Tobacco Smoke Exposure and Sleep Duration among U.S. Adolescents.

OBJECTIVES: Tobacco smoke exposure (TSE) and poor sleep are public health problems with their own set of consequences. This study assessed whether TSE was associated with sleep duration among U.S. adolescents. METHOD: We conducted a secondary analysis of 2013-2018 National Health and Nutrition Examination Survey data including 914 nontobacco-using adolescents ages 16-19 years. TSE measures included cotinine and self-reported home TSE groups including no home TSE, thirdhand smoke (THS) exposure, and secondhand smoke (SHS)+THS exposure. Sleep duration was assessed in hours and categorically as insufficient sleep (recommended hours). Weighted multiple linear regression and multinomial regression models were conducted. RESULTS: Adolescents with higher log-cotinine levels had higher number of sleep hours (ß = 0.31, 95%CI = 0.02,0.60) and were at increased odds of reporting excess sleep (AOR = 1.41, 95%CI = 1.40,1.42), but were at reduced odds of reporting insufficient sleep (AOR = 0.88, 95%CI = 0.87,0.89). Compared to adolescents with no home TSE, adolescents with home THS exposure and home SHS+THS exposure were at increased odds of reporting insufficient sleep (AOR = 2.27, 95%CI = 2.26,2.29; AOR = 2.75, 95%CI = 2.72,2.77, respectively) and excess sleep (AOR = 1.89, 95%CI = 1.87,1.90; AOR = 5.29, 95%CI = 5.23,5.34, respectively). CONCLUSIONS: TSE may affect insufficient and excess sleep duration among adolescents. Eliminating TSE may promote adolescent respiratory and sleep health.

Contamination of surfaces in children's homes with nicotine and the potent carcinogenic tobacco-specific nitrosamine NNK.

BACKGROUND: Tobacco smoke exposure (TSE) through secondhand and thirdhand smoke is a modifiable risk factor that contributes to childhood morbidity. Limited research has assessed surface TSE pollution in children's environments as a potential source of thirdhand smoke exposure, and none have examined levels of the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) on surfaces. OBJECTIVE: This study measured surface NNK and nicotine in children's homes and associations with sociodemographics and parent-reported TSE behaviors. We assessed correlations of surface NNK and nicotine with dust NNK, dust nicotine, and child cotinine. METHODS: Home surface wipe NNK and nicotine data from 84 children who lived with smokers were analyzed. Tobit and simple linear regression analyses were conducted to assess associations of surface NNK and nicotine with child characteristics. Spearman's (ρ) correlations assessed the strength of associations between environmental markers and child cotinine. RESULTS: Nearly half (48.8%) of children's home surfaces had detectable NNK and 100% had detectable nicotine. The respective geometric means (GMs) of surface NNK and nicotine loadings were 14.0 ng/m2 and 16.4 µg/m2. Surface NNK positively correlated with surface nicotine (ρ = 0.54, p < 0.001) and dust NNK (ρ = 0.30, p = 0.020). Surface nicotine positively correlated with dust NNK (ρ = 0.42, p < 0.001) and dust nicotine (ρ = 0.24, p = 0.041). Children with household incomes ≤$15,000 had higher surface NNK levels (GM = 18.7 ng/m2, p = 0.017) compared to children with household incomes >$15,000 (GM = 7.1 ng/m2). Children with no home smoking bans had higher surface NNK (GM = 18.1 ng/m2, p = 0.020) and surface nicotine (GM = 17.7 µg/m2, p = 0.019) levels compared to children with smoking bans (GM = 7.5 ng/m2, 4.8 µg/m2, respectively). IMPACT: Although nicotine on surfaces is an established marker of thirdhand smoke pollution, other thirdhand smoke contaminants have not been measured on surfaces in the homes of children living with smokers. We provide evidence that the potent carcinogenic tobacco-specific nitrosamine NNK was detectable on surfaces in nearly half of children's homes, and nicotine was detectable on all surfaces. Surface NNK was positively correlated with surface nicotine and dust NNK. Detectable surface NNK levels were found in homes with indoor smoking bans, indicating the role of NNK as a persistent thirdhand smoke pollutant accumulating on surfaces as well as in dust.

Distinguishing Exposure to Secondhand and Thirdhand Tobacco Smoke among U.S. Children Using Machine Learning: NHANES 2013-2016.

While the thirdhand smoke (THS) residue from tobacco smoke has been recognized as a distinct public health hazard, there are currently no gold standard biomarkers to differentiate THS from secondhand smoke (SHS) exposure. This study used machine learning algorithms to assess which combinations of biomarkers and reported tobacco smoke exposure measures best differentiate children into three groups: no/minimal tobacco smoke exposure (NEG); predominant THS exposure (TEG); and mixed SHS and THS exposure (MEG). Participants were 4485 nonsmoking 3-17-year-olds from the National Health and Nutrition Examination Survey 2013-2016. We fitted and tested random forest models, and the majority (76%) of children were classified in NEG, 16% were classified in TEG, and 8% were classified in MEG. The final classification model based on reported exposure, biomarker, and biomarker ratio variables had a prediction accuracy of 95%. This final model had prediction accuracies of 100% for NEG, 88% for TEG, followed by 71% for MEG. The most important predictors were the reported number of household smokers, serum cotinine, serum hydroxycotinine, and urinary 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL). In the absence of validated biomarkers specific to THS, comprehensive biomarker and questionnaire data for tobacco smoke exposure can distinguish children exposed to SHS and THS with high accuracy.

Sources of Tobacco Smoke Exposure and Their Associations With Serum Cotinine Levels Among US Children and Adolescents.

INTRODUCTION: We assessed tobacco smoke exposure (TSE) levels based on private and public locations of TSE according to race and ethnicity among US school-aged children ages 6-11 years and adolescents ages 12-17 years. AIMS AND METHODS: Data were from 5296 children and adolescents who participated in the National Health and Nutrition Examination Survey (NHANES) 2013-2018. Racial and ethnic groups were non-Hispanic white, black, other or multiracial, and Hispanic. NHANES assessed serum cotinine and the following TSE locations: homes and whether smokers did not smoke indoors (home thirdhand smoke [THS] exposure proxy) or smoked indoors (secondhand [SHS] and THS exposure proxy), cars, in other homes, restaurants, or any other indoor area. We used stratified weighted linear regression models by racial and ethnic groups and assessed the variance in cotinine levels explained by each location within each age group. RESULTS: Among 6-11-year-olds, exposure to home THS only and home SHS + THS predicted higher log-cotinine among all racial and ethnic groups. Non-Hispanic white children exposed to car TSE had higher log-cotinine (ß = 1.64, 95% confidence interval [CI] = 0.91% to 2.37%) compared to those unexposed. Non-Hispanic other/multiracial children exposed to restaurant TSE had higher log-cotinine (ß = 1.13, 95% CI = 0.23% to 2.03%) compared to those unexposed. Among 12-17-year-olds, home SHS + THS exposure predicted higher log-cotinine among all racial and ethnic groups, except for non-Hispanic black adolescents. Car TSE predicted higher log-cotinine among all racial and ethnic groups. Non-Hispanic black adolescents with TSE in another indoor area had higher log-cotinine (ß = 2.84, 95% CI = 0.85% to 4.83%) compared to those unexposed. CONCLUSIONS: TSE location was uniquely associated with cotinine levels by race and ethnicity. Smoke-free home and car legislation are needed to reduce TSE among children and adolescents of all racial and ethnic backgrounds. IMPLICATIONS: Racial and ethnic disparities in TSE trends have remained stable among US children and adolescents over time. This study's results indicate that TSE locations differentially contribute to biochemically measured TSE within racial and ethnic groups. Home TSE significantly contributed to cotinine levels among school-aged children 6-11 years old, and car TSE significantly contributed to cotinine levels among adolescents 12-17 years old. Racial and ethnic differences in locations of TSE were observed among each age group. Study findings provide unique insight into TSE sources, and indicate that home and car smoke-free legislation have great potential to reduce TSE among youth of all racial and ethnic backgrounds.