Tobacco Induced Diseases最新文献

{"title":"Impact of cigarette toxicants on sarcopenic obesity: An in silico network toxicology and molecular dynamics study.","authors":"Zijing Li, Daoyuan Li, Yuli Huang, Yushang Liu, Xinye Ouyang, Yufei Xu, Wenjuan Wu, Yanbiao Zhong, Maoyuan Wang","doi":"10.18332/tid/226887","DOIUrl":"10.18332/tid/226887","url":null,"abstract":"<p><strong>Introduction: </strong>Sarcopenic obesity (SO) is a geriatric metabolic syndrome characterized by muscle mass loss, muscle strength decline, and excessive fat accumulation. Nicotine and coal tar disrupt skeletal muscle homeostasis and lipid metabolism. This study aims to elucidate the relevant molecular mechanisms by which nicotine and coal tar trigger sarcopenic obesity using an integrated in silico approach.</p><p><strong>Methods: </strong>This in silico study was conducted in May 2026 using publicly available databases and computational platforms. Targets for nicotine, coal tar, and SO were retrieved from GeneCards and OMIM, and the intersection of targets was identified using Venny. KEGG enrichment was performed to detect key pathways. A protein-protein interaction (PPI) network was constructed via STRING, and the top 10 core genes were ranked by the Maximal Clique Centrality (MCC) algorithm in Cytoscape. Three GEO transcriptomic datasets (GSE290570, GSE262419, GSE226045) were used to cross-validate differentially expressed genes related to nicotine, coal tar, and SO. Molecular docking between nicotine and five core proteins was performed using CB-DOCK2, and 50 ns molecular dynamics simulations with GROMACS were used to assess complex stability via root-mean-square deviation (RMSD), root-mean-square fluctuation (RMSF), radius of gyration (Rg), solvent-accessible surface area (SASA), and hydrogen-bond analysis.</p><p><strong>Results: </strong>Twenty intersection targets were identified. Enriched pathways included MAPK, PI3K/Akt, p53, cholesterol metabolism, and ferroptosis. Five core genes (IL1β, IGF1, FGF2, CTNNB1, and CXCL12) were cross-validated by GEO transcriptomic data. Nicotine bound stably to CTNNB1, CXCL12, IGF1, and IL1β with binding energies ranging from -3.3 to -4.2 kcal/mol, whereas FGF2 showed a positive value (0.7). MD simulations confirmed that all complexes maintained structural stability throughout the 50 ns trajectory.</p><p><strong>Conclusions: </strong>Nicotine and coal tar may regulate core genes and inflammation- and metabolism-related pathways to promote SO progression. This study provides theoretical references for preventing tobacco exposure-induced SO.</p>","PeriodicalId":23202,"journal":{"name":"Tobacco Induced Diseases","volume":"24 ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13572993/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148971408","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biomarker-questionnaire discordance in secondhand smoke exposure among Korean children: A secondary analysis of the Korean National Environmental Health Survey, 2016-2017 and 2019-2020.","authors":"Hee-Jeong Lee, Sung-Il Cho","doi":"10.18332/tid/226880","DOIUrl":"10.18332/tid/226880","url":null,"abstract":"<p><strong>Introduction: </strong>Questionnaire-based assessment of secondhand smoke (SHS) exposure may not fully capture children's internal nicotine burden. We assessed concordance between parent-reported SHS exposure and urinary cotinine classifications and examined correlates of discordance by developmental stage and survey cycle.</p><p><strong>Methods: </strong>This secondary analysis included children aged 3-11years with urine specimens and parent-completed questionnaire data from two independent cross-sectional samples in the Korean National Environmental Health Survey (KoNEHS 2016-2017 and 2019-2020; N=2619). Pooled analyses were unweighted; cycle-specific weighting was examined in sensitivity analyses. Concordance between parent-reported SHS exposure (≥1 time/week) and urinary cotinine-based classifications at three prespecified thresholds [at or above the limit of detection (LOD), ≥3 ng/mL, and ≥5 ng/mL] was evaluated using sensitivity, specificity, Cohen's κ, and McNemar's test. Correlates of questionnaire-negative/biomarker-positive discordance were examined using multivariable logistic regression.</p><p><strong>Results: </strong>Concordance was negligible across thresholds and age groups (κ range: -0.02-0.01; McNemar p<0.001 for most strata). Sensitivity ranged from 7.1% to 16.1%, and at least 83.9% of biomarker-positive children were questionnaire-negative. Parent-reported SHS exposure was lower in Cycle 4 among children aged 3-5 and 6-8 years, whereas urinary cotinine concentrations were higher across all age groups. Among children aged 3-5 and 6-8 years without parent-reported SHS exposure, cotinine concentrations were higher in those with at least one current parental smoker than in those with no current parental smoker. At ≥LOD, questionnaire-negative/biomarker-positive discordance was associated with younger age (3-5 vs 9-11 years: adjusted odds ratio, AOR=1.64; 95% CI: 1.20-2.24) and with Cycle 4 (vs Cycle 3: AOR=2.09; 95% CI: 1.59-2.75).</p><p><strong>Conclusions: </strong>Parent-reported SHS exposure and urinary cotinine classifications showed marked discordance. These measures captured related but non-interchangeable information; urinary cotinine may complement questionnaires when characterizing children's internal nicotine burden.</p>","PeriodicalId":23202,"journal":{"name":"Tobacco Induced Diseases","volume":"24 ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13544052/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148897723","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring causal associations between multiple smoke exposures and neuroblastoma suppressor NBL1 via Mendelian randomization.","authors":"Siqi Xie, Shangeng Weng","doi":"10.18332/tid/226573","DOIUrl":"10.18332/tid/226573","url":null,"abstract":"<p><strong>Introduction: </strong>Neuroblastoma suppressor of tumorigenicity 1 (NBL1) is an established tumor suppressor and prognostic biomarker in neuroblastoma (NB). Although tobacco exposure is a well-known carcinogenic factor, its potential effect on NBL1 expression remains unclear. This two-sample Mendelian randomization (MR) study aimed to explore potential links between diverse smoking exposures, circulating NBL1 levels and NB risk.</p><p><strong>Methods: </strong>This study performed a two-sample MR analysis to investigate the causal effects of maternal smoking around birth (66 single-nucleotide polymorphisms, SNPs), household smoking exposure (17 SNPs), and smoking initiation (37 SNPs) on circulating NBL1 levels using large-scale GWAS summary statistics. Causal estimates were obtained using IVW, weighted median, and MR-Egger methods, with sensitivity, reverse MR, and validation analyses conducted to assess robustness and directionality.</p><p><strong>Results: </strong>No evidence of a causal association was observed between maternal smoking around birth or household smoking exposure and NBL1 levels. In contrast, genetically predicted smoking initiation was associated with lower NBL1 expression (IVW: OR=0.70; 95% CI: 0.50-0.99, p=0.04). The weighted median method failed to reach statistical significance (OR=0.642; 95% CI: 0.40-1.04, p=0.07), whereas MR-Egger regression yielded a non-significant estimate (OR=0.39; 95% CI: 0.06-2.56, p=0.34). Sensitivity analyses indicated no substantial pleiotropy or influential outliers. Reverse MR analysis provided no evidence that NBL1 influences smoking behavior. Additional validation analyses showed no causal association between smoking initiation and NB risk.</p><p><strong>Conclusions: </strong>Prenatal and household smoking exposures do not appear to affect NBL1 expression. Genetically predicted smoking initiation was associated with reduced NBL1 expression, but not with neuroblastoma risk.</p>","PeriodicalId":23202,"journal":{"name":"Tobacco Induced Diseases","volume":"24 ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13544053/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148897751","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Global, regional, and national burden of low-back pain attributable to smoking from 1990 to 2021: An age-period-cohort and joinpoint analysis of the Global Burden of Disease Study 2021.","authors":"Junkai Kou, Jianhua Ren, Aoying Min, Qi Hao, Shuo Li, Hengrui Chang, Xianzhong Meng","doi":"10.18332/tid/226563","DOIUrl":"10.18332/tid/226563","url":null,"abstract":"<p><strong>Introduction: </strong>Low-back pain (LBP) is the leading cause of disability worldwide. Although smoking is a well-established, modifiable risk factor that accelerates intervertebral disc degeneration, comprehensive spatiotemporal analyses of its attributable burden remain scarce. This study assessed the global burden of smoking-attributable LBP from 1990 to 2021, elucidating the underlying temporal dynamics and socioeconomic inequalities.</p><p><strong>Methods: </strong>Data were extracted from the Global Burden of Disease (GBD) study 2021. We evaluated absolute disability-adjusted life years (DALYs), age-standardized DALYs rate (ASDR), and estimated annual percentage change (EAPC) across 204 countries and territories. To disentangle temporal trends, age-period-cohort and joinpoint regression models were applied. The spatial-temporal relationship between the burden and the sociodemographic index (SDI) was also examined.</p><p><strong>Results: </strong>Globally, the absolute number of DALYs for smoking-attributable LBP increased by 29.6% to 8.67 million in 2021, primarily driven by population growth and aging. Conversely, the global ASDR decreased significantly by 35.8% to 99.95. Males bore a substantially higher burden than females, with biological risk peaking at 60-69 years (inverted U-shape). The ASDR trajectory exhibited a distinct inverted U-shaped relationship with SDI; while high-income nations experienced rapid declines (e.g. Denmark, EAPC= -2.29), the burden surged in specific developing regions (e.g. Afghanistan, EAPC=2.37). Joinpoint analysis revealed an accelerated global decline from 2016 to 2021 (annual percent change, APC= -1.70). Age-period-cohort modeling confirmed continuous monotonic reductions in both period and cohort relative risks, highlighting a profound 'generational dividend'.</p><p><strong>Conclusions: </strong>Despite continuous improvements in age-standardized rates driven by recent global tobacco control policies and younger birth cohorts, the absolute burden of smoking-attributable LBP continues to grow. Progress is alarmingly unequal, heavily favoring high-income countries while intensifying in developing nations. Global health strategies must prioritize equitable implementation of tobacco control in lower income regions and integrate cessation programs into occupational health initiatives and strengthening of targeted tobacco control policies, particularly in low- and middle-income regions.</p>","PeriodicalId":23202,"journal":{"name":"Tobacco Induced Diseases","volume":"24 ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13537002/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148881635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Socioeconomic inequality in any tobacco use versus current smoking across 66 DHS countries: Indirect implications for smokeless tobacco and oral cancer prevention.","authors":"Yin Tong, Hongtao Li, Xinyue Li, Mianjia Wan, Peng Zhou, Juncheng He, Kangwen Ming","doi":"10.18332/tid/226096","DOIUrl":"10.18332/tid/226096","url":null,"abstract":"<p><strong>Introduction: </strong>Smokeless tobacco use is a major preventable risk factor for lip and oral cavity cancer, with a particularly heavy burden in South and Southeast Asia. We aimed to quantify, across countries, whether the socioeconomic gradient of any tobacco use is more pro-poor than that of smoked tobacco alone, thereby indirectly assessing the additional inequality attributable to smokeless tobacco.</p><p><strong>Methods: </strong>In this secondary analysis of publicly available Demographic and Health Surveys (DHS) data (66 countries, survey years 1999-2024), supplemented by the WHO Global Health Observatory and World Bank indicators, we computed concentration indices (CIXs), the slope index of inequality (SII), and Wagstaff-normalized CIXs for smoking and any tobacco use across wealth, education level, and residence dimensions. Eligible observations were country-survey estimates stratified by wealth quintile, education level, or urban/rural residence, with complete data across all subgroups; national-total, age-, and region-only estimates were excluded. The core hypothesis was tested indirectly, via paired comparison of any-tobacco versus smoked-only CIXs (81 paired observations), because DHS smokeless indicators are available only as national aggregates. Wagstaff decomposition quantified the relative contributions of socioeconomic determinants.</p><p><strong>Results: </strong>The mean wealth-related CIX for smoking was -0.045 (SD=0.184), with 66% of estimates negative. The mean CIX for any tobacco use (-0.094) was significantly lower than for smoking alone (-0.060; paired ΔCIX= -0.033, 95% CI: -0.060 - -0.007, p=0.017), with 62% of pairs showing a more pro-poor gradient for any tobacco use. Education level and residence together accounted for >80% of explainable inequality in the decomposition analysis.</p><p><strong>Conclusions: </strong>The socioeconomic gradient of any tobacco use is significantly more pro-poor than that of smoking alone, suggesting that smokeless tobacco amplifies tobacco-related health inequality. These ecological findings suggest that tobacco-control monitoring may benefit from integrating smokeless tobacco into inequality surveillance; individual-level studies are needed before specific populations are targeted.</p>","PeriodicalId":23202,"journal":{"name":"Tobacco Induced Diseases","volume":"24 ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13532050/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148875984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Artificial intelligence and tobacco use: A bibliometric analysis 1997-2026.","authors":"Shengbo Wang, Jiahao Zhang, Liushen Chen","doi":"10.18332/tid/226603","DOIUrl":"10.18332/tid/226603","url":null,"abstract":"<p><strong>Introduction: </strong>Globally, tobacco use is a key public health issue. Exploring the impact of developing AI technologies on tobacco use and intervention will help promote the digital transformation of public health research. This study aims to map the trends, networks, and core themes of research at the intersection of artificial intelligence and tobacco use through visual analytics.</p><p><strong>Methods: </strong>In this study, a bibliometric analysis was conducted on 335 articles on AI and tobacco use in the Web of Science core collection from 1997 to 2026. The search cutoff date was 8 April 2026. Descriptive and visual analysis were conducted on the publication trend, cooperation network, keyword co-occurrence, clustering, and burst of this literature.</p><p><strong>Results: </strong>The speed of publication of literature in this field has increased significantly since 2018. In the cooperation network, national cooperation is dominated by the United States. Universities, rather than transnational institutions, significantly promote cooperation. The authors' cooperation network is more dispersed. The characteristics of interdisciplinary cooperation are obvious. The research hotspots focus on several aspects. These include machine learning prediction of smoking, dialogue AI and robot interventions, and NLP and social media monitoring. Other topics encompass the analysis of smoking-cessation behavior among youth groups, combined with AI, deep learning, and behavioral analysis; and the evaluation of tobacco characteristics, tobacco products, media, and health. Keyword hotspots and bursts reveal that the field has recently paid special attention to the intervention of cutting-edge technologies in smoking and smoking cessation behavior.</p><p><strong>Conclusions: </strong>Through data mining and visualization technology, this study reveals the overall evolution, interaction mode, and key fields of AI and tobacco use knowledge. The results provide an important framework for further research.</p>","PeriodicalId":23202,"journal":{"name":"Tobacco Induced Diseases","volume":"24 ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13524066/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148851666","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tobacco use and cognitive impairment: A bibliometric analysis of research trends and knowledge structure.","authors":"Shengyuan Xu, Shaojie Qi","doi":"10.18332/tid/226606","DOIUrl":"10.18332/tid/226606","url":null,"abstract":"<p><strong>Introduction: </strong>Smoking is recognized as a key preventable risk factor for dementia and has therefore received extensive research attention. However, the relationship between smoking and cognitive impairment is complex, involving methodological controversies such as residual confounding, the nicotine paradox, and selective survival bias. Despite the growing body of evidence, this interdisciplinary field still lacks systematic bibliometric analysis. The purpose of this study is to use bibliometric methods to map the knowledge structure, thematic evolution, and emerging frontiers in smoking and cognitive impairment research.</p><p><strong>Methods: </strong>Using the Web of Science core collection as the data source, 811 relevant English-language articles and reviews published from 1985 to 2026 were analyzed by bibliometrics. This article uses VOSviewer and CiteSpace to conduct co-occurrence and cluster analyses, burst detection, and thematic evolution analysis. It systematically examines the publication trends, collaboration networks, disciplinary distribution, keyword co-occurrence patterns, and research frontiers in this field.</p><p><strong>Results: </strong>Neuroscience and Public Health constitute the two core hub disciplines. The United States (293 publications), China (213), and England (131) dominate global research output. Keyword co-occurrence analysis revealed a four-dimensional research structure centered on disease outcome, tobacco exposure, epidemiological association, and preventive intervention. Burst detection identifies a three-stage evolution path from disease subtyping and population characteristics to prevention and intervention through mechanism exploration and exposure expansion. Prevention (burst strength = 4.20) and Intervention (3.85) are the keywords with the highest intensity after 2020. Observational studies predominated, while evidence from interventions and participation by low- and middle-income countries remained limited.</p><p><strong>Conclusions: </strong>The research on tobacco use and cognitive impairment has shifted from risk identification toward intervention validation, but observational research still dominates, and intervention evidence remains limited. Low- and middle-income countries remain under-represented in global evidence production.</p>","PeriodicalId":23202,"journal":{"name":"Tobacco Induced Diseases","volume":"24 ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13520597/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148841423","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of active and passive smoking with noncommunicable diseases in a large health check-up population: A cross-sectional study in Changzhi, Shanxi province, China.","authors":"Zhiyong Dou, Ping Wu, Lujie Wang, Jing Guo","doi":"10.18332/tid/226557","DOIUrl":"10.18332/tid/226557","url":null,"abstract":"<p><strong>Introduction: </strong>Tobacco smoke, encompassing both active smoking and secondhand smoke (SHS) exposure, constitutes a leading modifiable risk factor for the global burden of non-communicable diseases (NCDs). This study aimed to examine the association of active smoking and SHS with the presence of NCDs among health check-up populations, and to explore the dose-response association according to daily cigarette consumption and smoking duration.</p><p><strong>Methods: </strong>A cross-sectional study was conducted among 38906 adults aged ≥18 years who were local residents undergoing physical examination in Changzhi, Shanxi Province from January to December 2025. Questionnaire interviews were used to capture the demographics, lifestyle habits, tobacco smoke status (active smoking, SHS exposure, daily cigarette consumption, and smoking duration), and clinically diagnosed NCDs. Multivariable logistic regression estimated the adjusted odds ratios (AORs) and 95% confidence intervals (CIs), with adjustment for potential confounders. In this study, a p<0.05 was considered statistically significant.</p><p><strong>Results: </strong>The overall prevalence of current smoking was 27.3% (51.3% in men, 0.3% in women), and 26.2% of participants had at least one NCD. After full adjustment, active smoking remained independently associated with increased odds of NCDs (AOR=1.26; 95% CI: 1.18-1.35). A modest dose-response gradient was observed for smoking duration: compared with <5 years, the AORs were 1.24 (95% CI: 1.08-1.43) for 5-14 years, 1.23 (95% CI: 1.09-1.39) for 15-24 years, and 1.37 (95% CI: 1.19-1.58) for ≥25 years. Daily consumption of ≥20 cigarettes was modestly associated with elevated risk (AOR=1.13; 95% CI: 1.03- 1.25). Regarding SHS, the crude association was significant (OR=1.25; 95% CI: 1.16-1.35), but attenuated after adjusting for potential confounders (AOR=1.04; 95% CI: 0.95-1.13). In subgroup analyses, active smoking was associated with hypertension, diabetes, cardiovascular disease and dyslipidemia, and the doseresponse relationships were also observed for smoking duration.</p><p><strong>Conclusions: </strong>Active smoking independently increases the odds of prevalent NCDs, especially among long-term smokers. The attenuated effect of SHS highlights the challenge of isolating its independent role in observational settings. So comprehensive tobacco control strategies and targeted cessation interventions for long-term smokers are important.</p>","PeriodicalId":23202,"journal":{"name":"Tobacco Induced Diseases","volume":"24 ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13520596/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148841460","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Smoking-attributable burden of musculoskeletal disorders, 1990-2021, with exploratory projections to 2050: A secondary dataset analysis of the Global Burden of Disease Study 2021.","authors":"Zhihong Fu, Yunhui Zhang, Zhaojun Chen","doi":"10.18332/tid/226288","DOIUrl":"10.18332/tid/226288","url":null,"abstract":"<p><strong>Introduction: </strong>Musculoskeletal disorders (MSDs) are a leading source of disability worldwide, but the population-level burden attributable to smoking remains insufficiently characterized. The aim of this study was to quantify global, regional, and national smoking-attributable burden of MSDs from 1990 to 2021, and to explore socioeconomic inequalities and projections to 2050.</p><p><strong>Methods: </strong>This secondary dataset analysis used Global Burden of Disease Study 2021 estimates for smoking-attributable DALYs due to MSDs. Eligible estimates included both sexes combined, the risk factor smoking, the aggregate cause category of MSDs, all-age DALYs, age-standardized DALYs rate (ASDR), age-specific rates, global, sociodemographic index (SDI), regional, and national locations, for years 1990-2021. Temporal trends were summarized using estimated annual percentage change (EAPC) and joinpoint regression. Socioeconomic inequality, frontier performance, and exploratory autoregressive integrated moving average projections to 2050 were assessed; Bayesian age-period-cohort forecasts were used as sensitivity analysis for global DALYs.</p><p><strong>Results: </strong>Global smoking-attributable DALYs due to MSDs increased from 6.82 million (95% UI: 3.85-10.12) in 1990 to 8.89 million (95% UI: 4.72-13.68) in 2021, whereas ASDR decreased from 153.57 (95% UI: 85.94-228.28) to 102.44 (95% UI: 54.60-157.30). The global EAPC in ASDR was -1.20% (95% CI: -1.24 - -1.16). The largest relative increases in DALYs occurred in Middle-SDI regions (89.15%) and Low-SDI regions (71.71%). High-SDI regions retained the highest ASDR in 2021 (154.13; 95% UI: 81.19-231.32). Exploratory projections suggested that global ASDR may decline to 45.40 (95% UI: 29.06-61.74) by 2050, while DALYs may reach 7.53 million (95% UI: 4.12-10.93).</p><p><strong>Conclusions: </strong>Smoking-attributable MSDs remain a measurable component of global disability burden. The persistence of absolute burden despite declining ASDR may warrant greater consideration in future tobacco-related burden assessments and rehabilitation planning, while causal and policy interpretations warrant cautious interpretation as this is an ecological modelling study.</p>","PeriodicalId":23202,"journal":{"name":"Tobacco Induced Diseases","volume":"24 ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13520598/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148841445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reductions in smoking progression from 10th to 12th grade across 5 cohorts in Southern California 1995-2014.","authors":"Jessica L Barrington-Trimis, Afton Kechter, Jessica B Knapp, Feifei Liu, Kiros Berhane, Sandrah Eckel, James Sargent, Rob McConnell","doi":"10.18332/tid/217624","DOIUrl":"10.18332/tid/217624","url":null,"abstract":"<p><strong>Introduction: </strong>While initiation of adolescent cigarette smoking has declined in the last two decades, changes to smoking progression have not been examined.</p><p><strong>Methods: </strong>Survey data were from five cohorts of youth in Southern California (grade 12 in 1995, 1998, 2001, 2004, or 2014; n=2346). Among those who had smoked a cigarette by grade 10 (n=418), we modeled self-reported past-month, past-year, and lifetime number of cigarettes smoked in grade 12 as a function of grade 10 number of cigarettes and cohort (1995, 1998, 2001, 2004 vs 2014).</p><p><strong>Results: </strong>Smoking progression declined markedly over time. Among youth who had smoked by grade 10, the 1995 cohort smoked on average 23 times as many lifetime cigarettes by grade 12 as the 2014 cohort (adjusted rate ratio, ARR=22.9; 95% CI: 9.40-55.6). Similar findings were observed for the past year (ARR=30.1; 95% CI: 6.75-134) and the past month (ARR=12.1; 95% CI: 2.19-67.0) number of cigarettes smoked. Over time, females smoked less, but the pattern of decreasing progression in lifetime cigarettes smoked was more pronounced for females than males (lifetime, p for interaction <0.0001).</p><p><strong>Conclusions: </strong>The rate of progression among those initiating cigarette smoking in early high school decreased markedly over the two-decade period starting in 1995, suggesting that social or environmental factors may play a substantial role in the escalation of smoking through adolescence.</p>","PeriodicalId":23202,"journal":{"name":"Tobacco Induced Diseases","volume":"24 ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13459626/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148713516","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}