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BACKGROUND: Exposure to environmental tobacco smoke (ETS) has been associated with detectable levels of cotinine (a nicotine metabolite) in childrens saliva. However, tobacco smoke also contains toxic and essential trace metals, including chromium (Cr), copper (Cu), lead (Pb), manganese (Mn), nickel (Ni) and zinc (Zn). OBJECTIVE: The current study examines whether there is a relationship between ETS exposure, as gauged by salivary cotinine, and salivary levels of these metals in a subset (n = 238) of children from the Family Life Project. METHODS: Using inductively-coupled-plasma optical emission spectrophotometry, we measured levels of metals in saliva from children at ~90 months of age. Salivary cotinine was measured using a commercial immunoassay. RESULTS: We found that Cr, Cu, Mn, and Zn were detected in most samples (85-99%) with lower levels of detection for Pb and Ni (9.3% and 13.9% respectively). There were no significant differences in any of the metal concentrations between males and females, nor were levels associated with body mass index, although significant differences in salivary Cr and Mn by race, state and income-to-needs ratio were observed. Children with cotinine levels >1 ng/ml had higher levels of Zn (b = 0.401, 95% CI: 0.183 to 0.619; p = 0.0003) and Cu (b = 0.655, 95% CI: 0.206 to 1.104; p = 0.004) compared to children with levels 1 μg/L were more likely to have detectable levels of Pb in their saliva (b = 1.40, 95% CI: 0.424 to 2.459; p = 0.006) compared to children with cotinine levels

Abstract Environmental tobacco smoke (ETS) exposure has been shown to be associated with a variety of diseases, but evidence regarding the association between it and urinary incontinence (UI) is limited. Cotinine, a metabolite of nicotine in the human body, can more accurately quantify the level of human exposure to tobacco smoke. The study utilized data from seven survey cycles (2007-March 2020 Pre-pandemic) of the National Health and Nutrition Examination Survey (NHANES) program. Weighted multivariable logistic regression analysis, subgroup analysis, interaction tests, smooth curve fitting, and threshold effect models were used to analyze the relationship between serum cotinine and UI. Additionally, a 1:1 nearest neighbor propensity score matching (PSM) method was employed to minimize the impact of confounding factors. Before and after PSM, serum cotinine levels were higher in individuals with UI than those without (P

ObjectiveTo study the effect of maternal environmental tobacco smoke (ETS) exposure during pregnancy on the neurodevelopment of one-year-old rural infants in Yunnan province. MethodsA total of 385 newborns born between 2018 and 2019 in rural Xuanwei, Yunnan province, were recruited into a cohort and followed until 1 year of age. Ultra-high performance liquid chromatography-tandem mass spectrometry was used to determine urinary cotinine (UC) concentrations in samples collected from the mothers of the newborns in early, mid, and late pregnancy to assess maternal ETS exposure during pregnancy. The Bayley Scales of Infant and Toddler Development – Third Edition (BSID-III) was used to assess infant neurodevelopment. Multiple linear regression and logistic regression models were constructed to analyze the effect of ETS exposure during pregnancy on infant neurodevelopment. ResultsThe mean UC levels (median [25th percentile, 75th percentile] ng/mL) of the 385 mothers in early, mid, and late pregnancy were 2.94 (0.66, 6.28), 2.86 (0.58, 5.85), and 2.50 (0.39, 5.78), respectively, and ETS exposure in early, mid, and late pregnancy was reported by 80.26%, 81.04%, and 80.00% of the mothers, respectively. For the infants at 1 year of age, the BSID-III dimensional development scores were 99.17 ± 17.57 for cognition, 93.46 ± 15.44 for language, 93.66 ± 15.83 for motor, 109.03 ± 22.36 for social-emotional, and 87.83 ± 15.67 for adaptive behavior, with 9.35%, 22.60%, 18.44%, 6.49%, and 29.35% of the infants assessed having scores indicating delayed five-dimensional development. The results of the multiple linear regression analysis showed that maternal ETS exposure in early pregnancy was negatively correlated with BSID-III motor score in 1-year-old infants (β = – 0.239, 95% confidence interval [95%CI]: – 0.454, – 0.025). The results of logistic regression analysis showed that maternal ETS exposure in early pregnancy may increase the risk of delayed language development in 1-year-old infants (odds ratio = 3.497, 95%CI: 1.186, 10.309). ConclusionMaternal ETS exposure during early pregnancy may affect infant neurodevelopment one year after birth, particularly motor and language development.

Household smoking is one of the main sources of environmental tobacco smoke (ETS) exposure for children, a population considered to be at high risk for associated negative health outcomes. Several studies evidenced the occurrence of early effects related to ETS exposure, including the development of the oxidative stress process. The aim of this study was to evaluate the correlation between urinary levels of 8-oxo-7,8-dihydro-2-deoxyguanosine (8oxodGuo), a nucleic acid oxidation biomarker, and socio-demographic features and lifestyle factors in school children (aged 5–11 years). A cross-sectional study was conducted among 154 healthy children, residing in rural zones of central Italy. For each participant, one urine sample was analyzed by the HPLC-MS/MS technique to simultaneously quantify 8oxodGuo and cotinine (a biomarker of ETS exposure), while information on the children was collected using a questionnaire filled out by the parents. Urinary levels of 8oxodGuo was found to be significantly higher in children exposed to ETS compared to those not exposed (5.53 vs. 4.78 μg/L; p = 0.019). This result was confirmed by the significant association observed between urinary levels of cotinine and 8oxodGuo (r = 0.364, p < 0.0001). Additionally, children exposed to ETS with no smoking ban at home showed a further increased difference than those not exposed (6.35 μg/L vs. 4.78 μg/L; p = 0.008). Considering the great number of adverse effects on human health due to exposure to passive smoking, especially if this exposure begins early in life, it is essential to implement health promotion interventions in this area. [ABSTRACT FROM AUTHOR]

AbstractObjectiveMethodsResultsConclusionTo study associations between fractional exhaled nitric oxide (FeNO) and asthma, airway symptoms, sensitization to common allergens, outdoor pollution and home environment among 380 students in eight junior high schools in two areas in Indonesia.Data on health and home were collected by a face-to face interview before measuring FeNO and performing skin prick test against common allergens. Exploratory linear mixed and logistic regression models were employed.Geometric mean of FeNO was 17.8 ppb (GSD 2.09) and 139 students (36.6%) had elevated FeNO (>20 ppb). In total, 107 students (28.2%) were sensitized to house dust mite (HDM) (Der p1 or Der f1), 4 (1.1%) to cat and 3 (0.8%) to mold (Cladosporium or Alternaria). Moreover, 20 students (5.3%) had diagnosed asthma, 38 (10.0%) had current wheeze, and 107 (28.2%) had current rhinitis. HDM sensitization, diagnosed asthma, current wheeze, and current rhinitis were associated with FeNO. In total, 281 students (73.9%) had mold or dampness, 232 (61.1%) had environmental tobacco smoke (ETS) and 43 (11.3%) had other odor at home. Indoor mold or dampness and other odor at home were associated with FeNO. ETS was negatively associated with FeNO.HDM sensitization and elevated FeNO can be common among children in this part of Indonesia. The high prevalence of elevated FeNO indicate that undiagnosed childhood asthma is common. Dampness, mold and odor at home can be associated with increased FeNO while ETS can be associated with decreased FeNO. [ABSTRACT FROM AUTHOR]

Compared to cigarette smoke, heated tobacco product (HTP) aerosol contains significantly fewer and lower levels of harmful and potentially harmful constituents (HPHCs). However, the impact on environmental air is relatively unexplored. Therefore, this study compared levels of secondhand aerosol (SHA) constituents in air following glo HTP use with secondhand smoke (SHS) constituents following cigarette smoking in an environmental test chamber (ETC). Extracted ETC air samples following product use sessions were analyzed for 27 SHS/SHA constituents, including HPHCs. The use of glo HTPs resulted in significantly lower SHA HPHC levels in the ETC air relative to SHS HPHC levels from cigarette smoking. Some aerosol constituents (benzene, CO, formaldehyde, nicotine, respirable suspended particles, toluene, ethylbenzene, fine particulate matter, m- and p-cresol, o-cresol, pyridine, styrene, and ultraviolet particulate matter) were either below the limit of detection in ETC air or at significantly low levels following glo HTP use relative to cigarette smoking. Mean concentrations of the assessed constituents were at least 90 % lower following use of glo HTPs compared to smoking combustible cigarettes. These results suggest that glo HTP use would not contribute significantly to indoor air contamination and would reduce non-user exposure to HPHCs and other harmful constituents relative to combustible cigarettes. Such reductions in non-user exposure should be considered when assessing the tobacco harm reduction potential of glo HTPs.

Abstract Environmental tobacco smoke (ETS) is known to cause lung inflammatory and injurious responses. Smoke exposure is associated with the pathobiology related to lung fibrosis, whereas the mechanism that ETS exposure augments pulmonary fibrogenesis is unclear. We hypothesized that ETS exposure could exacerbate fibrotic responses via collagen dynamic dysregulation and complement activation. C57BL/6J and p16-3MR mice were exposed to ETS followed by bleomycin administration. ETS exposure exacerbated bleomycin-induced collagen and lysyl oxidase overexpression in the fibrotic lesion. ETS exposure also led to augmented bleomycin-induced upregulation of C3 and C3AR, which are pro-fibrotic markers. Moreover, overexpressed collagens and C3 levels were highly significant in males than females. The old mice (17 months old) were exposed to ETS and treated with bleomycin to induce fibrogenesis which is considered as an aging-associated disease. Fewer gene and protein dysregulations trends were identified between ETS exposure with the bleomycin group and the bleomycin alone group in old mice. Based on our findings, we suggested that ETS exposure increases the risk of developing severe lung fibrotic responses via collagen overexpression and lysyl oxidase-mediated collagen stabilization in the fibrotic lesion, and potentially affected the complement system activation induced by bleomycin. Further, male mice were more susceptible than females during fibrogenesis exacerbation. Thus ETS and bleomycin induced lung fibrotic changes via collagen-lysyl oxidase in an age-dependent mechanism.

Environmental tobacco smoke (ETS) is known to cause lung inflammatory and injurious responses. Smoke exposure is associated with the pathobiology related to lung fibrosis, whereas the mechanism that ETS exposure augments pulmonary fibrogenesis is unclear. We hypothesized that ETS exposure could exacerbate fibrotic responses via collagen dynamic dysregulation and complement activation. C57BL/6J and p16-3MR mice were exposed to ETS followed by bleomycin administration. ETS exposure exacerbated bleomycin-induced collagen and lysyl oxidase overexpression in the fibrotic lesion. ETS exposure also led to augmented bleomycin-induced upregulation of C3 and C3AR, which are pro-fibrotic markers. Moreover, overexpressed collagens and C3 levels were highly significant in males than females. The old mice (17 months old) were exposed to ETS and treated with bleomycin to induce fibrogenesis which is considered as an aging-associated disease. Fewer gene and protein dysregulations trends were identified between ETS exposure with the bleomycin group and the bleomycin alone group in old mice. Based on our findings, we suggested that ETS exposure increases the risk of developing severe lung fibrotic responses via collagen overexpression and lysyl oxidase-mediated collagen stabilization in the fibrotic lesion, and potentially affected the complement system activation induced by bleomycin. Further, male mice were more susceptible than females during fibrogenesis exacerbation. Thus ETS and bleomycin induced lung fibrotic changes via collagen-lysyl oxidase in an age-dependent mechanism. [ABSTRACT FROM AUTHOR]

Depression is associated with both environmental tobacco smoke (ETS) and inflammation. However, whether systemic inflammation mediates the ETS-depression relationship is unclear. We analyzed 19,612 participants from the 2009–2018 National Health and Nutrition Examination Survey (representing approximately 206,284,711 USA individuals), utilizing data of depressive symptoms (assessed by Patient Health Questionnaire-9), blood cotinine level (an ETS biomarker), dietary inflammatory index (DII, assessed by 24-h dietary recall) and inflammation, represented by immune-inflammation index (SII) and systemic inflammation response index (SIRI). Weighted multivariable logistic regression showed that a higher blood cotinine level is significantly associated with a higher depressive symptoms risk (OR = 1.79, 1.35–2.38). After adjusting for covariates, the effect in smokers (OR = 1.220, 95 % CI: 1.140–1.309) is larger than that in non-smokers (OR = 1.150, 95 % CI: 1.009–1.318). Compared to the lowest level, depressive symptoms risks in participants with the highest level of SII, SIRI and DII are 19 % (OR = 1.19, 1.05–1.35), 15 % (OR = 1.15, 1.01–1.31) and 88 % (OR = 1.88, 1.48–2.39) higher, respectively. Weighted linear regression demonstrated positive correlations of SII (β = 0.004, 0.001–0.006), SIRI (β = 0.009, 0.005–0.012) and DII (β = 0.213, 0.187–0.240) with blood cotinine level. Restricted cubic splines model showed a linear dose-response relationship between blood cotinine and depressive symptoms (P non-linear = 0.410), with decreasing risk for lower DII. And SII and SIRI respectively mediate 0.21 % and 0.1 % of the association between blood cotinine and depressive symptoms. Cross-sectional design, and lack of medication data for depression. Positive association of ETS (blood cotinine) with depressive symptoms risk is partly mediated by systemic inflammation, and anti-inflammatory diet could be beneficial. [Display omitted] • Environmental tobacco smoke increases risk of depressive symptoms and inflammation. • SII and SIRI partly mediate the effect of blood cotinine on depressive symptoms. • Low DII mitigates the association of blood cotinine with depressive symptoms. [ABSTRACT FROM AUTHOR]

Abstract Background Environmental tobacco smoke (ETS) exposure in children can cause delayed lung development and lifelong cardiovascular damage. The aim of this study was to measure ETS exposure in children in Israel in 2020–2021 using urinary cotinine (UC) measurements and to assess correlates of ETS exposure, including parental smoking. Methods In the framework of the National Human Biomonitoring Program, spot urine samples and questionnaire data were collected from 166 children aged 4–12 years, during the years 2020–2021. We collected urine samples in 233 adults, 69 of whom were parents of children included in the study. Parents of participating children were asked about parental smoking, child’s exposure to ETS and smoking policy at home. Cotinine and creatinine were measured in urine. Creatinine-adjusted and unadjusted urine cotinine (UC) geometric means were calculated. Associations between potential correlates and UC concentrations were analyzed in univariate and multivariate analyses. For 69 child-parent pairs, correlation between child and parental UC was analyzed. Results Based on urinary cotinine measurement, 65.2% of children of smokers are exposed to ETS, compared to 20.7% of children in non-smoking families. Greater numbers of smokers living in the home (beta = 1.27, p

Limited data are available on the effects of perinatal environmental tobacco smoke (ETS) exposure for early childhood influenza infection. The aim of the present study was to examine whether perinatal versus adult ETS exposure might provoke more severe systemic and pulmonary innate immune responses in mice inoculated with influenza A/Puerto Rico/8/34 virus (IAV) compared to phosphate-buffered saline (PBS). BALB/c mice were exposed to filtered air (FA) or ETS for 6 weeks during the perinatal or adult period of life. Immediately following the final exposure, mice were intranasally inoculated with IAV or PBS. Significant inflammatory effects were observed in bronchoalveolar lavage fluid of neonates inoculated with IAV (FA+IAV or ETS+IAV) compared to PBS (ETS+PBS or FA+PBS), and in the lung parenchyma of neonates administered ETS+IAV versus FA+IAV. Type I and III interferons were also elevated in the spleens of neonates, but not adults with ETS+IAV versus FA+IAV exposure. Both IAV-inoculated neonate groups exhibited significantly more CD4 T cells and increasing numbers of CD8 and CD25 T cells in lungs relative to their adult counterparts. Taken together, these results suggest perinatal ETS exposure induces an exaggerated innate immune response, which may overwhelm protective anti-inflammatory defenses against IAV, and enhances severity of infection at early life stages (e.g., in infants and young children).

Introduction: Studies on the relationship between environmental tobacco smoke (ETS) and gestational diabetes mellitus (GDM) are limited. In this study, we aimed to clarify the association between ETS at different trimesters of pregnancy and the risk of GDM among non‐smoking pregnant women. Methods: A total of 16,893 non‐smoking mothers from the Southwest Birth Cohort, China, were included in the final analyses. Exposure and outcome measures included self‐reported ETS status at different trimesters of pregnancy and GDM diagnosis. Multivariable logistic regression models were constructed to estimate the association between ETS and GDM. Results: The prevalence of ETS exposure was 25.7%. Compared with no ETS, ever ETS had an increased risk of GDM, with an adjusted odds ratio (95% confidence intervals) of 1.21 (1.09, 1.33). The association remained consistent at different trimesters of pregnancy ETS exposure. In the last trimester and with continuous ETS exposure, the risk of GDM increased significantly with the increase in the duration of the exposure. The risk of GDM associated with ever ETS during pregnancy significantly increased in mothers over 30 years old and pre‐pregnancy overweight (P for interaction <0.05). Conclusions: ETS exposure at different trimesters of pregnancy was associated with an increased risk of GDM among non‐smoking pregnant women. These findings emphasise the importance of preventing ETS exposure during pregnancy. [ABSTRACT FROM AUTHOR]

Indoor pollution and deposition dust (DD), in particular, are acquiring concern, due to long exposure time and importance of intake by humans through contact and ingestion. Hospitals look a special category of sites, owing to peculiar contaminants affecting them and to presence of people prone to adverse effects induced by toxicants. Four in-field campaigns aimed at understanding the chemical composition of DD were performed in five Italian hospitals. Measurements were performed before (autumn 2019), during (spring 2021), and after (winter 2022) the peak of SARS-CoV2 and when restrictions caused by pandemic were revoked (winter 2023). Parallel measurements were made outdoors (2022), as well as in a university and a dwelling. Targeted contaminants were n-alkanes and polycyclic aromatic hydrocarbons (PAHs), while iso- and anteiso-alkanes were analyzed to assess the impact of tobacco smoking. Total n-alkanes ranged from 3.9 ± 2.3 to 20.5 ± 4.2 mg/g, with higher percentages of short chain homologs in 2019. PAHs ranged from 0.24 ± 0.22 to 0.83 ± 0.50 mg/g, with light congeners (≤ 228 a.m.u.) always exceeding the heavy ones (≥ 252 a.m.u.). According to carbon preference indexes, alkanes originated overall from anthropogenic sources. Microorganisms resulted to affect a hospital, and tobacco smoke accounted for ~ 4–20‰ of DD mass. As for PAH sources, the diagnostic concentration ratios suggested the concourse of biological matter burning and vehicle emission. Benzo[a]pyrene equivalent carcinogenic and mutagenic potencies of depositions at hospitals ranged ~ 9–39 μg/g and ~ 15–76 μg/g, respectively, which seems of concern for health. DD composition in hospitals was different from that outside the premises, as well as that found at university and at dwelling. [ABSTRACT FROM AUTHOR]

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

Background and Objective: Indoor air pollution (IAP) and tobacco smoke exposure (ETS) are global health concerns contributing to the burden of childhood respiratory disease. Studies assessing the effects of IAP and ETS in preschool children are limited. We assessed the impact of antenatal and postnatal IAP and ETS exposure on lung function in a South African birth cohort, the Drakenstein Child Health Study. Methods: Antenatally enrolled mother–child pairs were followed from birth. Lung function measurements (oscillometry, multiple breath washout and tidal breathing) were performed at 6 weeks and 3 years. Quantitative antenatal and postnatal IAP (particulate matter [PM10], volatile organic compounds [VOC]) and ETS exposures were measured. Linear regression models explored the effects of antenatal and postnatal exposures on lung function at 3 years. Results: Five hundred eighty‐four children had successful lung function testing, mean (SD) age of 37.3 (0.7) months. Exposure to antenatal PM10 was associated with a decreased lung clearance index (p < 0.01) and postnatally an increase in the difference between resistance at end expiration (ReE) and inspiration (p = 0.05) and decrease in tidal volume (p = 0.06). Exposure to antenatal VOC was associated with an increase in functional residual capacity (p = 0.04) and a decrease in time of expiration over total breath time (tE/tTOT) (p = 0.03) and postnatally an increase in respiratory rate (p = 0.05). High ETS exposure postnatally was associated with an increase in ReE (p = 0.03). Conclusion: Antenatal and postnatal IAP and ETS exposures were associated with impairment in lung function at 3 years. Strengthened efforts to reduce IAP and ETS exposure are needed. Indoor air pollution (IAP) contributes to the high burden of childhood respiratory illness. We performed comprehensive lung function testing, showing both antenatal and postnatal IAP and environmental tobacco smoke exposure to be associated with impairment in lung function at 3‐years of age. This highlights the need for public health awareness and initiatives. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

PurposeThe detrimental effects of environmental tobacco smoke (ETS) on women’s reproductive health have been widely recognized. However, the detailed association between exposure to environmental tobacco smoke and the incidence of infertility remains under-explored. This investigation focuses on exploring this potential connection.MethodsFor this analysis, we extracted data from the US National Health and Nutrition Examination Survey (NHANES) database, covering the years 2013 to 2018, focusing on individuals with recorded serum cotinine levels and infertility information. ETS exposure and fertility status were analyzed as independent and dependent variables, respectively. We applied weighted multivariate logistic regression method to evaluate the impact of ETS on infertility, including subgroup analyses for more detailed insights.ResultsThe study encompassed 3,343 participants. Logistic regression analysis revealed a notable positive correlation between ETS exposure and infertility, with an odds ratio (OR) of 1.64 (95% Confidence Interval [CI]: 1.14–2.36). We observed a non-linear relationship between ETS exposure and infertility risk. Notably, infertility risk increased by 64% in serum cotinine levels above 0.136 compared to that in serum cotinine levels below 0.011. Further, subgroup analysis and interaction tests showed consistent results across different segments, underscoring the robustness of the ETS-infertility link.ConclusionOur findings suggest that environmental tobacco smoke exposure may be a contributing factor to infertility. These results reinforce the recommendation for women in their reproductive years to avoid ETS exposure, especially when planning for pregnancy.

Abstract Background Exposure to environmental tobacco smoke (ETS) is arguably the most ubiquitous and hazardous, even at very low levels, starting in early life. The objective of this study was to describe the state of research and future trends on ETS exposure and Children’s Health (CH) topics with bibliometrics and altmetrics. Methods An electronic search was performed in Scopus database on January 31, 2023. Consensus was arrived on 100 most-cited articles by two reviewers. These papers were then cross matched with citations harvested from Web of Science (WoS) and Google Scholar. Altmetric Attention Score (AAS) and Dimension counts were also collected. Analysis and network visualization of authors, countries, and keywords were generated using VOSviewer software. Results Among a total of 1107 articles published on ETS and CH, the 100 top-cited articles appeared in 54 journals, with Pediatrics (n = 12) contributing a maximum number of articles. The time period between 2000 and 2009 accounted for 44% of all publications. With respect to the research design employed across these studies, cross-sectional design took precedence over others accounting for approximately 40%. Predominantly, articles focused on childhood asthma; however, current research trends have shifted towards emerging fields such as children’s oral health and DNA methylation. Twitter, policy documents, and news outlets were the main platforms where outputs were discussed. The AAS was not associated with journal impact factor or access type. Weak correlations were observed between AAS and citation count in Scopus, WoS, and Google Scholar (r = 0.17 to 0.27) while a positive association existed between dimension count and the number of citations across all three databases (r = 0.84 to 0.98). Conclusion This study demonstrates the evolution, digital dissemination and research hotspots in the field of ETS and CH, predicting the possible future research directions. High-quality studies with more specific exposure classification are warranted to better understand the relationship between ETS and CH.

Household smoking is one of the main sources of environmental tobacco smoke (ETS) exposure for children, a population considered to be at high risk for associated negative health outcomes. Several studies evidenced the occurrence of early effects related to ETS exposure, including the development of the oxidative stress process. The aim of this study was to evaluate the correlation between urinary levels of 8-oxo-7,8-dihydro-2-deoxyguanosine (8oxodGuo), a nucleic acid oxidation biomarker, and socio-demographic features and lifestyle factors in school children (aged 5–11 years). A cross-sectional study was conducted among 154 healthy children, residing in rural zones of central Italy. For each participant, one urine sample was analyzed by the HPLC-MS/MS technique to simultaneously quantify 8oxodGuo and cotinine (a biomarker of ETS exposure), while information on the children was collected using a questionnaire filled out by the parents. Urinary levels of 8oxodGuo was found to be significantly higher in children exposed to ETS compared to those not exposed (5.53 vs. 4.78 μg/L; p = 0.019). This result was confirmed by the significant association observed between urinary levels of cotinine and 8oxodGuo (r = 0.364, p < 0.0001). Additionally, children exposed to ETS with no smoking ban at home showed a further increased difference than those not exposed (6.35 μg/L vs. 4.78 μg/L; p = 0.008). Considering the great number of adverse effects on human health due to exposure to passive smoking, especially if this exposure begins early in life, it is essential to implement health promotion interventions in this area.

BackgroundChildren's overall tobacco smoke exposure (TSE) consists of both inhalation of secondhand smoke (SHS) and ingestion, dermal uptake, and inhalation of thirdhand smoke (THS) residue from dust and surfaces in their environments.ObjectivesOur objective was to compare the different roles of urinary cotinine as a biomarker of recent overall TSE and hand nicotine as a marker of children's contact with nicotine pollution in their environments. We explored the differential associations of these markers with sociodemographics, parental smoking, child TSE, and clinical diagnoses.MethodsData were collected from 276 pediatric emergency department patients (Median age = 4.0 years) who lived with a cigarette smoker. Children's hand nicotine and urinary cotinine levels were determined using LC-MS/MS. Parents reported tobacco use and child TSE. Medical records were reviewed to assess discharge diagnoses.ResultsAll children had detectable hand nicotine (GeoM = 89.7ng/wipe; 95 % CI = [78.9; 102.0]) and detectable urinary cotinine (GeoM = 10.4 ng/ml; 95%CI = [8.5; 12.6]). Although hand nicotine and urinary cotinine were highly correlated (r = 0.62, p

Introduction Low parental education level and parental smoking are major risk factors for household secondhand smoke (SHS) exposure among adolescents. We investigated the trend in household SHS exposure according to sex, school, and parental education level to determine whether the decline in household SHS exposure over time depends on parental education level. Methods We used cross-sectional Korea Youth Risk Behavior datasets (2006–2020; 806829 subjects were eligible). We applied binary logistic regression to assess household SHS exposure trends and evaluated the interaction between period and parental education level. Results Household SHS exposure over 15 years has declined. The difference (0.121) was the smallest for male middle school students with low-educated parents. The slope for the estimated probability of household SHS exposure among students with high-educated parents was steeper than that for those with low-educated parents, except for female high school students (difference=0.141). Students with low-educated parents were at higher risk of household SHS exposure (male middle school students, adjusted odds ratio, AOR=1.52; 95% CI: 1.47–1.56; male high school students, AOR=1.42; 95% CI: 1.38–1.47; female middle school students, AOR=1.62; 95% CI: 1.58–1.67; female high school students, AOR=1.62; 95% CI: 1.57–1.67). The interaction between parental education level and period was significant. We also found a significant interaction between parental education level and parental smoking (other × present interaction, AOR=0.64; 95% CI: 0.60–0.67; low–low × present interaction, AOR=0.89; 95% CI: 0.83–0.95). Conclusions Changes in parental education level over time mainly contributed to changes in adolescents’ household SHS exposure. Adolescents with low-educated parents were at higher risk of household SHS exposure, with a slower decline. These gaps must be considered when creating and implementing interventions. Campaigns and community programs to prevent household SHS need to be emphasized among vulnerable adolescents.

Introduction Environmental tobacco smoke (ETS) is associated with several congenital anomalies, including non-syndromic orofacial clefts (NSOFCs). This systematic review aimed to update the literature on the association between ETS and NSOFCs. Methods Four databases were searched up to March 2022, and studies that evaluated the association between ETS and NSOFCs were selected. Two authors selected the studies, extracted the data, and evaluated the risk of bias. Comparing the association of maternal exposure to ETS and active parental smoking with NSOFCs allowed for the creation of pooled effect estimates for the included studies. Results Twenty-six studies were deemed eligible for this review, of which 14 were reported in a previous systematic review. Twenty five were case-control studies, and one was a cohort study. In total, these studies included 2142 NSOFC cases compared to 118129 controls. All meta-analyses showed an association between ETS and the risk of having a child with NSOFC, based on the cleft phenotype, risk of bias, and year of publication, with a pooled increased odds ratio of 1.80 (95% CI: 1.51–2.15). These studies had a marked heterogeneity, which decreased upon subgrouping based on the recent year of publication and the risk of bias. Conclusions ETS exposure was associated with more than a 1.5-fold increase in the risk of having a child with NSOFC, showing a higher odds ratio than paternal and maternal active smoking. TRIAL REGISTRATION The study is registered on the International Prospective Register of Systematic Reviews database # CRD42021272909.

Environmental tobacco smoke (ETS) exposure has been proven to induce digestive diseases such as hepatic steatosis, cirrhosis, and gastrointestinal cancer, yet little is known about the link between ETS exposure and constipation. This study aimed to investigate the impact of ETS exposure on the risk of chronic constipation in adults aged 20 years or older. This is a cross-sectional study based on population. A total number of 7705 participants from the National Health and Nutrition Examination Survey (NHANES) 2005–2010 were included. Cotinine, an alkaloid found in tobacco, serves as a reliable and precise biomarker for measuring exposure to ETS. Hence, the categorization of exposure to ETS was conducted based on serum cotinine levels, resulting in four distinct categories. The association between ETS exposure and the risk of constipation was assessed using multivariable restricted cubic spline and logistic regression with odds ratio (OR) and 95% confidence interval (CI). The weighted prevalence of constipation in this study was estimated to be 7.51% based on stool consistency, or 3.11% based on stool frequency. The fully adjusted models indicated a positive correlation between exposure to ETS and constipation as measured by stool frequency, among adults with poor dietary quality (OR (95% CI): moderate exposure: 2.49 (1.05, 5.94); high exposure: 2.36(1.13, 4.95), P for trend = 0.03), while no significant difference was observed in the subgroup with a higher healthy eating index. Furthermore, the log10-transformed serum cotinine level exhibited a non-linear inverted U-shaped association with constipation in individuals with poor dietary quality (P overall = 0.0207, P non-linear = 0.0427). Conversely, a J-shaped non-linear relationship was observed in the subgroup with a higher healthy eating index (P overall = 0.0028, P non-linear = 0.0036). Our results show that ETS exposure appears to be positively associated with stool frequency-related chronic constipation in adults with poor dietary quality. [ABSTRACT FROM AUTHOR]

Background: Exposure to environmental tobacco smoke (ETS) is arguably the most ubiquitous and hazardous, even at very low levels, starting in early life. The objective of this study was to describe the state of research and future trends on ETS exposure and Children's Health (CH) topics with bibliometrics and altmetrics. Methods: An electronic search was performed in Scopus database on January 31, 2023. Consensus was arrived on 100 most-cited articles by two reviewers. These papers were then cross matched with citations harvested from Web of Science (WoS) and Google Scholar. Altmetric Attention Score (AAS) and Dimension counts were also collected. Analysis and network visualization of authors, countries, and keywords were generated using VOSviewer software. Results: Among a total of 1107 articles published on ETS and CH, the 100 top-cited articles appeared in 54 journals, with Pediatrics (n = 12) contributing a maximum number of articles. The time period between 2000 and 2009 accounted for 44% of all publications. With respect to the research design employed across these studies, cross-sectional design took precedence over others accounting for approximately 40%. Predominantly, articles focused on childhood asthma; however, current research trends have shifted towards emerging fields such as children's oral health and DNA methylation. Twitter, policy documents, and news outlets were the main platforms where outputs were discussed. The AAS was not associated with journal impact factor or access type. Weak correlations were observed between AAS and citation count in Scopus, WoS, and Google Scholar (r = 0.17 to 0.27) while a positive association existed between dimension count and the number of citations across all three databases (r = 0.84 to 0.98). Conclusion: This study demonstrates the evolution, digital dissemination and research hotspots in the field of ETS and CH, predicting the possible future research directions. High-quality studies with more specific exposure classification are warranted to better understand the relationship between ETS and CH. [ABSTRACT FROM AUTHOR]

While there are legal regulations prohibiting smoking in indoor areas in Turkey, there is none for outdoor areas. Many non-smokers are exposed to environmental tobacco smoking against their will in Turkey. Numerous research efforts have documented the fact that environmental tobacco smoke poses risks to human health because it pollutes the environment by releasing dangerous chemicals into the air that non-smokers breathe. This means that tobacco smoking poses risks to a safe environment and people's lives. People have a right to the environment, as guaranteed by the Turkish Constitution. Since Stockholm Declaration, many countries have recognized that people have a right to a safe environment or that a safe environment is essential to the enjoyment of human rights, including Turkey. However, how non-smokers perceive of the impacts of environmental tobacco smoke on the enjoyment of the right to the environment enshrined within the Turkish legal system has not been studied to date. Accordingly, this research aims to explore how issues relating to environmental tobacco smoke can be approached from an environmental human rights perspective. To achieve this purpose, a qualitative case study was conducted in Istanbul. The results of this analysis show that non-smokers do not enjoy the right to the clean environment guaranteed by the Turkish Constitution due to the ETS. [ABSTRACT FROM AUTHOR]

Despite inititatives to reduce tobacco consumption, smoking remains a primary cause of death for both smokers and nonsmokers exposed to environmental tobacco smoke (ETS). The characteristics of some specific groups can make them more exposed to ETS or limit the benefit of prevention measures. This study investigated determinants of ETS in a population of young adult students, considered at higher risk of exposure due to their specific lifestyle. This cross‐sectional study involved 90 students aged 20 ± 1.7 years, from the University of Luxembourg, prior to the smoking ban enforcement in public places in the country. Participants reported their tobacco consumption and exposure to ETS at home and/or in public places, and provided a hair sample analyzed for nicotine and cotinine. Nicotine and cotinine were significantly higher in smokers than in nonsmokers' hair in general (median: 2.6 vs. 0.9 ng/mg and 87.1 vs. 22.5 pg/mg respectively). However, nonsmokers exposed to ETS at home and in public places had comparable concentrations to smokers (nic = 2.2 ng/mg; cot = 56.2 pg/mg), whereas unexposed nonsmokers presented significantly lower values (nic = 0.4 ng/mg, cot = 8.5 pg/mg). Nonsmokers exposed to ETS only at home presented higher values than nonsmokers only exposed in public places (nic: 1.3 vs. 0.8 ng/mg, cot: 70.4 vs. 15.0 pg/mg). The study shows the widespread exposure to ETS in this population, the importance of exposure assessment, and the relevance of hair analysis for this purpose. Results suggest that ETS can lead to equivalent exposure to active smoking and that exposure at home can highly contribute to ETS, which is not solved by smoking ban in public places. [ABSTRACT FROM AUTHOR]

Introduction The home is the primary source of children’s exposure to secondhand smoke. This study investigated the status and influencing factors of child exposure to secondhand smoke at home when people smoke in the household. Methods Participants with at least one child living in their household from 10 communities in Chongqing were recruited and provided a self-administered questionnaire using a multistage proportional random sampling design from June to August 2021. The chi-squared test and binary logistic regression analyses were used to identify influencing factors. Results The questionnaire completed by 1345 families showed that 631 (46.9%) families lived with smokers in their household, and 509 (80.7%) of those families reported that smoking occurred within the home while the children were present. Binary logistic regression analyses demonstrated that the time between waking up and household smokers having the first cigarette of the day (OR=0.44; 95% CI: 0.22–0.85), changes to smoking habits and behaviors within the last six months (OR=1.76; 95% CI: 1.06–2.90), attitudes towards tobacco control in the household (OR=2.91; 95% CI: 1.72–4.92), self-efficacy in maintaining a smoke-free home (OR=2.27; 95% CI: 1.36–3.79), having rules to maintain a smoke-free home (OR=3.25; 95% CI: 1.68–6.29), and the status of providing cigarettes to guests at home (OR=11.0; 95% CI: 1.33–90.8) were associated with exposure to SHS. Conclusions Education focusing on the impact of smoking on children’s health should be encouraged. Smoke-free homes should be established, and smoking restrictions in the household should be enacted. Therefore, information about the available tobacco-control services should be given to family members and be used properly. It is an effective way to decrease the risk of at-home exposure to SHS for children, to overcome any obstacles in tobacco control.

IntroductionEnvironmental exposure to lead (Pb) and cadmium (Cd) are risk factors for adverse health outcomes in children and adults. This study examined whether thirdhand smoke residue contributes to Pb and Cd in settled house dust.MethodsParticipants were 60 multiunit housing residents in San Diego, California. All had indoor smoking bans during the study period, and 55 were nonsmokers. Wipe samples from different surfaces and vacuum floor dust samples were analyzed for nicotine, a marker of thirdhand smoke, and for Pb and Cd using liquid chromatography-triple quadrupole mass spectrometry and inductively coupled plasma-mass spectrometry, respectively.ResultsExamined in each sample type separately, Pb and Cd loadings were significantly correlated (r = 0.73, vacuum floor dust; 0.52, floor wipes; 0.72, window sill/trough wipes; all p  0.30). Nicotine loading in dust was significantly correlated with Pb and Cd loading in dust (r = 0.49 for Pb; r = 0.39 for Cd, all p

Background: Secondhand smoke (SHS), a major indoor pollutant, is a significant risk factor for cardiovascular morbidity and mortality including arrhythmias and sudden cardiac death. Exposure to SHS can produce autonomic imbalance, as evidenced by reduced heart rate variability (HRV)-a clinical metric of cardiac vagal regulation. Currently, the mechanisms through which SHS changes the vagal preganglionic neuronal inputs to the heart to produce this remains unknown. Objectives: To characterize the effect of SHS on both the excitability and action potential (AP) characteristics of anatomically identified cardiac vagal neurons (CVNs) in the nucleus ambiguus and examine whether SHS alters small conductance calcium-activated potassium (SK) channel activity of these CVNs. Methods: Adult male mice were exposed to four weeks of filtered air or SHS (3 mg/m3) 6 h/day, 5 day/week. Using patch-clamp recordings on identified CVNs in brainstem slices, we determined neuronal excitability and AP characteristics with depolarizing step- and ramp-current injections. Results: Four weeks of SHS exposure reduced spiking responses to depolarizing current injections and increased AP voltage threshold in CVNs. Perfusion with apamin (20 nM) magnified these SHS-induced effects, suggesting reduced SK channel activity may serve to minimize the SHS-induced decreases in CVNs excitability. Medium afterhyperpolarization (a measurement of SK channel activity) was smaller in the SHS group, further supporting a lower SK channel activity. AP amplitude, rise rate, fast afterhyperpolarization amplitude (a measurement of voltage-gated channel activity), and decay rate were higher in the SHS group at membrane voltages more positive to 0 mV, suggesting altered inactivation properties of voltage-dependent channels underlying APs. Discussion: SHS exposure reduced neuronal excitability of CVNs with compensatory attenuation of SK channel activity and altered AP characteristics. Neuroplasticity of CVNs could blunt regulatory cardiac vagal signaling and contribute to the cardiovascular consequences associated with SHS exposure, including reduced HRV.

Exposure to environmental metals has been associated with health outcomes including respiratory health. Little is known about the impact of exposure to environmental metals on lung function among young children in general population. This study aimed to investigate the associations of exposure to metals with lung function among young children in a population-based cohort. A total of 1488 children aged 5–8 years attended a follow-up visit as part of the Longitudinal Investigation of Global Health in Taiwanese Schoolchildren (LIGHTS) cohort. We measured urinary samples of vanadium (median: 1.21 ng/mL; interquartile range (IQR): 0.73–1.98), manganese (median: 0.23 ng/mL; IQR: 0.13–0.47), arsenic (median: 40.51 ng/mL; IQR: 21.66–70.49), nickel (median: 1.09 ng/mL; IQR: 0.31–3.60), and cadmium (median: 0.26 ng/mL; IQR: 0.11–0.43) and performed lung function tests. Urinary vanadium concentrations were inversely associated with FVC (β coefficient for the highest quartile versus the other quartiles: −33.40, p = 0.001), FEV1 (β: −41.31, p

We examined independent and joint associations between prenatal and postnatal smoking exposure and the prevalence of wheeze and asthma among 3-year-old Japanese children. Sex differences were also investigated. Smoking exposure, allergic symptoms, and potential confounding factor data were collected using a self-administered questionnaire. Wheeze was defined on the basis of the International Study of Asthma and Allergies in Childhood criteria. Physician-diagnosed asthma was considered to be present if a physician had diagnosed the child with asthma any time before the survey was administered. There were 6402 pediatric participants in this study. Maternal smoking throughout pregnancy and household smoking exposure during the first year of life were associated with an increased prevalence of wheeze among girls but not boys (adjusted odds ratio (OR) [95% CI] = 2.00 [1.13–3.42] and 1.34 [1.07–1.68], respectively). Girls exposed to both prenatal maternal smoking and postnatal household smoking exposure had a significantly higher prevalence of wheeze and physician-diagnosed asthma compared with girls without these exposures (adjusted OR [95% CI] = 2.06 [1.39–3.01] and 1.86 [1.01–3.26], respectively). No association was observed between perinatal smoking exposure and the prevalence of wheeze or asthma among boys. Significant interactions between sex and smoking exposure affecting wheeze and asthma were also found (p for interaction = 0.0003 and 0.01, respectively). We found a positive association between perinatal smoking exposure and the prevalence of wheeze and asthma only among girls. Effects of perinatal smoking exposure on wheeze and asthma might be sex specific. Further research is required. [ABSTRACT FROM AUTHOR]

Objective The study aimed to better understand the perceptions of mothers of preterm infants regarding smoking behaviors and environmental tobacco smoke (ETS) exposure using qualitative methodology. Study Design Using a Grounded Theory approach, we conducted in-depth, semi-structured interviews with mothers of preterm infants, both smokers and nonsmokers. Using the Theory of Planned Behavior (TPB) as a conceptual framework for our questions, we conducted and analyzed interviews until theoretical saturation was reached. Analysis included an iterative coding process resulting in theme development. Results Our key themes aligned with the TPB domains of attitudes, perceived control, and social norms. Regarding attitudes, mothers expressed that smoking was bad for their infants and that preterm infants were more vulnerable than term infants. Regarding perceived control, mothers commented on their perceived ability to avoid ETS exposure with subthemes including strategies utilized to mitigate ETS exposure risk. Some mothers expressed difficulty avoiding ETS exposure, for example, when residing in high-density housing. Regarding perceived social norms, mothers whose family and friends were nonsmokers expressed ease avoiding ETS, while mothers whose family and friends were smokers expressed more difficulty avoiding ETS. Conclusion Mothers used a variety of behaviors within the domains of the TPB to reduce ETS exposures in their preterm infants which can inform future neonatal intensive care unit-based interventional strategies. Key Points Mothers felt ETS is harmful for preterm infants. Mothers reported strategies for ETS avoidance. Mothers reported barriers to ETS avoidance. TPB can frame mothers' ETS-related behaviors. [ABSTRACT FROM AUTHOR]

INTRODUCTION Environmental tobacco smoke (ETS) is associated with several congenital anomalies, including non-syndromic orofacial clefts (NSOFCs). This systematic review aimed to update the literature on the association between ETS and NSOFCs. METHODS Four databases were searched up to March 2022, and studies that evaluated the association between ETS and NSOFCs were selected. Two authors selected the studies, extracted the data, and evaluated the risk of bias. Comparing the association of maternal exposure to ETS and active parental smoking with NSOFCs allowed for the creation of pooled effect estimates for the included studies. RESULTS Twenty-six studies were deemed eligible for this review, of which 14 were reported in a previous systematic review. Twenty five were case-control studies, and one was a cohort study. In total, these studies included 2142 NSOFC cases compared to 118129 controls. All meta-analyses showed an association between ETS and the risk of having a child with NSOFC, based on the cleft phenotype, risk of bias, and year of publication, with a pooled increased odds ratio of 1.80 (95% CI: 1.51-2.15). These studies had a marked heterogeneity, which decreased upon subgrouping based on the recent year of publication and the risk of bias. CONCLUSIONS ETS exposure was associated with more than a 1.5-fold increase in the risk of having a child with NSOFC, showing a higher odds ratio than paternal and maternal active smoking. [ABSTRACT FROM AUTHOR]

Introduction Two known major risk factors for oral squamous cell carcinoma are smoking and alcohol consumption. Environmental tobacco smoke (also known as secondhand smoke) has been proven to be associated with the occurrence of lung and breast carcinoma. This study aimed to assess exposure to environmental tobacco smoke and its association with the development of oral squamous cell carcinomas. Methods Using a standardized questionnaire, 165 cases and 167 controls were asked about their demographic data and risk behaviors, including environmental tobacco smoke exposure. An environmental tobacco smoke score (ETS-score) was developed to semi-quantitatively record the previous exposure to ETS. Statistical analyses were performed with χ 2 test or Fishers exact test, and with ANOVA or Welch’s t-test as appropriate. An analysis was done using multiple logistic regression. Results Cases had a significantly increased previous exposure to environmental tobacco smoke compared to the controls (ETS-score: 36.69 ± 26.34 vs 13.92 ± 12.44; p

Introduction Alzheimer’s disease (AD) is a disease caused by many factors including occupational and environmental factors. Secondhand smoke (SHS) can affect cognitive function. However, there is limited recent epidemiological research on how SHS and occupational factors affect AD in Zhejiang province. Methods We established a cohort of an AD high-risk population. In 2018, a cohort of 1742 elderly aged ≥60 years was established. In 2020, the cohort was followed up, and a total of 1545 people participated in the two surveys. Data collection included demographic and economic information such as age, gender, occupation, education level etc., and relative health behavior information such as smoking, drinking and tea drinking, etc. Basic physical examination data included height, weight, blood pressure, etc. At the same time, related cognitive status was assessed. Cox proportional hazards regression models, both unadjusted and adjusted models, were used to determine associations between cohort characteristics and AD. Results The results showed that SHS exposure and occupational characteristics were associated with an increased risk of cognitive impairments in seniors. Subgroups who used to work as blue-collar workers, who never worked, who kept standing for most of the time at work, and who were engaged in hard physical labor prior to retirement, had high incidence rates of AD. Conclusions It was revealed that SHS, standing for most of the time and hard physical labor were associated risk factors of AD among seniors, compared with white-collar work. We recommend that the government establish a community supervisory mechanism to persuade smokers to quit or control smoking.

Abstract Background Epidemiological studies suggest that advanced paternal age impact offspring health, but its impact on respiratory health is unclear. This study aimed to investigate the association of paternal age with lung function and fraction of exhaled nitric oxide (FeNO) in children. Methods We analyzed data from 1330 single-born children (576 girls, 43.3%; mean age, 6.4 years), who participated in the Longitudinal Investigation of Global Health in Taiwanese Schoolchildren (LIGHTS) cohort and received measurements of lung function and FeNO at 6-year follow-up visits. Covariate-adjusted regression analyses were applied. Results Every 5-year increase in paternal age at birth was associated with 0.51% decrease in FEV1/FVC ratio (95% CI − 0.86 to − 0.15; p = 0.005) and 19.86 mL/s decrease in FEF75 (95% CI: − 34.07 to − 5.65; p = 0.006). Stratified analyses revealed that increasing paternal age at birth was associated with decreasing FEV1/FVC ratio and FEF75 only among children with prenatal exposure to environmental tobacco smoke (ETS) or not being breastfed. Sensitivity analyses using paternal age as a categorical variable found decreasing FEV1/FVC ratio and FEF75 in the groups of paternal age 35–39 and ≥ 40 years. There was no association of paternal age at birth with FeNO. Conclusion Our findings provide novel evidence linking advanced paternal age at birth with decreasing lung function in children at school age. Children with prenatal exposure to ETS or not being breastfed are more vulnerable to the adverse effect of advanced paternal age on childhood lung function. Further studies are warranted to confirm this novel adverse effect of advanced paternal age.

PurposeTo examine if secondhand smoke (SHS) is associated with elevated risk of type II diabetes among California teachers. We also aim to determine if overall and central obesity are mediators or effect modifiers of this association.MethodsUsing data from the California Teachers Study, conducted in 1995-2013 in California public schools, we obtained information on SHS exposure among 39,887 lifetime nonsmokers. The association between SHS and incident diabetes after 17 years of follow-up was assessed using Cox regression models. The mediation and modification effects of BMI and waist circumference on this association were tested.ResultsAt baseline, 70.2% of the nonsmokers reported exposure to SHS. Higher intensity, duration, and intensity-years of exposure to SHS were associated with higher multivariate adjusted risk of incident diabetes in a dose-response manner (hazard ratio = 1.28; 95% confidence interval, 1.11-1.48 for highest quartile vs. lowest quartile of exposure; P = .001 for trend). Participant's waist circumference (measured 2 years after baseline) could explain greater than 50% of the association between SHS and diabetes.ConclusionsSHS exposure is associated with increased risk of type II diabetes among nonsmokers of California teachers with obesity being a potentially important mediator but not an effect modifier for this association.

Prenatal tobacco exposure is a significant, preventable cause of childhood morbidity, yet little is known about exposure risks for many race/ethnic subpopulations. We studied active smoking and environmental tobacco smoke (ETS) exposure in a population-based cohort of 13 racially/ethnically diverse pregnant women: white, African American, Hispanic, Native American, including nine Asian/Pacific Islander subgroups: Chinese, Japanese, Korean, Filipino, Cambodian, Vietnamese, Laotian, Samoan, and Asian Indians (N = 3329). Using the major nicotine metabolite, cotinine, as an objective biomarker, we analyzed mid-pregnancy serum from prenatal screening banked in 1999⁻2002 from Southern California in an effort to understand differences in tobacco exposure patterns by race/ethnicity, as well as provide a baseline for future work to assess secular changes and longer-term health outcomes. Prevalence of active smoking (based on age- and race-specific cotinine cutpoints) was highest among African American, Samoan, Native Americans and whites (6.8⁻14.1%); and lowest among Filipinos, Chinese, Vietnamese and Asian Indians (0.3⁻1.0%). ETS exposure among non-smokers was highest among African Americans and Samoans, followed by Cambodians, Native Americans, Vietnamese and Koreans, and lowest among Filipinos, Japanese, whites, and Chinese. At least 75% of women had detectable cotinine. While for most groups, levels of active smoking corresponded with levels of ETS, divergent patterns were also found. For example, smoking prevalence among white women was among the highest, but the group's ETS exposure was low among non-smokers; while Vietnamese women were unlikely to be active smokers, they experienced relatively high ETS exposure. Knowledge of race/ethnic differences may be useful in assessing disparities in health outcomes and creating successful tobacco interventions.

IntroductionNon-smoking policies are strictly enforced in neonatal intensive care units (NICUs), which may still become contaminated by thirdhand smoke (THS), posing potential health risks to medically fragile infants. Study aims were to explore contamination routes by characterizing nicotine levels (THS proxy) found on the fingers of NICU medical staff and to assess finger-nicotine correlates.MethodsNICU medical staff were surveyed regarding smoking and electronic nicotine devices (ENDS) use/exposure, and household characteristics. Approximately 35% of staff were randomly selected for a finger-nicotine wipe. Three separate quantile regressions modeled percentiles associated with: presence of any finger nicotine, finger-nicotine levels above the median field blank level (i.e. 0.377 ng/wipe), and finger-nicotine levels two times the median blank.ResultsThe final sample size was 246 (n=260 approached; n=14 refusals). Over three-quarters (78.5%) reported some exposure to tobacco smoke or ENDS vapor/aerosols. After field-blank adjustments, the median nicotine level (ng/finger wipe) was 0.232 (IQR: 0.021-0.681) and 78.3% of medical staff had measurable finger-nicotine levels. Both being near smoking in friends'/family members' homes and finger-surface area were related to elevated finger-nicotine levels (p

Cigarette smoking continues to account for morbidity and mortality of millions around the globe. The adverse effects of active and passive smoking are well known and documented in the literature. Thirdhand smoke (THS) refers to the surface contamination produced by the emission of components in secondhand smoke (SHS) and by their products of chemical transformations, and the off-gassing of volatile components into the atmosphere. Because of its long-term detrimental effects on health, this involuntary and unaware intake of tobacco smoke components by those who are exposed to indoor areas, especially children, even in the absence of concurrent smoking, should be well addressed. This review gives an elaborated insight on the composition, sources, exposure and toxicity of THS along with its mitigation measures.

Abstract Background Particulate matter (PM) emission caused by tobacco combustion leads to severe health burdens worldwide. Second-hand smoke exposure is extraordinarily high in enclosed spaces (e.g., indoor rooms, car cabins) and poses a particular threat to the health of vulnerable individuals (e.g., children, elderly, etc.). This study aimed to establish a new measuring platform and investigate PM emissions under four different ventilation conditions inside a car cabin without exposing any person to harmful tobacco smoke. Methods PM concentrations were measured during the smoking of 3R4F reference cigarettes in a Mitsubishi Space Runner (interior volume 3.709 m3). The cigarettes were smoked with a machine, eliminating exposure of the researchers. Cigarettes were extinguished 4.5 min after ignition, and PM measurements continued until 10 min after ignition. Results High mean PM concentrations were measured for cigarettes without ventilation after 4.5 min (PM10: 1150 µg/m3, PM2.5: 1132 µg/m3, PM1: 861.6 µg/m3) and after 10 min (PM10: 1608 µg/m3, PM2.5: 1583 µg/m3, PM1: 1133 µg/m3). 3R4F smoked under conditions with turned on ventilation resulted in reduction of PM compared to those smoked without ventilation after 4.5 min (PM10:-47.5 to -58.4%, PM2.5:-47.2 to -58%, PM1:-39.6 to -50.2%) and after 10 min (PM10:-70.8 to -74.4%, PM2.5:-70.6 to -74.3%, PM1:-64.0 to -68.0%). Cigarettes smoked without ventilation generated high PM peaks at 4.5 min (PM10: 2207 µg/m3, PM2.5: 2166 µg/m3, PM1: 1421 µg/m3) and at 10 min (PM10: 1989 µg/m3, PM2.5: 1959 µg/m3, PM1: 1375 µg/m3). PM peaks of cigarettes smoked under different ventilation modes varied at 4.5 min (PM10: 630-845 µg/m3, PM2.5: 625-836 µg/m3, PM1: 543 - 693 µg/m3) and 10 min (PM10: 124 - 130 µg/m3, PM2.5: 124 - 129 µg/m3, PM1: 118 - 124 µg/m3). Conclusion The new measuring platform provides a safer way for researchers to investigate PM emissions of cigarettes. These data are comparable to published research and show that smoking in a parked vehicle with the windows closed generates harmful PM emissions even when the vehicle ventilation is in operation. Future studies should be carried out using the new measuring platform investigating PM exposure and PM distribution of in-vehicle smoking under a wide range of conditions.

INTRODUCTION Two known major risk factors for oral squamous cell carcinoma are smoking and alcohol consumption. Environmental tobacco smoke (also known as secondhand smoke) has been proven to be associated with the occurrence of lung and breast carcinoma. This study aimed to assess exposure to environmental tobacco smoke and its association with the development of oral squamous cell carcinomas. METHODS Using a standardized questionnaire, 165 cases and 167 controls were asked about their demographic data and risk behaviors, including environmental tobacco smoke exposure. An environmental tobacco smoke score (ETS-score) was developed to semi-quantitatively record the previous exposure to ETS. Statistical analyses were performed with χ² test or Fishers exact test, and with ANOVA or Welch's t-test as appropriate. An analysis was done using multiple logistic regression. RESULTS Cases had a significantly increased previous exposure to environmental tobacco smoke compared to the controls (ETS-score: 36.69 ± 26.34 vs 13.92 ± 12.44; p<0.0001). Comparing only the groups without additional active risk factors, exposure to environmental tobacco smoke was associated with a more than threefold higher likelihood of oral squamous cell carcinoma (OR=3.47; 95% CI: 1.31-10.55). Statistically significant differences in ETS-score were found for different tumor locations (p=0.0012) and different histopathological gradings (p=0.0399). A multiple logistic regression analysis confirmed exposure to environmental tobacco smoke as an independent risk factor for the development of oral squamous cell carcinomas (p<0.0001). CONCLUSIONS Environmental tobacco smoke is an important but yet underestimated risk factor for the development of oral squamous cell carcinomas. Further studies are needed to confirm the results, including the usefulness of the developed environmental tobacco smoke score for exposure. [ABSTRACT FROM AUTHOR]

Aim of the study was to assess the relationship between environmental tobacco smoke (ETS) and computed tomography-derived left ventricular global longitudinal strain (LV GLS) in patients with arterial hypertension. 103 non-smokers with AH were included in the study (age 67.73 ± 8.84 years). ETS exposure was assessed with the Second-Hand Smoke Exposure Scale (SHSES). LV GLS was measured on computed tomography using feature tracking technology. In accordance with SHSES scale patients were divided into subgroups: subgroup A—no ETS exposure, subgroup B—low ETS exposure, subgroup C—medium ETS exposure, and subgroup D—high ETS exposure. Peak of LV GLS was statistically significantly lower in subgroup D than in subgroup A. There was a negative correlation between the exposure to ETS expressed by the SHSES scale and peak of LV GLS (r = − 0.35, p < 0.05). Regression analysis showed that higher SHSES score, higher age, left ventricular hypertrophy, left ventricular diastolic dysfunction, and higher CAD-RADS are independent risk factors for lower peak of LV GLS values. On the contrary, the effective blood pressure control appeared to be independent protecting factor against lower peak of LV GLS values. In summary, there is an unfavorable weak relationship between ETS exposure estimated using the SHSES scale and LV GLS in hypertensive patients. [ABSTRACT FROM AUTHOR]

The study aimed to assess the association between environmental exposure and asthma among children between 3 and 12 years old in King Williams Town, South Africa. A quantitative case-control study was conducted at Grey Hospital to assess the association between environmental exposure and asthma among children who reside in King Williams Town. Of the total 566 study participants, 50.5% (286) had asthma while 49.5% did not. Socio-demographic factors associated with asthma in children were being within the age group 9–12 years (OR 1.74, CI 95% 1.09–2.78) and India ethnicity (OR 0.20, CI 95% 0.08–0.48). Factors associated with asthma were weight within 25–35 kg (OR 1.64, CI 95% 1.11–2.42) and BMI within 15–20 (OR 4.80, CI 95% 2.80–8.22). Environmental risk factors associated with asthma were indoor exposure to tobacco smoke from mothers of the participants (OR 5.45, CI 95% 3.08–9.65) and from fathers (OR 4.37; CI 95% 2.77–6.90). Abstaining from eating seafood appeared to be protective from developing asthma (OR 0.01; CI 95% 0.00–0.05). The study found no significant association between outdoor environmental exposures and childhood asthma. The age of participant, weight, BMI, exposure to environmental tobacco smoke (ETS), and eating seafood had significant correlations with childhood asthma. Strengthening the evaluation of children healthcare and encouraging smoking cessation among parents could reduce exposure to environmental asthma triggers among children. [ABSTRACT FROM AUTHOR]

Effects of environmental tobacco smoke (ETS) exposure on children and adolescent health outcomes have been attracted more and more attention. In the present study, we seek to examine the gender-specific difference association of environmental smoke exposure biomarkers and developmental disorders in children and adolescents aged 6–15 years. US nationally representative sample collected from the National Health and Nutrition Examination Survey (NHANES) 2007–2014 was enrolled (N = 4428). Developmental disorders (DDs) are defined as a positive answer to the question, "Does your child receive special education or early intervention services?" Serum cotinine and urinary 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) were utilized as acute and chronic exposure biomarkers of ETS, respectively. Participants with serum cotinine >0.015 ng/mL were considered as with acute ETS exposure, and participants with creatinine-adjusted NNAL >0.0006 ng/mL were considered as with chronic ETS exposure. A survey logistic regression model was used to estimate the association between ETS exposure biomarkers and DDs. Additive interaction was utilized to examine the interaction of gender and biomarkers of ETS. Overall, approximately 9% of children were defined as DDs, and 65% of children had serum cotinine and urinary NNAL levels above the limit of detection. In the adjusted models, the association of ETS exposure biomarkers with DDs was only observed in girls. Girls with low cotinine levels and high urinary NNAL levels had 2.074 (95% CI: 1.012–4.247) and 1.851 (95% CI: 1.049–3.265) times higher odds of being DDs than those without ETS exposure, respectively. However, the effects of boys and NNAL exposure on DDs have additively interacted. Our findings first provided strong evidence for gender differences in the association between two tobacco metabolites and DDs in children, disclosing the public health implications and economic burdens of environmental tobacco smoke exposure. [ABSTRACT FROM AUTHOR]