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1.
BMC Cardiovasc Disord ; 24(1): 292, 2024 Jun 05.
Article En | MEDLINE | ID: mdl-38840064

BACKGROUND: Tobacco use is recognized as a major cause of cardiovascular disease, which is associated with endothelial dysfunction. Endothelial function is evaluated using flow-mediated dilation (FMD), which is a noninvasive method. This meta-analysis aimed to investigate the association between smoking exposure and endothelial function evaluated using FMD values. METHODS: We searched the PubMed, Embase, Web of Science, and Cochrane Library databases for cohort studies of smokers or passive smokers that used FMD to assess endothelial function. The primary outcome of the study was the change in the rate of FMD. The risk of bias was evaluated using the Cochrane Collaboration tool and Newcastle-Ottawa Scale. Further, the weighted mean difference was used to analyze the continuous data. RESULTS: Overall, 14 of 1426 articles were included in this study. The results of these articles indicated that smoking is a major cause of endothelial dysfunction and altered FMD; a pooled effect size of - 3.15 was obtained with a 95% confidence interval of (- 3.84, - 2.46). Notably, pregnancy status, Asian ethnicity, or health status did not affect heterogeneity. CONCLUSIONS: We found that smoking has a significant negative impact on FMD, and measures such as medication or education for smoking cessation may improve endothelial function and reduce the risk of cardiovascular disease. TRIAL REGISTRATION: The meta-analysis was registered with PROSPERO on April 5th, 2023 (CRD42023414654).


Cardiovascular Diseases , Endothelium, Vascular , Vasodilation , Humans , Endothelium, Vascular/physiopathology , Female , Male , Middle Aged , Adult , Risk Assessment , Cardiovascular Diseases/physiopathology , Cardiovascular Diseases/diagnosis , Cardiovascular Diseases/etiology , Cardiovascular Diseases/epidemiology , Aged , Risk Factors , Tobacco Smoke Pollution/adverse effects , Predictive Value of Tests , Smoking/adverse effects , Smoking/physiopathology , Young Adult , Smokers , Brachial Artery/physiopathology , Brachial Artery/diagnostic imaging , Heart Disease Risk Factors
2.
Rev Prat ; 74(5): 526-528, 2024 May.
Article Fr | MEDLINE | ID: mdl-38833236

SMOKING AND TUBERCULOSIS. Tuberculosis and smoking are responsible for high mortality worldwide. Tuberculosis causes 9 million incident cases and 1.6 million deaths every year. Smoking increases the risk of infection by Mycobacterium tuberculosis and of severe tuberculosis disease with death or recurrence. Cessation of smoking improves the course of the disease, promoting adherence to anti-tuberculosis treatment and definitive cure. All health-care professionals involved in tuberculosis care must be involved to help smokers with tuberculosis to quit.


TABAC ET TUBERCULOSE. La tuberculose et le tabagisme sont à l'origine d'une importante mortalité dans le monde. La tuberculose cause 9 millions de cas incidents et 1,6 million de décès chaque année. Le tabagisme augmente les risques d'infection par Mycobacterium tuberculosis et de tuberculose maladie sévère avec décès ou récidive. L'arrêt du tabac améliore le cours de l'infection, favorisant l'adhésion des patients au traitement antituberculeux et la guérison définitive. Tous les professionnels de santé doivent s'investir dans la mission d'aide à l'arrêt du tabac des fumeurs atteints de tuberculose.


Smoking Cessation , Smoking , Tuberculosis , Humans , Tuberculosis/epidemiology , Tuberculosis/prevention & control , Smoking/adverse effects , Smoking/epidemiology , Smoking Cessation/methods , Risk Factors
3.
BMC Pulm Med ; 24(1): 264, 2024 Jun 01.
Article En | MEDLINE | ID: mdl-38824531

BACKGROUND: Smoking induces and modifies the airway immune response, accelerating the decline of asthmatics' lung function and severely affecting asthma symptoms' control level. To assess the prognosis of asthmatics who smoke and to provide reasonable recommendations for treatment, we constructed a nomogram prediction model. METHODS: General and clinical data were collected from April to September 2021 from smoking asthmatics aged ≥14 years attending the People's Hospital of Zhengzhou University. Patients were followed up regularly by telephone or outpatient visits, and their medication and follow-up visits were recorded during the 6-months follow-up visit, as well as their asthma control levels after 6 months (asthma control questionnaire-5, ACQ-5). The study employed R4.2.2 software to conduct univariate and multivariate logistic regression analyses to identify independent risk factors for 'poorly controlled asthma' (ACQ>0.75) as the outcome variable. Subsequently, a nomogram prediction model was constructed. Internal validation was used to test the reproducibility of the model. The model efficacy was evaluated using the consistency index (C-index), receiver operating characteristic (ROC) curve, calibration curve, and decision curve. RESULTS: Invitations were sent to 231 asthmatics who smoked. A total of 202 participants responded, resulting in a final total of 190 participants included in the model development. The nomogram established five independent risk factors (P<0.05): FEV1%pred, smoking index (100), comorbidities situations, medication regimen, and good or poor medication adherence. The area under curve (AUC) of the modeling set was 0.824(95%CI 0.765-0.884), suggesting that the nomogram has a high ability to distinguish poor asthma control in smoking asthmatics after 6 months. The calibration curve showed a C-index of 0.824 for the modeling set and a C-index of 0.792 for the self-validation set formed by 1000 bootstrap sampling, which means that the prediction probability of the model was consistent with reality. Decision curve analysis (DCA) of the nomogram revealed that the net benefit was higher when the risk threshold probability for poor asthma control was 4.5 - 93.9%. CONCLUSIONS: FEV1%pred, smoking index (100), comorbidities situations, medication regimen, and medication adherence were identified as independent risk factors for poor asthma control after 6 months in smoking asthmatics. The nomogram established based on these findings can effectively predict relevant risk and provide clinicians with a reference to identify the poorly controlled population with smoking asthma as early as possible, and to select a better therapeutic regimen. Meanwhile, it can effectively improve the medication adherence and the degree of attention to complications in smoking asthma patients.


Asthma , Nomograms , Smoking , Humans , Asthma/drug therapy , Asthma/physiopathology , Male , Female , Risk Factors , Adult , Middle Aged , Smoking/epidemiology , Smoking/adverse effects , ROC Curve , Logistic Models , China/epidemiology , Surveys and Questionnaires , Prognosis , Reproducibility of Results
4.
Sci Rep ; 14(1): 12727, 2024 06 03.
Article En | MEDLINE | ID: mdl-38830947

Coronary artery disease is a leading cause of morbidity and mortality worldwide. It occurs due to a combination of genetics, lifestyle, and environmental factors. Premature coronary artery disease (PCAD) is a neglected clinical entity despite the rising number of cases worldwide. This study aimed to investigate the risk factors of premature coronary artery disease. In this study, we searched articles that had studied the risk factors of premature coronary artery diseases from January 2000 to July 2022 in Saudi Arabia in Web of Science, Pub Med, Scopus, Springer, and Wiley databases. The final analysis is based on seven articles. The smoking prevalence was 39%, diabetes mellitus 41%, hypertension 33%, overweight and obesity 18%, family history of coronary artery disease (CAD) 19%, dyslipidemia 37%, and the prevalence range of low-density lipoprotein cholesterol was 33.8-55.0%. The results revealed a mortality prevalence of 4% ranging from 2 to 8% which is similar to the prevalence in older patients which was 2-10%. Smoking, diabetes mellitus, hypertension, family history of CAD, dyslipidemia, and overweight/obesity are significantly and positively associated with premature coronary artery diseases. The health authorities should design and implement an intensive and effective prophylactic plan to minimize the subsequent impact of PCAD on the young population. In addition, early diagnosis of PCAD has great value in providing timely treatment, managing the patients, and minimizing the burden of the disease.


Coronary Artery Disease , Humans , Saudi Arabia/epidemiology , Coronary Artery Disease/epidemiology , Coronary Artery Disease/mortality , Coronary Artery Disease/genetics , Risk Factors , Male , Prevalence , Female , Adult , Smoking/adverse effects , Smoking/epidemiology , Hypertension/epidemiology , Obesity/epidemiology , Obesity/complications , Dyslipidemias/epidemiology , Diabetes Mellitus/epidemiology , Diabetes Mellitus/mortality , Middle Aged
5.
BMC Musculoskelet Disord ; 25(1): 433, 2024 Jun 03.
Article En | MEDLINE | ID: mdl-38831392

This study presents a systematic literature review and meta-analysis of pseudarthrosis risk factors following lumbar fusion procedures. The odds ratio (OR) and 95% confidence interval (95% CI) were used for outcome measurements. The objective of this study was to identify the independent risk factors for pseudarthrosis after lumbar spinal fusion, which is crucial for mitigating morbidity and reoperation. Systematic searches in PubMed, Embase, and Scopus (1990-July 2021) were conducted using specific terms. The inclusion criteria included prospective and retrospective cohorts and case‒control series reporting ORs with 95% CIs from multivariate analysis. The quality assessment utilized the Newcastle-Ottawa scale. Meta-analysis, employing OR and 95% CI, assessed pseudarthrosis risk factors in lumbar fusion surgery, depicted in a forest plot. Of the 568 abstracts identified, 12 met the inclusion criteria (9 retrospective, 2006-2021). The 17 risk factors were categorized into clinical, radiographic, surgical, and bone turnover marker factors. The meta-analysis highlighted two significant clinical risk factors: age (95% CI 1.02-1.11; p = 0.005) and smoking (95% CI 1.68-5.44; p = 0.0002). The sole significant surgical risk factor was the number of fused levels (pooled OR 1.35; 95% CI 1.17-1.55; p < 0.0001). This study identified 17 risk factors for pseudarthrosis after lumbar fusion surgery, emphasizing age, smoking status, and the number of fusion levels. Prospective studies are warranted to explore additional risk factors and assess the impact of surgery and graft type.


Lumbar Vertebrae , Pseudarthrosis , Spinal Fusion , Humans , Spinal Fusion/adverse effects , Pseudarthrosis/etiology , Pseudarthrosis/epidemiology , Lumbar Vertebrae/surgery , Lumbar Vertebrae/diagnostic imaging , Risk Factors , Age Factors , Smoking/adverse effects
6.
Ren Fail ; 46(1): 2356024, 2024 Dec.
Article En | MEDLINE | ID: mdl-38832473

OBJECTIVE: Smoking has been suggested as a modifiable and cardiovascular risk factor for chronic kidney disease (CKD). Although long-term smoking has been associated with CKD, the potential relationship between its metabolite hydroxycotinine and CKD has not been clarified. METHODS: A total of 8,544 participants aged 20 years and above from the National Health and Nutrition Examination Survey (NHANES) 2017 - March 2020 were enrolled in our study. CKD was defined by estimated glomerular filtration rate (eGFR) < 60 mL/(min*1.73 m2). Serum hydroxycotinine was measured by an isotope-dilution high-performance liquid chromatography/atmospheric pressure chemical ionization tandem mass spectrometric (ID HPLC-APCI MS/MS) method with a lower limit of detections (LLOD) at 0.015 ng/mL. The non-linear relationship was explored with restricted cubic splines (RCS). Pearson's correlation coefficient and a multivariate logistic regression model were used for correlation analysis. RESULTS: Serum hydroxycotinine and eGFR were negatively correlated in both non-CKD group (r= -0.05, p < 0.001) and CKD group (r= -0.04, p < 0.001). After serum hydoxycotinine dichotominzed with LLOD, serum hydroxycotinine ≥ 0.015 ng/mL was negatively correlated with eGFR not only in non-CKD group (r = -0.05, p < 0.001) but also in CKD group (r = -0.09, p < 0.001). After adjusting for comprehensive confounders, results from the multivariate logistic regression analysis showed that participants with serum hydroxycotinine ≥ 0.015 ng/mL had increased odds of CKD (OR = 1.505, p < 0.001). CONCLUSIONS: Serum hydroxycotinine might be positively associated with CKD. Further study is warranted to find the right concentration of hydroxycotinine to measure the CKD.


Glomerular Filtration Rate , Nutrition Surveys , Renal Insufficiency, Chronic , Humans , Male , Renal Insufficiency, Chronic/blood , Female , Cross-Sectional Studies , Middle Aged , Adult , Aged , Tandem Mass Spectrometry , Risk Factors , Logistic Models , Chromatography, High Pressure Liquid , Smoking/epidemiology , Smoking/adverse effects , Biomarkers/blood , Cotinine/analogs & derivatives
7.
Sci Rep ; 14(1): 10550, 2024 05 08.
Article En | MEDLINE | ID: mdl-38719836

To investigate the influence of preoperative smoking history on the survival outcomes and complications in a cohort from a large multicenter database. Many patients who undergo radical cystectomy (RC) have a history of smoking; however, the direct association between preoperative smoking history and survival outcomes and complications in patients with muscle-invasive bladder cancer (MIBC) who undergo robot-assisted radical cystectomy (RARC) remains unexplored. We conducted a retrospective analysis using data from 749 patients in the Korean Robot-Assisted Radical Cystectomy Study Group (KORARC) database, with an average follow-up duration of 30.8 months. The cohort was divided into two groups: smokers (n = 351) and non-smokers (n = 398). Propensity score matching was employed to address differences in sample size and baseline demographics between the two groups (n = 274, each). Comparative analyses included assessments of oncological outcomes and complications. After matching, smoking did not significantly affect the overall complication rate (p = 0.121). Preoperative smoking did not significantly increase the occurrence of complications based on complication type (p = 0.322), nor did it increase the readmission rate (p = 0.076). There were no perioperative death in either group. Furthermore, preoperative smoking history showed no significant impact on overall survival (OS) [hazard ratio (HR) = 0.87, interquartile range (IQR): 0.54-1.42; p = 0.589] and recurrence-free survival (RFS) (HR = 1.12, IQR: 0.83-1.53; p = 0.458) following RARC for MIBC. The extent of preoperative smoking (≤ 10, 10-30, and ≥ 30 pack-years) had no significant influence on OS and RFS in any of the categories (all p > 0.05). Preoperative smoking history did not significantly affect OS, RFS, or complications in patients with MIBC undergoing RARC.


Cystectomy , Postoperative Complications , Robotic Surgical Procedures , Smoking , Urinary Bladder Neoplasms , Humans , Cystectomy/adverse effects , Cystectomy/methods , Male , Female , Urinary Bladder Neoplasms/surgery , Urinary Bladder Neoplasms/mortality , Urinary Bladder Neoplasms/pathology , Robotic Surgical Procedures/adverse effects , Robotic Surgical Procedures/methods , Aged , Smoking/adverse effects , Middle Aged , Postoperative Complications/epidemiology , Postoperative Complications/etiology , Retrospective Studies , Databases, Factual , Treatment Outcome , Republic of Korea/epidemiology , Preoperative Period
8.
Hipertens Riesgo Vasc ; 41 Suppl 1: S1-S85, 2024 Apr.
Article Es | MEDLINE | ID: mdl-38729667

Consensus statement on smoking and vascular risk About 22% of the Spanish population are daily smokers. Men are more likely to smoke than women. In Spain, women between 15-25 years of age smoke as much or more than men. Every smoker should be assessed for: physical dependence on nicotine (Fagerström test), social and psychological dependence (Glover Nilsson test), level of motivation to quit (Richmond test), probability of therapy success (Henri-Mondor and Michael-Fiore tests), and stage of behavioral change development (Prochaska and DiClementi). Advice on smoking cessation is highly cost-effective and should always be provided. Smoking is an enhancer of cardiovascular risk because it acts as a pathogen agent in the development of arteriosclerosis and is associated with ischemic heart disease, stroke, and peripheral artery disease. Smoking increases the risk of chronic lung diseases (COPD) and is related to cancers of the lung, female genitalia, larynx, oropharynx, bladder, mouth, esophagus, liver and biliary tract, and stomach, among others. Combined oral contraceptives should be avoided in women smokers older than 35 years of age due to the risk of thromboembolism. In smoking cessation, the involvement of physicians, nurses, psychologists, etc. is important, and their multidisciplinary collaboration is needed. Effective pharmacological treatments for smoking cessation are available. Combined treatments are recommended when smoker's dependence is high. For individuals who are unable to quit smoking, a strategy based on tobacco damage management with a total switch to smokeless products could be a less dangerous alternative for their health than continuing to smoke.


Smoking Cessation , Smoking , Humans , Female , Male , Adult , Smoking/adverse effects , Adolescent , Young Adult , Cardiovascular Diseases/prevention & control , Cardiovascular Diseases/etiology , Spain , Tobacco Use Disorder/therapy , Heart Disease Risk Factors
9.
PLoS One ; 19(5): e0302505, 2024.
Article En | MEDLINE | ID: mdl-38722836

BACKGROUND: Smoking has been associated with a higher risk of contracting pneumonia, but contradictory results have shown that smoking may or may not decrease the risk of dying in pneumonia. The aim of this study is to investigate how smoking is associated with contracting any infection and pneumonia and death. METHOD AND FINDINGS: Participants were drawn from the population-based Cohort of Swedish Men and the Swedish Mammography Cohort, which are representative of the Swedish population. Participants have answered detailed lifestyle questionnaires and have been followed in national registers, such as the Patient Register, Cause of Death register and Swedish Intensive Care Registry. The risks of contracting infection and pneumonia or dying in infection and pneumonia were assessed using Cox regression. Of 62,902 cohort participants, 25,297 contracted an infection of which 4,505 died; and 10,471 contracted pneumonia of which 2,851 died. Compared to never smokers, former smokers at baseline had hazard ratio (HR) 1.08 (95% confidence interval (CI) 1.05-1.12) of contracting and HR 1.19 (95% CI 1.11-1.28) of dying in infection and HR 1.17 (95% CI 1.12-1.23) of contracting and HR 1.16 (95% CI 1.06-1.27) of dying in pneumonia during follow-up. Compared to never smokers, current smokers at baseline had HR 1.17 (95% CI 1.13-1.21) of contracting infection and HR 1.64 (95% CI 1.52-1.77) dying in infection; HR 1.42 (95% CI 1.35-1.49) of contracting pneumonia and HR 1.70 (95% CI 1.55-1.87) of dying in pneumonia during follow-up. The risk of contracting and dying in infection and pneumonia increased in a dose-response manner with number of pack years smoked and decreased with years since smoking cessation. CONCLUSION: Smoking is associated with contracting and dying in any infection and pneumonia and the risk increases with pack years smoked, highlighting the importance of both primary prevention and smoking cessation.


Intensive Care Units , Pneumonia , Smoking , Humans , Male , Pneumonia/mortality , Pneumonia/epidemiology , Middle Aged , Smoking/adverse effects , Sweden/epidemiology , Aged , Female , Risk Factors , Bacterial Infections/mortality , Bacterial Infections/epidemiology , Adult , Cohort Studies , Proportional Hazards Models , Registries
10.
PLoS One ; 19(5): e0294898, 2024.
Article En | MEDLINE | ID: mdl-38701092

OBJECTIVE: The Global Adult Tobacco Survey conducted in India has divulged that 28.6% of the populace aged 15 years and above partakes in tobacco consumption in various modalities. Despite the availability of numerous studies on the correlation between smoking and hypertension, the nexus between tobacco smoking and hypertension remains enigmatic. Smoking has predominantly been linked to blood pressure, with scant investigations exploring the plausible association that may subsist between smoking and pulse pressure. METHODOLOGY: This study is based on secondary data analysis from the fifth National Family Health Survey (NFHS-5). 17 Field Agencies gathered information from 636,699 households, 724,115 women, and 101,839 men. The data related to only men was included and analysed in this present study. RESULTS: Male participants had a mean age of 32.2+1.2 years, an average waist circumference of 80.4+12.2 cm, and mean systolic and diastolic blood pressure of 123.4+13.8 mmHg and 80.5+10.2 mmHg. Daily smokers had a slightly higher likelihood of hypertension compared to non-smokers (OR = 1.2, p <0.001). Male quitters had significantly lower odds of hypertension (OR = 0.9, p <0.001). Quitters had reduced odds of narrow pulse pressure but increased odds of wide pulse pressure (OR = 0.81 and 1.14, respectively). CONCLUSION: The study found that regular smoking was associated with hypertension, while factors such as age, obesity, urban dwelling, wealth, and tribal residence were linked to increased blood pressure. Male quitters had a lower likelihood of hypertension, and middle-aged men and those with central obesity showed distinct associations with deranged pulse pressure.


Blood Pressure , Hypertension , Smoking , Humans , Male , Hypertension/epidemiology , Hypertension/etiology , India/epidemiology , Adult , Smoking/adverse effects , Smoking/epidemiology , Middle Aged , Health Surveys , Female , Adolescent , Young Adult , Risk Factors
11.
Sci Adv ; 10(18): eadl3747, 2024 May 03.
Article En | MEDLINE | ID: mdl-38701212

Early-life tobacco exposure serves as a non-negligible risk factor for aging-related diseases. To understand the underlying mechanisms, we explored the associations of early-life tobacco exposure with accelerated biological aging and further assessed the joint effects of tobacco exposure and genetic susceptibility. Compared with those without in utero exposure, participants with in utero tobacco exposure had an increase in Klemera-Doubal biological age (KDM-BA) and PhenoAge acceleration of 0.26 and 0.49 years, respectively, but a decrease in telomere length of 5.34% among 276,259 participants. We also found significant dose-response associations between the age of smoking initiation and accelerated biological aging. Furthermore, the joint effects revealed that high-polygenic risk score participants with in utero exposure and smoking initiation in childhood had the highest accelerated biological aging. There were interactions between early-life tobacco exposure and age, sex, deprivation, and diet on KDM-BA and PhenoAge acceleration. These findings highlight the importance of reducing early-life tobacco exposure to improve healthy aging.


Aging , Genetic Predisposition to Disease , Prenatal Exposure Delayed Effects , Humans , Female , Male , Prenatal Exposure Delayed Effects/genetics , Aging/genetics , Adult , Pregnancy , Nicotiana/adverse effects , Nicotiana/genetics , Smoking/adverse effects , Risk Factors , Middle Aged
12.
J Gastrointest Surg ; 28(5): 605-610, 2024 May.
Article En | MEDLINE | ID: mdl-38704197

BACKGROUND: Differential responses to neoadjuvant therapy (NAT) exist in pancreatic ductal adenocarcinoma (PDAC); however, contributing factors are poorly understood. Tobacco smoke is a common risk factor for PDAC, with nicotine-induced chemoresistance observed in other cancers. This study aimed to explore the potential association between tobacco use and NAT efficacy in PDAC. METHODS: A single-center, retrospective analysis was conducted that included all consecutive patients with PDAC who underwent surgical resection after NAT with a documented smoking history (N = 208). NAT response was measured as percentage fibrosis in the surgical specimen. Multivariable models controlled for covariates and survival were modeled using the Kaplan-Meier method. RESULTS: Postoperatively, major responses to NAT (>95% fibrosis) were less frequently observed in smokers than in nonsmokers (13.7% vs 30.4%, respectively; P = .021). Pathologic complete responses were similarly less frequent in smokers than in nonsmokers (2.1% vs 9.9%, respectively; P = .023). On multivariate analysis controlling for covariates, smoking history remained independently associated with lower odds of major fibrosis (odds ratio [OR], 0.25; 95% CI, 0.10-0.59; P = .002) and pathologic complete response (OR, 0.21; 95% CI, 0.03-0.84; P = .05). The median overall survival was significantly longer in nonsmokers than in smokers (39.1 vs 26.6 months, respectively; P = .05). CONCLUSION: Tobacco use was associated with diminished pathologic responses to NAT. Future research to understand the biology underlying this observation is warranted and may inform differential NAT approaches or counseling among these populations.


Carcinoma, Pancreatic Ductal , Neoadjuvant Therapy , Pancreatic Neoplasms , Smoking , Humans , Pancreatic Neoplasms/therapy , Pancreatic Neoplasms/pathology , Male , Female , Retrospective Studies , Middle Aged , Aged , Smoking/adverse effects , Smoking/epidemiology , Carcinoma, Pancreatic Ductal/therapy , Carcinoma, Pancreatic Ductal/mortality , Carcinoma, Pancreatic Ductal/pathology , Treatment Outcome , Fibrosis , Adenocarcinoma/therapy , Adenocarcinoma/pathology , Risk Factors , Kaplan-Meier Estimate
13.
BMC Public Health ; 24(1): 1238, 2024 May 06.
Article En | MEDLINE | ID: mdl-38711042

BACKGROUND: We conducted this meta-analysis to investigate the potential association between maternal smoking, alcohol and caffeinated beverages consumption during pregnancy and the risk of childhood brain tumors (CBTs). METHODS: A thorough search was carried out on PubMed, Embase, Web of Science, Cochrane Library, and China National Knowledge Internet to identify pertinent articles. Fixed or random effects model was applied to meta-analyze the data. RESULTS: The results suggested a borderline statistically significant increased risk of CBTs associated with maternal smoking during pregnancy (OR 1.04, 95% CI 0.99-1.09). We found that passive smoking (OR 1.12, 95% CI 1.03-1.20), rather than active smoking (OR 1.00, 95% CI 0.93-1.07), led to an increased risk of CBTs. The results suggested a higher risk in 0-1 year old children (OR 1.21, 95% CI 0.94-1.56), followed by 0-4 years old children (OR 1.12, 95% CI 0.97-1.28) and 5-9 years old children (OR 1.11, 95% CI 0.95-1.29). This meta-analysis found no significant association between maternal alcohol consumption during pregnancy and CBTs risk (OR 1.00, 95% CI 0.80-1.24). An increased risk of CBTs was found to be associated with maternal consumption of caffeinated beverages (OR 1.16, 95% CI 1.07-1.26) during pregnancy, especially coffee (OR 1.18, 95% CI 1.00-1.38). CONCLUSIONS: Maternal passive smoking, consumption of caffeinated beverages during pregnancy should be considered as risk factors for CBTs, especially glioma. More prospective cohort studies are warranted to provide a higher level of evidence.


Alcohol Drinking , Brain Neoplasms , Caffeine , Observational Studies as Topic , Prenatal Exposure Delayed Effects , Humans , Pregnancy , Female , Alcohol Drinking/adverse effects , Alcohol Drinking/epidemiology , Prenatal Exposure Delayed Effects/epidemiology , Brain Neoplasms/epidemiology , Brain Neoplasms/chemically induced , Brain Neoplasms/etiology , Child , Child, Preschool , Caffeine/adverse effects , Infant , Infant, Newborn , Smoking/epidemiology , Smoking/adverse effects , Risk Factors , Beverages/adverse effects
14.
BMC Oral Health ; 24(1): 535, 2024 May 06.
Article En | MEDLINE | ID: mdl-38711116

BACKGROUND: Periodontitis is a complex chronic inflammatory disease that is particularly associated with health-related conditions such as smoking, excessive drinking and depression. This research aimed to investigate the interaction between these lifestyles factors on periodontitis risk. METHODS: This study included participants who participated in the National Health and Nutrition Examination Survey in the United States between 2009 and 2014. They had completed oral health-periodontal examination, Smoking-Cigarette Use Questionnaire, Alcohol Use Questionnaire, and Patient Health Questionnaire. Periodontal clinical attachment loss (CAL) of 3 mm or more and Patient Health Questionnaire-9 (PHQ-9) of 10 scores or more were used to identify periodontitis and depression, respectively. Daily alcohol consumption in the past year was classified into three levels: low (1 drink or less), moderate (between 1 and 3 drinks), and heavy drinking (4 drinks or more), while smoking was defined as having smoked at least 100 cigarettes in one's lifetime. Then, the logistic regression combined with interaction models were used to analyze the independent and combined effects of smoking, drinking and depression on periodontitis risk. RESULTS: The results indicated a statistically significant multiplicative interaction between smoking and depression in relation to the development of periodontitis, both in the overall population (P = 0.03) and among male participants (P = 0.03). Furthermore, among individuals experiencing depression, smoking was found to significantly increase the prevalence of periodontitis by 129% in the younger age group compared to non-smokers (odds ratio [OR]: 2.29; 95% confidence interval [CI]: 1.10 to 4.76). However, the interaction between smoking and alcohol consumption was only significant among females (P < 0.05). There was a dose-dependent relationship between drinking frequency and smoking on periodontitis prevalence. In the smoking population, occasional drinking (OR: 1.70; 95% CI: 1.22 to 2.37) and regular drinking (OR: 2.28; 95% CI: 1.68 to 3.11) significantly increased the prevalence of periodontitis compared to individuals without these two factors. CONCLUSION: These results suggested that there were interactive effects between smoking, drinking and depression on periodontitis risk and policies aimed at healthy behaviours and mental health may be beneficial for our oral health.


Alcohol Drinking , Depression , Smoking , Humans , Male , Female , Alcohol Drinking/adverse effects , Alcohol Drinking/epidemiology , Smoking/adverse effects , Smoking/epidemiology , Middle Aged , Adult , Depression/epidemiology , United States/epidemiology , Risk Factors , Periodontitis/epidemiology , Nutrition Surveys , Aged , Periodontal Diseases/epidemiology , Young Adult , Surveys and Questionnaires
15.
BMC Pulm Med ; 24(1): 220, 2024 May 03.
Article En | MEDLINE | ID: mdl-38702679

BACKGROUND: Recent research suggests that periodontitis can increase the risk of chronic obstructive pulmonary disease (COPD). In this study, we performed two-sample Mendelian randomization (MR) and investigated the causal effect of periodontitis (PD) on the genetic prediction of COPD. The study aimed to estimate how exposures affected outcomes. METHODS: Published data from the Gene-Lifestyle Interaction in the Dental Endpoints (GLIDE) Consortium's genome-wide association studies (GWAS) for periodontitis (17,353 cases and 28,210 controls) and COPD (16,488 cases and 169,688 controls) from European ancestry were utilized. This study employed a two-sample MR analysis approach and applied several complementary methods, including weighted median, inverse variance weighted (IVW), and MR-Egger regression. Multivariable Mendelian randomization (MVMR) analysis was further conducted to mitigate the influence of smoking on COPD. RESULTS: We chose five single-nucleotide polymorphisms (SNPs) as instrumental variables for periodontitis. A strong genetically predicted causal link between periodontitis and COPD, that is, periodontitis as an independent risk factor for COPD was detected. PD (OR = 1.102951, 95% CI: 1.005-1.211, p = 0.039) MR-Egger regression and weighted median analysis results were coincident with those of the IVW method. According to the sensitivity analysis, horizontal pleiotropy's effect on causal estimations seemed unlikely. However, reverse MR analysis revealed no significant genetic causal association between COPD and periodontitis. IVW (OR = 1.048 > 1, 95%CI: 0.973-1.128, p = 0.2082) MR Egger (OR = 0.826, 95%CI:0.658-1.037, p = 0.1104) and weighted median (OR = 1.043, 95%CI: 0.941-1.156, p = 0.4239). The results of multivariable Mendelian randomization (MVMR) analysis, after adjusting for the confounding effect of smoking, suggest a potential causal relationship between periodontitis and COPD (P = 0.035). CONCLUSION: In this study, periodontitis was found to be independent of COPD and a significant risk factor, providing new insights into periodontitis-mediated mechanisms underlying COPD development.


Genome-Wide Association Study , Mendelian Randomization Analysis , Polymorphism, Single Nucleotide , Pulmonary Disease, Chronic Obstructive , Smoking , Humans , Pulmonary Disease, Chronic Obstructive/genetics , Pulmonary Disease, Chronic Obstructive/epidemiology , Risk Factors , Smoking/epidemiology , Smoking/adverse effects , Periodontitis/genetics , Periodontitis/epidemiology , Severity of Illness Index , Genetic Predisposition to Disease , Periodontal Diseases/genetics , Periodontal Diseases/epidemiology
16.
Clin Transl Med ; 14(5): e1679, 2024 May.
Article En | MEDLINE | ID: mdl-38706045

Metabolic abnormalities represent one of the pathological features of chronic obstructive pulmonary disease (COPD). Glutamic pyruvate transaminase 2 (GPT2) is involved in glutamate metabolism and lipid synthesis pathways, whilst the exact roles of GPT2 in the occurrence and development of COPD remains uncertain. This study aims at investigating how GPT2 and the associated genes modulate smoking-induced airway epithelial metabolism and damage by reprogramming lipid synthesis. The circulating or human airway epithelial metabolomic and lipidomic profiles of COPD patients or cell-lines explored with smoking were assessed to elucidate the pivotal roles of GPT2 in reprogramming processes. We found that GPT2 regulate the reprogramming of lipid metabolisms caused by smoking, especially phosphatidylcholine (PC) and triacylglycerol (TAG), along with changes in the expression of lipid metabolism-associated genes. GPT2 modulated cell sensitivities and survival in response to smoking by enhancing mitochondrial functions and maintaining lipid and energy homeostasis. Our findings provide evidence for the involvement of GPT2 in the reprogramming of airway epithelial lipids following smoking, as well as the molecular mechanisms underlying GPT2-mediated regulation, which may offer an alternative of therapeutic strategies for chronic lung diseases.


Lipidomics , Pulmonary Disease, Chronic Obstructive , Humans , Pulmonary Disease, Chronic Obstructive/metabolism , Pulmonary Disease, Chronic Obstructive/genetics , Lipidomics/methods , Smoking/adverse effects , Smoking/metabolism , Lipid Metabolism/genetics , Male , Female , Metabolomics/methods , Middle Aged
17.
Int J Chron Obstruct Pulmon Dis ; 19: 1011-1019, 2024.
Article En | MEDLINE | ID: mdl-38737192

Purpose: The prevalence of airflow obstruction in Japan is 3.8%-16.9%. This epidemiological study based on a large database aimed to reassess the prevalence of airflow obstruction in Japan and the diagnosis rate of chronic obstructive pulmonary disease (COPD). Patients and Methods: We used data regarding claims from the health insurance union and health checkups provided by JMDC. The present study included a subgroup of individuals aged ≥40 years who underwent health checkups involving spirometry between January and December 2019. The study endpoints were the prevalence of airflow obstruction, COPD diagnosis rate, disease stage, and respiratory function test results. Results: Among 102,190 participants, 4113 (4.0%) had airflow obstruction. The prevalence of airflow obstruction was 5.3% in men and 2.1% in women. Among the study population, 6.8% were current smokers, while 3.4% were never or former smokers. Additionally, the prevalence of COPD increased with age. Approximately 8.4% of participants with airflow obstruction were diagnosed with COPD. Regarding the COPD diagnosis status, participants with airflow obstruction who were diagnosed with COPD were at a more advanced stage than those not diagnosed. Finally, patients diagnosed with COPD had significantly lower FEV1/FVC and FEV1 (p < 0.0001; Wilcoxon rank sum test). Conclusion: The epidemiological study based on a large database determined the COPD diagnosis rate related to airflow obstruction. The COPD diagnosis rate was extremely low among individuals who underwent health checkups, indicating the need for increased awareness about this medical condition. Moreover, primary care physicians should identify patients with suspected COPD and collaborate with pulmonologists to facilitate the early detection of COPD and enhance the COPD diagnosis rate.


Pulmonary Disease, Chronic Obstructive , Spirometry , Humans , Pulmonary Disease, Chronic Obstructive/epidemiology , Pulmonary Disease, Chronic Obstructive/diagnosis , Pulmonary Disease, Chronic Obstructive/physiopathology , Male , Female , Japan/epidemiology , Middle Aged , Prevalence , Aged , Adult , Forced Expiratory Volume , Databases, Factual , Lung/physiopathology , Vital Capacity , Smoking/epidemiology , Smoking/adverse effects , Predictive Value of Tests , Severity of Illness Index
19.
Stomatologiia (Mosk) ; 103(2): 41-49, 2024.
Article Ru | MEDLINE | ID: mdl-38741534

OBJECTIVE: The aim of the sthudy. To study the influence of general and local factors on the regenerative potential of bone tissue to optimize augmentation mechanisms in the treatment of jaw atrophy. MATERIALS AND METHODS: The influence of general and local factors on the regenerative potential of the bone during the augmentation operation of the alveolar process (part) of the jaw in 68 patients was studied. The survival rate of dental implants and the incidence of complications after completion of dental rehabilitation in the long-term follow-up period (more than 5 years) were evaluated. 18 indicators were studied, which were evaluated by qualitative and quantitative methods. The study of the effect of indicators on regeneration was carried out using an accurate Fischer test for conjugacy tables. The assessment of the strength of the influence was calculated as the ratio of the chances of developing an unfavorable outcome of bone grafting and dental implantation. RESULTS: He highest chances of developing adverse outcomes were found in smoking patients with diabetes mellitus, high body mass index, low survival of bone walls, severe bone atrophy (5.6 and higher class according to Cawood & Howell), three-dimensional bone defect, in the absence of 3 or more bone walls, the presence of subcompensated and decompensated psychological state the patient. In the course of histological examination, the influence of these factors on the mechanisms of reparative osteogenesis morphologically manifested a lower degree of progress of regenerative processes and a lower degree of maturity of bone tissue. CONCLUSION: To reduce the chances of developing an unfavorable outcome, in the presence of negative general and local factors, it is not advisable to use dental implantation simultaneously with bone augmentation procedures. In order to reduce the pathophysiological impact of negative factors during sinus lifting, increase the proportion of autosteal material for potentiating the metabolic activity of bone tissue, as well as prescribe antioxidant, antihypoxant and membrane stabilizing therapy before surgery and in the early postoperative period.


Bone Regeneration , Humans , Male , Female , Middle Aged , Adult , Bone Transplantation , Alveolar Ridge Augmentation/methods , Dental Implants , Alveolar Process/surgery , Alveolar Process/pathology , Smoking/adverse effects
20.
PLoS One ; 19(5): e0303743, 2024.
Article En | MEDLINE | ID: mdl-38753732

BACKGROUND: Studies in general population reported a positive association between tobacco smoking and airflow obstruction (AFO), a hallmark of chronic obstructive pulmonary disease (COPD). However, this attempt was less addressed in silica dust-exposed workers. METHODS: This retrospective cohort study consisted of 4481 silicotic workers attending the Pneumoconiosis Clinic during 1981-2019. The lifelong work history and smoking habits of these workers were extracted from medical records. Spirometry was carried out at the diagnosis of silicosis (n = 4177) and reperformed after an average of 9.4 years of follow-up (n = 2648). AFO was defined as forced expiratory volume in one second (FEV1)/force vital capacity (FVC) less than lower limit of normal (LLN). The association of AFO with smoking status was determined using multivariate logistics regression, and the effect of smoking cessation on the development of AFO was evaluated Cox regression. RESULTS: Smoking was significantly associated with AFO (current smokers: OR = 1.92, 95% CI 1.51-2.44; former smokers: OR = 2.09, 95% CI 1.65-2.66). The risk of AFO significantly increased in the first 3 years of quitting smoking (OR = 1.23, 95% CI 1.02-1.47) but decreased afterwards with increasing years of cessation. Smoking cessation reduced the risk of developing AFO no matter before or after the confirmation of silicosis (pre-silicosis cessation: HR = 0.58, 95% CI 0.46-0.74; post-silicosis cessation: HR = 0.62, 95% CI 0.48-0.79). CONCLUSIONS: Smoking cessation significantly reduced the risk of AFO in the workers with silicosis, although the health benefit was not observed until 3 years of abstinence. These findings highlight the importance of early and long-term smoking cessation among silicotic or silica dust-exposed workers.


Pulmonary Disease, Chronic Obstructive , Silicosis , Smoking Cessation , Humans , Silicosis/epidemiology , Silicosis/etiology , Silicosis/complications , Silicosis/physiopathology , Male , Middle Aged , Retrospective Studies , Adult , Pulmonary Disease, Chronic Obstructive/epidemiology , Pulmonary Disease, Chronic Obstructive/etiology , Pulmonary Disease, Chronic Obstructive/physiopathology , Female , Occupational Exposure/adverse effects , Forced Expiratory Volume , Smoking/adverse effects , Spirometry , Vital Capacity , Cohort Studies
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