Tobacco Induced Diseases最新文献

Introduction: Approximately 5000 child deaths are attributed to secondhand smoke exposure (SHSe) annually, which is three times the number of childhood cancers combined. Infants, medically fragile infants, are highly vulnerable to the harmful effects of SHSe, including respiratory infections and sudden infant death syndrome. While having a home smoking ban may mitigate these risks, implementation remains a challenge for many families. Our primary aim was to explore the familial and sociocultural factors associated with smoking-ban initiation and maintenance in households with medically fragile infants.

Methods: Qualitative interviews were conducted with 20 mothers participating in a behavioral intervention from 2015 to 2016 aimed at reducing SHSe in infants discharged from a large urban, children's hospital in Houston, Texas. Interviews explored family structure, cultural influences, social networks, and smoking history. Thematic analysis was used to identify key themes.

Results: Three primary themes emerged: 1) Household structure and power dynamics - mothers in multigenerational homes often lacked authority to enforce smoking bans, especially when the primary authority figure was a smoker; 2) Sole responsibility - mothers felt burdened as the only advocates for SHSe reduction, often without support from other household members; and 3) Variable level of support for SHS bans - while emotional and logistical support was common during infants' hospital stays, this support rarely extended to smoking-related behavior change. Participants felt these factors significantly influenced smoking-ban initiation and sustainability.

Conclusions: Findings underscore the need to move beyond individual-level interventions and engage the broader household context. Intervention sessions should include all household members - particularly individuals who smoke - and incorporate collaborative care models that offer behavioral counseling, pharmacological aids (e.g. nicotine replacement therapy), and real-time feedback technologies. Tailoring interventions to reflect household power structures and support systems may enhance their effectiveness in reducing SHSe and protecting medically vulnerable infants.

Introduction: Tobacco exposure is a plausible accelerator of biological aging, yet population-level evidence and mechanisms remain insufficiently defined. We examined the association between serum cotinine and phenotypic age acceleration (PhenoAgeAccel), and assessed whether oxidative-stress biomarkers were related to the serum cotinine-PhenoAgeAccel association.

Methods: We conducted a cross-sectional, survey-weighted analysis of n=19744 adults from NHANES 2011-2018. PhenoAgeAccel was computed as the residual from regressing PhenoAge on chronological age. Multivariable linear regressions related serum cotinine to PhenoAgeAccel across hierarchical adjustment models. Restricted cubic splines assessed non-linearity. Mediation analysis was conducted to quantify the extent to which oxidative-stress biomarkers contribute to this association.

Results: Higher serum cotinine was associated with accelerated biological aging: each doubling of serum cotinine corresponded to a 0.22-year increase in PhenoAgeAccel (β=0.22; 95% CI: 0.16-0.29). Mediation analyses indicated that γ-glutamyl transferase (GGT) and uric acid (UA) statistically accounted for 9.5% of the association between serum cotinine and PhenoAgeAccel (p<0.001). Interactions were observed for sex and PIR, with stronger associations among women and participants with lower socioeconomic status. There was no evidence of non-linearity in the relationships of the serum cotinine with GGT, PhenoAgeAccel, or UA.

Conclusions: In this nationally representative cross-sectional study of US adults, higher serum cotinine levels were associated with greater phenotypic age acceleration. Oxidative-stress biomarkers were related to the observed association, although causal inferences cannot be drawn.

Introduction: Existing evidence on the association between smoking and hypertension (HTN) remains conflicting, and the potential role of systemic inflammation in mediating smoking-related mortality among hypertensive patients is poorly understood. This study aimed to investigate the association between smoking status, smoking volume, and HTN risk in a large, nationally representative sample. Furthermore, we sought to determine whether systemic inflammation, measured by the systemic inflammation index (SII), mediates the association between smoking and all-cause mortality in hypertensive individuals.

Methods: This cross-sectional, pooled secondary data analysis study utilized data from 10 cycles of the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2018. Data on smoking, covariates, and hypertension status were collected through standardized interviews, questionnaires, and laboratory/physical examinations. A total of 28967 participants were included after excluding those with incomplete data. Propensity score matching (PSM) analysis was employed to adjust for confounding factors such as age, gender, BMI, race, and other sociodemographic variables. Logistic regression and restricted cubic spline regression were used to assess the dose-response relationship between smoking and HTN. Mediation analysis was performed to evaluate the role of systemic inflammation, as measured by the systemic inflammation index (SII), in the increased mortality risk among hypertensive smokers.

Results: Smoking significantly increased the likelihood of HTN after adjusting for confounders (adjusted odds ration, AOR=1.18; 95% CI: 1.10-1.27). A dose-response relationship was observed, with individuals smoking >30 cigarettes/day having the highest likelihood of HTN (AOR=1.37; 95% CI: 1.07-1.75). PSM analysis confirmed these findings, showing a significant increase in HTN prevalence among smokers (p=0.045). Smoking was also associated with increased overall mortality in hypertensive patients (HR=1.993; 95% CI: 1.766-2.249). Mediation analysis revealed that systemic inflammation, as measured by SII, accounted for 87.70% of the increased mortality in hypertensive smokers (ACME=0.068, p<0.001).

Conclusions: This study establishes a significant association between smoking, HTN and mortality. The findings underscore a potential dose-response trend between cigarette consumption and HTN, with systemic inflammation playing a key role in mediating the higher mortality observed in hypertensive smokers. Interventions targeting smoking cessation and systemic inflammation may significantly reduce the burden of HTN-related morbidity and mortality.

Introduction: Tobacco use among adolescents is a concern in the Upper East Region of Ghana. We estimated the prevalence and identified factors contributing to single and multiple use of tobacco products among junior high school students in Ghana.

Methods: We conducted a cross-sectional analysis of a baseline survey of a school-based tobacco control intervention among adolescents in the Upper East Region of Ghana in 2022. A multi-stage cluster sampling approach was employed to identify the study sample, and data were collected using self-administered questionnaires. Current use of single tobacco products (at least one: cigarette, e-cigarette, shisha, or smokeless tobacco products) and multiple products (≥2 products) in the past 30 days was assessed. Multinomial logistic regression was used to assess the association of sociodemographic characteristics, perceptions towards tobacco's health risks, and exposure to tobacco products with single and multiple product use. Adjusted relative risk ratios (ARRR) and their corresponding 95% confidence intervals (CI) were computed.

Results: We surveyed 1328 adolescents, comprising an equal proportion of males (49.8%) and females (50.4%). One in five (21.7%) reported using tobacco products, with 11.5% using single products and 13.0% using multiple products. Shisha (13.6%), cigarettes (10.6%), e-cigarettes (8.2%), and smokeless tobacco (6.0%) were used. A number of factors were identified to be associated with tobacco use among adolescents.

Conclusions: One in five junior high school students used at least one form of tobacco product. Adolescent tobacco use is impacted by demographic factors and risk perceptions. Further studies are needed to better understand these associations.

Introduction: Japan is one of the countries most affected by both the global tobacco epidemic and disasters, which are often interrelated. This study aimed to analyze factors related to continuation of smoking or relapse after childbirth among women who smoked before pregnancy and inform approaches to help them continue smoking cessation in a post-disaster setting, such as that after the Fukushima nuclear accident.

Methods: We conducted a pooled analysis of secondary data collection from Fukushima prefecture-wide cross-sectional self-administered questionnaire-based surveys. Participants were recruited from women given a Maternal and Child Health Handbook by their city of residence in Fukushima Prefecture from 2013 to 2016. A total of 17211 responses to the Pregnancy and Birth Survey were analyzed. Women who smoked before pregnancy were divided according to smoking status during pregnancy and after childbirth, and then compared with those who did not smoke before pregnancy in terms of evacuation status, radiation risk perception, age, parity, subjective health, and depression tendency.

Results: A total of 16417 respondents did not smoke before pregnancy. Among those who smoked before pregnancy, 634 quit smoking during pregnancy and maintained cessation after childbirth, 182 quit smoking during pregnancy but relapsed afterward, 195 smoked during pregnancy but quit after childbirth, and 582 continued smoking during and after pregnancy. Age ≤24 years (AOR=2.36), multiparity (AOR=1.61), and depression tendency (AOR=1.85) were associated with relapse. Current evacuation status (AOR=1.65), radiation risk perception (AOR=0.55), age ≤24 years (AOR=2.19), multiparity (AOR=1.90), disease history (AOR=1.33), and depression tendency (AOR=1.85) were associated with continuation of smoking.

Conclusions: Previous smokers who continue smoking or relapse after childbirth need support that addresses complex underlying factors, including mental health. Continuation of smoking was particularly associated with disaster-related factors, suggesting that disaster-affected mothers need multifaceted support for health promotion.

Introduction: Tobacco use among adolescents continues to pose a major public-health challenge in Saudi Arabia. Despite national prevention efforts and declining smoking rates, many youths remain vulnerable to nicotine addiction and experimentation with emerging products such as shisha and e-cigarettes. Understanding factors that influence quit attempts and cessation awareness is essential to guide effective school- and community-based tobacco-control interventions. This study assessed the prevalence of quit attempts and identified behavioral and environmental correlates of cessation motivation among Saudi youth using data from the 2022 Global Youth Tobacco Survey.

Methods: A cross-sectional analysis was conducted using data from 6983 students aged 11-17 years who participated in the 2022 Global Youth Tobacco Survey. Weighted analyses described tobacco-use patterns and cessation behaviors. Chi-squared tests examined bivariate relationships, while multivariable logistic regression identified independent factors associated with quit attempts, including adjusting for age, sex, parental and peer smoking, and media exposure. Significance was defined as p<0.05.

Results: Approximately 33% of respondents had ever used tobacco or nicotine, and 10.8% were current users. Among those who used tobacco within the past 12 months (n=411), 77.4% had attempted to quit, 64% wanted to stop, and 79.8% had received advice to quit. Factors associated with quit attempts included having no close friends who smoke (AOR=4.38; 95% CI: 1.73-11.07), exposure to school-based anti-tobacco lessons (AOR=3.25; 95% CI: 1.51-6.99), noticing health warnings on shisha packs (AOR=2.59; 95% CI: 1.02-6.55), and exposure to tobacco imagery in media (AOR=3.19; 95% CI: 1.64-6.17).

Conclusions: Most Saudi youth who use tobacco express a desire to quit, and social context strongly influences their cessation behavior. Reinforcing school-based anti-tobacco education, expanding adolescent cessation programs, and strengthening policy enforcement could further reduce tobacco use and improve cessation outcomes among young people.

Introduction: Senescence of type II alveolar (AT-II) cells is involved in the pathogenesis of chronic obstructive pulmonary disease (COPD). We have reported that circRNA FOXO3 (circFOXO3) is upregulated after exposure to cigarette smoke (CS) and that circFOXO3 knockdown has protective effects on CS-induced inflammation. Here, we investigate whether circFOXO3 upregulation is involved in CS-induced AT-II cell senescence.

Methods: Within this experimental cell-based and animal study, the effects of circFOXO3 on CSE-induced senescence in AT-II cell line MLE12 were determined by senescence-associated β-galactosidase staining and western blotting analyses of p16 and p21 expression. Immunofluorescence staining was used to determine the expression of γ-H2AX to analyze DNA damage. Then the autophagy level of CSE-treated MLE12 cells was evaluated by western blotting analyses of LC3B and Beclin-1 expression. Furthermore, we analyzed interactions between circFOXO3 and E2F transcription factor 1 (E2F1) in RNA binding protein immunoprecipitation studies.

Results: Our results show that circFOXO3 knockdown suppressed CS extract (CSE)-induced senescence in the AT-II cell line MLE-12. Additionally, CSE-induced autophagy impairment was reduced by circFOXO3 knockdown, and the autophagy inhibitor 3-methyladenine abrogated the effects induced by circFOXO3 knockdown on cell senescence. Mechanistic investigations revealed that circFOXO3 interacts with E2F1 and suppresses its nuclear translocation. E2F1 knockdown reduced the positive regulation of circFOXO3 knockdown on autophagy and prevented the suppressive effects of circFOXO3 knockdown on cell senescence. Consistent with this, circFOXO3 knockdown mitigated CS-induced senescence in AT-II cells in vivo.

Conclusions: Overall, these findings suggest that CS-induced circFOXO3 upregulation promotes autophagy-dependent senescence of AT-II cells, leading to enhanced lung injury.

Introduction: Regular use of electronic nicotine delivery systems (ENDS) by people who smoke cigarettes may impact smoking trajectories. ENDS brands are used by different populations in different ways, but their associations with smoking cessation are not well understood. This study evaluated whether regular use of Juul or Alto ENDS differently impacted smoking abstinence one year later among adults who had smoked cigarettes.

Methods: This prospective cohort study surveyed a national sample of US adults who used ENDS in 2022-2023 and again after one year to assess cigarette smoking. Multivariable logistic regression models used data from 237 people who had smoked cigarettes in the past year and regularly used ENDS products Juul or Alto at baseline to examine the characteristics and behaviors associated with abstaining from cigarette smoking at follow-up at 12 months.

Results: Whereas no overall differences in smoking abstinence at follow-up at 12 months were found between adults who used Juul versus adults who used Alto, adults who used Juul and had quit smoking by baseline were more likely than their Alto-using counterparts to remain abstinent at follow-up at 12 months (AOR=7.07). Other characteristics that were associated with abstaining from cigarettes at follow-up included being 18-29 years (vs older) (AOR=3.64), identifying as White, non-Hispanic (vs another race/ethnicity) (AOR=3.03), not currently smoking at baseline (vs currently smoking) (AOR=20.25), using their Juul or Alto product to quit smoking or remain quit (AOR=2.77), and use of menthol cigarette flavors (vs tobacco flavor) (AOR=2.54).

Conclusions: This longitudinal study found limited differences in smoking abstinence after one year between those who regularly used Juul versus Alto. However, people who used ENDS products specifically to quit smoking were more likely to achieve smoking abstinence and there were important sociodemographic differences. Future research is needed to inform interventions to increase the likelihood that people who use ENDS completely stop smoking and eventually quit all consumer nicotine products.

Introduction: Gastrointestinal cancers remain a major global health issue, with tobacco use as a key factor. Understanding the impact of tobacco use on these cancers and its regional trends is essential for effective prevention strategies.

Methods: Using data from the Global Burden of Disease (GBD) study, we analyzed mortality and disability-adjusted life years (DALYs) related to tobacco from 1990 to 2021. Joinpoint regression estimated average annual percent change (AAPC), and ARIMA predicted disease burden up to 2036. Two-sample Mendelian randomization (MR) analysis with GWAS data, applied methods such as inverse variance weighting (IVW) and MR-Egger for causal inference.

Results: Esophageal cancer had the highest burden in 2021, with a mortality rate of 2.54 deaths per 100000 population and a DALY rate of 58.49 DALYs per 100000 population. Stomach cancer showed the most significant decrease, with mortality dropping from 2.81 to 1.25 deaths per 100000 population (AAPC= -2.58; 95% uncertainty interval, UI: -2.61- -2.55) and DALY rates decreasing from 71.71 to 29.01 DALYs per 100000 population (AAPC= -2.87; 95% UI: -2.90 - -2.84). The disease burden was higher in older males. ARIMA analysis showed a general decline in disease burden, though some regions had an increasing trend. MR analysis did not provide genetic evidence supporting an association between tobacco use and these cancers.

Conclusions: From 1990 to 2021, the global burden of gastrointestinal cancers linked to tobacco use showed a declining trend. However, mortality and DALY rates remain high, with significant regional, age, and gender differences, highlighting the need for continued tobacco control efforts.

Introduction: Osteoporosis (OP) is linked to smoking. Nicotine may disrupt bone homeostasis through various pathways, but its molecular mechanisms are unclear. This study aims to explore the molecular networks and key regulatory factors underlying nicotine-induced OP.

Methods: Nicotine toxicity was assessed via ProTox-3.0, with its Simplified Molecular Input Line Entry System (SMILES) structure retrieved from PubChem. Potential targets were predicted using five databases, including SuperPred. OP-related gene data (GSE56815) were extracted from Gene Expression Omnibus (GEO) and combined with GeneCards and Comparative Toxicogenomics Database (CTD) for target screening. Overlapping genes were identified by Venn diagram analysis, followed by protein-protein interaction (PPI) network construction. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed using HipLot, while Hallmark Gene Sets provided insights into key biological pathways. Core targets were screened via Cytoscape 3.9.1, and molecular docking was conducted using AutoDockTools 1.5.7.

Results: In all, 388 nicotine-associated targets and 1777 OP genes were predicted, with 116 overlapping. Enrichment analyses revealed associations with multiple signaling pathways, particularly those involving apoptosis and estrogen. Eight core targets, including SRC, BCL2, and CASP3, were identified. Molecular docking showed strong binding affinity (approximately -5 kcal/mol), with enhanced binding stability through hydrophobic interactions and hydrogen bonding.

Conclusions: This study suggests nicotine exacerbates OP by regulating key targets, such as CASP3 and ESR1, and pathways like apoptosis and estrogen signaling. These findings provide insights into the molecular mechanisms underlying nicotine's role in OP and potential therapeutic targets.