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To address the problems of unstable accuracy, low efficiency, and subjective influence of manual counting, a machine vision-based method to count the quantity of tobacco shreds is proposed for the first time. In this paper, the complex tobacco shred image is obtained by backlight imaging. The adaptive threshold segmentation method is used to segment tobacco shreds. The pixel area of the tobacco shred area is calculated by connected domain labelling. Second, independent tobacco shreds and adhesive tobacco shreds were identified based on the pixel area, and the quantity of segmented tobacco shreds was counted for the first time. Subsequently, in complex scenarios (such as tobacco shreds adhesive and overlapping), an image is usually obtained by manually drawing the contours of the adhesive and overlapping tobacco shreds on the basis of primary statistics. Finally, different individuals are distinguished, segmentation is completed, and tobacco shred quantity statistics are realised. The experimental results show that the average accuracy is 100.0 % for quantitative statistics of independent tobacco shred images. For tobacco shred images with adhesive and overlapping interference, the minimum accuracy is 90 %, and the accuracy increases with the increase in tobacco shred quantity. Furthermore, the efficiency of the tobacco shred quantity statistics conducted by the method in this paper was only affected by complex scenarios. Compared to artificial processing, the efficiency was increased by more than 100 %. The work in this paper can provide the technical basis for measuring the dimensions of tobacco shreds. [ABSTRACT FROM AUTHOR]

No consensus exists on the relative risk (RR) of lung cancer (LC) attributable to active smoking in China. This study aimed to evaluate the unified RR of LC attributable to active smoking among the Chinese population. A systematic literature search of seven databases was conducted to identify studies reporting active smoking among smokers versus nonsmokers in China. Primary articles on LC providing risk estimates with their 95% confidence intervals (CI s) for "ever" "former" or "current" smokers from China were selected. Meta-analysis was used to estimate the pooled RR of active smoking. Forty-four unique studies were included. Compared with that of nonsmokers, the pooled RR (95% CI) for "ever" "former" and "current" smokers were 3.26 (2.79–3.82), 2.95 (1.71–5.08), and 5.16 (2.58–10.34) among men, 3.18 (2.78–3.63), 2.70 (2.08–3.51), and 4.27 (3.61–5.06) among women, and 2.71 (2.12–3.46), 2.66 (2.45–2.88), and 4.21 (3.25–5.45) in both sexes combined, respectively. The RR of LC has remained relatively stable (range, 2–6) over the past four decades in China. Early quitting of smoking could reduce the RR to some extent; however, completely refraining from smoking is the best way to avoid its adverse effects. [ABSTRACT FROM AUTHOR]

Cardiac arrest is a severe heart anomaly that results in billions of annual casualties. Smoking is a specific hazard factor for cardiovascular pathology, including coronary heart disease, but data on smoking and heart death not earlier reviewed. The Heart Rate Variability (HRV) parameters used to predict cardiac arrest in smokers using machine learning technique in this paper. Machine learning is a method of computing experience based on automatic learning and enhances performances to increase prognosis. This study intends to compare the performance of logistical regression, decision tree, and random forest model to predict cardiac arrest in smokers. In this paper, a machine learning technique implemented on the dataset received from the data science research group MITU Skillogies Pune, India. To know the patient has a chance of cardiac arrest or not, developed three predictive models as 19 input feature of HRV indices and two output classes. These model evaluated based on their accuracy, precision, sensitivity, specificity, F1 score, and Area under the curve (AUC). The model of logistic regression has achieved an accuracy of 88.50%, precision of 83.11%, the sensitivity of 91.79%, the specificity of 86.03%, F1 score of 0.87, and AUC of 0.88. The decision tree model has arrived with an accuracy of 92.59%, precision of 97.29%, the sensitivity of 90.11%, the specificity of 97.38%, F1 score of 0.93, and AUC of 0.94. The model of the random forest has achieved an accuracy of 93.61%, precision of 94.59%, the sensitivity of 92.11%, the specificity of 95.03%, F1 score of 0.93 and AUC of 0.95. The random forest model achieved the best accuracy classification, followed by the decision tree, and logistic regression shows the lowest classification accuracy. [ABSTRACT FROM AUTHOR]

Scientific evidence about genetic and molecular changes in oral squamous cell carcinoma (OSCC) among smokers and non-smokers is inconclusive. This systematic review and meta-analysis assessed the effects of tobacco on the DNA of individuals with OSCC based on protein mutations. Electronic searches were conducted on PubMed, Ovid, Web of Science, and Scopus to identify observational studies published up to January/2022. The Joanna Briggs Institute tool was used for the critical appraisal of studies. The certainty of the evidence was evaluated. Twenty-three studies assessing 4,060 individuals (2,967 smokers vs. 1,093 non-smokers) were included in this review. Fifteen groups of proteins/genes were investigated. Analysis of the quality of articles revealed low risk of bias in most studies. The certainty of the evidence was very low. The meta-analysis confirmed no significant difference between smokers and non-smokers with respect to damage to GSTM1 (OR: 0.60; 95%CI: 0.30-1.18), GSTT1 (OR: 1.18; 95%CI:0.49-2.83), hydrolase proteins (Ku70 and Ku80) (OR: 0.74; 95%CI: 0.18-3.05), and transferase proteins (GSTM1, GSTT1, GSTM3) (OR: 0.74; 95%CI: 0.47-1.18). Most of the studies included showed that smokers are more likely to exhibit genetic instability. However, the meta-analysis revealed that smokers do not necessarily have more genetic alterations in the DNA than non-smokers. [ABSTRACT FROM AUTHOR]

Background: Current clinical classifications of olfactory function are based primarily upon a percentage of correct answers in olfactory identification testing. This simple classification provides little insight into etiologies of olfactory loss, associated comorbidities, or impact on the quality of life (QOL). Methods: Community-based subjects underwent olfactory psychophysical testing using Sniffin Sticks to measure threshold (T), discrimination (D), and identification (I). The cognitive screening was performed using Mini-Mental Status Examination (MMSE). Unsupervised clustering was performed based upon T, D, I, and MMSE. Post hoc differences in demographics, comorbidities, and QOL measures were assessed. Results: Clustering of 219 subjects, mean age 51 years (range 20-93 years) resulted in 4 unique clusters. Cluster 1 was the largest and predominantly younger normosmics. Cluster 2 had the worst olfaction with impairment in nearly all aspects of olfaction and decreased MMSE scores. This cluster had higher rates of smoking, heart disease, and cancer and had the worst olfactory-specific QOL. Cluster 3 had normal MMSE with relative preservation of D and I, but severely impaired T. This cluster had higher rates of smoking and heart disease with moderately impaired QOL. Cluster 4 was notable for the worst MMSE scores, but general preservation of D and I with moderate loss of T. This cluster had higher rates of Black subjects, diabetes, and viral/traumatic olfactory loss. Conclusion: Unsupervised clustering based upon detailed olfactory testing and cognitive testing results in clinical phenotypes with unique risk factors and QOL impacts. These clusters may provide additional information regarding etiologies and subsequent therapies to treat olfactory loss. [ABSTRACT FROM AUTHOR]

Scientometric analysis of a disease is often conducted to recognize research hotspots and investigate latest trends. In this brief report, we provide a scientometric overview of oral cancer research in Taiwan and mainland China. There were 1924 and 3853 articles on oral cancer research originating from Taiwan and mainland China, respectively. In Taiwan, the risk factors including areca/betel quid chewing, tobacco smoking, and alcohol use were the distinctive keywords. For basic research, genotype, reactive oxygen, p53, mitochondria and caspase-9 were the distinctive keywords. In mainland China, experiment methods such as genetic transfection, gene silencing, colony formation, tumor xenograft were the distinctive keywords. Epithelial mesenchymal transition, long untranslated RNA, protein function, uvomorulin, and Bcl-2 were the distinctive keywords of basic research. Collectively, we hope that these scientometric characteristics will aid clinicians and researchers for obtaining information on oral cancer and can be of guidance for future studies. [ABSTRACT FROM AUTHOR]

Copyright of Revista Ciência & Saúde Coletiva is the property of Associacao Brasileira de Pos-Graduacao em Saude Coletiva and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

• Social isolation and loneliness were associated with an increased risk of incident type 2 diabetes mellitus, regardless of genetic risk profile. • Persistent social isolation was associated with an increased type 2 diabetes mellitus risk. • Incident and persistent loneliness were associated with higher type 2 diabetes mellitus risks. • Loneliness might modify the association between social isolation and risk of incident type 2 diabetes mellitus. This study aimed to investigate the association of social isolation, loneliness, and their trajectory with the risk of developing type 2 diabetes mellitus (T2DM) across genetic risk. We included 439,337 participants (mean age 56.3 ± 8.1 years) enrolled in the UK Biobank study who were followed up until May 31, 2021. Social isolation and loneliness were self-reported and were further categorized into never, transient, incident, and persistent patterns. During a median follow-up of 12.7 years, 15,258 incident T2DM cases were documented. Social isolation (versus no social isolation: hazard ratio (HR) 95 % confidence interval (CI) 1.04 [1.00;1.09]) and loneliness (versus no loneliness: 1.26 [1.19;1.34]) were associated with an increased T2DM risk, independent of the genetic risk for T2DM. The interactions existed between social isolation and loneliness (P interaction < 0.05); the increased T2DM risk associated with social isolation was only significant among participants without loneliness. In the longitudinal analysis, only persistent social isolation (versus never social isolation: 1.22 [1.02;1.45]) was associated with an increased T2DM risk, whereas incident loneliness (versus never loneliness: 1.95 [1.40;2.71]) and persistent loneliness (2.00 [1.31;3.04]) were associated with higher T2DM risks. Social isolation and loneliness, especially their persistent pattern, were independently associated with an increased incident T2DM risk, irrespective of an individual's genetic risk. Loneliness modified the association between social isolation and incident T2DM. Hazard ratios adjusted for age, sex, ethnicity, assessment centers, current employment status, education, Townsend deprivation index, smoking status, alcohol consumption frequency, physical activity, TV watching time, healthy diet score, ever seeking help from physicians due to anxiety or depressive symptoms, antihypertensive medications use, and cholesterol medications use. CI, confidence interval; HR, hazard ratio. [Display omitted] [ABSTRACT FROM AUTHOR]

Tobacco smoking involves a high risk of human malignancies, including oral cancer, because it contains multiple carcinogens that cause genetic instability. Thus, a worse prognosis would be expected for cancer patients who are smokers. The aim of this study was to assess the DNA damage response through the expression of checkpoint kinase 2 (CHK2), H2A histone family member X (H2AX), and P53 among smokers and non-smokers with oral squamous cell carcinoma (OSCC). Associations between immunoexpression of proteins and clinicopathological data and histopathological grading were also analyzed. A total of 35 individuals (18 non-smokers and 17 smokers) with OSCC of the tongue and/or floor of the mouth were included. Immunohistochemistry for H2AX was conducted for the identification of double-strand breaks, CHK2, and P53 to evaluate the expression of this protein in cell cycle regulation. The sample consisted of 22 males and 13 females, with a mean age of 63.9±11.8 years. OSCC of non-smokers were well-differentiated tumors in 50% of the cases, and those of smokers were equally distributed into moderately differentiated and poorly differentiated tumors (35.3% each). Overall, 31 (88.6%) cases were CHK2-positive, 27 (77.1%) were H2AX-positive, and 23 (65.7%) were P53-positive, with no difference between smokers and non-smokers (p > 0.05). No association was found between proteins and clinicopathologic data (p > 0.05). Similarities in CHK2, H2AX, and P53 immunohistochemical staining patterns were observed between smokers and non-smokers, and immunoexpression was not associated with clinicopathological parameters. However, the findings indicated consistent expression of these proteins in OSCC. [ABSTRACT FROM AUTHOR]

Objective: To quantify and compare respiratory functions and further screen the oral mucosa of tobacco and non-tobacco users. Material and Methods: First control group, non-tobacco users (n=55); Second group, smokers’ group (n=168) who currently smoked cigarettes; Third group smokeless/chewing type, tobacco group (n=81); Fourth group, both smokeless and smoking type tobacco users (n=46). Fagerstrom Test for Nicotine Dependences (FTND) and Fagerström Test for Nicotine Dependence-Smokeless Tobacco (FTND-ST) instruments were used to assess nicotine dependence. Subsequently, spirometry and Toluidine Blue (TB) vital staining were performed. Chi-squared and one-way analysis of variance (ANOVA) were used for statistical analysis. Results: Fagerstrom test resulted in 48.8% of subjects with low dependency, followed by an increase in nicotine dependency from low to moderate (29.2%), moderate (15.6%), and highly dependent (6.4%) groups. All respiratory function tests and oral screening confirmed significant changes amongst tobacco and non-tobacco users. The forced vital capacity of non-smoker group was significantly different from other tobacco users’ group (p<0.05). Conclusion: Early effects of tobacco use can lead to complications with the respiratory system and oral cavity. Such data can be used to delineate the harm of tobacco and should be used to urge individuals to evade the utilization of tobacco. [ABSTRACT FROM AUTHOR]

Copyright of Revista Ciência & Saúde Coletiva is the property of Associacao Brasileira de Pos-Graduacao em Saude Coletiva and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Genetic data implicate IL-33 in asthma susceptibility. Itepekimab, a monoclonal antibody targeting IL-33, demonstrated clinical activity in asthma, with potential in chronic obstructive pulmonary disease (COPD). In this study we first aimed to test the hypothesis that genetic variants in the IL-33 pathway were also associated with COPD. On the basis of the strong association of IL-33 pathway genes with pulmonary diseases like asthma and COPD, we conducted this phase 2a trial to assess the safety and efficacy of itepekimab in patients with moderate-to-severe COPD on a stable regimen of triple-inhaled or double-inhaled background maintenance therapy. In this two-part study, genetic analyses of loss-of-function and gain-of-function variants in the IL-33 pathway, previously associated with asthma risk, were initially characterised for COPD. We then did a double-blind, phase 2a trial comparing itepekimab with placebo in patients with moderate-to-severe COPD despite standard therapy, at 83 study sites in ten countries. Patients aged 40–75 years who were current or former smokers, had been diagnosed with COPD for at least 1 year, and were on a stable regimen of triple-inhaled or double-inhaled background maintenance therapy, were randomly assigned (1:1) to receive itepekimab 300 mg or placebo, administered as two subcutaneous injections every 2 weeks for 24–52 weeks. The primary endpoint of the phase 2a trial was annualised rate of moderate-to-severe acute exacerbations of COPD during the treatment period. The key secondary outcome was change in prebronchodilator FEV 1 from baseline to weeks 16–24. Prespecified subgroup analyses were done for each of the endpoints, including by smoking status. Efficacy and safety analyses were done in all participants who received at least one dose of assigned treatment (modified intention-to-treat population). This trial is registered at ClinicalTrials.gov (NCT03546907). Genetic analyses demonstrated association of loss of function in IL33 with reduced COPD risk, and gain of function in IL33 and IL1RL1 variants with increased risk. Subsequent to this, in the phase 2 trial, 343 patients were randomly assigned to placebo (n=171) or itepekimab (n=172) from July 16, 2018, to Feb 19, 2020. Annualised rates of acute exacerbations of COPD were 1·61 (95% CI 1·32–1·97) in the placebo group and 1·30 (1·05–1·61) in the itepekimab group (relative risk [RR] 0·81 [95% CI 0·61–1·07], p=0·13), and least squares mean prebronchodilator FEV 1 change from baseline to weeks 16–24 was 0·0 L (SD 0·02) and 0·06 L (0·02; difference 0·06 L [95% CI 0·01–0·10], p=0·024). When analysis was restricted to former smokers, treatment with itepekimab was associated with nominally significant reductions in acute exacerbations of COPD (RR 0·58 [95% CI 0·39–0·85], p=0·0061) and FEV 1 improvement (least squares mean difference 0·09 L [0·02–0·15], p=0·0076) compared with placebo. Current smokers treated with itepekimab showed no treatment benefit versus placebo for exacerbations (RR 1·09 [0·74–1·61], p=0·65) or FEV 1 (least squares mean difference 0·02 [−0·05 to 0·09], p=0·54). Treatment-emergent adverse events (TEAEs) occurred in 135 (78%) patients in the itepekimab group and 136 (80%) in the placebo group. The most common TEAEs were nasopharyngitis (28 [16%] in the itepekimab group vs 29 [17%] in the placebo group), bronchitis (18 [10%] vs 14 [8%]), headache (14 [8%] vs 23 [13%]), and upper respiratory tract infection (13 [8%] vs 15 [9%]). The primary endpoint in the overall population was not met, subgroup analysis showed that itepekimab reduced exacerbation rate and improved lung function in former smokers with COPD. Two phase 3 clinical studies are ongoing to confirm the efficacy and safety profile of itepekimab in former smokers with COPD. Sanofi and Regeneron Pharmaceuticals. [ABSTRACT FROM AUTHOR]

Individual observations of risky behaviors present a paradox: individuals who take the most risks in terms of hazards (smoking, speeding, risky sexual behaviors) are also less likely to take risks when it comes to innovation, financial risks or entrepreneurship. Existing theories of risk-preferences do not explain these patterns. From a simple model, we argue that many decisions involving risk have a temporal dimension, and that this dimension is often the main determinant of individual choices. In many real life instances, risk taking amounts to damaging the individual's capital (whether embodied capital, financial capital, social reputation, etc.), which would affect her over a long period of time after the risky decision. In evolutionary terms, the marginal cost of this type of risky behavior depends on the relative importance of the future in the individual's fitness (e.g. her time horizon). Individuals with short time horizons will give less importance to a degradation of their capital because this degradation will be paid effectively for a shorter period of time. This approach explains patterns of behaviors observed across socio-economic groups and puts forward new approaches to prevent hazardous behaviors such as smoking. • From a simple model, we show that risk decisions reflect two types of preferences • "Hazardous behaviors" reflect a preference for short term gains rather than high variance • "Venture behaviors" reflect a preference for the variance of rewards • This accounts for the social distribution of risk behaviors observed in the literature [ABSTRACT FROM AUTHOR]

The smoking habit is particularly rife in South Africa, compared to the rest of the world. Although smoking rates in South Africa have been declining since the implementation of tobacco control measures in 1993, we still have an estimated eight million smokers in the country. Smoking has been associated with detrimental heath risks and related complications for decades, and such health issues are further compounded by the high incidence of tuberculosis and HIV/AIDS in the South African population. This article aims to provide an overview of the importance of smoking cessation, and the non-pharmacological and pharmacological measures aimed at successfully quitting the habit of smoking. [ABSTRACT FROM AUTHOR]

Genetic variation has an important role in the development of non-small-cell lung cancer (NSCLC). However, genetic factors for lung cancer have not been fully identified, especially in Chinese populations, which limits the use of existing polygenic risk scores (PRS) to identify subpopulations at high risk of lung cancer for prevention. We therefore aimed to identify novel loci associated with NSCLC risk, and generate a PRS and evaluate its utility and effectiveness in the prediction of lung cancer risk in Chinese populations. To systematically identify genetic variants for NSCLC risk, we newly genotyped 19 546 samples from Chinese NSCLC cases and controls from the Nanjing Medical University Global Screening Array Project and did a meta-analysis of genome-wide association studies (GWASs) of 27 120 individuals with NSCLC and 27 355 without NSCLC (13 327 cases and 13 328 controls of Chinese descent as well as 13 793 cases and 14 027 controls of European descent). We then built a PRS for Chinese populations from all reported single-nucleotide polymorphisms that have been reported to be associated with lung cancer risk at genome-wide significance level. We evaluated the utility and effectiveness of the generated PRS in predicting subpopulations at high-risk of lung cancer in an independent prospective cohort of 95 408 individuals from the China Kadoorie Biobank (CKB) with more than 10 years' follow-up. We identified 19 susceptibility loci to be significantly associated with NSCLC risk at p≤5·0 × 10−8, including six novel loci. When applied to the CKB cohort, the PRS of the risk loci successfully predicted lung cancer incident cases in a dose-response manner in participants at a high genetic risk (top 10%) than those at a low genetic risk (bottom 10%; adjusted hazard ratio 1·96, 95% CI 1·53–2·51; p trend =2·02 × 10−9). Specially, we observed consistently separated curves of lung cancer events in individuals at low, intermediate, and high genetic risk, respectively, and PRS was an independent effective risk stratification indicator beyond age and smoking pack-years. We have shown for the first time that GWAS-derived PRS can be effectively used in discriminating subpopulations at high risk of lung cancer, who might benefit from a practically feasible PRS-based lung cancer screening programme for precision prevention in Chinese populations. National Natural Science Foundation of China, the Priority Academic Program for the Development of Jiangsu Higher Education Institutions, National Key R&D Program of China, Science Foundation for Distinguished Young Scholars of Jiangsu, and China's Thousand Talents Program. [ABSTRACT FROM AUTHOR]

Background: Tobacco smoking is one of the determinants of health and social challenges in Uganda. Although ample information exists about smoking prevalence, less is known about the determinants particularly in the leading tobacco-growing regions of the country. Data and methods: Secondary data were extracted from the 2016 Uganda Demographic and Health Survey dataset. The un-weighted and weighted samples were 16,800 and 14,791 respectively. Tobacco-smoking status, the outcome variable, was dichotomized into those who smoked and those who never smoked. Binary logistic regression was used to model the dichotomous outcome variable against a combination of predictor variables. Findings: Overall being male, having low education, belonging to the poor wealth quintile and being of advanced age increased the odds of tobacco-smoking. Conclusion: Sex, level of education, wealth index and age predicted tobacco-smoking. We recommend strengthening educational programmes, increased advocacy for reducing tobacco-smoking and improvement of socioeconomic status of the population. [ABSTRACT FROM AUTHOR]

A growing number of young people smoke electronic (e-) cigarettes, presenting an emerging challenge to tobacco control. Analyses are needed to better understand the dynamics of mutual transitions between e-cigarette and conventional combustible (c-) cigarette smoking to advance evidence-based tobacco control. In this study we modeled the nonlinear dynamics of c- and ecigarette smoking behavior transitions using the 2014 National Youth Tobacco Survey (NYTS) data. A model with five Markov-Chain transition stages linked by 21 transitional paths/probabilities was constructed, guided by the probabilistic discrete event systems (PDES) theory. The Moore-Penrose generalized inverse matrix was used to solve the proposed model that was under-determined. The estimated transitional probabilities indicate that each year, 7-8% of middle school students and 11% of high school students initiated smoking. E-cigarettes were more attractive then c-cigarettes but the behavior of smoking c-cigarettes was more stable than that of smoking e-cigarettes. Female students were more likely to remain as quitters or ex-smokers while male students were more likely to relapse and smoke again. Findings of this nonlinear dynamics modelling indicate potential increases in both e- and c-cigarette smoking among U.S. middle and high school students if no further measures are taken. The PDESbased approach is effective to investigate the nonlinear dynamics of mutual transitions of two risk behaviors in adolescents with one wave cross-sectional data. [ABSTRACT FROM AUTHOR]

Background: Smoking remains a highly significant preventable global public health problem. In this context, digital interventions offer great advantages in terms of a lack of biological side effects, possibility of automatic delivery, and consequent human resource savings relative to traditional interventions. Such interventions have been studied in randomized controlled trials (RCTs) but have not been systematically reviewed with the inclusion of text-based and multiplatform-based interventions. In addition, this area has not been evaluated from the perspective of the psychological theoretical basis of intervention. Objective: The aim of this paper is to assess the efficiency of digital interventions in RCT studies of smoking cessation and to evaluate the effectiveness of the strategies used for digital interventions. Methods: An electronic search of RCTs was conducted using PubMed, Embase, and the Cochrane Library by June 30, 2021. Eligible studies had to compare automated digital intervention (ADI) to the use of a self-help guideline or no intervention. Participants were current smokers (aged 16 years or older). As the main outcome, abstinence after endpoint was extracted from the studies. Systematic review and meta-analysis were conducted to assess the efficiency of ADIs. Metaregressions were conducted to assess the relationship between intervention theory and effectiveness. Results: A total of 19 trials (15,472 participants) were included in the analysis. The overall abstinence rate (95% CI) at the endpoint was 17.8% (17.0-18.7). The overall risk ratio of the intervention group compared to the controls at the endpoint was 17.8% (17.0-18.7). Cochrane risk-of-bias tool for randomized trials (ROB 2) suggested that most of the studies had a low risk of bias (56.3%). Psychological theory–related constructs or predictors, which refer to other theory-based concepts (rather than only behavioral theory) such as craving or anxiety, are associated with effectiveness. Conclusions: This study found that ADI had a clear positive effect compared to self-help guidelines or to no intervention, and effectiveness was associated with theory-related constructs or predictors. ADIs should be promoted by policy makers and clinical practitioners to address the huge gap between the need for smoking cessation and availability of traditional treatment resources. Possible increases in ADI efficiency may be achieved by optimally integrating psychotherapeutic theories and techniques. Trial Registration: PROSPERO CRD42021256593; https://www.crd.york.ac.uk/prospero/display%5frecord.php?RecordID=256593 J Med Internet Res 2022;24(11):e38206 doi:10.2196/38206 [ABSTRACT FROM AUTHOR]

Objective To update the estimated prevalence rates of smoking and examine major metabolic diseases associated with smoking status in Chinese adults. Methods Using a complex, multistage, probability sampling design, we recruited a nationally representative sample of 98,658 Chinese adults aged ≥18 years in 2010. Information on current, former, never, and passive smoking status was obtained using a standard questionnaire. All estimates were weighted to represent the overall Chinese adult population. Results The estimated proportion of current smokers was 28.3% for Chinese adults aged ≥18 years. The corresponding values of former and passive smokers were 5.1% and 21.4%, respectively. Additionally, former smokers were found to have a less favorable metabolic risk profile among all categories of smoking status in both men and women. The prevalence of metabolic diseases such as diabetes and hypertension also increased with a greater number of smoking pack-years in men. Conclusion The prevalences of current smoking and passive smoking remain high in Chinese adults. [ABSTRACT FROM AUTHOR]

Limited studies have examined associations between air pollutants exposure and renal function, especially in China, with the most extensive chronic kidney disease (CKD) disease burden worldwide. This study examines associations between long-term exposure to ambient PM 2.5 , NO 2 , CO, O 3 , SO 2 and renal function. We included 80,225 participants aged 30–79 years from the baseline data of the China Multi-Ethnic Cohort (CMEC) study. Three-year average concentrations of PM 2.5 , NO 2 , CO, O 3 , and SO 2 were estimated using satellite-based spatiotemporal models. Renal function is determined by the estimated glomerular filtration rate (eGFR) using Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation. After adjusting for covariates, generalized propensity scores (GPS) weighting regression was used to estimate associations between ambient air pollutants and renal function. An increase of 0.1 mg/m3 CO (OR [odds ratio] =1.20 95% CI [confidence interval], 1.05–1.37) was positively associated with CKD. An increase of 1 μg/m3 in SO 2 (1.07, 1.00–1.14) concentration was positively associated with CKD. An increase of 10 μg/m3 in PM 2.5 (1.17, 0.99–1.38), NO 2 (1.12, 0.83–1.51) and O 3 (1.10, 0.81–1.50) concentration was not associated with CKD. These effects are stronger in those younger than 65, smoking and with low BMI. In this study, we found that long-term exposure to ambient CO and SO 2 were positively associated with CKD. Gaseous pollutants should also arouse the concern of relevant departments. [Display omitted] • A positive association between long-term exposure to ambient CO, SO 2 and CKD was observed. • Smoking, age and BMI modified the above association. • The generalized propensity scores weighting method was used to obtain approximate causal associations. • Gaseous pollutants such as CO and SO 2 should also arouse the concern of relevant departments. [ABSTRACT FROM AUTHOR]

The purpose of this review is to describe the existing literature regarding the relationship between the vaginal microbiome, human papillomavirus persistence, and cervical cancer risk, as well as to discuss factors that mediate these relationships. Data suggest that alterations in the vaginal microbiome affect the risk of human papillomavirus infection and persistence, which has downstream effects on cervical dysplasia and cancer risk. The homeostatic Lactobillus species L. crispatus, L. gasseri, L. jensenii act to promote a healthy vaginal environment, while L. iners and pathogens causing bacterial vaginosis are associated with increased inflammation, human papillomavirus infection, cervical dysplasia, and potentially cancer. There are, however, still several large gaps in the literature, particularly related to the modifiable and non-modifiable factors that affect the vaginal microbiome and ensuing risk of pre-cancerous and cancerous lesions. Evidence currently suggests that endogenous and exogenous hormones, tobacco products, and sexual practices influence vaginal microbiome composition, but the nuances of these relationships and how changes in these factors affect dysplasia risk are yet to be delineated. Other studies examining how diet, exercise, race, socioeconomic status, and genetic factors influence the vaginal microbiome are difficult to interpret in the setting of multiple confounders. Future studies should focus on how changes in these modulatory factors might promote a healthy vaginal microbiome to prevent or treat dysplasia in the lower female genital tract. [ABSTRACT FROM AUTHOR]

The article discusses the resistance to quitting smoking among low income smokers in France. Topics include statistics on smokers in France, social manifestations of smoking in France and in comparison with other countries, and the social integration of low income smokers and their lack of inclination to quit smoking.

Background: Facebook can be a suitable platform for public health interventions. Facebook users can express their reaction to the given social media content in many ways using interaction buttons. The analysis of these interactions can be advantageous in increasing reach and engagement of public health interventions.Objective: This research aimed at understanding how Facebook users' interactions correlate with organic reach and engagement regarding the same smoking cessation support contents.Methods: The study population consisted of Facebook users who were reached by a public smoking cessation support page without advertising. We included 1025 nonpaid Facebook posts (N=1025) which used smoking cessation strategies based on a motivational interviewing counseling style. The following data were collected from the "Post Details": the number of people who saw the given nonpaid content (organic reach) which consisted of fan and nonfan reach according to previous "page like" activity; each rate of "engagement indicators" (such as the symbols of "like," "love," "haha," "wow," "sad," "angry"; or other interactions: "shares," "comments," "clicks"); and the rate of negative Facebook interactions (eg, "post hides" or "unlike of page"). Overall, these data were analyzed with the Spearman correlation method.Results: Surprisingly, we found a significant negative correlation between organic reach and the "like" reaction (rs=-0.418; P<.001). The strongest significant positive correlations of organic reach were observed with the "haha" reaction (rs=0.396; P<.001), comments (rs=0.368; P<.001), and the "love" reaction (rs=0.264; P<.001). Furthermore, nonfan reach correlated positively with "shares" (rs=0.388; P<.001) and clicks (rs=0.135; P<.001), while fan reach correlated positively with the "haha" reaction (rs=0.457; P<.001), comments (rs=0.393; P<.001), and the "love" reaction (rs=0.310; P<.001). Contrary to expectations, the "like" reaction was sharply separated by significant negative correlations from "wow" (rs=-0.077; P=.013), "sad" (rs=-0.120; P<.001), "angry" reactions (rs=-0.136; P<.001), and comments (rs=-0.130; P<.001). Additionally, a high rate of negative Facebook interactions was significantly associated with "wow" (rs=0.076; P=.016) and "sad" reactions (rs=0.091; P=.003).Conclusions: This study has shown that it is possible to hypothesize a disadvantage of the "like" reaction and advantages of other interactions (eg, the "haha" reaction or "comments") in content algorithmic ranking on Facebook. In addition, the correlational analysis revealed a need of a further categorization to fan-specific interactions (eg, "haha" or "love" reactions) and nonfan-specific interactions (eg, "shares" and "clicks"). Regarding the direction of the correlations, these findings suggest that some interactions (eg, negative Facebook interactions, "wow," "sad," and "angry" reactions) may decrease the engagement, while other interactions ("like," "love," "haha" reactions, "shares," and "clicks") may increase the engagement during Facebook-based smoking cessation interventions. This hypothesis-generating research offers an important insight into the relationship between organic reach, engagement, and Facebook users' interactions for public health professionals who design Facebook-based interventions. [ABSTRACT FROM AUTHOR]

Genetic effects are suspected to influence cadmium internal dose. Our objective was to assess genetic determinants of urine cadmium in American Indian adults participating in the Strong Heart Family Study (SHFS). Urine cadmium levels and genotyped short tandem repeat (STR) markers were available on 1936 SHFS participants. We investigated heritability, including gene-by-sex and smoking interactions, and STR-based quantitative trait locus (QTL) linkage, using a variance-component decomposition approach, which incorporates the genetic information contained in the pedigrees. We also used available single nucleotide polymorphisms (SNPs) from Illumina's Metabochip and custom panel to assess whether promising QTLs associated regions could be attributed to SNPs annotated to specific genes. Median urine cadmium levels were 0.44 μg/g creatinine. The heritability of urine cadmium concentrations was 28%, with no evidence of gene-by-sex or -smoking interaction. We found strong statistical evidence for a genetic locus at chromosome 16 determining urine cadmium concentrations (Logarithm of odds score [LOD] = 3.8). Among the top 20 associated SNPs in this locus, 17 were annotated to ABCC1 (p-values from 0.0002 to 0.02), and attenuated the maximum linkage peak by a ∼40%. Suggestive QTL signals (LOD>1.9) in chromosomes 2, 6, 11, 14, and 19, showed associated SNPs in the genes NDUFA10 , PDE10A , PLEKHA7 , BAZ1A and CHAF1A , respectively. Our findings support that urinary cadmium levels are heritable and influenced by a QTL on chromosome 16, which was explained by genetic variation in ABCC1. Studies with extended sets of genome-wide markers are needed to confirm these findings and to identify additional metabolism and toxicity pathways for cadmium. [Display omitted] • Genetic effects are suspected to influence cadmium internal dose. • We used data from 1936 Strong Heart Family Study participants. • The heritability of urine cadmium concentrations was ∼30%. • A QTL on chromosome 16 was associated with urine cadmium levels (LOD score = 3.8). • SNPs in ABCC1 attenuated the maximum linkage peak by a ∼40%. [ABSTRACT FROM AUTHOR]

Since the first report by Perry et al. (1955), most studies affirmed the hypertensive effects of cadmium (Cd) in humans. Nonetheless, conclusions between studies remain inconsistent. The aim of this study was to reevaluate the evidence for a potential relationship between Cd exposure and altered blood pressure and/or hypertension, focusing on studies published between January 2010 and March 2020. We reviewed all observational studies from database searches (PubMed and SCOPUS) on Cd exposure and blood pressure or hypertension. We extracted information from studies that provided sufficient data on population characteristics, smoking status, exposure, outcomes, and design. Thirty-eight studies met our inclusion criteria; of those, twenty-nine were cross sectional, three case control, five cohort and one interventional study. Blood or urinary Cd levels were the most commonly used biomarkers. A positive association between blood Cd levels and blood pressure and/or hypertension was identified in numerous studies at different settings. Limited number of representative population-based studies of never-smokers was observed, which may have confounded our conclusions. The association between urinary Cd and blood pressure and/or hypertension remains uncertain due to conflicting results, including inverse relationships with lack of strong mechanistic support. We point to the urgent need for additional longitudinal studies to confirm our findings. • We performed a systematic review on the effects of human Cd exposure and altered blood pressure and/or hypertension. • Observational studies were reviewed from database searches published between January 2010 and March 2020. • A positive association between blood Cd levels and blood pressure and/or hypertension was identified. • The association between urinary Cd and blood pressure and/or hypertension remains uncertain. • Future population-wide longitudinal studies, as well as studies in non-smoking populations are needed. [ABSTRACT FROM AUTHOR]