, in cases where they do, are more likely to quit [30,31].
Our research has confirmed that even after controlling SHS exposure at home and in public, many children still faced serious consequences of their parents’ smoking habits. This indicates that while the prohibition of smoking at home and in public show a highly negative correlation with children’s exposure to SHS [28,30], these policies alone cannot fully protect them from the adverse effects of SHS exposure due to parental smoking. The fact that children living with parents who smoke may explain such a phenomenon because they have a higher degree of exposure to SHS than children of non-smokers, even if they live in a house where indoor smoking is prohibited [32]. The World Health Organization states that there is no safe level of exposure to SHS, a pollutant that causes serious illnesses in adults and children. Hence, the only effective way to protect the population from the harmful effects of exposure to SHS is to maintain a 100% non-smoking environment [33]. Implementing physical measures or anti-smoking measures at home, such as the opening of windows or doors or removing cigarette smoke using a ventilator fan, is ineffective in preventing children’s exposure to cigarette smoke. This is because only a completely non-smoking environment can prevent SHS exposure in the home [12,32]. Furthermore, it is necessary to persuade the family to abstain from smoking. Providing counseling to parents regarding the harmful effects of SHS exposure and recommending that they quit smoking may reduce SHS exposure, but not completely eliminate it. Therefore, a comprehensive national anti-smoking policy is required. This should include the provision of services and implementation of preventive programs to support smoking cessation, including cessation treatment and counseling, strong smoking regulations in public places, and regulations on tobacco prices and taxes.
This study has some limitations. First, we used cross-sectional data. Therefore, the cause and effect and the direction of the relationships observed cannot be determined. Second, the results of this study were based on self-reported data. Thus, the number of cigarettes smoked may have been underestimated or overestimated, and some survey questions may be subject to recall bias. Third, despite our efforts to control for confounding factors, not all covariates affecting NNAL and cotinine concentrations may have been considered. Notwithstanding these limitations, our study has important implications. The results can be generalized because the research was conducted using the nationally representative and highly reliable Korea National Health and Nutrition Examination Survey (KNHANES) data. Our findings also support previous results. We targeted school-age children and thus minimized the bias related to smoking status. Further, we controlled for both SHS exposure in public and at home. These factors were not well-considered in previous studies. Furthermore, while analyses based on cotinine measurements were commonly performed in previous studies, our research is meaningful in that we additionally analyzed the concentration of NNAL, which has a longer half-life.
Our study demonstrated that children with parents who smoked are at a higher risk of exposure to SHS, implying that individual efforts to avoid smoking in the presence of children may be an insufficient alternative. Comprehensive national anti-smoking policies that include the provision of anti-smoking services are needed. Furthermore, price- and non-price-related measures should be implemented to persuade parents to quit smoking. Furthermore, cessation treatment and counseling and an increase in cigarette prices and taxes are also required.