Prenatal tobacco smoke exposure and risk for cognitive delays in infants born very premature.

Prenatal tobacco smoke exposure (TSE) and prematurity are independent risk factors for abnormal neurodevelopment. The objectives were to compare differences in Bayley-III cognitive, language, and motor scores at 2 years corrected age (CA) in 395 infants born very preterm (≤ 32 weeks gestation) with and without prenatal TSE. We performed multivariable linear regression analyses to examine associations between prenatal TSE and neurodevelopmental outcomes and a mediation analysis to estimate direct effects of prenatal TSE on outcomes and indirect effects through preterm birth. In total, 50 (12.6%) infants had prenatal TSE. Infants with prenatal TSE had lower mean [95% CI] Cognitive score (82.8 [78.6, 87.1]) vs. nonexposed infants (91.7 [90.1, 93.4]). In children with and without prenatal TSE, there were significant differences in mean [95% CI] Language scores (81.7 [76.0, 87.4] vs. 92.4 [90.2, 94.6], respectively) and mean [95% CI] Motor scores (86.5 [82.2, 90.7] vs. 93.4 [91.8, 95.0], respectively); scores remained significant after controlling for confounders. Preterm birth indirectly mediated 9.0% of the total effect of prenatal TSE on Cognitive score (P = NS). However, 91% of the remaining total effect was significant and attributable to TSE's direct harmful effects on cognitive development (ß = - 5.17 [95% CI - 9.97, - 0.38]). The significant association is largely due to TSE's direct effect on cognitive development and not primarily due to TSE's indirect effect on preterm birth.

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.

Assessment of the Smoke Free Families Tobacco Screening, Counseling, and Referral Program in Pediatric Primary Care Practices.

OBJECTIVE: The Smoke Free Families (SFF) program trained pediatric providers to use an SFF tool during well-child visits (WCVs) of infants ≤12 months to "Ask" caregivers about tobacco use, "Advise" smokers to quit, and "Refer" smokers to cessation services (AAR). The primary objectives were to assess the prevalence and changes in caregiver tobacco use after being screened and counseled by providers using the SFF tool. A secondary objective was to examine providers' AAR behavior facilitated by using the SFF tool. METHODS: Pediatric practices participated in 1 of 3 6-9-month SFF program waves. Over the 3 waves, all initial SFF tools completed on caregivers during their infant's WCV were evaluated for the caregiver and household tobacco use and providers' AAR rates. An infant's first and next WCV was matched to determine changes in caregiver tobacco product use. RESULTS: In total, the SFF tool was completed at 19,976 WCVs; 2081 (18.8%) infants were exposed to tobacco smoke. A total of 834 (74.1%) caregivers who smoked received counseling: 786 (69.9%) were advised to quit, 700 (62.2%) were given cessation resources, and 198 (17.6%) were referred to the Quitline. In total, 230 (27.6%) of caregivers who smoked had a second visit; 58 (25.2%) self-reported that they quit using tobacco. Among cigarette users (n = 183), 89 (48.6%) reported that they used fewer cigarettes or quit at their infants' second WCV. CONCLUSIONS: Systematic use of the SFF AAR tool during infants' WCVs could improve the health of caregivers and children, resulting in decreases in tobacco-related morbidity.

Inflammatory marker levels in children with tobacco smoke exposure.

BACKGROUND: Tobacco smoke exposure (TSE) has inflammatory and immunosuppressive effects which may be associated with altered levels of inflammatory markers and pediatric illnesses. OBJECTIVE: The primary objective was to examine the associations of cotinine-confirmed and parent-reported child TSE patterns and discharge diagnoses with C-reactive protein (CRP), IL-8, and IL-10 in 0-11-year-old pediatric emergency department (PED) patients who lived with ≥ 1 smoker. METHODS: Saliva samples were obtained from 115 children with a mean (SD) age of 3.5 (3.1) years during the PED visit (T0). Saliva was analyzed for cotinine, CRP, IL-8, and IL-10. Parents self-reported their children's TSE patterns; children's medical records were reviewed to identify and categorize discharge diagnoses. Linear regression models were utilized to find T0 associations of cotinine-confirmed and parent-reported child TSE patterns, and PED diagnoses with each inflammatory marker. All models were adjusted for child race/ethnicity, child sex, annual household income, and housing type. The TSE models also adjusted for child discharge diagnosis. RESULTS: At T0, the geometric mean (GeoM) of cotinine was 4.1 ng/ml [95 %CI = 3.2-5.2]; the GeoMs of CRP, IL-8, and IL-10 were 3,326 pg/ml [95 %CI = 2,696-4,105], 474 pg/ml [95 %CI = 386-583], and 1.1 pg/ml [95 %CI = 0.9-1.3], respectively. Parent-reported child TSE patterns were positively associated with ln-transformed CRP levels, while adjusting for the covariates (ß^ = 0.012 [95 %CI:0.004-0.020], p = 0.037). In the parent-reported child TSE pattern model, there were significant positive associations between the covariate of child age with CRP and IL-8 levels (p = 0.028 and p < 0.001, respectively). Children with a bacterial diagnosis had higher IL-8 levels (p = 0.002) compared to the other diagnosis groups. CONCLUSIONS: Results indicate that parent-reported child TSE increases the expression of CRP in ill children and supports prior work demonstrating that IL-8 is higher in children with TSE who have bacterial infections. These findings should be examined in future research with ill children with and without TSE.

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.

Neonatal AVPR1a Methylation and In-Utero Exposure to Maternal Smoking.

(1) Introduction: Epigenetic changes have been proposed as a biologic link between in-utero exposure to maternal smoking and health outcomes. Therefore, we examined if in-utero exposure to maternal smoking was associated with infant DNA methylation (DNAm) of cytosine-phosphate-guanine dinucleotides (CpG sites) in the arginine vasopressin receptor 1A AVPR1a gene. The AVPR1a gene encodes a receptor that interacts with the arginine vasopressin hormone and may influence physiological stress regulation, blood pressure, and child development. (2) Methods: Fifty-two infants were included in this cohort study. Multivariable linear models were used to examine the effect of in-utero exposure to maternal smoking on the mean DNAm of CpG sites located at AVPR1a. (3) Results: After adjusting the model for substance use, infants with in-utero exposure to maternal smoking had a reduction in DNAm at AVPR1a CpG sites by -0.02 (95% CI -0.03, -0.01) at one month of age. In conclusion, in-utero exposure to tobacco smoke can lead to differential patterns of DNAm of AVPR1a among infants. Conclusions: Future studies are needed to identify how gene expression in response to early environmental exposures contributes to health outcomes.

Changes and stability of hand nicotine levels in children of smokers: Associations with urinary biomarkers, reported child tobacco smoke exposure, and home smoking bans.

BACKGROUND: Exposure to thirdhand smoke (THS) residue takes place through inhalation, ingestion, and dermal transfer. Hand nicotine levels have been proposed to measure THS pollution in the environment of children, but little is known about its variability and stability over time and correlates of change. OBJECTIVES: The goal was to determine the stability of hand nicotine in comparison to urinary biomarkers and to explore factors that influence changes in hand nicotine. METHODS: Data were collected from 0 to 11-year-old children (Mean age = 5.9) who lived with ≥1 tobacco smokers (N = 129). At a 6-week interval, we collected repeated measures of hand nicotine, four urinary biomarkers (cotinine, trans-3'-hydroxycotinine, nicotelline N-oxides, and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol), and parent-reported child tobacco smoke exposure (TSE). Dependent sample t-tests, correlations, and multivariable regression analyses were conducted to examine the changes in child TSE. RESULTS: Hand nicotine levels (r = 0.63, p < 0.001) showed similar correlations between repeated measures to urinary biomarkers (r = 0.58-0.71; p < 0.001). Different from urinary biomarkers, mean hand nicotine levels increased over time (t(113) = 3.37, p < 0.001) being significantly higher in children from homes without smoking bans at Time 2 (p = 0.016) compared to Time 1 (p = 0.003). Changes in hand nicotine correlated with changes in cotinine and trans-3'-hydroxycotinine (r = 0.30 and r = 0.19, respectively, p < 0.05). Children with home smoking bans at Time 1 and 2 showed significantly lower hand nicotine levels compared to children without home smoking bans. DISCUSSION: Findings indicate that hand nicotine levels provide additional insights into children's exposure to tobacco smoke pollutants than reported child TSE and urinary biomarkers. Changes in hand nicotine levels show that consistent home smoking bans in homes of children of smokers can lower THS exposure. Hand nicotine levels may be influenced by the environmental settings in which they are collected.

Electronic cigarette use and cigarette smoking associated with inadequate sleep duration among U.S. young adults.

OBJECTIVE: Nicotine use can influence inadequate sleep, but less is known about the associations of exclusive and dual use of electronic cigarettes (e-cigarettes) with combustible cigarettes in U.S. young adults. This study assessed the associations between current exclusive e-cigarette use, exclusive cigarette smoking, and dual e-cigarette and combustible cigarette use and inadequate sleep duration among U.S. young adults. METHODS: We performed a secondary analysis of 2020 Behavioral Risk Factor Surveillance System (BRFSS) data including 13,978 U.S. young adults ages 18-24 years. Inadequate sleep duration was assessed categorically using the National Sleep Foundation's age-specific recommendations that define <7 h as inadequate sleep. Weighted logistic regression models were performed while adjusting for participants' sex, race/ethnicity, education level, annual household income level, body mass index, current physical activity, mental health status, disability status, current alcohol use, and current smokeless tobacco use. RESULTS: Concerning use patterns, 11.8% of young adults were exclusive e-cigarette users, 4.7% were exclusive cigarette smokers, and 3.8% were dual e-cigarette and combustible cigarette users. Exclusive e-cigarette users (adjusted odds ratio [AOR] = 1.41, 95% confidence interval [CI] = 1.16-1.72), exclusive cigarette smokers (AOR = 1.63, 95%CI = 1.22-2.18), and dual product users (AOR = 2.03, 95%CI = 1.44-2.86) were at increased odds of having inadequate sleep duration compared to non-users, while adjusting for the covariates. Additionally, dual product users were at increased odds (AOR = 1.52, 95%CI = 1.06-2.19) of reporting inadequate sleep duration compared to exclusive e-cigarette users, while adjusting for the covariates. CONCLUSIONS: Current e-cigarette and cigarette use may influence inadequate sleep among U.S. young adults. Tobacco cessation efforts may encourage increased sleep health.

"I Don't Want My Child to Be a Guinea Pig": Reasons for Non-Participation in a Parental Tobacco Cessation Trial in the Pediatric Emergency Department Setting.

(1) Background: Pediatric emergency department (PED) settings are opportune venues in which to recruit parental smokers into tobacco cessation interventions. However, the barriers associated with parents' participation in PED-based cessation trials are unknown. The objective was to explore parents' reasons for non-participation in a PED-based tobacco cessation trial. (2) Methods: We employed the framework method and conducted a qualitative data analysis of parental smokers who were eligible to participate in a PED-based tobacco cessation trial and did not choose to participate (n = 371). (3) Results: Two main themes emerged about reasons for non-participation: (a) Not interested in participating in a research study, and (b) concerns specific to the study. Parents had various reasons for not participating in the cessation trial including not being interested in quitting, parents' health and well-being, parents' beliefs about research, and time required for the study and follow-up visits. (4) Conclusion: General disinterest and specific study-related concerns were touted as reasons for non-participation in a PED-based tobacco cessation trial. Given the potential reductions in tobacco-related morbidity to both parents and children that tobacco control interventions can facilitate, future tobacco interventions should consider alterations in study design and recruitment strategies to encourage all eligible parental smokers to participate.

Policy-relevant differences between secondhand and thirdhand smoke: strengthening protections from involuntary exposure to tobacco smoke pollutants.

Starting in the 1970s, individuals, businesses and the public have increasingly benefited from policies prohibiting smoking indoors, saving thousands of lives and billions of dollars in healthcare expenditures. Smokefree policies to protect against secondhand smoke exposure, however, do not fully protect the public from the persistent and toxic chemical residues from tobacco smoke (also known as thirdhand smoke) that linger in indoor environments for years after smoking stops. Nor do these policies address the economic costs that individuals, businesses and the public bear in their attempts to remediate this toxic residue. We discuss policy-relevant differences between secondhand smoke and thirdhand smoke exposure: persistent pollutant reservoirs, pollutant transport, routes of exposure, the time gap between initial cause and effect, and remediation and disposal. We examine four policy considerations to better protect the public from involuntary exposure to tobacco smoke pollutants from all sources. We call for (a) redefining smokefree as free of tobacco smoke pollutants from secondhand and thirdhand smoke; (b) eliminating exemptions to comprehensive smoking bans; (c) identifying indoor environments with significant thirdhand smoke reservoirs; and (d) remediating thirdhand smoke. We use the case of California as an example of how secondhand smoke-protective laws may be strengthened to encompass thirdhand smoke protections. The health risks and economic costs of thirdhand smoke require that smokefree policies, environmental protections, real estate and rental disclosure policies, tenant protections, and consumer protection laws be strengthened to ensure that the public is fully protected from and informed about the risks of thirdhand smoke exposure.

The Associations of Trans-3'-Hydroxy Cotinine, Cotinine, and the Nicotine Metabolite Ratio in Pediatric Patients with Tobacco Smoke Exposure.

(1) Background: Trans-3'-hydroxy cotinine (3HC) and cotinine (COT) are tobacco smoke exposure (TSE) biomarkers and the 3HC/COT ratio is a marker of CYP2A6 activity, an enzyme which metabolizes nicotine. The primary objective was to assess the associations of these TSE biomarkers with sociodemographics and TSE patterns in children who lived with ≥1 smoker. (2) Methods: A convenience sample of 288 children (mean age (SD) = 6.42 (4.8) years) was recruited. Multiple linear regression models were built to assess associations of sociodemographics and TSE patterns with urinary biomarker response variables: (1) 3HC, (2) COT, (3) 3HC+COT sum, and (4) 3HC/COT ratio. (3) Results: All children had detectable 3HC (Geometric Mean [GeoM] = 32.03 ng/mL, 95%CI = 26.97, 38.04) and COT (GeoM = 10.24 ng/mL, 95%CI = 8.82, 11.89). Children with higher cumulative TSE had higher 3HC and COT (ß^ = 0.03, 95%CI = 0.01, 0.06, p = 0.015 and ß^ = 0.03, 95%CI = 0.01, 0.05, p = 0.013, respectively). Highest 3HC+COT sum levels were in children who were Black (ß^ = 0.60, 95%CI = 0.04, 1.17, p = 0.039) and who had higher cumulative TSE (ß^ = 0.03, 95%CI = 0.01, 0.06, p = 0.015). Lowest 3HC/COT ratios were in children who were Black (ß^ = -0.42, 95%CI = -0.78, -0.07, p = 0.021) and female (ß^ = -0.32, 95%CI = -0.62, -0.01, p = 0.044). (4) Conclusion: Results indicate that there are racial and age-related differences in TSE, most likely due to slower nicotine metabolism in non-Hispanic Black children and in younger children.

Current tobacco use patterns associated with healthcare utilization among non-Hispanic Black and Hispanic men with chronic conditions.

INTRODUCTION: Tobacco use disparities persist among U.S. adults who are male, racially/ethnically diverse, and have chronic conditions. This study assessed current tobacco use patterns associated with past year healthcare utilization among non-Hispanic Black and Hispanic men ≥40 years old with ≥1 chronic condition. METHODS: Data were collected from a sample of 1,904 non-Hispanic Black and Hispanic men from across the U.S. using an internet-delivered survey. Participants were categorized into four tobacco use groups: nontobacco users, exclusive cigarette smokers, dualtobacco users (cigarettes + one other tobacco product), and polytobacco users (cigarettes + ≥2 other tobacco products). Logistic regression analyses were conducted to assess current tobacco use patterns with past year primary care visits, emergency department (ED) visits, and overnight hospital stays. Adjusted models included participants' age, race/ethnicity, education level, marital status, health insurance coverage, body mass index, and number of chronic conditions. RESULTS: Relative to nontobacco users, exclusive cigarette smokers were at decreased odds of having a past year primary care visit (adjusted odds ratio [AOR] = 0.68, 95% confidence interval [CI] = 0.47-0.99). Exclusive cigarette smokers (AOR = 1.66, 95%CI = 1.25-2.19), dualtobacco users (AOR = 1.75, 95%CI = 1.23-2.50), and polytobacco users (AOR = 4.10, 95%CI = 2.46-6.84) were at increased odds of having a past year ED visit compared to nontobacco users. Additionally, polytobacco users were at increased odds of having a past year overnight hospital stay (AOR = 2.72, 95%CI = 1.73-4.29) compared to nontobacco users. CONCLUSIONS: Findings suggest current tobacco use patterns are uniquely associated with past year healthcare utilization among non-Hispanic Black and Hispanic men, while taking into consideration important factors including complex disease profiles.

Tobacco Smoke Exposure and Gastrointestinal Problems Among US Children.

This study examined the association between home tobacco smoke exposure (TSE) status and gastrointestinal problems in the past 12 months among US children. We conducted a secondary analysis of the 2018-2019 National Survey of Children's Health cross-sectional data including 20 149 children aged 4 to 10 years. Weighted logistic regression models unadjusted and adjusted for child and family covariates were fitted. Overall, 12.3% of children had home thirdhand smoke (THS) exposure only and 1.8% had home secondhand smoke (SHS) and THS exposure. Unadjusted (odds ratio [OR] = 1.70, 95% confidence interval [CI] = 1.32-2.20) and adjusted (adjusted odds ratio [AOR] = 1.51, 95% CI = 1.14-1.99) logistic regression results indicated that relative to children with no home TSE, children with home THS exposure only were at increased odds of having frequent or chronic difficulty with gastrointestinal problems over the past 12 months. Interventions are critically needed to promote smoking cessation among household members who live with children in order to reduce levels of SHS and THS in their homes.

Associations of household tobacco smoking status with childhood temperament among U.S. preschool-aged children.

BACKGROUND: This study investigated the association between household tobacco smoking status and temperament among U.S. 3-5-year-olds. METHODS: A secondary analysis of 2019-2020 National Survey of Children's Health data (N = 11,100) was conducted. Temperament dimensions of effortful control (characterized by attention focusing), negative affectivity (characterized by anger and soothability), and surgency (characterized by activity level and shyness) were assessed. Weighted ordinal regression models were conducted while adjusting for child and family covariates. RESULTS: Approximately 13 % of children lived with smokers. Compared to children who did not live with smokers, children living with smokers displayed behaviors of poorer effortful control and were more likely to be easily distracted (AOR = 1.59, 95%CI = 1.24-2.04) and less likely to keep working on tasks until finished (AOR = 0.56, 95%CI = 0.44-0.71). Children living with smokers displayed behaviors of greater negative affectivity and were at increased odds of being angry or anxious when transitioning between activities (AOR = 1.50, 95%CI = 1.13-1.98) and losing their temper when things did not go their way (AOR = 1.53, 95%CI = 1.20-1.96), and were at decreased odds of calming down quickly when excited (AOR = 0.54, 95%CI = 0.42-0.70). Children living with smokers displayed behaviors of poorer surgency and were less likely to play well with others (AOR = 0.58, 95%CI = 0.45-0.76) and sit still compared to same-aged children (AOR = 0.56, 95%CI = 0.44-0.71). LIMITATIONS: The NSCH uses a cross-sectional survey design; longitudinal associations and objective measures could not be assessed. However, the NSCH is nationally representative and results are generalizable to U.S. 3-5-year-olds. CONCLUSIONS: Findings suggest household tobacco smoking influences temperament in early childhood. Results signify the need to promote household tobacco cessation.

Prenatal tobacco smoke exposure and risk of brain abnormalities on magnetic resonance imaging at term in infants born very preterm.

BACKGROUND: Prenatal tobacco smoke exposure and preterm birth are associated with abnormal brain and neurodevelopmental outcomes in infants. Studies that can disentangle indirect mediating effects from direct effects of prenatal tobacco smoke exposure on sensitive early brain magnetic resonance imaging biomarkers in very preterm infants are needed. OBJECTIVE: This study aimed to determine whether prenatal tobacco smoke exposure in preterm infants posed any direct effects on magnetic resonance imaging-determined global brain abnormality score and secondary measures of brain abnormalities after removing any indirect mediating effects of preterm birth on neurostructural outcomes. STUDY DESIGN: We examined brain magnetic resonance imaging findings collected at 39 to 44 weeks postmenstrual age from a prospective cohort of 395 infants born very preterm (gestational age of ≤32 weeks). The primary outcome was global brain abnormality score, and the secondary outcomes were global efficiency of structural connectome, diffuse white matter abnormality volume, total brain tissue volume, total gray and white matter volumes, and cerebellar volume. Maternal reports of smoking during pregnancy were obtained. We performed multivariable linear regression analyses to examine the association between prenatal tobacco smoke exposure and our magnetic resonance imaging outcomes, controlling for prospectively collected confounders. Moreover, we performed a mediation analysis to estimate the direct effects of prenatal tobacco smoke exposure on brain abnormalities and any indirect effects through preterm birth. RESULTS: Overall, 12.6% of infants had prenatal tobacco smoke exposure. Infants with prenatal tobacco smoke exposure had a higher median global brain abnormality score than nonexposed infants (7 [interquartile range, 0-41] vs 5 [interquartile range, 0-34]; P≤.001); the findings remained significant (P<.001) after controlling for antenatal confounders. Global efficiency (P<.001), diffuse white matter volume (P=.037), and total brain tissue volume (P=.047) were significantly different between TSE groups in multivariable analyses. On mediation analysis, preterm birth mediated between 0% and 29% of the indirect effect of prenatal tobacco smoke exposure on several measures of brain abnormality outcomes. Thus, prenatal tobacco smoke exposure had a direct adverse effect between 71% and 100% on brain injury or abnormal development. CONCLUSION: Our study has identified multiple adverse effects of prenatal tobacco smoke exposure on sensitive and objective measures of neonatal brain injury and abnormal development; most cases seemed to be a direct effect of prenatal tobacco smoke exposure on fetal brain development. The results underscored the significant adverse neurostructural effects of prenatal tobacco smoke exposure to tobacco smoke pollutants.

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.

Carcinogenic and tobacco smoke-derived particulate matter biomarker uptake and associated healthcare patterns among children.

BACKGROUND: The objective was to assess the associations of child tobacco smoke exposure (TSE) biomarkers (urinary cotinine, NNAL, and nicotelline N-oxides) and parent-reported smoking and child TSE patterns with total hospital visits, pediatric emergency department (PED) visits, urgent care (UC), revisits, and hospital admissions among 0-9-year-olds. METHODS: A convenience sample of PED/UC patients (N = 242) who presented to a large, US children's hospital who had baseline urine samples assayed for the TSE biomarkers of interest were included. Biomarker levels were log-transformed, and linear and Poisson regression models were built. RESULTS: The geometric means of child cotinine, creatinine-adjusted NNAL, and N-oxide levels were 11.2 ng/ml, 30.9 pg/mg creatinine, and 24.1 pg/ml, respectively. The mean (SD) number of daily cigarettes smoked by parents was 10.2 (6.1) cigarettes. Each one-unit increase in log-NNAL levels was associated with an increase in total UC visits (aRR = 1.68, 95% CI = 1.18-2.39) among 0-9-year-olds, while controlling for the covariates. Each one-unit increase in child log-NNAL/cotinine ratio (×103) values was associated with an increase in total hospital visits (aRR = 1.39, 95% CI = 1.10-1.75) and UC visits (aRR = 1.56, 95% CI = 1.14-2.13) over 6 months. CONCLUSION: Systematic screening for child TSE should be conducted during all hospital visits. The comprehensive assessment of TSE biomarkers should be considered to objectively measure young children's exposure. IMPACT: Higher levels of cotinine, a widely used tobacco smoke exposure biomarker, have been associated with higher healthcare utilization patterns among children. Less is known on the associations of carcinogenic and tobacco smoke-derived particulate matter biomarker uptake with child healthcare utilization patterns. This study assessed the associations of several biomarkers with healthcare utilization patterns among pediatric emergency department patients ages 0-9 years who lived with tobacco smokers. Higher urinary NNAL biomarker levels, in individual and ratio form with cotinine, increased children's risk for urgent care visits over 6 months. Higher parent-reported cumulative child tobacco smoke exposure increased children's risk for hospital admissions.

Exposure to Polycyclic Aromatic Hydrocarbons and adverse reproductive outcomes in women: current status and future perspectives.

OBJECTIVES: Polycyclic Aromatic Hydrocarbons (PAHs) are ubiquitous, toxic environmental chemicals that can cause adverse reproductive health effects. The objectives of this mini-review are to highlight the adverse reproductive outcomes due to PAH exposure with the main focus on polycystic ovary syndrome (PCOS) and premature ovarian failure (POF) and to provide perspectives on future research needs. CONTENT: We reviewed studies that have reported the adverse reproductive outcomes associated with PAHs exposures in women through a comprehensive search of bibliographic databases and gray literature sources. In addition, potentially modifiable sources of exposure to PAHs and associated reproductive outcomes were also investigated. SUMMARY: A total of 232 papers were retrieved through a comprehensive search of bibliographic databases, out of which three studies met the eligibility criteria and were included in the review. Results showed that exposure to PAHs is associated with adverse reproductive outcomes defined as PCOS, POF, and reproductive hormone imbalance. Sources of PAH exposure associated with adverse reproductive outcomes include active and passive tobacco smoking, specific cooking methods, and pesticides. OUTLOOK: Future studies are warranted to examine the mechanisms by which PAHs result in adverse reproductive endpoints in women. Further, environmental exposures that are potentially modifiable such as exposure to tobacco smoke, may contribute to PAH exposure, and these exposures should be targeted in future policies and interventions.

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.

Smartphone Apps Targeting Youth Tobacco Use Prevention and Cessation: An Assessment of Credibility and Quality.

Purpose of Review: The goals of this study were to identify smartphone apps targeting youth tobacco use prevention and/or cessation discussed in the academic literature and/or available in the Apple App Store and to review and rate the credibility of the apps. We took a multiphase approach in a non-systematic review that involved conducting parallel literature and App Store searches, screening the returned literature and apps for inclusion, characterizing the studies and apps, and evaluating app quality using a standardized rating scale. Recent Findings: The negative consequences of youth tobacco use initiation are profound and far-reaching. Half of the youth who use nicotine want to quit, but quit rates are low. The integration of smartphone apps shows promise in complementing and enhancing evidence-based youth tobacco prevention and treatment methods. Summary: Consistent with prior reviews, we identified a disconnect between apps that are readily accessible and those that have an evidence base, and many popular apps received low quality scores. Findings suggest a need for better integration between evidence-based and popular, available apps targeting youth tobacco use.