Environmental Tobacco Smoke Exposure Research Articles

Impact of Comprehensive Smoking Bans on the Health of Infants and Children

As evidence of the negative effects of environmental tobacco smoke (ETS) has mounted, an increasingly popular public policy response has been to impose restrictions on smoking through 100% smoke-free bans (comprehensive smoking bans). Yet sparse information exists regarding the impact these smoking bans at the state and local levels have on the health of children and infants. A rationale for expansion of smoke-free laws implicitly presumes that potential public health gains from reducing adult cigarette consumption and declines in adult ETS exposure extend to children. However, if smokers compensate by shifting their consumption of cigarettes from public venues that impose a comprehensive smoking ban to smoking at home, then these policies may have a harmful effect on children and infants. This study provides estimates of how comprehensive smoking bans impact the venue of smoking, and the health of children and infants. Using models that exploit state- and county-level changes to smoking ban legislation over time, estimates suggest that smoking bans have improved the health of both infants and children, mainly through implementation of more comprehensive bans. Further, we find no evidence of displacement among smokers (both smokers with and without children in the household), and actually find that the bans had a positive spillover effect in terms of reducing smoking inside the home – an effect which may further explain the improvement in infant and children’s health. Our effect magnitudes imply that expanding comprehensive coverage from 60% (current level) to 100% of the population can prevent between approximately 1,110 – 1,750 low birthweight births among low-educated mothers, resulting in economic cost savings of about $71 – $111 million annually. Health improvements among older children add to these economic benefits.

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.

Early life exposure to coal mine fire and tobacco smoke affect subclinical vascular function

ObjectiveTo evaluate whether vascular health in young children was associated with exposure to a 6-week episode of coal mine fire smoke or environmental tobacco smoke (ETS) in a retrospective cohort...

Epidemiological evidence relating environmental smoke to COPD in lifelong non-smokers: a systematic review

Background: Some evidence suggests environmental tobacco smoke (ETS) might cause chronic obstructive pulmonary disease (COPD). We reviewed available epidemiological data in never smokers. Methods: We identified epidemiological studies providing estimates of relative risk (RR) with 95% confidence interval (CI) for various ETS exposure indices. Confounder-adjusted RRs for COPD were extracted, or derived using standard methods. Meta-analyses were conducted for each exposure index, with tests for heterogeneity and publication bias. For the main index (spouse ever smoked or nearest equivalent), analyses investigated variation in RR by location, publication period, study type, sex, diagnosis, study size, confounder adjustment, never smoker definition, and exposure index definition. Results: Twenty-eight relevant studies were identified; nine European or Middle Eastern, nine Asian, eight American and two from multiple countries. Five were prospective, seven case-control and 16 cross-sectional. The COPD definition involved death or hospitalisation in seven studies, GOLD stage 1+ criteria in twelve, and other definitions in nine. For the main index, random-effects meta-analysis of 33 heterogeneous (p<0.001) estimates gave a RR of 1.20 (95%CI 1.08-1.34). Higher estimates for females (1.59,1.16-2.19, n=11) than males (1.29,0.94-1.76, n=7) or sexes combined (1.10,0.99-1.22, n=15 where sex-specific not available), and lower estimates for studies of 150+ cases (1.08,0.97-1.20, n=13) partly explained the heterogeneity. Estimates were higher for Asian studies (1.34,1.08-1.67, n=10), case-control studies (1.55,1.04-2.32, n=8), and COPD mortality or hospitalisation (1.40,1.12-1.74, n=11). Some increase was seen for severer COPD (1.29,1.10-1.52, n=7). Dose-response evidence was heterogeneous. Evidence for childhood (0.88,0.72-1.07, n=2) and workplace (1.12,0.77-1.64, n=4) exposure was limited, but an increase was seen for overall adulthood exposure (1.20,1.03-1.39, n=17). We discuss study weaknesses that may bias estimation of the association of COPD with ETS. Conclusions: Although the evidence suggests ETS increases COPD, study weaknesses and absence of well-designed large studies preclude reliable estimation of the effect. More definitive evidence is required.

Cigarette Smoke Condensate Exposure Changes RNA Content of Extracellular Vesicles Released from Small Airway Epithelial Cells

Exposure to environmental tobacco smoke (ETS) is a known risk factor for the development of chronic lung diseases, cancer, and the exacerbation of viral infections. Extracellular vesicles (EVs) have been identified as novel mediators of cell–cell communication through the release of biological content. Few studies have investigated the composition/function of EVs derived from human airway epithelial cells (AECs) exposed to cigarette smoke condensate (CSC), as surrogates for ETS. Using novel high-throughput technologies, we identified a diverse range of small noncoding RNAs (sncRNAs), including microRNA (miRNAs), Piwi-interacting RNA (piRNAs), and transfer RNA (tRNAs) in EVs from control and CSC-treated SAE cells. CSC treatment resulted in significant changes in the EV content of miRNAs. A total of 289 miRNAs were identified, with five being significantly upregulated and three downregulated in CSC EVs. A total of 62 piRNAs were also detected in our EV preparations, with five significantly downregulated and two upregulated in CSC EVs. We used TargetScan and Gene Ontology (GO) analysis to predict the biological targets of hsa-miR-3913-5p, the most represented miRNA in CSC EVs. Understanding fingerprint molecules in EVs will increase our knowledge of the relationship between ETS exposure and lung disease, and might identify potential molecular targets for future treatments.

White Blood Cell Count and Risk of Incident Lung Cancer in the UK Biobank.

The contribution of measurable immunological and inflammatory parameters to lung cancer development remains unclear, particularly among never smokers. We investigated the relationship between total and differential white blood cell (WBC) counts and incident lung cancer risk overall and among subgroups defined by smoking status and sex in the United Kingdom (UK). We evaluated 424 407 adults aged 37-73 years from the UK Biobank. Questionnaires, physical measurements, and blood were administered and collected at baseline in 2006-2010. Complete blood cell counts were measured using standard methods. Lung cancer diagnoses and histological classifications were obtained from cancer registries. Multivariable Cox regression models were used to estimate the hazard ratio (HR) and 95% confidence intervals of incident lung cancer in relation to quartiles (Q) of total WBC and subtype-specific counts, with Q1 as the reference. There were 1493 incident cases diagnosed over an average 7-year follow-up. Overall, the highest quartile of total WBC count was statistically significantly associated with elevated lung cancer risk (HRQ4 = 1.67, 95% CI = 1.41 to 1.98). Among women, increased risks were found in current smokers (n cases / n = 244 / 19 464, HRQ4 = 2.15, 95% CI = 1.46 to 3.16), former smokers (n cases / n = 280 / 69 198, HRQ4 = 1.75, 95% CI = 1.24 to 2.47), and never smokers without environmental tobacco smoke exposure (ncases / n = 108 / 111 294, HRQ4 = 1.93, 95% CI = 1.11 to 3.35). Among men, stronger associations were identified in current smokers (ncase s / n = 329 / 22 934, HRQ4 = 2.95, 95% CI = 2.04 to 4.26) and former smokers (nc ases / n = 358/71 616, HRQ4 = 2.38, 95% CI = 1.74 to 3.27) but not in never smokers. Findings were similar for lung adenocarcinoma and squamous cell carcinoma and were driven primarily by elevated neutrophil fractions. Elevated WBCs could potentially be one of many important markers for increased lung cancer risk, especially among never-smoking women and ever-smoking men.

Association between environmental tobacco smoke exposure across the first four years of life and manifestation of externalizing behavior problems in school-aged children.

Extensive literature in human and animal models has documented an association between maternal smoking during pregnancy and externalizing behavior in offspring. It remains unclear; however, the extent to which postnatal environmental smoke exposure is associated with behavioral development, particularly for children whose mothers did not smoke during pregnancy. The present study examined whether magnitude of exposure to environmental smoke across the first four years of life demonstrated a linear association with later externalizing symptoms. Exposure was quantified through salivary cotinine measured when children were 6, 15, 24, and 48months of age, providing a more accurate quantification of realized exposure than can be estimated from parental report of cigarettes smoked. Data were available for n=1,096 (50% male; 44% African American) children recruited for the Family Life Project, a study of child development in areas of rural poverty. Analyses indicate a linear association between cotinine and children's symptoms of hyperactivity and conduct problems. This association remained significant after controlling for family poverty level, parental education, parental history of ADHD, hostility, depression, caregiver IQ, and obstetric complications. Furthermore, this association was unchanged when excluding mothers who smoked during pregnancy from the model. Findings are consistent with animal models demonstrating an effect of environmental exposure to nicotine on ongoing brain development in regions related to hyperactivity and impulsivity, and highlight the importance of mitigating children's exposure to environmental smoke, including sources that extend beyond the parents.

Environmental Tobacco Smoke Affects Lung Function of Preschoolers With Asthma Even After a Decade

To evaluate whether early tobacco smoke exposure has a long-term effect on lung function.Children (n = 105; mean age: 5.62 years) with a history of wheeze and bronchodilator response had been previously enrolled for a study evaluating the association between maternal smoking and preschool asthma. Children could not have taken corticosteroids in the previous 6 months nor have had a respiratory tract infection in the previous 2 weeks. These children were evaluated at a follow-up visit 10 years after the initial enrollment (n = 64; mean age: 14.22 years).The cohort in this study had been assessed at enrollment for environmental tobacco smoke exposure by urinary cotinine and questionnaires. At both enrollment and the 10-year follow-up, fractional exhaled nitric oxide (FeNO), impulse oscillometry (IOS), blood eosinophil counts, and allergic sensitization to indoor and outdoor aeroallergens were assessed. At the 10-year follow-up, children also performed spirometry and a methacholine challenge. Results were compared between enrollment and follow-up.At the 10-year follow-up, fewer children wheezed in the previous year (11% vs 83%), whereas more children had positive allergy testing results (92% vs 70%). Blood eosinophil count, FeNO, and total respiratory system resistance (resistance at 5 Hz [R5]), one of the IOS indices, were all decreased at follow-up. Forty-three percent of parents stopped smoking during the 10 years. Approximately one-third of children reported asthma symptoms and the need for asthma medications in the previous 2 months at the follow-up visit. None reported smoking. Being overweight correlated with forced expiratory volume in 1 second and/or forced vital capacity and the IOS indices (R5 and area under reactance), at the follow-up visit but did not correlate with the preschool urinary cotinine levels. However, preschool urinary cotinine levels did significantly correlate with increased FeNO scores, blood eosinophils, and R5 and decreased reactance (by 5) at the follow-up. No significant correlation was seen with forced expiratory volume in 1 second or methacholine challenge.Early tobacco smoke exposure is linked to the presence of airway inflammation and decreased lung function in older children with a history of asthma.Limitations included the lack of a control asthma group without preschool exposure to tobacco smoke, the small sample size, and lack of interval assessment during the 10-year period to evaluate the potential confounding effect of other environmental factors, socioeconomic factors, or the development of other comorbidities. The study also did not consider whether aeroallergen sensitization had an impact on lung function over time. IOS is not as commonly performed as spirometry for the assessment of asthma, so the use of IOS in assessing and managing asthma in a clinical practice needs further validation. Nevertheless, this study provides further proof that early exposure to tobacco smoke in childhood potentially has long-term negative health effects.

Association between environmental tobacco smoke exposure and risk of type 2 diabetes mellitus in Chinese female never smokers: A population-based cohort study.

Evidence for the association between environmental tobacco smoke (ETS) exposure and the risk of type 2 diabetes mellitus (T2DM) is limited. The aim of this study was to investigate this association in female never smokers. We analyzed 28 177 female participants of the China Kadoorie Biobank (CKB) in the Suzhou area, who were never smokers and had no diabetes. ETS exposure was defined as being exposed to other people's tobacco smoke either at home, workplace, or in public places at least 1 d/wk. Cox proportional hazard regression models were used to assess the association between ETS exposure and incident T2DM according to the frequency and duration of ETS exposure. A total of 774 incident cases of T2DM were identified during a median 7.3-year follow-up. Compared with no ETS exposure, hazard ratios (95% CIs) for all ETS exposure, daily, and ≥14 h/wk ETS exposure were 1.17 (1.00-1.37), 1.23 (1.04-1.46), and 1.25 (1.03-1.53), respectively. Moreover, a positive dose-response relationship was observed between ETS exposure level and T2DM (all P <.05 for trend). This prospective study suggests that ETS exposure increases the risk of T2DM incidence with dose-response relationship in female never smokers. Thus, reducing ETS exposure may help decrease the burden of T2DM in Chinese females.

The Association of Environmental Tobacco Smoke Exposure and Inflammatory Markers in Hospitalized Children.

Background: Environmental tobacco smoke (ETS) exposure is associated with altered cytokine levels in children. We sought to examine ETS exposure prevalence and the relationship between ETS exposure and cytokine levels in a sample of hospitalized children. (2) Methods: Inflammatory markers (IL-8, IL-1β, IL-10, and TNF-α) and cotinine were measured in saliva of hospitalized, nonsmoking children (N = 112). To assess the association between ETS exposure and immune system response, we built a multivariate regression model including the four inflammatory markers as the response variables and cotinine, age, sex, and discharge diagnosis as explanatory variables while assessing possible interaction effects. (3) Results: Mean age (SD) was 5.8(5.0) years; Geometric Mean (GeoM) cotinine = 1.8 [95% CI = 1.4–2.2]. Children with non-inflammatory other diagnoses had lower IL-10 (p = 0.003) and TNF-α (p = 0.009) levels than children with inflammatory other diagnoses. Children with asthma (p = 0.01) and bacterial illnesses and/or pneumonia (p = 0.002) had higher IL-8 levels. Independent of diagnosis, there was a significant curvilinear association between cotinine and IL-1β (p = 0.002) reflecting no association for cotinine levels <5 ng/mL and a positive association for >5 ng/mL. (4) Conclusions: Children with higher ETS exposure levels have higher IL-1β levels regardless of age, sex, and diagnosis. ETS exposure may increase pro-inflammatory immune responses in children and may interfere with native immune responses and the ability to heal and fight infection.

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.

Further Insights on Predictors of Environmental Tobacco Smoke Exposure during the Pediatric Age.

Background: The smoking ban in public places has reduced Environmental Tobacco Smoke (ETS) exposure for non-smokers, but despite this, domestic environments still remain places at high risk of exposure, and, today, about 40% of children worldwide are exposed to ETS at home. The aims of the study are to investigate the contribution of several factors on ETS exposure among a group of Italian children and to evaluate the changes in smoking precautions adopted at home when the smoker is the mother, the father, or both parents, respectively. Methods: A cross-sectional study was performed on a sample of 519 Italian schoolchildren. Information was collected via a questionnaire. Results: 41.4% of the participants lived with at least one smoker. Almost half of the children exposed to ETS lived with one or more smokers who do not observe any home smoking ban. Lower maternal or paternal educational levels significantly increase the risk of ETS exposure at home and the “worst case” is represented by both parents who smoke. Conclusions: More effective preventive interventions are needed to protect children from ETS exposure. Some interventions should be specifically dedicated to smokers with a low educational level and to mothers that smoke.

Environmental tobacco smoke exposure affects the QT interval during early infancy

Environmental tobacco smoke exposure affects the QT interval during early infancy

P4387Environmental tobacco smoke exposure affects the QT interval during early infancy

Abstract Background The association between long QT interval and sudden infant death syndrome (SIDS) has been clearly established. Environmental tobacco smoke (ETS) exposure is associated with increased risk for SIDS. However, there has been little focus on the relationship between the QT interval and ETS exposure during early infancy. To clarify this, we examined the QT interval with ETS exposure during early infancy. Methods Electrocardiographic study was performed in 624 infants (age: 1–5 months) who have been exposed to tobacco smoking since intrauterine life and 1119 age-matched children without ETS exposure. QT data were extracted from the electrocardiogram monitor built-in echocardiogram. Recordings from lead II on the monitor ECG were used to measure the QT interval. The QT intervals of 5 consecutive beats were measured manually. The QT interval was measured on the first, second, third, fourth, and fifth month. The corrected QT interval (QTc) was calculated by dividing the QT interval by the square root of the RR interval (Bazett's formula). The data of the number of cigarettes per day were collected by a questionnaire. Results In the total study population, the mean QTc showed the highest peak at the second month. The mean QTc at the first and second month (399±21 and 402±18 msec) was significantly longer (p&lt;0.05) than that at the third, fourth, and fifth month (394±19, 393±21, and 392±22 msec) as shown in Figure 1A. The mean QTc in ETS infants at the first, second and third month was significantly greater than that in infants without ETS (404±20 vs. 397±21 msec, 407±19 vs. 399±17 msec and 404±17 vs. 390±18 msec, p&lt;0.01, respectively), but the mean QTc at the fourth and fifth was similar in the 2 groups as shown in Figure 1B. The QTc increased significantly as the category of number of cigarettes per day increased, with a significant prolongation as of the category 6–10 cigarettes per day as shown in Figure 1C. Figure 1 Conclusions The present study indicates that the QT interval during early infancy lengthens by ETS exposure. Further study is needed as to whether QT prolongation associated with ETS exposure is a risk factor for SIDS.

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.

Associations between Environmental Tobacco Smoke Exposure in Early Life and Astigmatism among Chinese Preschool Children.

This study aimed to investigate the association between environmental exposure to tobacco smoke (ETS) during early life and astigmatism in Chinese preschool children. In this cross-sectional study, information concerning prenatal and postnatal ETS exposure at three stages of early life (during pregnancy, from birth to one year and from one to three years), visual problems of children and parents (including a confirmed diagnosis of astigmatism), socio-demographics and perinatal characteristics were obtained from 27,890 parent-reported questionnaires. Logistic regression analyses were undertaken to yield adjusted odds ratios (OR) for assessing their associations. After adjusting for the potential confounders, children were more likely to exhibit astigmatism when they were exposed to ETS during pregnancy + from one to three years [OR (95% CI) = 1.37 (1.02, 1.84)], or from birth to one year + from one to three years [OR (95% CI) = 1.36 (1.11, 1.66)], or during pregnancy + from birth to one year + from one to three years old [OR (95% CI) = 1.29 (1.16, 1.45)], compared to children without ETS exposure at any stage of early life. In Chinese preschool children, prenatal and postnatal astigmatism was associated with ETS exposure; the greater the ETS dose, the greater the astigmatism risk.

Variability of exposure to PM2.5 related to indoor pollution sources in low socio-economic urban households, Durban, South Africa

TPS 722: Low and middle income countries: indoor air pollutants, Exhibition Hall, Ground floor, August 28, 2019, 3:00 PM - 4:30 PM Abstract Background: The goal of PM2.5 indoor assessment for use in epidemiological studies is to estimate indoor levels over time and space. Because of logistical constraints, very few studies have been conducted to assess the reproducibility of indoor PM2.5 measurements. Objective: To evaluate PM2.5 variability in urban households of mothers participating in the Mother and Child in the Environment birth cohort study in Durban, South Africa. Methods: Indoor PM2.5 samples were collected in warm season and cold season from 30 homes across Durban. Four measurements of PM2.5 were undertaken in each house within a 2 week interval using Airmetrics miniVol samplers. We fitted a mixed effects model to estimate the variation of PM2.5 and to determine the determinants of this variance. Results: PM2.5 levels ranged from 1.5 to 302 µg/m3. Levels were highest (mean (SD) =60.8 (70.8) µg/m3) during the cold season and lowest (mean (SD)=43.5 (45.8) µg/m3) during the warm season. Within-home variation dominated the total variability. The results showed that PM2.5 predictors such as active smoking, environmental tobacco smoke exposure and seasonal indicators were significant determinants of PM2.5 variation (R2=0.71), contributing to 2.5–81.4% of the variability. Conclusions: The results suggest that within home variance in PM2.5 levels influence total variability more than factors affecting PM2.5 levels variance between homes over time.

Investigating the effect of England's smoke-free private vehicle regulation on changes in tobacco smoke exposure and respiratory disease in children: a quasi-experimental study

Comprehensive tobacco control policies can help to protect children from tobacco smoke exposure and associated adverse respiratory health consequences. We investigated the impact of England's 2015 regulation that prohibits smoking in a private vehicle with children present on changes in environmental tobacco smoke exposure and respiratory health in children. In this quasi-experimental study, we used repeated cross-sectional, nationally representative data from the Health Survey for England from Jan 1, 2008, to Dec 31, 2017, of children aged up to 15 years. We did interrupted time series logistic or ordinal regression analyses to assess changes in prevalence of self-reported respiratory conditions, prevalence of self-reported childhood tobacco smoke exposure (children aged 8-15 years only), and salivary cotinine levels (children aged 2 years or older) before and after implementation of the smoke-free private vehicle regulation on Oct 1, 2015. Children who were considered active smokers were excluded from the analyses of salivary cotinine levels. Our primary outcome of interest was self-reported current wheezing or asthma, defined as having medicines prescribed for these conditions. Analyses were adjusted for underlying time trends, quarter of year, sex, age, Index of Multiple Deprivation quintile, and urbanisation level. 21 096 children aged 0-15 years were included in our dataset. Implementation of the smoke-free private vehicle regulation was not associated with a demonstrable change in self-reported current wheezing or asthma (adjusted odds ratio 0·81, 95% CI 0·62-1·05; p=0·108; assessed in 13 369 children), respiratory conditions (1·02, 0·80-1·29; p=0·892; assessed in 17 006 children), or respiratory conditions probably affecting stamina, breathing, or fatigue (0·75, 0·47-1·19; p=0·220; assessed in 12 386 children). Self-reported tobacco smoke exposure and salivary cotinine levels generally decreased over the study period. There was no additional change in self-reported tobacco smoke exposure in cars among children aged 8-15 years following the legislation (0·77, 0·51-1·17; p=0·222; assessed in 5399 children). We observed a relative increase in the odds of children having detectable salivary cotinine levels post legislation (1·36, 1·09-1·71; p=0·0074; assessed in 7858 children) and levels were also higher (1·30, 1·04-1·62; p=0·020; ordinal variable). Despite introduction of the regulation, one in 20 children still reported being regularly exposed to tobacco smoke in cars and one in three still had detectable salivary cotinine levels. We found no demonstrable association between the implementation of England's smoke-free private vehicle regulation and changes in children's self-reported tobacco smoke exposure or respiratory health. There is an urgent need to develop more effective approaches to protect children from tobacco smoke in various places, including in private vehicles. Netherlands Lung Foundation, Erasmus MC, Farr Institute, Health Data Research UK, Asthma UK Centre for Applied Research, Academy of Medical Sciences, and Newton Fund.

Source profile and excess cancer risk evaluation of environmental tobacco smoking under real conditions, China

To demonstrate the chemical characteristics and carcinogenic risk of environmental tobacco smoke (ETS) emission, replicate PM2.5 samples were collected via volunteers smoking nine different brands of Chinese cigarettes. The source profile of ETS was established with an abundance of inorganic and organic chemical compositions, source signatures were recognized, and a comparison of excess cancer risk of heavy metals versus polycyclic aromatic hydrocarbons (PAHs) was completed. The results showed that organic carbon (OC), element carbon (EC) and potassium (K) were the primary components in the ETS profile; chromium (Cr), lead (Pb) and cadmium (Cd) were the most abundant heavy metals; and PAHs were mainly distributed in middle molecular weight (MMW) and high molecular weight (HMW) ranges. Benz(a)anthracene (BaA), benzo(b)fluoranthene (BbF) and chrysene (CHR) could distinguish ETS from cooking/outdoor stationary sources as source-related markers. The ranking of excess cancer risk of heavy metals was Cr > Cd > arsenic (As) > Pb > nickel (Ni) and that of PAHs was benzo(a)pyrene (BaP) > BaA > BbF > indeno(1,2,3-cd)pyrene (IND) > CHR. The comparison revealed that the totality of excess cancer risk of heavy metals was 785 times higher than that of PAHs, indicating that the harmful health effect caused by inorganic compositions during ETS exposure should attract public attention.

Prevalence of Involuntary Environmental Cannabis and Tobacco Smoke Exposure in Multi-Unit Housing.

No research has examined the prevalence of involuntary cannabis exposure in the home within the context of multi-unit housing (MUH). The 2017 cycle of the Centre for Addiction and Mental Health Monitor population RDD survey included measures of environmental cannabis smoke (ECS) and environmental tobacco smoke (ETS) for Ontario, Canada. These ECS measures were defined for those who did not live in a detached dwelling self-reporting noticing any tobacco or cannabis smoke enter the home from a neighboring unit or from outside the building at least once in the past 6 months. Overall, 6.6% (95% CI: 4.5–9.5%) and 7.5% (9% CI: 5.4–10.4%) of the population reported being exposed to ETS and ECS in MUH respectively. Individuals exposed to ECS were single, had used cannabis in the past 12 months, and had lower household incomes. The prevalence of involuntary exposure to cannabis smoke is similar to exposure to tobacco smoke. Exposure correlates were primarily associated with characteristics of those who lived in MUH who tend to be members of more vulnerable populations.