Childhood Environmental Tobacco Smoke Research Articles

Metal mixture exposures and serum lipid levels in childhood: the Rhea mother-child cohort in Greece.

Growing evidence suggests that cardiovascular disease develops over the lifetime, often beginning in childhood. Metal exposures have been associated with cardiovascular disease and important risk factors, including dyslipidemia, but prior studies have largely focused on adult populations and single metal exposures. To investigate the individual and joint impacts of multiple metal exposures on lipid levels during childhood. This cross-sectional study included 291 4-year-old children from the Rhea Cohort Study in Heraklion, Greece. Seven metals (manganese, cobalt, selenium, molybdenum, cadmium, mercury, and lead) were measured in whole blood using inductively coupled plasma mass spectrometry. Serum lipid levels included total cholesterol, triglycerides, high-density lipoprotein (HDL) cholesterol, and low-density lipoprotein (LDL) cholesterol. To determine the joint and individual impacts of child metal exposures (log2-transformed) on lipid levels, Bayesian kernel machine regression (BKMR) was employed as the primary multi-pollutant approach. Potential effect modification by child sex and childhood environmental tobacco smoke exposure was also evaluated. BKMR identified a positive association between the metal mixture and both total and LDL cholesterol. Of the seven metals examined, selenium (median 90.6 [IQR = 83.6, 96.5] µg/L) was assigned the highest posterior inclusion probability for both total and LDL cholesterol. A difference in LDL cholesterol of 8.22 mg/dL (95% CI = 1.85, 14.59) was observed when blood selenium was set to its 75th versus 25th percentile, holding all other metals at their median values. In stratified analyses, the positive association between selenium and LDL cholesterol was only observed among boys or among children exposed to environmental tobacco smoke during childhood. Growing evidence indicates that cardiovascular events in adulthood are the consequence of the lifelong atherosclerotic process that begins in childhood. Therefore, public health interventions targeting childhood cardiovascular risk factors may have a particularly profound impact on reducing the burden of cardiovascular disease. Although growing evidence supports that both essential and nonessential metals contribute to cardiovascular disease and risk factors, such as dyslipidemia, prior studies have mainly focused on single metal exposures in adult populations. To address this research gap, the current study investigated the joint impacts of multiple metal exposures on lipid concentrations in early childhood.

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 115,663 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 age 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, n=112; MoBa, n=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 to 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.

Involuntary tobacco smoke exposures from conception to 18 years increase midlife cardiometabolic disease risk: a 40-year longitudinal study.

Few population studies have sufficient follow-up period to examine early-life exposures with later life diseases. A critical question is whether involuntary exposure to tobacco smoke from conception to adulthood increases the risk of cardiometabolic diseases (CMD) in midlife. In the Collaborative Perinatal Project, serum-validated maternal smoking during pregnancy (MSP) was assessed in the 1960s. At a mean age of 39 years, 1623 offspring were followed-up for the age at first physician-diagnoses of any CMDs, including diabetes, heart disease, hypertension, or hyperlipidemia. Detailed information on their exposure to environmental tobacco smoke (ETS) in childhood and adolescence was collected with a validated questionnaire. Cox regression was used to examine associations of in utero exposure to MSP and exposure to ETS from birth to 18 years with lifetime incidence of CMD, adjusting for potential confounders. We calculated midlife cumulative incidences of hyperlipidemia (25.2%), hypertension (14.9%), diabetes (3.9%), and heart disease (1.5%). Lifetime risk of hypertension increased by the 2nd -trimester exposure to MSP (adjusted hazard ratio: 1.29, 95% confidence interval: 1.01-1.65), ETS in childhood (1.11, 0.99-1.23) and adolescence (1.22, 1.04-1.44). Lifetime risk of diabetes increased by joint exposures to MSP and ETS in childhood (1.23, 1.01-1.50) or adolescence (1.47, 1.02-2.10). These associations were stronger in males than females, in never-daily smokers than lifetime ever smokers. In conclusion, early-life involuntary exposure to tobacco smoke increases midlife risk of hypertension and diabetes in midlife.

Passive Smoking And The Health Of Children: A Primary Concern In Pakistan.

Dear Madam, Environmental tobacco smoke (ETS), also referred to as second-hand, involuntary, or passive smoke, is produced from the combustion of tobacco products or puffed out by active smokers. The smoke emitted from the tip of a cigarette contains about two times the concentration of nicotine, five times the concentration of Carbon monoxide, and 50 times the concentration of ammonia than active smoke1. Furthermore, amongst the exposed population, children are far more susceptible to complications associated with ETS due to their manner of exposure and developmental physiology. According to the 2014 Global Adult Tobacco Survey for Pakistan, 43.3% of households were exposed to ETS, with a significant amount of children included in that percentage2. Thus, children's health is more detrimentally impacted by ETS than adults. Exposure of children to ETS in domestic and public settings risks a higher occurrence of respiratory and middle-ear diseases. According to numerous studies, dose-dependent exposure to ETS directs more frequent and severe asthma attacks accompanied by wheezing. Moreover, it is observed that school-aged individuals who live in a smoking household tend to develop a range of lung diseases, including bronchitis, bronchiolitis, and pneumonia. Their lungs become weak, resulting in impaired pulmonary function3. With reference to a population-based cohort study conducted by Lovasi et al. (ref 4), it was evident that childhood ETS exposure from 2 or more smokers compared with none is linked with early emphysema in adulthood4. In addition, constant ETS exposure leads to swelling and obstruction of the eustachian tube, which interferes with pressure equalization leading to pain, fluid accumulation, and infection. Ear infections and middle ear fluid are the most common causes of hearing loss in children. Being the primary reason behind several disease, ETS is also known to cause acute effects on cardiovascular function in children. Compelling evidence demonstrates that childhood ETS exposure risks the accumulation of factors associated with cardiovascular diseases, including obesity, dyslipidemia, and imbalanced systolic and diastolic blood pressure5. [Exposure to hazardous chemicals found in ETS, for instance, benzopyrene, is known to accelerate the development of atherosclerosis]. Moreover, studies show convincing evidence that hypertension is common in children exposed to ETS at home. It is also observed that hypertension is a common risk factor for cardiovascular disease and cardiovascular stress hyperactivity in children with smoking parents. ---Continue

Lung function and cognitive ability in children: a UK birth cohort study

BackgroundDecreased adult lung function is associated with subsequent impairment in cognition. A similar relationship in early life could be of great policy importance, since childhood cognitive ability determines key adult...

Cigarette Smoking and Asthma

Cigarette smoking is a well-know health hazard, probably not least for patients suffering from asthma. This review gives a short overview concerning the effects of passive and active smoking on the inception and outcome with regard to longitudinal changes in lung function and mortality for patients with asthma. Substantial evidence suggests that smoking affects asthma adversely. Exposure to environmental tobacco smoke in children, especially maternal smoking, may be a significant risk factor for asthma. Environmental tobacco exposure in patients with established asthma is not only associated with more severe symptoms, but also with lower quality of life, reduced lung function, and increased health care utilisation for asthma, including hospital admissions. Active smoking appears not to be a significant risk factor for asthma, but it is associated with worse outcome with regard to both longitudinal changes in lung function and asthma-related mortality. Based on the current knowledge, it therefore seems of utmost importance to encourage patients with asthma not to smoke. In line with this, patients with asthma should be given full support in their right to a smoke-free environment.

Use of urinary cotinine and cotinine/creatinine ratio as a biomarker of environmental tobacco exposure

Purpose: Exposure to Environmental Tobacco Smoke (ETS) remains a worldwide public health problem. The purpose of this study was to investigate the relationship between parents' smoking habits at home and children's exposure to environmental tobacco smoke by measuring urinary cotinine levels and urine cotinine/creatinine ratios in children.
 Materials and Methods: This case-control typed analytical study was conducted with 357 children in the 0-18 age group. The case group consisted of 180 children exposed to environmental cigarette smoke. As the control group, it consisted of 177 healthy children and non-smoking in their family. The levels of cotinine and creatinine in spot urinary were analyzed in both groups.
 Results: The urinary cotinine level of the children was found to be statistically higher in those whose parents were smokers, female gender, fathers with a low educational level, and those with 3 or fewer rooms in the house. The urinary cotinine/creatinine ratio of the children was found to be statistically higher in those whose parents were smokers (15.91 pg/mg (1.54-147.54) vs 7.90 pg/mg (1.29-68.52)), female gender (13.19 pg/mg (1.79-115.07) vs 10.45 pg/mg (1.29-147.54)). Urinary cotinine levels in the ETS exposed group were affected 1042 times more than in the ETS unexposed group [OR:1042,462, 95% CI (139.821.839-7772.246)]. 
 Conclusion: In the present study, urinary cotinine levels were found to be higher in children exposed to tobacco smoke than in children not exposed to tobacco smoke. In the light of these results, urinary cotinine can be used as a biomarker to evaluate exposure to ETS in children. Educating parents is essential to raising their awareness of exposure to ETS and teaching the right behaviors to protect children's health, especially in the home environment.

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.

The Association between the Occurrence of Asthma and Antecedents of Exposure to Environmental Tobacco Smoke in the Previous Year in Children: An Incidence-Density Study.

In previous studies, the strength of the association between childhood asthma and environmental tobacco smoke (ETS) differed depending on the way ETS was assessed and the type of study conducted. We investigated the relationship between asthma occurrence in children and recent exposure to ETS based on an incidence-density study driven by the explicit formulation of a theoretical design. Additionally, we assessed whether the relationship is modified by perinatal ETS exposure and parental inhalation atopy. The event was conceptualized as ‘first doctor’s diagnosis of asthma’. Population time was probed by sampling population moments. Exposure to ETS was conceptualized as recent exposure (1 year prior to diagnosis or at sampling) and perinatal exposure (in utero and/or during the first year of life). Thirty-nine events and 117 population moments were included. There was no indication for effect modification by perinatal exposure to ETS or parental inhalation atopy. After adjustment for confounding, an association was observed between occurrence of a first asthma diagnosis and recent ETS exposure: incidence-density ratio 4.94 (95% confidence interval 1.21, 20.13). Asthma occurrence in children is associated with recent exposure to ETS, and this association seems not to be modified by perinatal ETS exposure or parental inhalation atopy.

Parental Knowledge, Attitude, and Practice on Tobacco Use, Smoking Cessation, and Children's Environmental Tobacco Smoke Exposure.

Background: Environmental tobacco smoke (ETS) exposure in children ranks one of the major public health problems in our time. Poor parental knowledge, attitude, and practice (KAP) on ETS often contribute to worse exposure of the kids. Thus, we aimed to document parental KAP regarding tobacco use, smoking cessation and children's ETS exposure, and to analyse how knowledge and attitude relate to practice.Methods: Self-administered KAP questionnaires were distributed to smoking parents recruited from the pediatric unit at the Prince of Wales Hospital, which provides pediatric service to a population of 1.2 million in Hong Kong. The 60-item questionnaire had a range of 0–38 for knowledge, 0–44 for attitude, and 0–40 for practice. Descriptive analyses were performed for KAP response, regression analyses were performed for the exploration of associations and identification of predictive indicators.Results: 145 smoking parents (mean age: 38.0 ± 6.7 yrs.; male: 85.5%) were included. Less than half (39.3%) of them reported a smoke-free policy at home. Among those parents who had private cars, less than half (45.2%) of them had smoke-free policy in their car that they never smoked in the car. Only 25.5% of the participants correctly answered ≥70% of the knowledge questions, and 11.8 % of the participants gave favorable responses to ≥70% of the attitude questions. The total knowledge and the total attitudes score were positively associated (r = 0.49, 95% CI: 0.35–0.79, p < 0.001), yet they were only modestly correlated with parental practice on children's ETS exposure. By multivariate regressions, potential predictive factors for more favorable parental KAP included higher household income, lower parental nicotine dependence level and breastfeeding practice.Conclusions: Parental KAP related to tobacco use and children's ETS exposure needs improvement to address the significant gap between recommended and actual practice. The weak association between knowledge and practice suggested that parental education alone is not adequate to combat ETS exposure in children.

Impact of early life exposures on COPD in adulthood: A systematic review and meta-analysis.

Early life represents a critical period for the development and growth of the lungs. Adverse exposures in this stage may drive the development of chronic obstructive pulmonary disease (COPD). Thus, we quantitatively evaluated the impact of different early life exposures on COPD in adulthood. The PubMed, Embase and Cochrane Library electronic databases were searched for articles published from January 2001 to October 2020. A total of 30 studies (795,935 participants) met the criteria and were included in the review. We found a significant association of COPD with childhood serious respiratory infections, pneumonia or bronchitis (pooled adjusted OR [aOR], 2.23 [95% CI, 1.63-3.07]). The probability of COPD was increased 3.45-fold for children with than without asthma (pooled aOR, 3.45 [95% CI, 2.37-5.02]). In addition, the probability of COPD was associated with maternal smoking (pooled aOR, 1.42 [95% CI, 1.17-1.72]), any child maltreatment (pooled aOR, 1.30 [95% CI, 1.18-1.42]) and low birth weight (pooled aOR, 1.58 [95% CI, 1.08-2.32]) but not childhood environmental tobacco smoke exposure (pooled aOR, 1.15 [0.83-1.61]) or premature birth (pooled aOR, 1.17 [95% CI, 0.87-1.58]). Furthermore, subgroup analyses revealed that probability was increased for only women with childhood physical abuse, sexual abuse and exposure to intimate partner violence. Factors resulting in COPD in adults could trace back to early life. Childhood respiratory disease, maltreatment, maternal smoking and low birth weight increase the risk of COPD. Promising advances in prevention strategies for early life exposures could markedly decrease the risk of COPD.

Smoking habit in parents and exposure to environmental tobacco smoke in elementary school children of Milan

IntroductionChildren with smoking parents are potentially exposed to Environmental Tobacco Smoke (ETS). The aims of this study were: 1) to assess ETS exposure in Milan schoolchildren, by measuring urinary cotinine (COT-U), 2) to compare the parents' perception of children ETS exposure, with the actual ETS exposure measured by COT-U, 3) to explore the factors influencing COT-U, including smoking bans at home, the season, and children characteristics. MethodsOne-hundred school children (7–11 years) and their parents were recruited for the study in Spring 2018 (n = 81) and in Winter 2019 (n = 94), 75 children participated to both campaigns, for a sum of 175 observations. A questionnaire was submitted to parents to collect information about smoking habits in the house. COT-U was measured by LC-MS/MS in spot urine sample collected in the morning from children. ResultsDetectable COT-U levels were found in 42% and 57% of children, in spring and winter, in contrast with 17% and 13% of parents acknowledging ETS exposure. Children living with smokers or e-cigarette users (vapers) (30% of the participants) had higher COT-U levels than children not living with smokers or vapers (median 0.67, 0.46, and <0.1 μg/L in spring, and 0.98, 0.85, and 0.11 μg/L in winter, respectively). Increasingly higher COT-U levels were observed in children living in homes where smoking was completely banned, allowed in the external parts of the home, or allowed in some rooms. The multiple regression analysis confirmed the positive significant effect of living with smokers, a partial smoking ban and absence of smoking ban at home, the winter season, and BMI as determinants of COT-U. ConclusionETS exposure resulted in measurable urinary cotinine in children. Smoking parents underestimate exposure to ETS of their children. Living with smokers is a determinant of COT-U, only slightly mitigated by adopting partial smoking ban.

Abstract P201: Early Life Exposure To Environmental Tobacco Smoke And Cardiometabolic Diseases In Middle Age: A 4-decade Follow-up Study Of The Collaborative Perinatal Project

Introduction: Environmental tobacco smoke (ETS) is a major source of indoor air pollution and has been associated with cardiovascular diseases (CVD) risks. There is little research on the associations of ETS exposure in early life with CVD risks in later life. Hypothesis: We hypothesized that ETS exposures in the uterus, childhood, and teenage increase midlife CVD risks. Methods: For 1,623 offspring born in 1959-1966 at two sites from the Collaborative Perinatal Project, we defined intrauterine ETS exposure in each trimester if the mother smoked (1-19 or ≥20 cigs/day). ETS exposure in each year from birth to 18 years was quantified by total daily-average hours of parents smoking weighted by daily packs from a questionnaire at the adult follow-up (mean age: 39 years). Ever diagnoses of diabetes (cumulative incidence: 3.0%), heart diseases (1.5%), hypertension (17.3%), and high cholesterol (25.3%) until adult follow-up were reported. Cardiometabolic diseases (CMD, cumulative incidence: 35.4%) were defined as any diagnosis. We estimated odds ratio (OR) for CMD by ETS exposures in each trimester adjusting for prenatal factors (maternal SES, pre-pregnancy BMI, parity, newborn sex); additionally adjusted for maternal smoking in pregnancy, birth weight, and gestational age for ETS exposure from birth to 18 years. We also stratified the analyses by adult smoking status. Results: Exposure to ≥20 cigs/day in the 1 st (OR: 1.52, 95% CI: 1.02-2.26) and 2 nd (OR: 1.50, 95% CI: 1.01-2.24) trimester was significantly associated with hypertension compared to none exposure, and the associations were stronger in adult offspring who were smokers. Among the 70% of participants who reported childhood ETS exposure, the average exposure was 8.5 smoker-hours/day and 10.5 smoker-hour*packs/day (HP/Day), with a declining trend from birth to 18 years. ETS exposure (per SD increment) in early life from birth to 18 years, separately or cumulatively (OR=1.24, 95% CI: 1.07-1.43), was associated with higher odds of adult hypertension. ETS exposure in teenage (11-18 years, OR=1.26, 95% CI: 1.05-1.50), but not in childhood (birth to 10 years, OR=1.18, 95% CI: 0.96-1.45), was associated with higher odds of a combination of adult heart disease and diabetes, which was more striking in adult non-smokers than smokers. Odds of adult CMD increased by 13% (95% CI: 1%-28%) for each SD (about 10 HP/Day) increment in ETS in the whole childhood and by 16% (95% CI: 3%-30%) in teenage. The results for smoker-hours/day were similar to those for smoker-hour*packs/day. Conclusions: Intrauterine exposure to maternal smoking and ETS exposures (time and total amount) from birth to 18 years increase the risk of adult hypertension. ETS exposure in early life may also increase the risk of adult cardiometabolic diseases. Teenage may be a sensitive window for elevated risk of adult heart diseases and diabetes associated with ETS exposure.

Early life multiple exposures and child cognitive function: A multi-centric birth cohort study in six European countries

Epidemiological studies mostly focus on single environmental exposures. This study aims to systematically assess associations between a wide range of prenatal and childhood environmental exposures and cognition. The study sample included data of 1298 mother-child pairs, children were 6–11 years-old, from six European birth cohorts. We measured 87 exposures during pregnancy and 122 cross-sectionally during childhood, including air pollution, built environment, meteorology, natural spaces, traffic, noise, chemicals and life styles. The measured cognitive domains were fluid intelligence (Raven's Coloured Progressive Matrices test, CPM), attention (Attention Network Test, ANT) and working memory (N-Back task). We used two statistical approaches to assess associations between exposure and child cognition: the exposome-wide association study (ExWAS) considering each exposure independently, and the deletion-substitution-addition algorithm (DSA) considering all exposures simultaneously to build a final multiexposure model. Based on this multiexposure model that included the exposure variables selected by ExWAS and DSA models, child organic food intake was associated with higher fluid intelligence (CPM) scores (beta = 1.18; 95% CI = 0.50, 1.87) and higher working memory (N-Back) scores (0.23; 0.05, 0.41), and child fast food intake (−1.25; −2.10, −0.40), house crowding (−0.39; −0.62, −0.16), and child environmental tobacco smoke (ETS) (−0.89; −1.42, −0.35), were all associated with lower CPM scores. Indoor PM2.5 exposure was associated with lower N-Back scores (−0.09; −0.16, −0.02). Additional associations in the unexpected direction were found: Higher prenatal mercury levels, maternal alcohol consumption and child higher perfluorooctane sulfonic acid (PFOS) levels were associated with better cognitive performance; and higher green exposure during pregnancy with lower cognitive performance. This first comprehensive and systematic study of many prenatal and childhood environmental risk factors suggests that unfavourable child nutrition, family crowdedness and child indoor air pollution and ETS exposures adversely and cross-sectionally associate with cognitive function. Unexpected associations were also observed and maybe due to confounding and reverse causality.

The Intersection Between Adverse Childhood Experiences and Environmental Tobacco Smoke in U.S. Households With Children.

Environmental tobacco smoke (ETS) is a potent risk factor for secondhand smoke (SHS) exposure. Research reveals, moreover, that children who are exposed to SHS are at an increased risk of disease and premature mortality. Limited research, however, has examined whether households with children experiencing accumulating adverse childhood experiences (ACEs) are also more likely to be characterized by ETS-particularly in the form of family members smoking inside the housing unit. The current study employs a nationally representative sample of 102 341 households with children from the three most recent cohorts of National Survey of Children's Health. Both multinomial logistic regression and a strategic comparison approach are used to examine the association between ACEs and ETS categories. A large majority of households characterized by ETS report one or more ACEs, while households without ETS are largely void of ACEs. Findings indicate that this association is not merely a function of general family member smoking, as ACEs are strongly and uniquely associated with family smoking inside the housing unit-above and beyond family members smoking more generally. Households exhibiting an accumulation of ACEs may benefit from interventions providing resources and education supporting smoke-free home environments. Such families may also be screened and referred through existing family and parenting programs administered in the home environment (eg, home visiting). Public health initiatives designed to mitigate child adversities from early life stages may help reduce ETS in housing units-thereby diminishing the risk of secondhand smoke (SHS) exposure among children.

Systematic Review of Behaviour Change Techniques within Interventions to Reduce Environmental Tobacco Smoke Exposure for Children.

Children are particularly vulnerable to environmental tobacco smoke (ETS). There is no routine support to reduce ETS in the home. We systematically reviewed trials to reduce ETS in children in order to identify intervention characteristics and behaviour change techniques (BCTs) to inform future interventions. We searched Medline, EMBASE, CINAHL, PsycINFO, ERIC, Cochrane Central Register of Controlled Trials, and Cochrane Tobacco Addiction Group Specialised Register from January 2017 to June 2020 to update an existing systematic review. We included controlled trials to reduce parent/caregiver smoking or ETS in children <12 years that demonstrated a statistically significant benefit, in comparison to less intensive interventions or usual care. We extracted trial characteristics; and BCTs using Behaviour Change Technique Taxonomy v1. We defined “promising” BCTs as those present in at least 25% of effective interventions. Data synthesis was narrative. We included 16 trials, of which eight were at low risk of bias. All trials used counselling in combination with self-help or other supporting materials. We identified 13 “promising” BCTs centred on education, setting goals and planning, or support to reach goals. Interventions to reduce ETS in children should incorporate effective BCTs and consider counselling and self-help as mechanisms of delivery.

Gene-Environment Interaction between the IL1RN Variants and Childhood Environmental Tobacco Smoke Exposure in Asthma Risk.

(1) Background: Variants of the interleukin-1 receptor antagonist (IL1RN) gene, encoding an anti-inflammatory cytokine, are associated with asthma. Asthma is a chronic inflammatory disease of the airway influenced by interactions between genetic variants and environmental factors. We discovered a gene–environment interaction (GEI) of IL1RN polymorphisms with childhood environmental tobacco smoke (ETS) exposure on asthma susceptibility in an urban adult population. (2) Methods: DNA samples from the NYU/Bellevue Asthma Registry were genotyped for tag SNPs in IL1RN in asthma cases and unrelated healthy controls. Logistic regressions were used to study the GEI between IL1RN variants and childhood ETS exposures on asthma and early onset asthma, respectively, adjusting for population admixture and other covariates. (3) Results: Whereas the rare genotypes of IL1RN SNPs (e.g., GG in SNP rs2234678) were associated with decreased risk for asthma among those without ETS exposure (odds ratio OR = 0.215, p = 0.021), they are associated with increased risk for early onset asthma among those with childhood ETS (OR = 4.467, p = 0.021). (4) Conclusions: We identified a GEI between polymorphisms of IL1RN and childhood ETS exposure in asthma. Analysis of GEI indicated that childhood ETS exposure disrupted the protective effect of some haplotypes/genotypes of IL1RN for asthma and turned them into high-risk polymorphisms for early onset asthma.

Early Life Multiple Exposures and Child Cognitive Function: A Multi-Centric Birth Cohort Study in Six European Countries

Background: Epidemiological studies on environmental risk factors for cognitive outcomes mostly focus on single environmental exposures or exposure families. The present study aims to systematically assess associations between a wide range of prenatal and childhood environmental exposures and cognitive functioning. Methods:The study sample included 1,298 children, aged 6-11 years, from six European birth cohorts. We measured 87 exposures during pregnancy and 122 cross-sectionally during childhood, including air pollution, built environment, meteorology, natural spaces, traffic, noise, chemicals and life styles. The measured cognitive domains were fluid intelligence (Raven's Coloured Progressive Matrices test, CPM), attention function (Attention Network Test, ANT) and working memory (N-Back task). We used two statistical approaches to assess associations between exposure and child cognition: the exposome-wide association study (ExWAS) considering each exposure independently, and the deletion-substitution-addition algorithm (DSA) considering all exposures simultaneously to build a final multiexposure model. Findings: Based on multiexposure model, child organic food intake was associated with higher fluid intelligence (CPM) scores (beta=1.18; 95% CI=0.50, 1.87) and higher working memory (N-Back) scores (0.23; 0.05, 0.41), and child fast food intake (-1.25; -2.10, -0.40), house crowding (-0.39; -0.62, -0.16), and child environmental tobacco smoke (ETS) (-0.89; -1.42, -0.35), were all associated with lower CPM scores. Indoor PM 2.5 exposure was associated with lower N-Back scores (-0.09; -0.16, -0.02). Additional associations in the unexpected direction were also found. Namely, higher prenatal mercury levels, maternal alcohol consumption and child higher perfluorooctane sulfonic acid (PFOS) levels were associated with better cognitive performance and higher green exposure during pregnancy with lower cognitive performance. Interpretation:This first comprehensive and systematic study of many prenatal and childhood environmental risk factors suggests that unfavourable child nutrition, family crowdedness and child indoor air pollution and ETS exposures adversely affect cognitive function. Unexpected associations were also observed and maybe due to confounding and reverse causality. Funding:European Community’s Seventh Framework Programme (FP7/2007-206) under grant agreement no 308333 – the HELIX project. Declaration of Interests: The authors have no conflicts of interest to declare. Ethics Approval Statement: The ethics committee for each cohort approved the consent form. We obtained written informed consent for all participants, signed by the parent.

Environmental Tobacco Smoke Exposure in Relation to Family Characteristics, Stressors and Chemical Co-Exposures in California Girls.

Childhood environmental tobacco smoke (ETS) exposure is a risk factor for adverse health outcomes and may disproportionately burden lower socioeconomic status groups, exacerbating health disparities. We explored associations of demographic factors, stressful life events, and chemical co-exposures, with cotinine levels, among girls in the CYGNET Study. Data were collected from families of girls aged 6–8 years old in Northern California, through clinic exams, questionnaires and biospecimens (n = 421). Linear regression and factor analysis were conducted to explore predictors of urinary cotinine and co-exposure body burdens, respectively. In unadjusted models, geometric mean cotinine concentrations were higher among Black (0.59 ug/g creatinine) than non-Hispanic white (0.27), Asian (0.32), or Hispanic (0.34) participants. Following adjustment, living in a rented home, lower primary caregiver education, and lack of two biologic parents in the home were associated with higher cotinine concentrations. Girls who experienced parental separation or unemployment in the family had higher unadjusted cotinine concentrations. Higher cotinine was also associated with higher polybrominated diphenyl ether and metals concentrations. Our findings have environmental justice implications as Black and socio-economically disadvantaged young girls experienced higher ETS exposure, also associated with higher exposure to other chemicals. Efforts to reduce ETS and co-exposures should account for other disparity-related factors.

Smoking habit in parents and exposure to environmental tobacco smoke in elementary school children of Milan

Abstract Introduction Children with smoking parents are potentially exposed to Environmental Tobacco Smoke (ETS). The aims of this study were: 1) to assess ETS exposure in Milan schoolchildren, by measuring urinary cotinine (COT-U), 2) to compare the parents' perception of children ETS exposure, with the actual ETS exposure measured by COT-U, 3) to explore the factors influencing COT-U, including smoking bans at home, the season, and children characteristics. Methods One-hundred school children (7–11 years) and their parents were recruited for the study in Spring 2018 (n = 81) and in Winter 2019 (n = 94), 75 children participated to both campaigns, for a sum of 175 observations. A questionnaire was submitted to parents to collect information about smoking habits in the house. COT-U was measured by LC-MS/MS in spot urine sample collected in the morning from children. Results Detectable COT-U levels were found in 42% and 57% of children, in spring and winter, in contrast with 17% and 13% of parents acknowledging ETS exposure. Children living with smokers or e-cigarette users (vapers) (30% of the participants) had higher COT-U levels than children not living with smokers or vapers (median 0.67, 0.46, and Conclusion ETS exposure resulted in measurable urinary cotinine in children. Smoking parents underestimate exposure to ETS of their children. Living with smokers is a determinant of COT-U, only slightly mitigated by adopting partial smoking ban.