New Aminobiphenylcysteine Derivatives in Globin and Urine of Rats Dosed with 4-Aminobiphenyl, a Tobacco Smoke Carcinogen.

The 4-biphenylnitrenium ion (BPN), a reactive metabolic intermediate of the tobacco smoke carcinogen 4-aminobiphenyl (4-ABP), can react with nucleophilic sulfanyl groups in glutathione (GSH) as well as in proteins. The main site of attack of these S-nucleophiles was predicted using simple orientational rules of aromatic nucleophilic substitution. Thereafter, a series of presumptive 4-ABP metabolites and adducts with cysteine were synthesized, namely, S-(4-amino-3-biphenyl)cysteine (ABPC), N-acetyl-S-(4-amino-3-biphenyl)cysteine (4-amino-3-biphenylmercapturic acid, ABPMA), S-(4-acetamido-3-biphenyl)cysteine (AcABPC), and N-acetyl-S-(4-acetamido-3-biphenyl)cysteine (4-acetamido-3-biphenylmercapturic acid, AcABPMA). Then, globin and urine of rats dosed with a single ip dose of 4-ABP (27 mg/kg b.w.) was analyzed by HPLC-ESI-MS2. ABPC was identified in acid-hydrolyzed globin at levels of 3.52 ± 0.50, 2.74 ± 0.51, and 1.25 ± 0.12 nmol/g globin (mean ± S.D.; n = 6) on days 1, 3, and 8 after dosing, respectively. In the urine collected on day 1 (0-24 h) after dosing, excretion of ABPMA, AcABPMA, and AcABPC amounted to 1.97 ± 0.88, 3.09 ± 0.75, and 3.69 ± 1.49 nmol/kg b.w. (mean ± S.D.; n = 6), respectively. On day 2, excretion of the metabolites decreased by one order of magnitude followed by a slower decrease on day 8. Regarding the possible formation of AcABPC from ABPC, N-acetylation of the amino group at the biphenyl moiety prior to that at cysteine appears to be very unlikely. Thus, the structure of AcABPC indicates the involvement of N-acetyl-4-biphenylnitrenium ion (AcBPN) and/or its reactive ester precursors in in vivo reactions with GSH and protein-bound cysteine. ABPC in globin might become an alternative biomarker of the dose of toxicologically relevant metabolic intermediates of 4-ABP.

Interaction between Occupational and Non-Occupational Arsenic Exposure and Tobacco Smoke on Lung Cancerogenesis: A Systematic Review.

Although a higher lung cancer risk has been already associated with arsenic exposure, the contribution of arsenic and its compounds to the carcinogenic effects of other agents, such as tobacco smoke, is not well characterized. This systematic review examined the relationship between occupational and non-occupational arsenic exposure and tobacco smoking on lung cancer risk using papers published from 2010 to 2022. Two databases, PUBMED and Scifinder, were used for the searches. Among the sixteen human studies included, four were about occupational exposure, and the others were about arsenic in drinking water. Furthermore, only three case-control studies and two cohort studies evaluated an additive or multiplicative interaction. The interaction between arsenic exposure and tobacco smoke seems to be negligible at low arsenic concentrations (<100 µg/L), while there is a synergistic effect at higher concentrations. Finally, it is not yet possible to assess whether a linear no-threshold (LNT) model for lung cancer risk can be applied to the co-exposure to arsenic and tobacco smoke. Although the methodological quality of the included studies is good, these findings suggest that rigorous and accurate prospective studies on this topic are highly needed.

Smoking and passive smoking increases mortality through mediation effect of cadmium exposure in the United States.

Cigarette smoking is one of the leading causes of preventable and premature death worldwide. Even worse, many people are generally exposed to passive smoking, which leads to several respiratory diseases and related mortalities. Considering, more than 7000 compounds are included in cigarettes, their combustion results intoxicants that have deleterious effects on health. However, there is a lack of research analyzing the effects of smoking and passive smoking on all-cause and disease-specific mortality through its chemical compounds including heavy metals. Thus, this study aimed to evaluate the effect of smoking and passive smoking on all-cause and disease-specific mortality mediated by cadmium, one of the representative smoking-related heavy metals using data from the National Health and Nutrition Examination Survey (NHANES) 1999-2018 in the United States. We found that current smoking and passive smoking was related to increased risk of all-cause, CVD-related, and cancer-related mortality. Notably, passive smoking showed a synergistic effect with smoking status on the risk of mortality. In particular, current smokers with passive smoking had the highest risk of all-cause and disease-specific deaths. In addition, the accumulation of cadmium in the blood due to smoking and passive smoking mediates the increased risk of all-cause mortality. Further studies are needed to monitor and treat cadmium toxicity to improve smoking-related mortality rates.

Tobacco Smoke Exposure According to Location of Home Smoking in Israel: Findings from the Project Zero Exposure Study.

Young children are particularly vulnerable to harms from tobacco smoke exposure (TSE). This study aimed to compare TSE: (1) between children who live in smoking families and those who do not; and (2) among children who live in smoking households with varying smoking locations. The data came from two studies that were conducted concurrently in Israel (2016-2018). Study 1: a randomized controlled trial of smoking families (n = 159); Study 2: a cohort study of TSE among children in non-smoking families (n = 20). Hair samples were collected from one child in each household. Baseline hair nicotine data were analyzed for 141 children in Study 1 and 17 children in Study 2. Using a logistic regression analysis (exposed vs. not exposed as per laboratory determination) and a linear regression (log hair nicotine), we compared TSE between: (1) children in Study 1 vs. Study 2; (2) children in families with different smoking locations in Study 1: balcony; garden, yard, or other place outside of the home; or inside the home (designated smoking areas within the home (DSAs) or anywhere). A higher proportion of children living in smoking households were measurably exposed to tobacco smoke (68.8%) compared to children living in non-smoking households (35.3%, p = 0.006). Among children from smoking families, 75.0% of those whose parents smoked in the house were exposed, while 61.8% of children whose parents restricted smoking to the porch (n = 55) were exposed, and 71.4% of those whose parents smoked outside the home (including gardens and yards) (n = 42) were exposed. In univariable and multivariable models, smoking location was not significantly associated with exposure. The majority of children in smoking families were measurably exposed to TSE, even if smoking was restricted to designated areas in the home, balconies, orgarden/yard/other outdoor areas. Reducing population smoking rates, particularly among parents, restricting smoking to at least 10 meters from homes and children, and denormalizing smoking around others are recommended to reduce population-level child TSE and tobacco-attributable disease and death.

Associations between smoke exposure and osteoporosis or osteopenia in a US NHANES population of elderly individuals.

Background: Tobacco exposure is considered to be a risk factor for reduced bone mineral density (BMD), which may result in osteopenia. Cotinine, a metabolite of nicotine, is commonly utilized as a marker of tobacco exposure. Nevertheless, there are limited clinical data on the associations between osteoporosis (OP) or osteopenia and smoking status or serum cotinine level. Methods: We thoroughly examined the NHANES cross-sectional data from 2005 to 2010, 2013 to 2014, and 2017 to 2018. Multivariate logistic regression models were applied to assess the associations among smoking status and serum cotinine levels as well as OP and osteopenia. The relationships between serum cotinine level and OP and osteopenia were also assessed using the restricted cubic spline (RCS) method. Results: A total of 10,564 participants were included in this cross-sectional study. The mean age of the study population was 64.85 ± 9.54 years, and the patients were predominantly male (51.9%). We found that the relationships between higher serum cotinine levels (≥3 ng/ml) and the prevalence of osteoporosis (Model 1: OR=2.27 [1.91-2.69]; Model 2: OR=2.03 [1.70-2.43]; Model 3: OR=2.04 [1.70-2.45]; all p for trend <0.001) remained significant after adjustment for covariates by applying the lowest serum cotinine levels (<0.05 ng/ml) as the reference. Similar results were observed for current smokers, who were more likely to develop OP compared with nonsmokers (Model 1: OR=2.30 [1.90-2.79]; Model 2: OR=2.16 [1.77-2.64]; Model 3: OR=2.16 [1.77-2.65]). Moreover, higher serum cotinine levels were found to be strongly and positively correlated with the prevalence of osteopenia (OR=1.60 [1.42-1.80]). A similar relationship was observed between current smokers and the prevalence of osteopenia compared with nonsmokers (OR=1.70 [1.49-1.94]). RCS regression also showed that serum cotinine levels were nonlinearly and positively correlated with OP and osteopenia, with inflection points of 5.82 ng/ml and 3.26 ng/ml, respectively. Conclusion: This study showed that being a smoker was associated with the prevalence of OP or osteopenia compared with being a nonsmoker and that there was a strong nonlinear positive dose-response relationship between serum cotinine levels and OP and osteopenia.

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

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

Transcriptome characterization of human gingival mesenchymal and periodontal ligament stem cells in response to electronic-cigarettes.

The potential toxicities and threats of electronic cigarettes (E-cigs) on periodontal health remain elusive. Gingival mesenchymal stem cells (GMSCs) and periodontal ligament stem cells (PDLSCs) contribute to cell differentiation and regeneration for periodontium as well as inflammatory modulation. However, the effects of E-cig exposure on periodontal tissues, particularly GMSCs and PDLSCs, and the underlying epigenetic mechanisms remain largely unknown. In this study, we conducted RNA-seq analysis to examine the transcriptome of human GMSCs and PDLSCs exposed to four types of E-cigs (aerosol and liquid with tobacco and menthol flavor) and conventional tobacco smoke in vitro. Our results showed that E-cig exposure primarily impacted the immunoregulation and inflammatory responses to pathogenic microorganisms in GMSCs, and the microenvironment, differentiation and response to corticosteroid in PDLSCs, which were significantly different from the damage effects caused by tobacco smoke. Additionally, we discovered a large number of differentially expressed non-coding RNAs among the different E-cig exposure methods and flavors. We also noticed that in GMSCs, CXCL2 was especially down-regulated by E-cig aerosol exposure whereas up-regulated by E-liquid exposure compared to control. Of note, the enhancer elements near CXCL2 and other genes located at Chromosome 4 contributed to the transcription activity of these genes, and KDM6B was remarkably elevated in response to E-liquid exposure. Lastly, we conducted ChIP-seq analysis to confirm that the elevated gene transcription by E-liquids was due to the weakened H3K27me3 at genome-wide enhancer elements in GMSCs, but not at promoter regions. Taken together, our results characterized the diverse gene expression profiles of GMSCs and PDLSCs in response to E-cigs with different exposure methods and flavors in vitro, and indicated a novel mechanism of KDM6B-mediated H3K27me3 on enhancers for gene transcription regulation. Our data could be served as a resource for emphasizing the understanding of E-cigs in periodontal health.

Prevalence and influencing factors of wheeze and asthma among preschool children in Urumqi city: a cross-sectional survey.

To investigate the prevalence and indoor environmental influencing factors of wheeze and asthma among preschool children in Urumqi, Xinjiang, China to provide a strong basis for prevention and control. In August 2019, a cross-sectional study involving 8153 preschool children was conducted in 60 kindergartens in Urumqi. The ALLHOME-2 questionnaire was used for childhood wheeze and asthma survey, and the dampness in buildings and health (DBH) questionnaire was used for the childhood home dwelling and living environment survey. Multivariate unconditional logistic regression was then used to analyze the potential influencing factors of childhood asthma and wheeze. The prevalence of wheeze and asthma in children was 4.7% and 2.0%, respectively. Multivariate unconditional logistic regression results suggested that ethnicity other than the Han Chinese (odds ratio (OR) 1.39, 95% confidence interval (CI) 1.05-1.84), caesarean section (OR 1.24, 95% CI 1.00-1.53), family history of asthma (OR 5.00, 95% CI 3.36-7.44), carpet or floor bedding at home (OR 1.40, 95% CI 1.05-1.87), purchasing new furniture in the mother's residence during pregnancy (OR 1.58, 95% CI 1.06-2.36), pet keeping in the residence at aged 0-1 year (OR 1.55, 95% CI 1.13-2.13), passive smoking by child in the current residence (OR 1.35, 95% CI 1.01-1.80), and having mould or hygroma in the child's residence at aged 0-1 year (OR 1.72, 95% CI 1.12-2.64) were risk factors for wheeze. In addition, Girls (OR 0.73, 95% CI 0.59-0.90) was a protective factor for wheeze. Caesarean section (OR 1.46, 95% CI 1.06-2.00), family history of asthma (OR 7.06, 95% CI 4.33-11.53), carpet or floor bedding at home (OR 2.20, 95% CI 1.50-3.23), and pet keeping in the residence at aged 0-1 year (OR 1.64, 95% CI 1.04-1.83) were risk factors for asthma, whereas Girls (OR 0.58, 95% CI 0.42-0.80) was a protective factor for asthma. This survey indicates that the purchase of new furniture, the placement of carpet or floor bedding in the child's residence, the pets keeping, room dampness or moldy phenomena, and passive smoking may all contribute to an elevated risk of wheeze or asthma in children.

Tobacco exposure in adults and children with proteinuric glomerulopathies: a NEPTUNE cohort study.

BACKGROUND: Tobacco exposure has been recognized as a risk factor for cardiovascular disease (CVD) and progression of kidney disease. Patients with proteinuric glomerulopathies are at increased risk for cardiovascular morbidity and mortality. Multiple studies have linked tobacco exposure to CVD and chronic kidney disease, but the relationships between smoking and proteinuric glomerulopathies in adults and children have not been previously explored. METHODS: Data from the Nephrotic Syndrome Study Network (NEPTUNE), a multi-center prospective observational study of participants with proteinuric glomerulopathies, was analyzed. 371 adults and 192 children enrolled in NEPTUNE were included in the analysis. Self-reported tobacco exposure was classified as non-smoker, active smoker, former smoker, or exclusive passive smoker. Baseline serum cotinine levels were measured in a sub-cohort of 178 participants. RESULTS: The prevalence of active smokers, former smokers and exclusive passive smoking among adults at baseline was 14.6%, 29.1% and 4.9%, respectively. Passive smoke exposure was 16.7% among children. Active smoking (reference non-smoking) was significantly associated with greater total cholesterol among adults (ß 17.91 95% CI 0.06, 35.76, p = 0.049) while passive smoking (reference non-smoking) was significantly associated with greater proteinuria over time among children (ß 1.23 95% CI 0.13, 2.33, p = 0.03). Higher cotinine levels were associated with higher baseline eGFR (r = 0.17, p = 0.03). CONCLUSION: Tobacco exposure is associated with greater risk for CVD and worse kidney disease outcomes in adults and children with proteinuric glomerulopathies. Preventive strategies to reduce tobacco exposure may help protect against future cardiovascular and kidney morbidity and mortality in patients with proteinuric glomerulopathies.

A harm reduction model for environmental tobacco smoke exposure among Bangladeshi rural household children: A modified Delphi technique approach.

This paper aimed to develop a harm reduction model to reduce exposure to environmental tobacco smoke among children of rural households in Bangladesh. A mixed-methods exploratory sequential design has been applied, and data has been collated from six randomly selected villages of Munshigonj district, Bangladesh. The research was divided into three phases. In the first phase, the problem was identified through key informant interviews and a cross-sectional study. In the second phase, the model was developed by focus group discussion, and in the third phase, the model was evaluated through the modified Delphi technique. The data was analyzed by thematic analysis and multivariate logistic regression in phase one, qualitative content analysis for phase two, and descriptive statistics in phase three. The key informant interviews showed attitude toward environmental tobacco smoke, lack of awareness, inadequate knowledge as a reason and smoke-free rules, religious beliefs, social norms, and social awareness as preclusion of environmental tobacco smoke. The cross-sectional study detected that households with no smoker (OR 0.006, 95% CI 0.002-0.021), high implantation of smoke-free household rules (OR 0.005, 95% CI 0.001-0.058), moderate (OR 0.045, 95% CI 0.004-0.461) to strong (OR 0.023, 95% CI 0.002-0.224) influence of social norm and culture along with neutral (OR 0.024, 95% CI 0.001-0.510) and positive (OR 0.029, 95% CI 0.001-0.561) peer pressure had been significantly associated with environmental tobacco smoke exposure. The final components of the harm reduction model consist of a smoke-free household, social norms and culture, peer support, social awareness and religious practice identified by the FGDs and modified Delphi technique.

Mechanisms and Consequences of Variable TRPA1 Expression by Airway Epithelial Cells: Effects of TRPV1 Genotype and Environmental Agonists on Cellular Responses to Pollutants in Vitro and Asthma.

BACKGROUND: Transient receptor potential ankyrin-1 [transient receptor potential cation channel subfamily A member 1 (TRPA1)] and vanilloid-1 [transient receptor potential cation channel subfamily V member 1 (TRPV1)] detect inhaled irritants, including air pollutants and have roles in the development and exacerbation of asthma. OBJECTIVES: This study tested the hypothesis that increased expression of TRPA1, stemming from expression of the loss-of-function TRPV1 (I585V; rs8065080) polymorphic variant by airway epithelial cells may explain prior observations of worse asthma symptom control among children with the TRPV1 I585I/V genotype, by virtue of sensitizing epithelial cells to particulate materials and other TRPA1 agonists. METHODS: TRP agonists, antagonists, small interfering RNA (siRNA), a nuclear factor kappa light chain enhancer of activated B cells (NF-κB) pathway inhibitor, and kinase activators and inhibitors were used to modulate TRPA1 and TRPV1 expression and function. Treatment of genotyped airway epithelial cells with particulate materials and analysis of asthma control data were used to assess consequences of TRPV1 genotype and variable TRPA1 expression on cellular responses in vitro and asthma symptom control among children as a function of voluntarily reported tobacco smoke exposure. RESULTS: A relationship between higher TRPA1 expression and function and lower TRPV1 expression and function was revealed. Findings of this study pointed to a mechanism whereby NF-κB promoted TRPA1 expression, whereas NF-κB-regulated nucleotide-binding oligomerization domain, leucine rich repeat and pyrin domain containing 2 (NLRP2) limited expression. Roles for protein kinase C and p38 mitogen activated protein kinase were also demonstrated. Finally, the TRPV1 I585I/V genotype was associated with increased TRPA1 expression by primary airway epithelial cells and amplified responses to selected air pollution particles in vitro. However, the TRPV1 I585I/V genotype was not associated with worse asthma symptom control among children exposed to tobacco smoke, whereas other TRPA1 and TRPV1 variants were. DISCUSSION: This study provides insights on how airway epithelial cells regulate TRPA1 expression, how TRPV1 genetics can affect TRPA1 expression, and that TRPA1 and TRPV1 polymorphisms differentially affect asthma symptom control. https://doi.org/10.1289/EHP11076.

Thirdhand Smoke May Promote Lung Adenocarcinoma Development through HN1.

Thirdhand smoke (THS) refers to residual tobacco smoking pollutants that can be adsorbed to indoor surfaces and dust and persist for years after active smoking. THS-related chemicals such as N-nitrosonornicotine (NNN) and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) are tobacco-specific lung carcinogens that involved in lung cancer development and progression. In this study, we computed the differentially expressed genes (DEGs) between THS and paired control samples. THS-related overexpressed genes (OEs) were overlapped with OEs of lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC). Survival analyses of these overlapped genes were performed using LUAD and LUSC data. 6 genes were selected for validation based on their expression levels and prognostic value. Hematological and neurological expressed 1 (HN1) was further selected due to its novelty in LUAD research. The potential roles of HN1 in LUAD were explored in several ways. In summary, HN1 is overexpressed in THS samples and is associated with the prognosis of patients with LUAD. It may promote cancer progression through several pathways and could serve as a potential therapeutic target especially for THS-related LUAD. In-depth mechanistic studies and clinical trials are warranted.

Age-dependent effects of tobacco smoke and nicotine on cognition and the brain: A systematic review of the human and animal literature comparing adolescents and adults.

Cigarette smoking is often initiated during adolescence and an earlier age of onset is associated with worse health outcomes later in life. Paradoxically, the transition towards adulthood also marks the potential for recovery, as the majority of adolescents are able to quit smoking when adulthood emerges. This systematic review aimed to evaluate the evidence from both human and animal studies for the differential impact of adolescent versus adult repeated and long-term tobacco and nicotine exposure on cognitive and brain outcomes. The limited human studies and more extensive yet heterogeneous animal studies, provide preliminary evidence of heightened fear learning, anxiety-related behaviour, reward processing, nicotinic acetylcholinergic receptors expression, dopamine expression and serotonin functioning after adolescent compared to adult exposure. Effects of nicotine or tobacco use on impulsivity were comparable across age groups. These findings provide novel insights into the mechanisms underlying adolescents' vulnerability to tobacco and nicotine. Future research is needed to translate animal to human findings, with a focus on directly linking a broader spectrum of brain and behavioural outcomes.

Smoke-Free Policies and Resident Turnover: An Evaluation in Massachusetts Public Housing From 2009‒2018.

INTRODUCTION: Smoke-free policies (SFP) in multi-unit housing are a promising tool for reducing exposure to tobacco smoke among residents. Concerns about increased housing instability due to voluntary or involuntary transitions induced by SFPs have been a primary barrier to greater widespread adoption. The impact of SFP implementation on transitions out of public housing in federally funded public housing authorities in Massachusetts was evaluated. METHODS: Tenancy data from the Department of Housing and Urban Development were used to determine the time from admission to transitioning out of public housing based on a cohort study design. Periods of exposure to SFPs were defined based on dates of SFP implementation at each PHA. Multi-level Cox regression models were fit to estimate the effects of SFPs on the hazard of transitioning, adjusting for household- and PHA-level characteristics. Analyses were conducted in 2021‒2022. RESULTS: There were 44,705 households with a record of residence in Massachusetts PHAs over 2009‒2018. Over this period, despite increasing adoption of SFPs among the PHAs, rates of transition remained steady at around 5‒8 transitions per 1,000 household-months. There was no overall association between exposure to SFPs and transitions among the full sample (adjusted HR=0.99, 95% CI=0.95, 1.04, p=0.794). However, the association varied significantly by age group, race/ethnicity, timing of SFP adoption, and era of admission. CONCLUSIONS: Adoption of SFPs in public housing had a minimal overall impact on turnover for households in Massachusetts, though disparities in the impact were observed between different demographic and PHA-level subgroups.

Concentrations of Transition Metal Ions in Rat Lungs after Tobacco Smoke Exposure and Treatment with His-Leu Dipeptide.

Tobacco smoking is deleterious to the lungs because it exposes them to many toxic substances. These include transition metal ions, such as cadmium. However, there is a lack of information about the influence of endogenous metal-binding peptides, such as His-Leu (HL), on the lung distribution of transition metals in smokers. To address this, we administered HL subcutaneously to rats exposed to tobacco smoke for six weeks, then we measured the concentrations of transition metal ions in the lungs. We found that exposure to tobacco smoke elevates the concentrations of Cd(II) and Cu(II). Administration of the HL peptide, whose elevation is a consequence of angiotensin receptor blocker anti-hypertension therapy, increases the concentration of Fe in the lungs of rats exposed to smoke. These findings suggest that smoking is a risk factor for patients receiving angiotensin receptor blockers to treat hypertension.

Decrease in Secondhand Smoke Exposure in Work and Public Places among Adults in the Philippines: An Analysis of the Global Adult Tobacco Survey, 2009 and 2015.

The implementation of several tobacco control policies in the Philippines may have contributed to a decrease in secondhand smoke (SHS) exposure. We examined changes in SHS exposure at work and in public places between 2009 and 2015 among adults aged ≥15 years and interpreted these results within the tobacco policy landscape in the Philippines. We analyzed the Philippines Global Adult Tobacco Survey 2009 and 2015 data. We examined marginal effects in logistic regression to get the adjusted prevalence of SHS exposure at five work and public places, controlling for selected characteristics. We calculated adjusted prevalence ratios and adjusted prevalence differences between 2009 and 2015. Adjusted prevalence of SHS exposure decreased from 2009 to 2015 by 19% (5.7 percentage points) at work, 45% (11.2 percentage points) in government buildings, 48% (3.2 percentage points) in healthcare facilities, 29% (8.2 percentage points) in restaurants, and 33% (19.9 percentage points) on public transportation. Although the prevalence of SHS exposure at work and in public places decreased significantly between 2009 and 2015, a substantial proportion of adults remain exposed to SHS. This study highlights the importance of continued implementation, enforcement, monitoring, and evaluation of tobacco control and prevention measures in the Philippines.

Eating Behaviors, Lifestyle, and Ischemic Stroke: A Lebanese Case-Control Study.

BACKGROUND: Stroke is the second leading cause of death and the third leading cause of disability on a global scale. Most clinicians tend to underestimate the importance of diet and inadequate or dysfunctional eating attitudes in patients with a complicated relationship with food. Concerned about the potential of an independent Lebanese approach, and also because prior international research has revealed a link between eating intake or choice and ischemic stroke risk, it was considered vital to broaden the scope of the literature and evaluate further the association of disordered eating attitudes and focus on the distinct relationship with food in the case of orthorexia nervosa (ON) in the Lebanese community. Consequently, the purpose of the present study is to investigate the potential association between pre-existing disordered eating attitudes, specifically ON, and ischemic stroke risk, with an emphasis on the evidence supporting a Mediterranean-style diet. METHODS: This research is a case-control survey study involving 113 Lebanese individuals with ischemic stroke and 451 age-(within 5 years) and sex-matched controls recruited from several hospitals in Lebanon (April 2020-April 2021). RESULTS: According to the findings of our first regression model, living 100 m from a crowded road (adjusted odds ratio [aOR]: 3.421, 95% confidence interval [CI]: 1.585-7.387), living 100 m from an electricity generator (aOR: 3.686, 95% CI: 1.681-8.085), higher waterpipe dependence (aOR: 1.204, 95% CI: 1.117-1.297), higher exposure to passive smoking (aOR: 2.651, 95% CI: 2.051-3.426), being married (aOR: 3.545, 95% CI: 1.297-9.689), having a low educational attainment (aOR: 0.239, 95% CI: 0.084-0.679), vigorous physical activity (aOR: 1.003, 95% CI: 1.001-1.006), and having more inappropriate eating (aOR: 1.040, 95% CI: 1.006-1.074) were all associated with higher odds of having ischemic stroke. Furthermore, atrial fibrillation (aOR: 2.945, 95% CI: 1.010-8.585), diabetes (aOR: 2.550, 95% CI: 1.169-5.561), heart diseases (aOR: 6.193, 95% CI: 2.196-17.463), and hypertension (aOR: 2.744, 95% CI: 1.049-7.180) were also linked to an increased risk of stroke. Moreover, having more orthorexia nervosa tendencies (aOR: 1.123, 95% CI: 1.021-1.235) was related to a higher odds of having an ischemic stroke, whereas better adherence to the MeD was significantly linked (aOR: 0.691, 95% CI: 0.583-0.819) to lower odds of ischemic stroke. CONCLUSIONS: Ischemic stroke patients were more likely to have disordered eating attitudes and orthorexic behaviors. Furthermore, the MeD has been found to be beneficial in reducing ischemic stroke risk. Despite the study's focus, outdoor pollution, waterpipe dependence, and passive smoking were linked to ischemic stroke. In summary, this review suggests that improving one's nutritional status and making a few lifestyle changes are key stroke prevention and treatment methods.

Asymptomatic nasopharyngeal bacterial carriage, multi-drug resistance pattern and associated factors among primary school children at Debre Berhan town, North Shewa, Ethiopia.

BACKGROUND: Nasopharyngeal carriage of bacteria is the main source for transmission of pathogens across individuals and horizontal spread of organisms in the community. It is an important risk factor for the acquisition of community-acquired respiratory tract infection. It is the major public health problem among children. The asymptomatic carriage of nasopharyngeal bacteria is different globally, particularly in Africa, carriage is higher in children and decreases with increasing age, 63.2% in children less than 5 years, 42.6% in children 5-15 years, and 28.0% in adults older than 15 years. OBJECTIVE: The aims of this study was to determine asymptomatic nasopharyngeal bacterial carriage, multi-drug resistance pattern and associated factors among primary school children at Debre Berhan town, North Shewa, Ethiopia. METHODS: Institutional based cross-sectional study was conducted at Debre Berhan town primary schools from February 1 to April 30, 2021. Primarily, the schools were stratified into two strata, public and private primary schools. From a total of sixteen government and fourteen private primary schools, five government and five private schools were selected by using a simple random sampling technique. Socio-demographic variables and potential risk factors were assessed using a structured questionnaire. A total of 384 nasopharyngeal swab samples were collected using sterile swabs aseptically; and inoculated on Blood agar, Chocolate agar, MacConkey agar, and Mannitol salt agar. The colony was characterized to isolate bacteria, and bacterial identification was performed by Gram reaction, hemolysis patterns, colonial characteristics and pigmentation, catalase test, coagulase test, mannitol fermentation test, oxidase test, fermentation of carbohydrates, H2S production, motility, formation of indole, triple sugar iron agar (TSI), citrate utilization, lysine decarboxylase or methyl red vogues proskur utilization, urea hydrolysis and satellitism tests. Antimicrobial sensitivity tests were performed by using modified Kirby-Bauer disk diffusion method. Data were entered into statistical package Epi data 4.0.0.6 and transferred to and analyzed using SPSS software version-23. P value of < 0.05 with Odds ratio (OR) and 95% confidence interval (CIs) was considered as statistically significant. RESULTS: The overall prevalence of nasopharyngeal carriage of bacterial isolate was 35.7% (95% CI 30.7-40.7%). The predominant isolates were Staphylococcus aureus 54.5% followed by coagulase-negative Staphylococcus 35.8%, and Streptococcus pyogens 4.5%. Most bacterial isolates were susceptible to chloramphenicol, ciprofloxacin, gentamycin, nitrofurantoin, azithromycin, ciprofloxacin; and the overall multidrug resistance pattern of isolated bacteria was 62.03% out of 137 bacterial isolates. Numbers of rooms ≤ 2 per house [AOR = 5.88, 95%CI 1.26-27.57], having history of hospitalization [AOR = 4.08, 95%CI 1.45-11.53], passive smoking [AOR = 4.87, 95%CI 1.49-15.97], family size of > 5 members [AOR = 2.17, 95%CI 1.24-3.81], and number of students in the classroom [AOR = 2.35,95%CI 1.37-4.02] were statistically significant associated risk factors for nasopharyngeal bacteria carriage. CONCLUSION: Asymptomatic nasopharyngeal bacteria carriage in children is alarming for community-acquired infection. The overall multidrug resistance was very high. The risk of the carriage was increased with having a history of passive smoking, being in large family size and number of students per class. Longitudinal follow-up studies would be helpful for better understanding the infection risk in bacterial pathogen carriers.

[Tobacco smoking and cancer risk]. / Tabakrauchen und Krebsrisiko.

Smoking tobacco is the most important and potentially modifiable risk factor for cancer in Germany. Combining tobacco with alcohol can multiply cancer risks. Up to 30 % of cancer deaths are due to tobacco smoking. 23,3 % of 18-64 year-old Germans are current smokers; in addition, 11 % of the population are regularly exposed to secondhand tobacco smoke. Tobacco smoking is causally associated with oropharyngeal, laryngeal, nose, paranasal sinus, lung, esophageal, gastric, pancreatic, hepatocellular, biliary, colorectal, kidney, ureter, urinary bladder, uterine cervix and ovary cancers and leukemia. Smokers should be supported to stop smoking and join programmes of cancer screening. Smoking cessation effectively reduces tobacco-associated cancer risk.

The Association between Exposure to Second-Hand Smoke and Disease in the Chinese Population: A Systematic Review and Meta-Analysis.

Objective: To analyze the association between exposure to second-hand smoke (SHS) and 23 diseases, categorized into four classifications, among the Chinese population. Methods: We searched the literature up to June 30, 2021, and eligible studies were identified according to the PECOS format: Participants and Competitors (Chinese population), Exposure (SHS), Outcomes (Disease or Death), and Study design (Case-control or Cohort). Results: In total, 53 studies were selected. The odds ratio (OR) for all types of cancer was 1.79 (1.56-2.05), and for individual cancers was 1.92 (1.42-2.59) for lung cancer, 1.57 (1.40-1.76) for breast cancer, 1.52 (1.12-2.05) for bladder cancer, and 1.37 (1.08-1.73) for liver cancer. The OR for circulatory system diseases was 1.92 (1.29-2.85), with a value of 2.29 (1.26-4.159) for stroke. The OR of respiratory system diseases was 1.76 (1.13-2.74), with a value of 1.82 (1.07-3.11) for childhood asthma. The original ORs were also shown for other diseases. Subgroup analyses were performed for lung and breast cancer. The ORs varied according to time period and were significant during exposure in the household; For lung cancer, the OR was significant in women. Conclusion: The effect of SHS exposure in China was similar to that in Western countries, but its definition and characterization require further clarification. Studies on the association between SHS exposure and certain diseases with high incidence rates are insufficient.