Tobacco Smoke Exposure In Children Research Articles

Role of parental smoking and environmental tobacco smoke exposure in childhood cancer: A study using hair cotinine analysis and questionnaires.

In the etiology of childhood cancers, many genetic and environmental factors play a role. One of these factors could be cigarette smoking, and the main source of tobacco smoke exposure of children is parental smoking. However, establishing a causal relationship between parental smoking and childhood cancers has proven challenging due to difficulties in accurately detecting tobacco smoke exposure METHODS: To address this issue, we used hair cotinine analysis and a questionnaire to get information about tobacco smoke exposures of pediatric cancer patients and healthy children. A total of 104 pediatric cancer patients and 99 healthy children participated in our study. Parental smoking behaviors (pre-conceptional, during pregnancy, and current smoking) and environmental tobacco smoke (ETS) exposures of children are compared. We have found no differences between two groups by means of maternal smoking behaviors. However, the rates of paternal pre-conceptional smoking and smoking during pregnancy were significantly low in cancer patients (p<.05). These data suggest that social desirability bias among fathers of cancer patients may have contributed to this discrepancy. According to questionnaire, cancer patients had significantly lower ETS exposures than healthy children (p<.05). However, ETS exposure assessment through cotinine analysis demonstrated that cancer patients had higher exposure to ETS compared to healthy children (p<.001). Our findings provide evidence supporting the potential role of smoking as a risk factor for childhood cancers. This study also revealed that questionnaires could cause biases. We suggest that cotinine analysis along with validated questionnaires can be used to prevent biases in studies of tobacco smoke in the etiology of childhood cancers.

Association of Zinc Intake, Tobacco Smoke Exposure, With Metabolic Syndrome: Evidence from NHANES 2007-2018.

The objective was to explore the effect modification of zinc (Zn) intake levels on the relationship of tobacco smoke exposure and risk of metabolic syndrome (MetS) in children and adolescents. We used data from 2007-2018 National Health and Nutrition Examination Survey (N = 3701). MetS was considered as main endpoint. Weighted multivariable logistic regression models showed that high cotinine level (≥ 0.05ng/mL) was associated with increased odds of MetS [odds ratio = 1.54, 95% confidence interval: 1.01, 2.36], and the association between Zn intake levels and MetS did not demonstrate statistical significance. Importantly, the multiplicative interaction term between low Zn intake (≤ 4.89mg/1000kcal) and high cotinine level was related to higher odds of MetS (p-value for interaction 0.018). For the group with low Zn intake, high cotinine level was associated with increased odds of MetS. However, there was no significant relationship between cotinine levels and MetS risk in the group with high Zn intake. The effect modification by Zn intake on the relationship of tobacco smoke exposure and risk of MetS is significant in individuals who had a sedentary time of ≥ 6h, identified as non-Hispanic White, or resided in households with smokers. In short, low Zn intake may potentiate the association of tobacco smoke exposure and MetS risk in children and adolescents.

Tobacco Smoke Exposure in Early Childhood and Later Risk of Inflammatory Bowel Disease: A Scandinavian Birth Cohort Study.

To examine the association between early-life smoking exposure and later risk of inflammatory bowel disease [IBD]. We followed 115663 participants from the Norwegian Mother, Father and Child [MoBa] and All Babies in Southeast Sweden [ABIS] cohorts from birth [1997-2009] through 2021. IBD was identified through national patient registers. Validated questionnaire data defined maternal smoking during pregnancy, maternal environmental tobacco smoke [ETS] exposure during pregnancy, and child ETS exposure by ages 12 and 36 months. Cox regression was used to estimate adjusted hazard ratios [aHRs] for sex, maternal age, education level, parental IBD, and origin. Cohort-specific estimates were pooled using a random-effects model. During 1 987 430 person-years of follow-up, 444 participants developed IBD [ABIS, 112; MoBa, 332]. Any vs no maternal smoking during pregnancy yielded a pooled aHR of 1.30 [95% CI = 0.97-1.74] for offspring IBD. Higher level of maternal smoking during pregnancy (compared with no smoking, average ≥6 cigarettes/day: pooled aHR = 1.60 [95% CI = 1.08-2.38]) was associated with offspring IBD, whereas a lower smoking level was not (average 1-5 cigarettes/day: pooled aHR = 1.09 [95% CI = 0.73-1.64]). Child ETS exposure in the first year of life was associated with later IBD (any vs no ETS, pooled aHR = 1.32 [95% CI = 1.03-1.69]). Estimates observed for child ETS exposure by 36 months were similar but not statistically significant. In this prospective Scandinavian cohort study, children exposed to higher levels of maternal smoking during pregnancy or ETS during the first year of life were at increased risk of later IBD.

Association between parental smoking and child exposure to environmental tobacco smoke in Israel

BackgroundEnvironmental tobacco smoke (ETS) exposure in children can cause delayed lung development and lifelong cardiovascular damage. The aim of this study was to measure ETS exposure in children in Israel in 2020–2021 using urinary cotinine (UC) measurements and to assess correlates of ETS exposure, including parental smoking.MethodsIn the framework of the National Human Biomonitoring Program, spot urine samples and questionnaire data were collected from 166 children aged 4–12 years, during the years 2020–2021. We collected urine samples in 233 adults, 69 of whom were parents of children included in the study. Parents of participating children were asked about parental smoking, child’s exposure to ETS and smoking policy at home. Cotinine and creatinine were measured in urine. Creatinine-adjusted and unadjusted urine cotinine (UC) geometric means were calculated. Associations between potential correlates and UC concentrations were analyzed in univariate and multivariate analyses. For 69 child-parent pairs, correlation between child and parental UC was analyzed.ResultsBased on urinary cotinine measurement, 65.2% of children of smokers are exposed to ETS, compared to 20.7% of children in non-smoking families. Greater numbers of smokers living in the home (beta = 1.27, p < 0.01), and low maternal education (beta = − 2.32, p < 0.01) were associated with higher levels of UC in a multivariate analysis. Spearman correlations showed a positive moderate correlation between UC in 69 child–parent pairs (r = 0.52, p < 0.01).ConclusionsIn order to reduce child exposure to ETS, smoking parents should be urgently targeted for smoking cessation and smoke-free home interventions. Further interventions are needed to protect all children from ETS.

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

BackgroundExposure 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. ObjectivesThe goal was to determine the stability of hand nicotine in comparison to urinary biomarkers and to explore factors that influence changes in hand nicotine. MethodsData 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. ResultsHand 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. DiscussionFindings 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.

Evaluation of urine cotinine levels in children with chronic cough

Bacground: Our study was planned to reveal the objective relation between urine cotinine level and tobacco smoke exposure in children suffering from chronic cough.&#x0D; Methods: Between ages 5-18 years, 58 patients with chronic cough with no underlying specific cause and 54 healthy individuals were included in the study. &#x0D; Results: There was a statistically significant difference between urine cotinine levels of cases those who exposed and unexposed (based on the declaration of parents) to tobacco smoke (p

Eliminating children's tobacco smoke exposure: a pathway to bioverified abstinence among low-income maternal smokers in the Babies Living Safe and Smokefree (BLiSS) trial.

Identifying behavioral pathways to smoking cessation in high-risk populations, such as low-income maternal smokers, could reduce tobacco disparities. The previous"BLiSS" multilevel intervention trial demonstrated efficacy of the BLiSS intervention in facilitating low-income maternal smokers' bioverified abstinence. This present study examined four putative pathways measured at 3-month end of treatment (Time 2) that could account for the observed intervention effect on smoking abstinence through 12 months (Time 2 - Time 3). Nutritionists in community clinics delivering safety net nutrition promotion programs across Philadelphia, Pennsylvania, USA, were trained by trial principal investigators to deliver a brief tobacco intervention informed by the American Academy of Pediatrics best practice guidelines ("Ask, Advise, Refer [AAR]"). After referral, 396 eligible participants were randomized to either a multimodal behavioral intervention (AAR + MBI) or a parallel attention control (AAR + control). Random effects regression analysis tested mediation. Elimination of children's tobacco smoke exposure (TSE) at Time 2 was the only significant mediator of longitudinal smoking abstinence through Time 3. AAR + MBI mothers were more likely to eliminate their children's TSE by Time 2 (OR = 2.11, 95%CI 1.30, 3.42), which was significantly associated with Time 3 abstinence (OR = 6.72, CI 2.28, 19.80). Modeling showed a significant total effect of AAR + MBI on abstinence (OR = 6.21, CI 1.86, 20.71), a direct effect of AAR + MBI on abstinence (OR = 4.80, CI 1.45, 15.94) and an indirect effect through TSE elimination (OR = 1.29, CI 1.06, 1.57). Integrating smoking cessation interventions with counseling prior to the quit attempt that is designed to facilitate adoption of smokefree home policies and efforts to eliminate children's TSE could enhance the likelihood of long-term abstinence in populations of smokers with elevated challenges quitting smoking.

Prenatal and Childhood Smoke Exposure Associations with Cognition, Language, and Attention-Deficit/Hyperactivity Disorder

To assess the relationships of prenatal and childhood smoke exposure with specific neurodevelopmental and behavioral problems during early childhood. A subsample (n=386) of mother-child dyads from the Newborn Epigenetic Study (NEST) prebirth cohort participated in the study. Cotinine concentrations were used to objectively measure prenatal and childhood smoke exposure when youth were aged 3-13years. Multivariable regression models were used to estimate associations of prenatal and childhood cotinine concentrations with performance on the National Institutes of Health (NIH) Toolbox and attention-deficit/hyperactivity disorder and behavioral symptoms, measured using the Behavior Assessment System for Children, 2nd edition (BASC-2). After adjusting for confounders, childhood cotinine concentrations were associated with poorer cognitive performance on tasks measuring cognitive flexibility (B=-1.29; P=.03), episodic memory (B=-0.97; P=.02), receptive language development (B=-0.58; P=.01), and inhibitory control and attention (B=-1.59; P=.006). Although childhood cotinine concentration was associated with higher levels of attention problems (B=0.83; P=.004) on the BASC-2, after adjustment for confounders, the association is nonsignificant. Although associations for maternal cotinine concentrations were null, an interaction was detected between prenatal and childhood cotinine concentrations on the NIH Toolbox Picture Vocabulary Task (P=.02). Our findings suggest that childhood tobacco smoke exposure may lead to poorer attention regulation and language acquisition, complex visual processing ability, and attention problems.

Child Tobacco Smoke Exposure, Indoor Home Characteristics, and Housing Stability among a National Sample of U.S. Children.

(1) Objectives: To examine the associations of child tobacco smoke exposure (TSE) with home quality and housing instability. (2) Methods. A secondary analysis of 32,066 U.S. 0-11-year-old children from the 2018-2019 National Survey of Children's Health was conducted. Child home TSE status was defined as: no TSE: child lived with no smokers; thirdhand smoke (THS) exposure only: child lived with a smoker(s) who did not smoke indoors; and secondhand smoke (SHS) and THS exposure: child lived with a smoker(s) who smoked indoors. Home quality was assessed by the presence of mold or pesticide use and housing instability was assessed by home ownership, frequency of moves, and number of household members. We conducted weighted multivariable logistic regression and linear regression models while adjusting for important child covariates. (3) Results: In total, 12.3% had home THS exposure only and 1.6% had home SHS and THS exposure. Compared to children with no home TSE, children with home SHS and THS exposure were 2.60 times more likely (95%CI = 1.73, 3.92) to have mold inside their homes; 1.57 times more likely (95%CI = 1.09, 2.26) to live in homes where pesticides were used ≥1 time during the past 12-months; and more likely to have more frequent moves (β = 1.06, 95%CI = 0.62, 1.50). (4) Conclusions: Children with home TSE have higher rates of mold, pesticide use, frequent moves, and household members compared to children with no home TSE. Children with TSE should also be screened for home quality and housing instability and provided with appropriate interventions and resources.

Antecedents of Self-Efficacy to Achieve Smoking-Behavior-Change Goals among Low-Income Parents Enrolled in an Evidence-Based Tobacco Intervention.

Previous studies have shown that greater self-efficacy (SE) to modify smoking behaviors during treatment improves long-term post-treatment outcomes. Little is known about factors that might enhance SE for smoking abstinence and for reducing children’s tobacco smoke exposure (TSE). The present study investigated hypothesized predictors of end-of-treatment SE to abstain from smoking and to protect children from TSE by conducting secondary multiple regression analyses of data (N = 327) from the Kids Safe and Smokefree (KiSS) behavioral intervention trial. KiSS aimed to reduce parental smoking and child TSE in urban, low-income, and minority communities. The results showed that partner support and initiating a planned quit attempt during treatment were positively related to SE to abstain from smoking and to reduce children’s TSE (all p’s < 0.001) at the end of treatment (EOT). Further, lower baseline nicotine dependence and the use of nicotine replacement were related to higher SE to abstain from smoking at EOT (p < 0.01), whereas more restrictive residential smoking rules and lower children’s TSE at baseline was associated with higher SE to reduce children’s TSE at EOT (all p’s < 0.05). These findings inform theory and future intervention design, identifying individual and social-environmental factors that might enhance smoking-behavior-change SE.

Urinary cotinine and exposure to passive smoke in children and adolescents in Germany – Human biomonitoring results of the German Environmental Survey 2014–2017 (GerES V)

Passive smoking is a preventable and significant cause of many serious health problems, with children being particularly at risk. In the fifth German Environmental Survey (GerES V), conducted from 2014 to 2017, information reflecting the extent of passive smoke exposure in children and adolescents was collected by interview-based questionnaires and human biomonitoring (HBM) analyses of cotinine in urine from 2260 participants, aged 3–17 years. Based on these population-representative data, we describe current passive smoke exposure stratified by different subgroups and identify specific exposure determinants using multivariate logistic regression. The questionnaire data revealed that 42% of children and adolescents lived with at least one smoker in the household. Quantifiable concentrations of cotinine could be detected in 56% of the participants. The overall median concentration of cotinine was 0.2 μg/L, with children and adolescents of low socioeconomic status found to be a group particularly affected by passive smoke with higher cotinine concentrations (median = 1.2 μg/L). In the multiple analysis, the most significant predictor of cotinine levels derived from the questionnaire was passive smoking at home (odds ratio (OR) 13.07 [95CI: 4.65, 36.70]). However, parental smoking and passive smoking among friends and relatives could also be identified as independent factors influencing elevated cotinine levels. The comparison between the previous cycle GerES IV (2003–2006) on 3–14-year-olds and GerES V shows that tobacco smoke exposure of children decreased significantly. This decrease is likely an effect of extensive non-smoker protection laws being enforced 2007–2008 on federal and state level. This is reflected by a halving of urinary cotinine concentrations. Nevertheless, our results indicate that passive smoke is still a relevant source of harmful pollutants for many children and adolescents in Germany, and thus support the need for further efforts to reduce passive smoke exposure, especially in the private environment.

Exposure to parental smoking and cardiac structure and function in adulthood: the Cardiovascular Risk in Young Finns Study.

The relationship between childhood tobacco smoke exposure and cardiac structure and function in midlife is unclear. We investigated the association between parental smoking with cardiac structure and function in adulthood. 1250 participants (56.5% female) from the Cardiovascular Risk in Young Finns Study who had data on parental smoking and/or serum cotinine, a biomarker of exposure to tobacco smoke, at baseline 1980 (age 3-18 years) and echocardiography performed in 2011. Parental smoking hygiene (i.e., smoking in the vicinity of children) was categorized by parental smoking and serum cotinine levels in offspring. Dimensions of the left ventricle, diastolic and systolic function, and cardiac remodeling were used as outcomes. Analyses were adjusted for sex, age, and covariates (blood pressure (BP), serum lipids, body mass index, socioeconomic status, smoking (only in adulthood)) in childhood and adulthood. Parental smoking was not associated with systolic or diastolic function in adulthood. Participants exposed to parental smoking (odds ratio (OR) 1.90, 95%CI 1.23-2.92), hygienic parental smoking (OR 1.74, 95%CI 1.12-2.71), and non-hygienic parental smoking (OR 1.88, 95%CI 1.02-3.45) had higher odds of concentric remodeling (relative wall thickness >85th sex-specific percentile without left ventricular hypertrophy). These associations were attenuated after adjustment for child and adult covariates in the non-hygienic parental smoking group. Exposure to parental smoking in childhood was associated with a higher likelihood of concentric remodeling and thicker left ventricular and interventricular septal walls in midlife, which was not improved by parents who smoked hygienically. Parental smoking was not related to systolic or diastolic function in this relatively young population.

Hand nicotine as an independent marker of thirdhand smoke pollution in children's environments

BackgroundHand nicotine (HN) levels measure children's exposure to tobacco smoke pollutants from thirdhand and secondhand smoke. HN is associated with urinary and salivary cotinine, but the associations of HN with other tobacco smoke exposure (TSE) markers remain unknown. ObjectivesWe compared levels of HN and four urinary TSE biomarkers: cotinine, trans-3′-hydroxycotinine (3HC), nicotelline N-oxides, and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), and children's sociodemographic and TSE patterns. We also examined if HN is a plausible pathway for children's exposure to active smoking. MethodsData were collected from 175 non-smoking patients (Mean (SD) age = 5.4 (3.4) years) who lived with ≥1 cigarette smoker(s). HN and TSE biomarker levels were determined using LC-MS/MS. Multivariate and multivariable regression analyses were conducted to examine associations between TSE markers and parent-reported measures, controlling for sociodemographics. ResultsOf the five markers of TSE, cotinine (R2 = 0.221; p = 0.003) and HN (R2 = 0.247; p = 0.001) showed the strongest overall associations. Of the five markers, only cotinine showed significantly higher levels among Black children (β^=0.307,p<0.05) independent of age, reported exposure, and home smoking bans. Cotinine (β^=0.010,p<0.05), NNAL (β^=0.012,p<0.05), and HN (β^=0.011,p<0.05) showed significant positive associations with reported exposure independent of race, age, and home smoking bans. NNAL (β^=−0.285,p<0.05) and HN (β^=−0.336,p<0.05), but not cotinine, 3HC, and N-oxides, showed significantly lower levels among children who lived in homes with smoking bans. Child age, hand surface area, home smoking ban, and reported exposure independently accounted for 21 % of the variance in HN levels (p = 0.002). HN accounted for 30 % of the variance in cotinine independent of child race and child age. DiscussionHN levels were associated with modifiable tobacco-related behaviors and shows promise as a marker of sources of THS pollution in a child's environment not captured by measurement of urinary cotinine alone. HN levels provide additional information about TSE, complementing other biomarkers when assessing children's overall TSE.

Financial Insecurity and Food Insecurity among U.S. Children with Secondhand and Thirdhand Smoke Exposure.

Objectives: Smokers with financial and food insecurity may find it difficult to quit smoking and reduce their children’s tobacco smoke exposure (TSE). The objective was to examine the associations between child TSE and financial and food insecurity among U.S. school-aged children. Methods: We examined the 2018–2019 National Survey of Children’s Health data on 17,484 children 6–11 years old. Children were categorized into TSE groups: (1) No TSE: did not live with a smoker; (2) thirdhand smoke (THS) exposure alone: lived with a smoker who did not smoke inside the home; or (3) secondhand smoke (SHS) and THS exposure: lived with a smoker who smoked inside the home. We conducted weighted logistic, ordinal, and linear regression analyses to assess the relationships between child TSE status and financial and food insecurity, adjusting for covariates. Results: Overall, 13.1% and 1.8% of children had THS exposure alone and SHS and THS exposure, respectively. Compared to children with no TSE, children with THS exposure alone were at 2.17 increased odds (95% CI = 1.83, 2.58, p < 0.001) and children with SHS and THS exposure were at 2.24 increased odds (95% CI = 1.57, 3.19, p < 0.001) of having financial insecurity. Children with THS exposure alone were at 1.92 increased odds (95% CI = 1.58, 2.33, p < 0.001) and children with SHS and THS exposure were at 2.14 increased odds (95% CI = 1.45, 3.16, p < 0.001) of having food insecurity. Conclusions: Children with TSE are at increased risk of experiencing financial and food insecurity. When developing tobacco interventions, a holistic approach to tobacco control that addresses ways to decrease financial and food hardships may improve outcomes.

Association between objective measures and parent-reported measures of child tobacco smoke exposure: A secondary data analysis of four trials.

INTRODUCTIONTobacco smoke exposure (TSE) harms children and adults. Studies of childhood TSE exposure often relies on parental reports, but may benefit from objective measures. The objective of our study was to study the relationship between reported and objective measures of TSE.METHODSWe analyzed data from four intervention trials, conducted in clinical or community settings, to identify objective measures most closely associated with parent-reported measures and the optimal set of parent-reported measures for predicting objective measures. We also assessed whether there was a learning curve in reported exposure over time, and the importance of replicate biomarker measures.RESULTSCorrelations between objective and parent-reported measures of child TSE were modest at best, ranging from zero to 0.41. Serum cotinine and urinary cotinine were most strongly associated with parental reports. Parental questions most closely related to biomarkers were number of cigarettes and home smoking rules; together these formed the best set of predictive questions. No trial included all objective measures and all questions, precluding definitive statements about relative advantages. Within-subject repeatability of biomarker measures varied across studies, suggesting that direct pilot data are needed to assess the benefit of replicate measurements.CONCLUSIONSImprovements in objective and parent-reported child exposure measurements are needed to accurately monitor child TSE, evaluate efforts to reduce such exposure, and better protect child health.

Unintentional Tobacco Smoke Exposure in Children.

Secondhand smoke (SHS) exposure increases the prevalence and severity of sinopulmonary diseases in children. The primary source of SHS exposure in children is through adults who live in the same house; however, the level of exposure may vary based on the adult smoking habits at home. This prospective cross-sectional study in Alberta, Canada, investigated the relationship between self-reported caregiver smoking, location, outdoor temperature and children’s’ urine cotinine: creatinine ratio (CCR), a marker of nicotine metabolism. Participants aged 0–9 were recruited from the Child Health Clinics at the Misericordia Community Hospital in Edmonton, Alberta, from 8 January to 24 February 2016 and 30 June to 18 August 2016. Participant CCR levels were compared to caregiver-reported smoking location and environmental factors such as temperature and season. Of the 233 participants who reported smoking status, 21% reported smoking, in keeping with local smoking rates. More participants smoked indoors during the winter than the summer; however, some families limited indoor smoking to a garage. Of the 133 parent–child dyads who provided smoking information and a child urine sample, 18 had an elevated cotinine:creatinine ratio, suggestive of significant tobacco smoke exposure, 15 of whom were from homes that reported smoking. Age < 1 year and number of cigarettes smoked in the home weekly were risks for significant exposure while season, outdoor temperature and smoking location in the home did not reach significance. Smokers should be counseled to protect children, particularly infants, from exposure by limiting the number of cigarettes smoked and isolating smoking to outside the home. Segregated areas such as a garage may provide a useful harm mitigation strategy for indoor smokers, provided the garage does not share ventilation or is not in close proximity to high-traffic areas of the home.

Monthly Motivational Interview Counseling and Nicotine Replacement Therapy for Smoking Parents of Pediatric Patients: A Randomized Controlled Trial.

BackgroundParental smoking is the dominant source of passive smoke exposure in the pediatric population. The current randomized controlled trial (RCT) study aimed to evaluate the effectiveness of a multi-component smoking reduction intervention in parental smoking reduction and children's environmental tobacco smoke exposure reduction in clinical settings.MethodsA single-blinded, 6-month randomized controlled trial recruited smoking parents (N = 210) of children who attended the pediatric wards or clinics at the Prince of Wales Hospital. Participants allocated to the intervention group (n = 105) received monthly motivational interviews on smoking reduction with emphasis on health hazards related to children's passive smoke exposure, 8-week nicotine replacement therapy, and referral to smoking cessation service if the parents preferred. The control group (n = 105) received simple verbal advice on smoking cessation. Primary outcomes were parental urine cotinine validated and self-reported ≥50% smoking reduction rates at 6 months.ResultsSmoking parents in the intervention group had significantly more biochemically validated ≥50% smoking reduction than the control: 27.1 vs. 10.0% (OR = 3.34, 95% CI: 1.16–9.62, P = 0.02). The rate of self-reported ≥50% smoking reduction was also significantly higher in the intervention group than the control: 51.9 vs. 20.2% (OR = 4.40, 95% CI: 2.38–8.12, P < 0.001). For secondary outcomes, the rate of parental self-reported smoking cessation was higher in the intervention arm: 10.5 vs. 1.0% (OR = 12.17, 95% CI: 1.54–96.07, P < 0.001), however, no differences were detected in biochemically validated cessation and changes in children's passive smoke exposure between the groups.ConclusionMonthly smoking reduction counseling together with nicotine replacement therapy is more effective than simple verbal cessation advice in the smoking reduction for parents of pediatric patients. However, this study did not demonstrate differences in smoking cessation or reduction in children's passive smoke exposure with a 6-month follow-up. Achievement of a smoke-free environment remains challenging.Trial RegistrationClinicaltrials.gov, identifier: NCT03879889.

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

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. 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. 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. 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. 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.

Disparities in Neighborhood Characteristics among U.S. Children with Secondhand and Thirdhand Tobacco Smoke Exposure.

(1) Background: Home tobacco smoke exposure (TSE) and negative neighborhood characteristics adversely affect children’s overall health. The objective was to examine the associations of child TSE status and neighborhood characteristics among U.S. school-aged children. (2) Methods: We conducted a secondary analysis of the 2018–2019 National Survey of Children’s Health (NSCH) data including 17,300 U.S. children ages 6–11 years old. We categorized children’s home TSE status into: (a) no TSE: child did not live with a smoker; (b) thirdhand smoke (THS) exposure alone: child lived with a smoker who did not smoke inside the home; and (c) secondhand smoke (SHS) and THS exposure: child lived with a smoker who smoked inside the home. We conducted a series of weighted linear and logistic regression analyses to assess the associations between child TSE status and neighborhood characteristics, adjusting for covariates. (3) Results: Overall, 13.2% and 1.7% of children were exposed to home THS alone and home SHS and THS, respectively. Compared to children with no TSE, children with home THS exposure alone and children with home SHS and THS exposure had a significantly lower total number of neighborhood amenities and children with SHS and THS exposure had a significantly higher total number of detracting neighborhood elements. (4) Conclusions: Children with TSE demonstrate disparities in the characteristics of the neighborhood in which they live compared to children with no TSE. TSE reduction interventions targeted to children with TSE who live in these neighborhoods are warranted.

Multilevel Intervention for Low-Income Maternal Smokers in the Special Supplemental Nutrition Program for Women, Infants, and Children (WIC).

Objectives. To test the efficacy of Babies Living Safe and Smokefree (BLiSS), a multilevel intervention initiated in a citywide safety net health system to improve low-income maternal smokers' abstinence and reduce child tobacco smoke exposure. Methods. This randomized controlled trial in Philadelphia, Pennsylvania (2015-2020), recruited low-income maternal smokers who received a brief smoking intervention (Ask, Advise, Refer [AAR]) from nutrition professionals in the Special Supplemental Nutrition Program for Women, Infants, and Children before randomization to (1) a multilevel intervention (AAR + multimodal behavioral intervention [MBI]; n = 199) or (2) an attention control intervention (AAR + control; n = 197). Results. AAR + MBI mothers had significantly higher 12-month bioverified abstinence rates than did AAR + control mothers (odds ratio [OR] = 9.55; 95% confidence interval [CI] = 1.54, 59.30; P = .015). There were significant effects of time (b = -0.15; SE = 0.04; P < .001) and condition by time (b = -0.19; SE = 0.06; P < .001) on reported child exposure favoring AAR + MBI, but no group difference in child cotinine. Presence of other residential smokers was related to higher exposure. Higher baseline nicotine dependence was related to higher child exposure and lower abstinence likelihood at follow-up. Conclusions. The multilevel BLiSS intervention was acceptable and efficacious in a population that experiences elevated challenges with cessation. Public Health Implications. BLiSS is a translatable intervention model that can successfully improve efforts to address the persistent tobacco-related burdens in low-income communities. Trial Registration. ClinicalTrials.govidentifier: NCT02602288. (Am J Public Health. 2022;112(3):472-481. https://doi.org/10.2105/AJPH.2021.306601).