Early life exposure to secondhand tobacco smoke and eating behaviors at age 12 years.

BACKGROUND: Prenatal or early childhood secondhand tobacco smoke (SHS) exposure increases obesity risk. However, the potential mechanisms underlying this association are unclear, but obesogenic eating behaviors are one pathway that components of SHS could perturb. Our aim was to assess associations of prenatal and early childhood SHS exposure with adolescent eating behaviors. METHODS: Data came from a prospective pregnancy and birth cohort (N = 207, Cincinnati, OH). With multiple informant models, we estimated associations of prenatal (mean of 16 and 26 weeks of gestation maternal serum cotinine concentrations) and early childhood cotinine (average concentration across ages 12, 24, 36, and 48 months) with eating behaviors at age 12 years (Child Eating Behaviors Questionnaire). We tested whether associations differed by exposure periods and adolescent's sex. Models adjusted for maternal and child covariates. RESULTS: We found no statistically significant associations between cotinine measures and adolescent's eating behaviors. Yet, in females, prenatal cotinine was associated with greater food responsiveness (ß: 0.23; 95% CI: 0.08, 0.38) and lower satiety responsiveness (ß: -0.14; 95% CI: -0.26, -0.02); in males, prenatal and postnatal cotinine was related to lower food responsiveness (prenatal: ß: -0.25; 95% CI: -0.04, -0.06; postnatal: ß: -0.36; 95% CI: -0.06, -0.11). No significant effect modification by sex or exposure window was found for other eating behaviors. CONCLUSION: Prenatal and early childhood SHS exposures were not related to adolescent's eating behavior in this cohort; however, biological sex may modify these associations.

Effect of twice daily inhaled albuterol on cardiopulmonary exercise outcomes, dynamic hyperinflation, and symptoms in secondhand tobacco-exposed persons with preserved spirometry and air trapping: a randomized controlled trial.

BACKGROUND: In tobacco-exposed persons with preserved spirometry (active smoking or secondhand smoke [SHS] exposure), air trapping can identify a subset with worse symptoms and exercise capacity. The physiologic nature of air trapping in the absence of spirometric airflow obstruction remains unclear. The aim of this study was to examine the underlying pathophysiology of air trapping in the context of preserved spirometry and to determine the utility of bronchodilators in SHS tobacco-exposed persons with preserved spirometry and air trapping. METHODS: We performed a double-blinded placebo-controlled crossover randomized clinical trial in nonsmoking individuals at risk for COPD due to exposure to occupational SHS who had preserved spirometry and air trapping defined as either a residual volume-to-total lung capacity ratio (RV/TLC) > 0.35 or presence of expiratory flow limitation (EFL, overlap of tidal breathing on maximum expiratory flow-volume loop) on spirometry at rest or during cardiopulmonary exercise testing (CPET). Those with asthma or obesity were excluded. Participants underwent CPET at baseline and after 4-week trials of twice daily inhalation of 180 mcg of albuterol or placebo separated by a 2-week washout period. The primary outcome was peak oxygen consumption (VO2) on CPET. Data was analyzed by both intention-to-treat and per-protocol based on adherence to treatment prescribed. RESULTS: Overall, 42 participants completed the entire study (66 ± 8 years old, 91% female; forced expiratory volume in 1 s [FEV1] = 103 ± 16% predicted; FEV1 to forced vital capacity [FVC] ratio = 0.75 ± 0.05; RV/TLC = 0.39 ± 0.07; 85.7% with EFL). Adherence was high with 87% and 93% of prescribed doses taken in the treatment and placebo arms of the study, respectively (P = 0.349 for comparison between the two arms). There was no significant improvement in the primary or secondary outcomes by intention-to-treat or per-protocol analysis. In per-protocol subgroup analysis of those with RV/TLC > 0.35 and ≥ 90% adherence (n = 27), albuterol caused an improvement in peak VO2 (parameter estimate [95% confidence interval] = 0.108 [0.014, 0.202]; P = 0.037), tidal volume, minute ventilation, dynamic hyperinflation, and oxygen-pulse (all P < 0.05), but no change in symptoms or physical activity. CONCLUSIONS: Albuterol may improve exercise capacity in the subgroup of SHS tobacco-exposed persons with preserved spirometry and substantial air trapping. These findings suggest that air trapping in pre-COPD may be related to small airway disease that is not considered significant by spirometric indices of airflow obstruction.

Pre- and postnatal exposure to secondhand tobacco smoke and cardiometabolic risk at 12 years: Periods of susceptibility.

BACKGROUND: To identify periods of heightened susceptibility to the association of secondhand tobacco smoke (SHS) exposure with cardiometabolic (CM) risk at age 12 years. METHODS: We used data from 212 adolescents from the HOME Study, a prospective pregnancy and birth cohort in Cincinnati, OH. Using multiple informant models, we estimated associations of maternal serum cotinine (mean of concentrations at 16 and 26 weeks of pregnancy) and children's serum cotinine concentrations (mean of concentrations at ages 1, 2, 3, and 4 years) with a CM risk summary score constructed of five risk components measured at age 12 years. We determined if these associations differed for pre- and postnatal exposure periods, and adolescent's sex. RESULTS: We found some evidence that the cotinine-outcome associations differed by exposure period and sex. Postnatal, but not prenatal, cotinine was associated with higher CM risk scores and individual CM risk component values (interaction p-values = 0.04 to 0.35). Each 10-fold increase in postnatal cotinine was associated with 0.57 (95% CI: 0.32, 1.45), 0.09 (95% CI: 0.13, 0.31), 0.14 (-0.08, 0.35), 0.07 (95% CI: 0.34, 0.48), and 0.11 (95% CI: 0.04, 0.27) higher CM risk, HOMA-IR, TG to HDL-C ratio, leptin to adiponectin ratio, and visceral fat area. Postnatal cotinine was associated with higher visceral fat area among females but not males (sex × period × cotinine interaction p-value = 0.01). CONCLUSIONS: Serum cotinine concentrations during the postnatal period had greater influence on adolescent's CM risk compared to the prenatal period, and these associations may be sex-specific. This study reinforces the need for ongoing public health interventions to minimize children's exposure to SHS.

Time trend of exposure to secondhand tobacco smoke and polycyclic aromatic hydrocarbons between 1995 and 2019 in Germany - Showcases for successful European legislation.

Starting in 2002, regulations and legislative amendments in Germany focused on the non-smoker protection with several measures to reduce exposure to secondhand tobacco smoke (SHS). The present work aimed to evaluate the relationship between polycyclic aromatic hydrocarbons (PAHs) and SHS exposure and to determine to which extent enforced non-smoking regulations and smoking bans affected the exposure of the non-smoking population in Germany since their implementation in the early 2000s until today. For this purpose, cotinine and selected monohydroxylated PAHs (OH-PAHs) were analyzed by means of (UP)LC-MS/MS in 510 24-h-urine samples of the Environmental Specimen Bank collected over a time span of 24 years from 1995 to 2019. Median urinary cotinine levels were found to steadily and significantly decline by 82% from 1995 to 2019. A significant decrease of urinary 3-hydroxybenzo[a]pyrene (19%), 1-OH-pyrene (39%), 1-naphthol (66%), 1- (17%), 2- (25%), and 3-OH-phenanthrene (22%) was also observed throughout the same time span. The decline in urinary levels of cotinine and several OH-PAHs can most likely be attributed to smoking bans and regulations limiting SHS and PAH exposure. This study therefore emphasizes the relevance of human biomonitoring to investigate the exposure of humans to chemicals of concern, assess the effectiveness of regulatory measures, and help policies to enforce provisions to protect public health.

Early life stress, prenatal secondhand smoke exposure, and the development of internalizing symptoms across childhood.

BACKGROUND: Prior findings relating secondhand tobacco smoke (SHS) exposure and internalizing problems, characterized by heightened anxiety and depression symptoms, have been equivocal; effects of SHS on neurodevelopment may depend on the presence of other neurotoxicants. Early life stress (ELS) is a known risk factor for internalizing symptoms and is also often concurrent with SHS exposure. To date the interactive effects of ELS and SHS on children's internalizing symptoms are unknown. We hypothesize that children with higher exposure to both prenatal SHS and ELS will have the most internalizing symptoms during the preschool period and the slowest reductions in symptoms over time. METHODS: The present study leveraged a prospective, longitudinal birth cohort of 564 Black and Latinx mothers and their children, recruited between 1998 and 2006. Cotinine extracted from cord and maternal blood at birth served as a biomarker of prenatal SHS exposure. Parent-reported Child Behavior Checklist (CBCL) scores were examined at four timepoints between preschool and eleven years-old. ELS exposure was measured as a composite of six domains of maternal stress reported at child age five. Latent growth models examined associations between SHS, ELS, and their interaction term with trajectories of children's internalizing symptoms. In follow-up analyses, weighted quintile sum regression examined contributions of components of the ELS mixture to children's internalizing symptoms at each time point. RESULTS: ELS interacted with SHS exposure such that higher levels of ELS and SHS exposure were associated with more internalizing symptoms during the preschool period (ß = 0.14, p = 0.03). The interaction between ELS and SHS was also associated with a less negative rate of change in internalizing symptoms over time (ß=-0.02, p = 0.01). Weighted quintile sum regression revealed significant contributions of maternal demoralization and other components of the stress mixture to children's internalizing problems at each age point (e.g., age 11 WQS ß = 0.26, p < 0.01). CONCLUSIONS: Our results suggest that prior inconsistencies in studies of SHS on behavior may derive from unmeasured factors that also influence behavior and co-occur with exposure, specifically maternal stress during children's early life. Findings point to modifiable targets for personalized prevention.

The contribution of secondhand tobacco smoke to blood lead levels in US children and adolescents: a cross-sectional analysis of NHANES 2015-2018.

BACKGROUND: Lead is a major developmental neurotoxicant in children, and tobacco smoke has been suggested as a source of lead exposure in vulnerable populations. This study evaluates the contribution of secondhand tobacco smoke (SHS) to blood lead levels (BLLs) in children and adolescents. METHODS: We analyze data from 2,815 participants aged 6-19 years who participated in the National Health and Nutrition Examination Survey (2015-2018) to investigate the association between serum cotinine levels and BLLs. A multivariate linear regression was conducted to estimate geometric means (GMs) and the ratios of GMs after adjusting for all covariates. RESULTS: The geometric means of BLLs in study participants aged 6 - 19 years were 0.46 µg/dl (95% CI 0.44, 0.49). After adjusting for relevant participant characteristics, the geometric means of BLLs were 18% (BLL 0.48 µg/dl, 95% CI 0.45, 0.51) and 29% (BLL 0.52 µg/dl, 95% CI 0.46, 0.59) higher in participants who had intermediate serum cotinine levels (0.03 - 3 ng/mL) and those who had high serum cotinine levels (> 3 ng/mL) respectively, compared to participants who had low serum cotinine levels (BLL 0.41 µg/dl, 95% CI 0.38, 0.43). CONCLUSIONS: SHS exposure may be a source of BLLs in US children and adolescents. Efforts to reduce lead exposure in children and adolescents should include strategies to reduce SHS exposure.

Secondhand tobacco smoke and severity in wheezing children: Nasal oxidant stress and inflammation.

OBJECTIVES: Prenatal and postnatal smoke exposures are associated with many lung diseases in children due to impaired lung function, increased inflammation, and oxidative stress. We aimed to determine the influence of secondhand tobacco smoke exposure on the levels of nasal glutathione, IL-8, IL-17, MMP-9, and TIMP-1, as well as serum surfactant protein-D (SP-D) in wheezy children. METHODS: We enrolled 150 children with recurrent wheezing and recorded wheezing characteristics at enrollment. We measured the levels of serum cotinine, SP-D, nasal glutathione, IL-8, IL-17, MMP-9, and TIMP-1. Serum cotinine levels between 3 and 12 ng/mL, and above 12 ng/mL were defined as lower and higher level secondhand tobacco smoke exposure, respectively. The ANOVA test, Pearson's correlation analysis and multivariate analysis with a linear regression test were used for the statistical analysis. RESULTS: Ninety-one children had been exposed to lower level secondhand tobacco smoke, while 24 children were exposed to higher level secondhand tobacco smoke. Thirty-five children were not exposed to cigarette smoke. Wheezing symptom scores were higher in exposed children (p = 0.03). Levels of other biomarkers showed no significant difference. CONCLUSIONS: Secondhand tobacco smoke exposure is associated with more severe respiratory symptoms in wheezing children. However, levels of nasal or serum inflammatory markers fail to explain this association, either because of different mechanical factors in the process or due to low levels of the biomarkers especially in nasal secretions.

Babies Living Safe & Smokefree: randomized controlled trial of a multilevel multimodal behavioral intervention to reduce low-income children's tobacco smoke exposure.

BACKGROUND: Addressing children's tobacco smoke exposure (TSE) remains a public health priority. However, there is low uptake and ineffectiveness of treatment, particularly in low-income populations that face numerous challenges to smoking behavior change. A multilevel intervention combining system-level health messaging and advice about TSE delivered at community clinics that disseminate the Special Supplemental Nutrition Program for Women, Infants and Children (WIC), combined with nicotine replacement and intensive multimodal, individual-level behavioral intervention may improve TSE control efforts in such high-risk populations. METHODS/DESIGN: This trial uses a randomized two-group design with three measurement points: baseline, 3-month and 12-month follow-up. The primary outcome is bioverified child TSE; the secondary outcome is bioverified maternal quit status. Smoking mothers of children less than 6 years old are recruited from WIC clinics. All participants receive WIC system-level intervention based on the "Ask, Advise, Refer (AAR)" best practices guidelines for pediatrics clinics. It includes training all WIC staff about the importance of maternal tobacco control; and detailing clinics with AAR intervention prompts in routine work flow to remind WIC nutrition counselors to ask all mothers about child TSE, advise about TSE harms and benefits of protection, and refer smokers to cessation services. After receiving the system intervention, mothers are randomized to receive 3 months of additional treatment or an attention control intervention: (1) The multimodal behavioral intervention (MBI) treatment includes telephone counseling sessions about child TSE reduction and smoking cessation, provision of nicotine replacement therapy, a mobile app to support cessation efforts, and multimedia text messages about TSE and smoking cessation; (2) The attention control intervention offers equivalent contact as the MBI and includes nutrition-focused telephone counseling, mobile app, and multimedia text messages about improving nutrition. The control condition also receives a referral to the state smoking cessation quitline. DISCUSSION: This study tests an innovative community-based, multilevel and integrated multimodal approach to reducing child TSE in a vulnerable, low-income population. The approach is sustainable and has potential for wide reach because WIC can integrate the tobacco intervention prompts into routine workflow and refer smokers to free evidence-based behavioral counseling interventions, such as state quitlines. TRIAL REGISTRATION: Clinicaltrials.gov NCT02602288 . Registered 9 November 2015.

Secondhand Tobacco Smoke and COPD Risk in Smokers: A COPDGene Study Cohort Subgroup Analysis.

BACKGROUND: Exposure to secondhand tobacco smoke (SHS) can be a risk factor for chronic obstructive pulmonary disease (COPD), but its role among relatively heavy smokers with potential co-exposure to workplace vapors, gas, dust, and fumes (VGDF) has not been studied. METHODS: To estimate the contribution of SHS exposure to COPD risk, taking into account smoking effects and work-related exposures to VGDF, we quantified SHS based on survey responses for 1400 ever-employed subjects enrolled in the COPDGene study, all current or former smokers with or without COPD. Occupational exposures to VGDF were quantified based on a job exposure matrix. The associations between SHS and COPD were tested in multivariate logistic regression analyses adjusted for age, sex, VGDF exposure, and cumulative smoking. RESULTS AND DISCUSSION: Exposures to SHS at work and at home during adulthood were associated with increased COPD risk: odds ratio (OR) = 1.12 (95% confidence interval [CI]: 1.02-1.23; p = 0.01) and OR = 1.09 (95%CI: 1.00-1.18; p = 0.04) per 10 years of exposure adjusted for smoking and other covariates, respectively. In addition, subjects with employment histories likely to entail exposure to VGDF were more likely to have COPD: OR = 1.52 (95%CI: 1.16-1.98; p < 0.01) (adjusted for other covariates). While adult home SHS COPD risk was attenuated among the heaviest smokers within the cohort, workplace SHS and job VGDF risks persisted in that stratum. CONCLUSION: Among smokers all with at least 10 pack-years, adult home and work SHS exposures and occupational VGDF exposure are all associated with COPD.

Routine screening of hospital patients for secondhand tobacco smoke exposure: a feasibility study.

OBJECTIVE: Secondhand tobacco smoke (SHS) exposure causes over 40,000 deaths per year, but healthcare systems rarely address this risk factor. In September 2012, Massachusetts General Hospital initiated routine inpatient screening for SHS exposure by adding a question to the nurses' computerized admission assessment form ("Is smoking allowed in your home or car?"). We measured the implementation of this screening question over 1year. METHODS: Multivariable analysis of hospital records of adult and pediatric admissions (N=35,701) from September 1, 2012 to August 31, 2013, to assess screening question completion and identify characteristics of nonsmokers who may be exposed to SHS. RESULTS: Nurses entered "Yes" or "No" to the screening question for 91% of 34,295 adult admissions and 86% of 1406 pediatric admissions. Among nonsmokers, smoking in the home or car was allowed for 3% of adult admissions and 4% of pediatric admissions. Adults admitted for psychiatric diagnoses, children admitted for asthma, and patients with Medicaid insurance had higher odds of exposure to SHS in their home or car. CONCLUSION: Routine screening of SHS among hospitalized patients by nurses is feasible. Doing so offers hospitals an opportunity to intervene and to promote smoke-free policies in patients' homes and cars.

Occupational secondhand smoke is the main determinant of hair nicotine concentrations in bar and restaurant workers.

OBJECTIVE: To evaluate the relative contribution of occupational vs. non-occupational secondhand tobacco smoke exposure to overall hair nicotine concentrations in non-smoking bar and restaurant employees. METHOD: We recruited 76 non-smoking employees from venues that allowed smoking (n=9), had mixed policies (smoking and non-smoking areas, n=13) or were smoke-free (n=2) between April and August 2008 in Santiago, Chile. Employees used personal air nicotine samplers during working and non-working hours for a 24-h period to assess occupational vs. non-occupational secondhand tobacco smoke exposure and hair nicotine concentrations to assess overall secondhand tobacco smoke exposure. RESULTS: Median hair nicotine concentrations were 1.5 ng/mg, interquartile range (IQR) 0.7 to 5.2 ng/mg. Time weighted average personal air nicotine concentrations were higher during working hours (median 9.7, IQR 3.3-25.4 µg/m(3)) compared to non-working hours (1.7, 1.0-3.1 µg/m(3)). Hair nicotine concentration was best predicted by personal air nicotine concentration at working hours. After adjustment, a 2-fold increase in personal air nicotine concentration in working hours was associated with a 42% increase in hair nicotine concentration (95% confidence interval 14-70%). Hair nicotine concentration was not associated with personal air nicotine concentration during non-working hours (non-occupational exposure). CONCLUSIONS: Personal air nicotine concentration at working hours was the major determinant of hair nicotine concentrations in non-smoking employees from Santiago, Chile. Secondhand tobacco smoke exposure during working hours is a health hazard for hospitality employees working in venues where smoking is allowed.

The impact of secondhand smoke on failure of Helicobacter pylori therapy is not inferior to that of smoking.

BACKGROUND: Previous studies have shown the associations between smoking and failure to eradicate Helicobacter pylori (H. pylori), but less is known about the impact of secondhand tobacco smoke (SHS) on H. pylori eradication. METHODS: Between July 2022 to July 2023, 646 patients who received proton pump inhibitor (PPIs) as first-line H. pylori eradication therapy were recruited for the study. Information was obtained via the hospital database and a telephone questionnaire. Univariate and multivariate regression analysis were used to examine risk factors of H. pylori eradication failure. RESULTS: This was a single-center retrospective study consisting of 646 patients who received PPIs as first-line H. pylori eradication therapy. This included 122 smokers, 165 never-smokers with SHS, and 359 never-smokers with no SHS exposure. Compared with subjects in the "eradication success" group, those in the "eradication failure" group tended to have higher prevalence of smoke consumption and have higher prevalence of SHS exposure. In binary logistic regression analysis, smoking (OR 3.409, 95 % CI: 1.782- 6.522, P < 0.001) and SHS (OR 3.188, 95 % CI: 1.726-5.886, P < 0.001) were independent predictors of eradication failure. In addition, never-smokers with SHS exposure and smoking had similar effects on H. pylori eradication (OR, 0.893; 95 % CI, 0.464 to 1.717, P value = 0.734). CONCLUSION: Both smoking and SHS are independent risk factors for H. pylori eradication failure. Furthermore, the impact of SHS is not inferior to smoking.

Association between secondhand smoke exposure and incident heart failure: The Multi-Ethnic Study of Atherosclerosis (MESA).

AIMS: There are no studies on the association between secondhand smoke (SHS) exposure and incident heart failure (HF). This cohort study aimed to examine the associations of self-reported and urinary cotinine-assessed SHS exposure with incident HF. METHODS AND RESULTS: This study included 5548 non-active smoking participants aged 45-84 years and free of known cardiovascular diseases and HF at baseline who self-reported SHS exposure time in the Multi-Ethnic Study of Atherosclerosis (MESA) at baseline (2000-2002). A cohort subset of 3376 non-active smoking participants underwent urinary cotinine measurements. HF events were verified by medical records or death certificates and ascertained from baseline through 2019. Multivariable Cox proportional hazards regression analysis was used with adjustment for demographic variables, traditional cardiovascular risk factors, physical activity, tobacco pack-years and medications. During a median follow-up of 17.7 years, 353 and 196 HF events were identified in the self-report cohort and cohort subset, respectively. In the self-report cohort, compared with the SHS unexposed group (0 h/week), the highest tertile of the SHS exposed group (7-168 h/week) was not associated with incident HF (hazard ratio [HR] 0.70, 95% confidence interval [CI] 0.49-1.00; p = 0.052). In contrast, in the cohort subset, participants with detectable urinary cotinine >7.07 ng/ml had a higher risk of incident HF than those with undetectable urinary cotinine ≤7.07 ng/ml (HR 1.45, 95% CI 1.03-2.06; p = 0.034). There were no significant heterogeneities in HF risk by age, sex, race/ethnicity, or past smoking status. CONCLUSION: Secondhand smoke exposure reflected by modestly increased urinary cotinine (>7.07 ng/ml) rather than self-report in non-active smokers was associated with a 40-50% higher risk of any HF event.

Exposure to household secondhand tobacco smoke and the odds of developing atopic dermatitis among adolescents: A causal mediation analysis.

INTRODUCTION: Exposure to household secondhand tobacco smoke (SHS) among adolescents has been shown to be associated with atopic dermatitis, and affects disproportionality females. However, the mechanisms underlying this link are uncertain. This study sought to identify modifiable factors that mediate the relationship between household SHS exposure and atopic dermatitis among adolescents. METHODS: During October 2015, a cross-sectional study was conducted using the ISAAC questionnaire for data collection from adolescents enrolled in nine high schools of Hawalli - one of the six governorates of Kuwait. Data were collected on sociodemographic characteristics, self-reported tobacco smoking among adolescents, household SHS exposure (≥1 smokers at home vs none), self-reported asthma and atopic dermatitis. For causal mediation analysis an inverse odds-weighting approach was used. RESULTS: Of 746 participants, 74.8% were Kuwaiti, 50.1% were female, 12.4% were regular daily smokers and 54.1% had household SHS exposure, which was more common among Kuwaiti (79.6%) than non-Kuwaiti (20.4%) adolescents. The prevalences of self-reported asthma and atopic dermatitis were 20.6% and 14.9%, respectively. After adjusting for the pre-exposure covariates (i.e. sex and nativity), household SHS exposure had a significant (p=0.043) total effect, non-significant (p=0.133) natural direct effect, and marginally insignificant (p=0.058) natural indirect effect, which were jointly mediated by asthma status and adolescent's self-reported smoking status, with a proportion of mediated risk to atopic dermatitis of 29.6%. CONCLUSIONS: Asthma and self-tobacco smoking among adolescents not only directly affected but also mediated household SHS exposure effect on atopic dermatitis risk. Voluntarily adopting a smoke-free home rule may minimize household SHS exposure, reduce the odds of developing asthma, and deter the initiation of tobacco smoking among adolescents. Such an effort will likely mitigate the atopic dermatitis risk among adolescents in this and other similar settings. If implemented, future studies may contemplate evaluating the impact of such intervention.

Secondhand tobacco smoke exposure in homes and vehicles in youth: disparities among racial, and sexual and gender minorities.

Background: Secondhand smoke exposure (SHSe) among youth is a serious public health concern, leading to an increased risk of conditions such as asthma and respiratory infections. However, there is little research on SHSe among vulnerable populations, such as racial and sexual minorities. Understanding the factors associated with youth SHSe in homes and vehicles is crucial to developing better protective policies. Methods: This study utilized 2020 data from the National Youth Tobacco Survey, a representative sample of middle- and high-school students in the US. The primary outcomes were youth SHSe at home and while riding in a vehicle. Multinomial regression models were used to assess factors associated with SHSe. Results: The data included 9,912 students enrolled in grades 6 through 12 in the United States who reported never using any form of tobacco. Non-Hispanic Black students living with someone who does not use any form of tobacco products were significantly more likely to experience moderate [OR = 2.1 (1.1-3.9), p = 0.03] and severe [OR = 5.1 (2.2-11.7), p < 0.001] secondhand smoke exposure (SHSe) in homes compared to their non-Hispanic White counterparts. Heterosexual female students had lower odds of reporting moderate SHSe in the home compared to heterosexual males [OR = 0.7 (0.6-0.99), p = 0.02], whereas bisexual females had two-fold increased odds of severe SHSe in homes [OR = 2.0 (1.2-3.4), p = 0.01]. Conclusion: Significant efforts are needed to develop targeted interventions to reduce SHSe in homes and vehicles, particularly in these vulnerable populations.

Translating pediatric primary care best practice guidelines for addressing tobacco in the WIC system.

Tobacco smoke exposure (TSE) adversely affects child health. Intervention research on reducing childhood TSE and uptake of evidence-based smoking cessation programs has had limited reach in high-risk communities. Intervening in clinics delivering the Special Supplemental Nutrition Program for Women, Infants, and Children (WIC) could address overlapping public health priorities essential for healthy child development-nutrition and smoke-free environments. The Babies Living Safe and Smokefree (BLiSS) trial addresses existing gaps by implementing and evaluating a WIC in-clinic evidence-based training based on Ask, Advise, and Refer (AAR) guidelines. WIC nutrition staff (n = 67) completed surveys pre- and post-training as part of the larger BLiSS trial. Staff sociodemographic data, knowledge, and attitudes about maternal smoking and child TSE prevention, and AAR practices in clinic were collected using self-administered surveys. Pre-post outcomes were assessed using bivariate statistics and multiple regression models. Controlling for baseline AAR-related practices and other covariates, nutrition managers were more likely to engage in post-training AAR practices than nutrition assistants. Sociodemographics and smoking status were not related to post-training AAR. Lower perceived barriers and higher reported frequency of tobacco intervention practices at baseline were associated with higher engagement in post-test AAR practices. WIC-system interventions aimed at reducing child TSE and maternal tobacco smoking may be more effective if nutrition management-level staff are involved in assessment and by addressing barriers related to TSE among nutrition assistants. Findings suggest that WIC in-clinic training may help to increase self-efficacy for staff engagement in brief screening, intervention, and referral practices.

Intervention research on reducing childhood tobacco smoke exposure (TSE) and uptake of evidence-based smoking cessation programs has had limited reach in high-risk communities. Intervening in clinics delivering the Special Supplemental Nutrition Program for Women, Infants, and Children (WIC) could address overlapping public health priorities essential for healthy child development­nutrition and smoke-free environments. The Babies Living Safe and Smokefree (BLiSS) trial implemented and evaluated training on evidence-based guidelines in WIC clinics to nutrition managers and nutrition assistants. Findings suggest that WIC in-clinic training may help to increase self-efficacy for staff engagement in brief screening, intervention, and referral practices. Further, our results indicate that interventions aimed at reducing child TSE and maternal tobacco smoking may be more effective if nutrition management-level staff are involved in assessment and by addressing barriers related to TSE among nutrition assistants.

Intervening With Smoking Parents of Inpatients to Reduce Exposure: The INSPIRE Randomized Controlled Trial.

BACKGROUND: Hospitalized children have high rates of tobacco smoke exposure; parents who smoke may be receptive to interventions during their child's hospitalization. OBJECTIVE: We tested the efficacy of a smoking cessation intervention for parents of hospitalized children. METHODS: We conducted a randomized, single-blind clinical trial from 12/14-5/18 at the Children's Hospital Colorado. Hospitalized children who had a parent who smoked tobacco were eligible. INTERVENTION: Intervention participants received motivational interviewing sessions, 2 weeks of nicotine replacement therapy; both groups received referral to the Quitline Consenting parents completed a questionnaire; urine was collected from the child for measurement of cotinine. Our primary outcome was: 1) increase in reporting "no one is allowed to smoke anywhere" in the home (smoke-free home rule). Additional outcomes included: 2) change in child's cotinine from baseline to 1 year, and 3) parental quitting at 1 year. Data were analyzed using Chi-square and t tests for bivariable data, and multivariable logistic and linear regression. RESULTS: Of 1641 eligible families approached, 252 were randomized (15%); 149 families had follow-up data at 12 months (59%). In the adjusted analysis, there was no difference between the groups in smoke free home rules, or child cotinine level; in an intention-to-treat analysis, 15% in the intervention group versus 8% of controls reported quit (p=0.07). CONCLUSIONS: A smoking cessation intervention can be delivered to parents of hospitalized children. While hospitalization provides an opportunity to help parents quit smoking, more efficient and effective engagement strategies are needed to optimize tobacco control success.

Elastin Degradation and Lung Function Deterioration with Remote Secondhand Tobacco Smoke Exposure in Never-smokers.

Background: Prolonged past exposure to secondhand tobacco smoke (SHS) in never-smokers is associated with abnormal lung function and reduced diffusing capacity suggestive of an associated lung tissue injury and damage. The mechanisms by which past SHS exposure may contribute to lung tissue damage are unknown. Elastin is a major constituent of extracellular matrix in lung parenchyma. Objective: To determine whether past exposure to SHS is associated with ongoing lung tissue damage as indicated by elevated elastin degradation products that are linked to lung function. Methods: We measured the plasma levels of elastin degradation markers (EDM) from 193 never-smoking flight attendants with a history of remote SHS exposure in aircraft cabins and 103 nonsmoking flight attendants or sea-level control participants without such history of cabin SHS exposure and examined those levels versus their lung function with adjustment for covariates. The cabin SHS exposure was estimated based on airline employment history and years of the smoking ban enactment. Results: The median [interquartile range] plasma EDM level for all participants was 0.30 [0.24-0.36] ng/mL with a total range of 0.16-0.65 ng/mL. Plasma EDM levels were elevated in those with a history of exposure to cabin SHS compared to those not exposed (0.33±0.08 versus 0.26±0.06 ng/mL; age- and sex-adjusted P<0.001). In those with a history of cabin SHS exposure, higher EDM levels were associated with a lower diffusing capacity (parameter estimate [PE] 95% [confidence interval(CI)]=4.2 [0.4-8.0] %predicted decrease per 0.1 ng/mL increase in EDM; P=0.030). Furthermore, EDM levels were inversely associated with forced expiratory volume in 1 second (FEV1), FEV1 to forced vital capacity (FVC) ratio , and forced expiratory flow rate between 25% and 75% ( FEF25%-75%) (PE [95%CI]=5.8 [2.1-9.4], 4.0 [2.2-5.7], and 12.5 [5.8-19.2] %predicted decrease per 0.1 ng/mL increase in EDM, respectively; P<0.001). Plasma EDM mediated a substantial fraction of the association of SHS with FEV1, FVC, and FEF25%-75% (P<0.05). Conclusions: Long after past exposure to SHS, there is ongoing elastin degradation beyond what is expected from the aging process, which likely contributes to lower lung function and a reduced pulmonary capillary bed as seen in chronic obstructive pulmonary disease (COPD).

Comparison of lung cancer aggressiveness in patients who never smoked compared to those who smoked.

OBJECTIVES: To determine whether radiographic measures of tumor aggressiveness differ by smoking status. MATERIALS AND METHODS: All patients diagnosed with non-small-cell lung cancer(NSCLC) ≤ 30 mm in maximum diameter, without clinical evidence of metastasis who had both pre-treatment PET scans and two CT scans at least 90 days apart in a prospective cohort, the Initiative for Early Lung Cancer Research on Treatment(IELCART) at Mount Sinai between 2016 and 2020 were identified. Comparison of two measures of tumor aggressiveness, positron emission tomography(PET) SUVmax and tumor volume doubling time(VDT) by smoking status was performed. RESULTS: Of 417 patients identified, 158 patients had pre-treatment PET scans and at least two CT scans available. The two measures of tumor aggressiveness, SUVmax and VDT values were significantly different between patients who had never smoked and those who smoked: patients who never smoked had lower median SUVmax[2.5(IQR: 1.1-4.8) vs. 4.2(IQR:2.1-9.2),p = 0.002] and longer median VDT[(372.6 days vs. 225.6 days,p = 0.001)] compared to those who smoked. Using multivariable analyses, when adjusting for age and sex alone, SUVmax(p = 0.004) and VDT(p = 0.0001) remained significantly different by smoking status. The final multivariable analysis, adjusted for all three co-variates(sex, age and tumor histology) showed no significant difference in SUVmax and VDT by smoking status [SUVmax(p = 0.25) and VDT(p = 0.06)]. CONCLUSION: Smoking history does not influence VDT or PET SUVmax measures of lung cancer aggressiveness.

Actigraphy informs distinct patient-centered outcomes in Pre-COPD.

BACKGROUND: Actigraphy can provide useful patient-centered outcomes for quantification of physical activity in the "real-world" setting. METHODS: To characterize the relationship of actigraphy outputs with "in-laboratory" measures of cardiopulmonary function and respiratory symptoms in pre-COPD, we obtained actigraphy data for 8 h/day for 5 consecutive days a week before in-laboratory administration of respiratory questionnaires, PFT, and CPET to a subgroup of subjects participating in the larger study of the health effects of exposure to secondhand tobacco smoke who had air trapping but no spirometric obstruction (pre-COPD). Using machine learning approaches, we identified the most relevant actigraphy predictors and examined their associations with symptoms, lung function, and exercise outcomes. RESULTS: Sixty-one subjects (age = 66±7 years; BMI = 24±3 kg/m2; FEV1/FVC = 0.75 ± 0.05; FEV1 = 103 ± 17 %predicted) completed the nested study. In the hierarchical cluster analysis, the activity, distance, and energy domains of actigraphy, including moderate to vigorous physical activity, were closely correlated with each other, but were only loosely associated with spirometric and peak exercise measures of oxygen consumption, ventilation, oxygen-pulse, and anaerobic threshold (VO2AT), and were divergent from symptom measures. Conversely, the sedentary domain clustered with respiratory symptoms, air trapping, airflow indices, and ventilatory efficiency. In Regression modeling, sedentary domain was inversely associated with baseline lung volumes and tidal breathing at peak exercise, while the activity domains were associated with VO2AT. Respiratory symptoms and PFT data were not associated with actigraphy outcomes. DISCUSSION: Outpatient actigraphy can provide information for "real-world" patient-centered outcomes that are not captured by standardized respiratory questionnaires, lung function, or exercise testing. Actigraphy activity and sedentary domains inform of distinct outcomes.