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

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

Active and passive smoking and breast cancer in Japan: a pooled analysis of nine population-based cohort studies.

BACKGROUND: Epidemiological studies have shown inconsistent results regarding the link between smoking and breast cancer risk, despite the biological plausibility of a positive association. METHODS: Participants were 166 611 women from nine prospective cohort studies in Japan which launched in 1984-1994 and followed for 8-22 years. Information on smoking and secondhand smoke was obtained through self-administered baseline questionnaires. Breast cancer was defined as code C50 according to the International Classification of Diseases for Oncology, 3rd Edition or the International Classification of Diseases, 10th Revision. After adjusting for several potential confounders, relative risks for breast cancer were calculated in the individual studies according to the current or previous status of active and passive smoking using Cox regression, followed by a summary estimate of hazard ratios using random-effects meta-analyses. RESULTS: Of the 60 441 participants who reported being premenopausal and 106 170 who reported being postmenopausal at baseline, 897 and 1168 developed breast cancer during follow-up, respectively. Compared with never smokers, current smokers had a higher risk of developing breast cancer before the age of 50 years. In addition, ever smokers who started smoking at 30 years of age or younger, or who started smoking before first childbirth, had a higher risk of developing breast cancer before the age of 50 years. No association between adulthood or childhood exposure to secondhand smoke and breast cancer was observed. CONCLUSION: Smoking may increase the risk of premenopausal breast cancer, and smoking earlier in life might be especially harmful. The impact of secondhand smoke needs further investigation.

Tobacco control interventions for populations living in subsidised, low-income housing: a scoping review.

OBJECTIVES: People living in subsidised low-income housing are more likely to smoke and experience secondhand smoke exposure compared to the general population. While tobacco control interventions have yielded substantial population health benefits, people living in subsidised housing experience a greater burden of tobacco-related harms. We synthesised existing peer-reviewed and grey literature to determine tobacco control interventions that have been implemented in subsidised housing globally, and to understand their impact on smoking and secondhand smoke exposure. METHODS: We searched five databases for peer-reviewed research, and Google Advanced for grey literature. We adhered to the JBI Scoping Review Methodology and Preferred Reporting Items for Systematic reviews and Meta-Analyses extension for Scoping Reviews (PRISMA-ScR) checklist. RESULTS: Fifty-seven sources met the eligibility criteria. The most common type of intervention was mandatory smoking bans covering all indoor spaces (n = 32), followed by cessation-focused interventions (n = 19). Interventions that indirectly addressed smoking were the least common (n = 6). Our findings suggest smoking bans can increase smoking cessation and reduce secondhand smoke exposure, especially if implemented alongside cessation support strategies. CONCLUSION: Tobacco control interventions targeting subsidised housing demonstrate positive effects on tobacco-related outcomes for residents and provide an important opportunity to address health disparities. Future research should examine the long-term impacts of the interventions, including potential unintended consequences, in varied subsidised housing contexts.

Tobacco smoke condensate-induced senescence in endothelial cells was ameliorated by colchicine treatment via suppression of NF-κB and MAPKs P38 and ERK pathways activation.

Smoking is the major cause of cardiovascular diseases and cancer. It induces oxidative stress, leading to DNA damage and cellular senescence. Senescent cells increase the expression and release of pro-inflammatory molecules and matrix metalloproteinase, which are known to play a vital role in the initiation and progression of cardiovascular diseases and metastasis in cancer. The current study investigated the smoking induced cellular senescence and employed colchicine that blocked senescence in endothelial cells exposed to tobacco smoke condensate. Colchicine prevented oxidative stress and DNA damage in tobacco smoke-condensate-treated endothelial cells. Colchicin reduced ß-gal activity, improved Lamin B1, and attenuated cell growth arrest markers P21 and P53. Colchicine also ameliorated the expression of SASP factors and inhibited the activation of NF-kB and MAPKs P38 and ERK. In summary, colchicine inhibited tobacco smoke condensate-induced senescence in endothelial cells by blocking the activation of NF-kB and MAPKs P38 and ERK.

Secondhand smoke prevention through the perceptions of pregnant women with smoking family members: a Thailand study.

PURPOSE: Pregnant women with smoking family members are at risk of exposure to second-hand smoke, which leads to adverse pregnancy outcomes. Second-hand smoke prevention is thus important but remains less understood based on pregnant women's perceptions. This study aimed to describe the perceptions of pregnant women on second-hand smoke prevention. METHODS: This study employed a qualitative descriptive approach. Data collection was performed between July and August 2023 through in-depth interviews with 17 pregnant women purposively selected from a province in central Thailand. The verbatim transcribed data were analysed using thematic analysis. RESULTS: Five themes emerged: unclear understanding of second-hand smoke; influences shaping perceptions related to second-hand smoke; attempt to prevent second-hand smoke exposure; barriers to prevention of second-hand smoke exposure; and needs related to prevention of second-hand smoke exposure. CONCLUSION: The findings provide insights into second-hand smoke prevention from the perception of pregnant women with smoking family members. Healthcare professionals need to design interventions tailored to pregnant women's needs and involve smoking family members. It is necessary to develop and incorporate clinical guidelines into standard prenatal care to support healthcare personnel in identifying, assessing, educating, and mitigating the issue of second-hand smoking exposure.

Epidemiology and risk factors of oral frailty among older people: an observational study from China.

OBJECTIVES: This study aimed to compare the prevalence of oral frailty among community-dwelling older people in Nanjing, China with the usage of different measurements, and to investigate the potential risk factors of oral frailty. DESIGN: Cross-sectional study. SETTING AND PARTICIPANTS: A total of 338 community-dwelling older people in Nanjing, China were recruited. METHODS: Oral frailty was measured based on the Oral Frailty Index-8 (OFI-8) scale and other measurement methods including the number of natural teeth (TN), repetitive saliva-swallowing test (RSST), and oral diadochokinesis (ODK). The chi-square test and the binary logistic regression analysis were performed to identify potential risk factors for oral frailty. RESULTS: There were 310 participants included in the analysis. Prevalence of oral frailty by using the OFI-8, OFI-8 + TN, OFI-8 + ODK, OFI-8 + TN + ODK and RSST measurement methods were 69.0%, 27.4%, 51.9%, 21.0% and 2.9%, respectively. Passive smoking (OR = 2.04; 95%CI 1.03-4.03), being widowed/unmarried (OR1 = 2.53; 95%CI 1.25-5.10; OR2 = 2.94; 95%CI 1.12-7.77), pre-frailty (OR = 1.76; 95%CI 1.03-3.01), frailty (OR = 3.01; 95%CI 1.39-6.54), and aged 80 years and above (OR = 3.99; 95%CI 1.35-11.81) were found to be risk factors of oral frailty by the usage of the four kinds of measurement methods. CONCLUSIONS AND IMPLICATIONS: The definition and diagnostic criteria of oral frailty are strongly needed to be unified in future research. Only subjective assessment is not enough for assessing oral frailty. Among objective indicators, RSST is not suitable as a screening method for oral frailty. In addition, objective indicators including TN and ODK should be valued for early screening and preventive interventions. The risk factors of oral frailty include physical frailty, passive smoking, and being widowed.

A systematic review of second-hand smoking mass media campaigns (2002-2022).

BACKGROUND: Second-hand smoking (SHS) increases the risk of chronic disease in adults and poses a serious health threat to children. Mass media campaigns are instrumental in raising awareness and reducing SHS exposure. There is a need to identify recent SHS mass media campaigns and assess their sustainability in terms of knowledge, attitudes, and behavioural changes. This systematic review summarises the characteristics and outcomes of mass media campaigns on SHS prevention. METHODS: PubMed, Embase, Web of Science, and grey literature were searched in November 2022 for SHS campaigns implemented between 2016 and 2022. The eligibility criteria included campaigns on the dangers or effects of SHS with any target group, dissemination medium, study design, or language. The database search identified 1,413 peer-reviewed titles, of which 82 full-texts were screened, with 14 meeting the eligibility criteria. The grey literature search identified 9,807 sources, of which 61 were included. We extracted data on the campaign characteristics, metrics, and smoking-related outcomes. The JBI critical appraisal tool was used to assess the risk of bias of the included studies. RESULTS: We found 73 SHS campaigns conducted between 2002 and 2022, across 50 countries. The campaigns reached 378 million people. The reported recall rates range from 8 to 76%. Of the 11 studies that reported smoking-related outcomes, 10 reported increased knowledge in understanding SHS risks (73-85%), five reported an increased prevalence of smoke-free homes, and two reported an increase in number of participants persuading others to quit smoking. Two studies reported a decrease in overall smoking, whereas three studies observed a reduction in smoking in the presence of children. CONCLUSION: The available data provide some support for the effectiveness of SHS campaigns in reducing smoking behaviours in homes and around children. However, the certainty of evidence was low due to the lack of a control group and the substantial heterogeneity in the outcomes assessed. Future campaigns need comprehensive evaluation and reporting to reduce publication bias.

Recent tobacco smoking, restaurant and in-car secondhand smoke exposure are associated with depressive symptoms among young adults: a population-based cross-sectional analysis.

The purpose of this study was to evaluate the association between recent tobacco smoking, household secondhand smoke exposure, confined space secondhand smoke exposure and depressive symptoms in young adults after adjustments for each other. Data from NHANES 2013-2018 were extracted. A total of 4129 young adults age 18-35 years (mean age 26.11 ± 5.39 years, 2021 males and 2108 females) were included. Depressive symptoms were screened by PHQ-9. Recent tobacco smoking was assessed through question "smoked tobacco in the last 5 days?". Household secondhand smoke exposure was assessed through question "living with a smoker who smoked inside the house?". Confined space secondhand smoke exposure was assessed by SSEQ. Binary logistic regression models were performed to analyze the associations. Significant association were observed in recent tobacco smoking (OR = 1.593, 95% CI 1.318-1.926) and confined space secondhand smoke exposure (OR = 1.399, 95% CI 1.185-1.651), but not in household secondhand smoke exposure (P = 0.108). Among the different settings of confined space secondhand smoke exposure, restaurant (OR = 1.732, 95% CI 1.120-2.678) and in-car (OR = 1.350, 95% CI 1.102-1.652) exposure were significantly associated with depressive symptom after after fully adjustments.

Airway inflammation in a novel mouse model of asthma-COPD overlap induced by co-exposure to papain and tobacco smoke.

Asthma and chronic obstructive pulmonary disease (COPD) are respiratory diseases associated with airway inflammation, which is the main pathogenesis. Although their causes and characteristics differ, in some cases, asthma and COPD may coexist in the same patient in a condition called asthma-COPD overlap (ACO). The prognosis of ACO is more unfavourable than those of asthma or COPD alone, without any treatment strategies demonstrating efficacy. Owing to its intricate spectrum of features, the detailed pathogenesis of how ACO exacerbates respiratory features remains unclear. In this study, we exposed papain-induced asthma model mice to tobacco smoke to establish an ACO mouse model, in which features of airway inflammation observed in both asthma and COPD were incorporated. This model exhibited distinctive mixed and corticosteroid-resistant airway inflammation and emphysematous changes that are characteristic of ACO. The novel mouse model established here is expected to significantly contribute to elucidating the mechanisms of the broad pathologies of ACO and identifying potential therapeutic targets.

Combined and sequential exposure to prenatal second hand smoke and postnatal maternal distress is associated with cingulo-opercular global efficiency and attention problems in school-age children.

BACKGROUND: Prenatal exposure to secondhand (environmental) tobacco smoke (SHS) is associated with adverse neurodevelopmental outcomes, including altered functional activation of cognitive control brain circuitry and increased attention problems in children. Exposure to SHS is more common among Black youth who are also disproportionately exposed to socioeconomic disadvantage and concomitant maternal distress. We examine the combined effects of exposure to prenatal SHS and postnatal maternal distress on the global efficiency (GE) of the brain's cingulo-opercular (CO) and fronto-parietal control (FP) networks in childhood, as well as associated attention problems. METHODS: Thirty-two children of non-smoking mothers followed in a prospective longitudinal birth cohort at the Columbia Center for Children's Environmental Health (CCCEH) completed magnetic resonance imaging (MRI) at ages 7-9 years old. GE scores were extracted from general connectivity data collected while children completed the Simon Spatial Incompatibility functional magnetic resonance imaging (fMRI) task. Prenatal SHS was measured using maternal urinary cotinine from the third trimester; postnatal maternal distress was assessed at child age 5 using the Psychiatric Epidemiology Research Interview (PERI-D). The Child Behavior Checklist (CBCL) measured Attention and Attention Deficit Hyperactivity Disorder (ADHD) problems at ages 7-9. Linear regressions examined the interaction between prenatal SHS and postnatal maternal distress on the GE of the CO or FP networks, as well as associations between exposure-related network alterations and attention problems. All models controlled for age, sex, maternal education at prenatal visit, race/ethnicity, global brain correlation, and mean head motion. RESULTS: The prenatal SHS by postnatal maternal distress interaction term associated with the GE of the CO network (ß = 0.673, Bu = 0.042, t(22) = 2.427, p = .024, D = 1.42, 95% CI [0.006, 0.079], but not the FP network (ß = 0.138, Bu = 0.006, t(22) = 0.434, p = .668, 95% CI [-0.022, 0.033]). Higher GE of the CO network was associated with more attention problems (ß = 0.472, Bu = 43.076, t(23) = 2.780, p = .011, D = 1.74, n = 31, 95% CI [11.024, 75.128], n = 31) and ADHD risk (ß = 0.436, Bu = 21.961, t(29) = 2.567, p = .018, D = 1.81, 95% CI [4.219, 39.703], n = 30). CONCLUSIONS: These preliminary findings suggest that sequential prenatal SHS exposure and postnatal maternal distress could alter the efficiency of the CO network and increase risk for downstream attention problems and ADHD. These findings are consistent with prior studies showing that prenatal SHS exposure is associated with altered function of brain regions that support cognitive control and with ADHD problems. Our model also identifies postnatal maternal distress as a significant moderator of this association. These data highlight the combined neurotoxic effects of exposure to prenatal SHS and postnatal maternal distress. Critically, such exposures are disproportionately distributed among youth from minoritized groups, pointing to potential pathways to known mental health disparities.

Ultrastructural changes of lung tissue under conditions of experimental obesity and smoking.

Obesity can cause respiratory disorders inflicted by adipose tissue accumulation and the numerous cytokines adipocytes produce. Smoking is, first of all, associated with a wide range of lung diseases characterized by diffuse changes in the lung tissue and a decrease in the respiratory volume of the lungs. The study aimed to investigate the ultrastructural changes in the lungs of sexually mature male rats under conditions of experimental obesity and smoking. The total sample of experimental animals consisted of 120 rats, divided into four groups: the control group (n=30) - conditionally healthy rats fed on a standard diet; a group of rats subjected to isolated exposure to tobacco smoke (n=30); a group of experimentally obese rats (n=30) and a group of experimentally obese rats simultaneously exposed to tobacco smoke (n=30) - feeding using a high-fat diet with exposure to a chamber with tobacco smoke. The revealed ultrastructural features of the lungs in the group of rats with experimental obesity and the group of rats with experimental obesity that were simultaneously exposed to tobacco smoke did not differ qualitatively, which indicates that pathological changes in the ultrastructure of the lung tissue developed regardless of the presence or absence of a direct damaging effect on the lung tissue of passive smoking.

Association between Outdoor and Indoor Air Pollution Sources and Atopic Eczema among Preschool Children in South Africa.

The objective of the study was to investigate the association between outdoor and indoor air pollution sources and atopic eczema among preschool children in South Africa. A cross-sectional design, following the International Study of Asthma and Allergies in Childhood (ISAAC) Phase III protocol, was applied. The study was conducted in Mabopane and Soshanguve Townships in the City of Tshwane Metropolitan Municipality in Gauteng, South Africa. A total population of 1844 preschool children aged 7 years and below participated in the study; 1840 were included in the final data analysis. Data were analyzed using multilevel logistic regression analysis. The prevalence of eczema ever (EE) and current eczema symptoms (ESs) was 11.9% and 13.3%, respectively. The use of open fires (paraffin, wood, or coal) for cooking and heating increased the likelihood of EE (OR = 1.63; 95% CI: 0.76-3.52) and current ESs (OR = 1.94; 95% CI: 1.00-3.74). Environmental tobacco smoke (ETS) exposure at home increased the likelihood of EE (OR = 1.66; 95% CI: 1.08-2.55) and current ESs (OR = 1.61; 95% CI: 1.07-2.43). Mothers or female guardians smoking cigarettes increased the likelihood of EE (OR = 1.50; 95% CI: 0.86-2.62) and current ESs (OR = 1.23; 95% CI: 0.71-2.13). The use of combined building materials in homes increased the likelihood of EE, and corrugated iron significantly increased the likelihood of current ESs. The frequency of trucks passing near the preschool children's residences on weekdays was found to be associated with EE and current ESs, with a significant association observed when trucks passed the children's residences almost all day on weekdays. Atopic eczema was positively associated with exposure to outdoor and indoor air pollution sources.

Perception of harm is strongly associated with complete ban on in-home cannabis smoking: a cross-sectional study.

BACKGROUND: Perception of health risk can influence household rules, but little is known about how the perception of harm from cannabis secondhand smoke (cSHS) is related to having a complete ban on in-home cannabis smoking. We examined this association among a nationally representative sample of United States adults. METHODS: Respondents were 21,381 adults from the cross-sectional Marijuana Use and Environmental Survey recruited from December 2019-February 2020. Perceived harm of cSHS exposure (extremely harmful, somewhat harmful, mostly safe, or totally safe) and complete ban of cannabis smoking anywhere in the home (yes or no) were self-reported. Logistic regression for survey-weighted data estimated covariate-adjusted odds ratios (OR) and 95% confidence intervals (CI) for the association between perceived harm of cSHS and complete ban on in-home cannabis smoking. Stratified subgroup analyses (by cannabis smoking status, cannabis use legalization in state of residence, and children under age 6 living in the home) were conducted to quantify effect measure modification of the association between perception of harm and complete ban. RESULTS: A complete ban on in-home cannabis smoking was reported by 71.8% of respondents. Eight percent reported cSHS as "totally safe"; 20.5% "mostly safe"; 38.3% "somewhat harmful"; and 33.0% "extremely harmful". Those who reported cSHS as "extremely harmful" had 6 times the odds of a complete ban on in-home cannabis smoking (OR = 6.0, 95%CI = 4.9-7.2) as those reporting smoking as "totally safe". The odds of a complete ban were higher among those reporting cSHS as "somewhat harmful" (OR = 2.6, 95%CI = 2.2-3.1) or "mostly safe" (OR = 1.4, 95%CI = 1.2-1.7) vs those reporting cSHS as "totally safe". In each subgroup of cannabis smoking status, state cannabis use legalization, and children under the age of 6 living in the home, perceived harm was associated with a complete ban on in-home cannabis smoking. CONCLUSIONS: Our study demonstrates perceiving cSHS as harmful is strongly associated with having a complete in-home cannabis smoking ban. With almost a third of US adults perceiving cSHS as at least "mostly safe", there is strong need to educate the general population about potential risks associated with cSHS exposure to raise awareness and encourage adoption of household rules prohibiting indoor cannabis smoking.

Impacts of environmental tobacco smoke on the onset and progression of multiple sclerosis: a systematic review.

BACKGROUND: Unlike cigarette smoking, environmental tobacco smoke (ETS) has not been as well described as an environmental risk for Multiple sclerosis (MS) nor as a risk factor for disease progression. OBJECTIVE: We systematically reviewed the association between ETS and the risk of onset and/or progression of MS. METHODS: We systematically screened MedLine/PubMed, Science Direct, LILACs, and SciELO searching for publications between January 1st, 2010, and July 5, 2021, with the following keywords: "multiple sclerosis and smoking"; "multiple sclerosis and passive smoking"; "multiple sclerosis and secondhand smoking". RESULTS: Fifteen articles were included in this review, which consisted of systematic reviews with meta-analysis (N = 2), systematic reviews (N = 2), and observational studies (N = 11). Both meta-analyses reported an impact of ETS on MS onset among secondhand smokers. One of the systematic reviews selected two observational studies showing the association between ETS and MS development, and one study that did not find a significant association between ETS and the risk of MS development. The other systematic review identified selected eight articles showing a relationship between ETS and MS. Seven observational studies reported higher odds of MS onset when associated with ETS. Four observational studies did not show a relationship between ETS and MS onset or progression. CONCLUSION: Most articles showed a positive association between ETS exposure and the risk of developing MS. On the other hand, an association between ETS and a higher risk for MS progression could not be established.

ANTECEDENTES: Ao contrário do tabagismo ativo, o fumo passivo (FP) não é tão bem estabelecido como risco para o desenvolvimento de esclerose múltipla (EM) nem como um fator de risco para a progressão da doença. OBJETIVO: Revisamos sistematicamente a associação entre FP e o risco de aparecimento e/ou progressão da EM. MéTODOS: Fizemos uma triagem sistemática nas bases de dados MedLine/PubMed, Science Direct, LILACs e SciELO em busca de publicações entre 1° de janeiro de 2010 e 5 de julho de 2021 com as seguintes palavras-chave: "multiple sclerosis and smoking"; "multiple sclerosis and passive smoking"; "multiple sclerosis and secondhand smoking". RESULTADOS: Quinze artigos foram incluídos nesta revisão, que consistiu em revisões sistemáticas com metanálise (N = 2), revisões sistemáticas (N = 2) e estudos observacionais (N = 11). As metanálises relataram um impacto do FP no surgimento da EM entre fumantes passivos. Um revisão sistemática selecionou dois estudos observacionais mostrando a associação entre FP e desenvolvimento de EM, e um estudo que não encontrou associação significativa entre FP e o risco de desenvolvimento de EM. Outra revisão sistemática identificou oito artigos selecionados mostrando uma relação entre FP e EM. Sete estudos observacionais relataram maiores chances de aparecimento de EM quando associados a FP. Quatro estudos observacionais não mostraram uma relação entre FP e o desenvolvimento ou progressão da EM. CONCLUSãO: A maioria dos artigos mostrou uma associação positiva entre a exposição ao FP e o risco de desenvolver EM. Por outro lado, não foi possível estabelecer uma associação entre FP e maior risco de progressão da EM.

The application of a self-designed microfluidic lung chip in the assessment of different inhalable aerosols.

Microfluidic-based assessment platforms have recently attracted considerable attention and have been widely used for evaluating in vitro toxic effects. In the present study, we developed an original real-time aerosol exposure system, which focused on a self-designed microfluidic chip, in order to evaluate the toxicological effects following exposure to inhalable aerosols. The three-layer structured microfluidic chip enables real-time aerosol exposure at the gas-liquid interface. The comprehensive detection of toxic effect biomarkers based on this assessment platform encompasses transcriptomics, in situ fluorescence detection, and the identification of extracellular secretagogues. Correspondingly, the effects of selected inhalable aerosols such as cigarette smoke (CS), heated tobacco product smoke (HS), and electronic cigarette smoke (ES) on gene expression profiles, cell viability, intracellular biomarkers (reactive oxygen species and nitric oxide), apoptosis (caspase-3/7 activity), and extracellular biomarkers (IL-8, IL-1ß, TNF-α, and malondialdehyde) in the BEAS-2B cells present on the chip were investigated. Following exposure to aerosols derived from CS, HS, and ES, the transcriptome analysis revealed differential expression in these cells. In addition, the overlapping DEGs from the different treatment groups were found to be primarily associated with stimuli and inflammatory responses. Correspondingly, each of the three categories of selected inhalable aerosols was confirmed to induce significant changes in biomarkers that were associated with toxic effects. These results suggest that the original real-time aerosol exposure system centered around a self-designed chip can be applied to the toxic effect evaluation of inhalable aerosol exposure.

Low levels of nicotine and cotinine but not benzo[a]pyrene induce human trophoblast cell proliferation.

E-cigarettes use constitutes a source of thirdhand nicotine exposure. The increasing use of electronic cigarettes in homes and public places increases the risk of exposure of pregnant women to thirdhand nicotine. The effects of exposure of pregnant women to very low levels of nicotine have not been studied in humans but detrimental in experimental animals. The objective of this study is to investigate the effect of nanomolar concentrations of nicotine and its metabolite cotinine on the proliferation of JEG-3, a human trophoblast cell line. We also studied the proliferative effect of nanomolar concentrations of benzo[a]pyrene (B[a]P), a polycyclic hydrocarbon in tobacco smoke, for comparison. We treated JEG-3 cells in culture with nanomolar concentrations of nicotine, cotinine, and B[a]P. Their effect on cell proliferation was determined, relative to untreated cells, by MTT assay. Western blotting was used to assess the mitogenic signaling pathways affected by nicotine and cotinine. In contrast to the inhibitory effects reported with higher concentrations, we showed that nanomolar concentrations of nicotine and cotinine resulted in significant JEG-3 cell proliferation and a rapid but transient increase in levels of phosphorylated ERK and AKT, but not STAT3. Biphasic, non-monotonic effect on cell growth is characteristic of endocrine disruptive chemicals like nicotine. The mitogenic effects of nicotine and cotinine potentially contribute to increased villous epithelial thickness, seen in placentas of some smoking mothers. This increases the diffusion distance for oxygen and nutrients between mother and fetus, contributing to intrauterine growth restriction in infants of smoking mothers.

Unraveling the link: environmental tobacco smoke exposure and its impact on infertility among American women (18-50 years).

Purpose: The 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. Methods: For 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. Results: The 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. Conclusion: Our 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.

Secondhand smoke increases the risk of developing chronic obstructive pulmonary disease.

Smoking is the most important risk factor for chronic obstructive pulmonary disease (COPD), however evidence from large-scale studies on whether secondhand smoke (SHS) increases the risk of COPD is still lacking. We conducted this large longitudinal study to investigate the association between SHS and the development of COPD. This is a longitudinal study. Data on 6519 subjects who were never-smokers, had no history of COPD, and had complete lung function records were extracted from the Taiwan Biobank. They were divided into two groups according to SHS exposure: no exposure and exposure groups. Data were collected when participants enrolled in the study and during regular follow-up. Cox proportional hazards regression models were used to estimate the relative risk (RR) and 95% confidence interval (CI) for the association between SHS and the risk of developing COPD. At 48 months of follow-up, 260 (4%) participants in the no exposure group and 34 (7%) participants in the exposure group developed COPD. The RR of incident COPD development was significantly higher in the exposure group than that in the no exposure group after adjusting for confounders (RR = 1.49; 95% CI 1.04 to 2.14; P value = 0.031). There is a dose-response relationship between the duration of exposure to SHS and the risk of incident COPD, which demonstrates that an additional hour of exposure to SHS per week was associated with a 1.03-fold increased likelihood of developing COPD after adjusting for confounders (RR = 1.03; 95% CI 1.00 to 1.05; P value = 0.027). SHS exposure contributes to the development of COPD. This finding can help raise awareness of the harms of SHS and provide a reference for formulating anti-smoking policies.

Correlation analysis between smoke exposure and serum neurofilament light chain in adults: a cross-sectional study.

BACKGROUND: Smoke exposure is a prevalent and well-documented risk factor for various diseases across different organ systems. Serum neurofilament light chain (sNfL) has emerged as a promising biomarker for a multitude of nervous system disorders. However, there is a notable paucity of research exploring the associations between smoke exposure and sNfL levels. METHODS: We conducted a comprehensive analysis of the National Health and Nutrition Examination Survey (NHANES) cross-sectional data spanning the years 2013 to 2014. Serum cotinine levels were classified into the following three groups: < 0.05, 0.05-2.99, and ≥ 3 ng/ml. Multiple linear regression models were employed to assess the relationships between serum cotinine levels and sNfL levels. Additionally, we utilized restricted cubic spline analyses to elucidate the potential nonlinear relationship between serum cotinine and sNfL levels. RESULTS: A total of 2053 participants were included in our present research. Among these individuals, the mean age was 47.04 ± 15.32 years, and males accounted for 48.2% of the total study population. After adjusting the full model, serum cotinine was positively correlated with sNfl in the second group (ß = 0.08, 95%CI 0.01-0.15) and in the highest concentration of serum cotinine (ß = 0.10, 95%CI 0.01-0.19) compared to the group with the lowest serum cotinine concentrations. Current smokers, in comparison to non-smokers, exhibited a trend toward elevated sNfL levels (ß = 0.07, 95%CI 0.01-0.13). Furthermore, subgroup analyses revealed interactions between serum cotinine levels and different age groups (P for interaction = 0.001) and gender stratification (P for interaction = 0.015) on sNfL levels. CONCLUSION: The study suggested that serum cotinine was significantly and positively associated with sNfl levels in adult participants. Furthermore, current smokers tend to exhibit elevated sNfL levels. This research sheds light on the potential implications of smoke exposure on neurological function impairment and underscores the importance of further exploration in this area.

Effect of children secondhand smoke exposure associated with GABA concentration: Influence from parents who are extremely heavy smokers in urban households.

BACKGROUND: Secondhand smoke (SHS) poses the most considerable health risk to children in urban households. However, limited evidence exists regarding the impact of children exposure to SHS on gamma-aminobutyric acid (GABA) levels. This study aimed to investigate the level of cotinine and GABA and their association with variables related to children exposed to SHS. METHODS: A cross-sectional analysis was conducted to assess urinary cotinine and GABA levels in respondents. The study involved 85 participants aged 2-4 years who resided with parents exhibiting heavy smoking habits in urban households in Bangkok, Thailand. Urinary cotinine and GABA concentrations were utilized as biomarkers and measured using an enzyme-linked immunosorbent assay kit. An independent t-test was employed to compare contributing factors with urinary cotinine metabolites. Spearman's correlation test was utilized to assess the relationship between cotinine metabolites and GABA concentration. RESULTS: The study found a correlation between urinary cotinine metabolites and GABA concentration among children's (r = 0.260, p-value = 0.016), particularly influenced by parents exhibiting extreme heavy smoking in urban households. Male children exhibited significantly higher urinary cotinine metabolite concentrations than females (p-value = 0.040). Moreover, significantly elevated levels of cotinine metabolites (57.37 ± 10.27 ng/ml) were observed in households where parents engaged in extreme heavy smoking. CONCLUSIONS: This research establishes a link between urinary cotinine metabolite levels and GABA concentration among children exposed to extreme heavy smoking by their parents in urban households. Consequently, smoking might impact neurobehavioral effects, potentially leading to insomnia. The study emphasizes the importance of promoting and safeguarding non-smokers from exposure to SHS in indoor workplaces, public spaces, and households, advocating for the implementation of smoke-free public health regulations.