To our knowledge, this is the first study to assess the association between biologically confirmed SHS exposure and mental disorder symptoms in a nationally representative sample of US children and adolescents. Secondhand smoke exposure was positively associated with symptoms of DSM-IV MDD, GAD, ADHD, and conduct disorder, but not panic disorder, among the total sample of nonsmokers even after adjusting for age, sex, race/ethnicity, poverty, migraine, asthma, hay fever, maternal smoking during pregnancy, and allostatic load. However, this association differed across sex and race/ethnicity subpopulations, with the most apparent associations noted for male sex and non-Hispanic white race/ethnicity. Serum cotinine level was also positively associated with DSM-IV ADHD diagnosis; however, the association between serum cotinine level and ADHD diagnosis was attributed to maternal smoking during pregnancy. Serum cotinine level was associated with ADHD symptoms only among participants without an ADHD diagnosis.
Both SHS exposure and poor mental health are major public health problems among children and adolescents. Exposure to tobacco smoke among young children has been associated with several short-term and long-term health effects, including sudden infant death syndrome,27
among others. Furthermore, 2 longitudinal studies36,37
showed that maternal smoking is associated with increased risk of behavioral problems even after adjusting for confounding factors. The findings presented herein provide additional evidence on the harmful effects of SHS exposure on children and adolescents. Our results are consistent with data from previous cross-sectional5,6
studies in adults and suggest that exposure to SHS may precipitate the onset of or exacerbate mental disorder symptoms. Data herein further suggest that this association may differ across sex and race/ethnicity subgroups.
There are known variations in the prevalence, patterns of use, and outcomes of smoking across sex and race/ethnicity strata.38
Individual differences by sex and race/ethnicity in the associations between SHS exposure and DSM-IV
symptoms may be explained by variations in cotinine metabolism39,40
or by other biological, social, or environmental factors that vary across sex and race/ethnicity strata and were unaccounted for in the models herein. However, our results also suggest that male sex and non-Hispanic white race/ethnicity may somehow confer greater vulnerability to mental health effects of SHS exposure. Future research is needed to clarify the biological or psychological mechanisms of associations between SHS exposure and mental health, as well as potential reasons for differential associations across sex and race/ethnicity strata.
In the case of ADHD diagnosis, our study findings differ from those of a 2010 study by Xu et al.41
They also used the 2001 to 2004 NHANES and found that serum cotinine level was positively associated with ADHD diagnosis among Mexican American children but was not associated with ADHD diagnosis among non-Hispanic white and black children even after adjusting for maternal smoking during pregnancy. The study by Xu et al had methodological limitations; ADHD was measured using a single-item question that asked parents whether a health care professional had ever diagnosed their child as having ADHD, and they did not use a cotinine cutoff point to measure SHS exposure. The differences in results between the 2 studies may be related to these measurement variations. Furthermore, current cigarette smokers were more likely to be retained in the analyses by Xu et al. Our findings suggest that the association between SHS exposure and ADHD diagnosis is attributable to in utero tobacco exposure. Recent results from a large longitudinal study by Ekblad et al42
suggest that in utero tobacco exposure may lead to adverse psychiatric conditions. A recent study by Cho et al43
among children in 5 Korean cities also found a positive association between SHS exposure and ADHD symptoms. Therefore, the association between SHS exposure and ADHD symptoms may only be significant at the subthreshold level vs at the diagnostic level.
Several limitations to our study must be considered when interpreting the results. These include the cross-sectional design, our inability to control for some potential confounders, and the possibility that intermittent smokers were included in the analyses. There is no established cutoff point for nonsmokers among persons younger than 12 years,22
and intermittent smokers of any age could have been retained in our analysis if they did not smoke in the 24 to 36 hours before their NHANES blood draw. Some of these participants would not have had detectable serum cotinine levels at the time of their NHANES participation because of the short half-life of this measure.44
Furthermore, we did not control for alcohol consumption because data on alcohol consumption in participants younger than 12 years were not collected in the NHANES. Another potential confounder that we were unable to control for in our analysis is maternal psychiatric history.45–47
That is, children with depressed mothers are more likely to have poor mental health.45–47
In addition, the source of SHS exposure is unknown (eg, mother, father, or other), and illicit drug use was not considered a covariate. Finally, our models included adjustment for allostatic load as a proxy control for psychological stress, which has been shown to be associated with risk of psychiatric symptoms.7,8
However, controlling for allostatic load did not weaken associations between serum cotinine level and DISC-IV symptoms, so it remains unclear if this measure appropriately controlled for psychological stress.
Despite these limitations, findings in the present study provide critical and much-needed data on associations of biologically confirmed SHS exposure with DSM-IV
symptoms in a nationally representative sample of US children and adolescents. Our results have important public health implications. Only 26 states in the United States have banned smoking in all public places (such as bars and restaurants), despite evidence that comprehensive public smoking bans lead to reduced incidence of cardiovascular and respiratory conditions.48
Similar improvements in population-level mental health may be possible.49
Efforts to ban smoking in public places where children and adolescents are present, including all child care settings and schools, should continue, as well as increased efforts to develop interventions targeted directly at parents and designed to prevent SHS exposure in the homes of children and adolescents.50,51
Given the critical developmental period of childhood and adolescence, the effects of policy to reduce or ban smoking in public places and in the home may help prevent or reduce the progression of illness in at-risk individuals and alleviate the heavy burden of illness attributable not only to tobacco use but also to mental disorders.