Role Of Tobacco Smoking Research Articles

The role of tobacco smoking in antineutrophil cytoplasmic antibody-associated vasculitis: a systematic review.

Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitides (AAV) are a group of systemic pauci-immune necrotising vasculitides involving small vessels, characterised by the presence of specific ANCA autoantibodies directed to leukocyte proteinase 3 (PR3-ANCA) or myeloperoxidase (MPO-ANCA) and subdivided into three clinical entities: granulomatosis with polyangiitis (GPA), microscopic polyangiitis (MPA) and eosinophilic granulomatosis with polyangiitis (EGPA). The aetiology of AAV is unknown and many genetic, epigenetic and environmental factors have been reported to be involved in pathogenesis. Smoking is widely recognised as a risk factor for the development of many autoimmune diseases, such as rheumatoid arthritis and systemic lupus erythematosus. This systematic review will analyse known data about the role of smoking in the development, clinical presentation and outcome of AAV. Articles that examined interactions between tobacco smoking and AAV (GPA, MPA, EGPA) were included. All articles selected were in English. No limitation on publication date was established. Case reports were excluded. The systematic search was performed using PubMed/Medline and Cochrane Library databases. The search provided a total of 131 articles. Three studies were added, obtained from the review of the reference lists of articles. 70 were removed because they were duplicated or written in languages other than English. The title and abstract of 64 articles were screened. Of these, 30 were excluded as the title and/or abstract did not meet the inclusion criteria. Thus, 34 remained for full-text review, of which 8 were excluded. 26 articles were therefore included in this review. The role of smoking in AAV development is unclear. AAV patients current smoking appear appear to be younger and more frequently males, with a lower prevalence of EGPA and MPA than GPA. Ever smokers show higher relapse rate. Smoking seems to be associated with a higher risk of cardiovascular events during follow-up. Smokers incur an increased risk of infections. Finally, many data support smoking as a risk factor for end stage renal disease and mortality in AAV patients. Current data support the hypothesis that smoking influences prevalence, clinical phenotype and prognosis of ANCA-associated vasculitis. However, further studies are required to fully determine its role.

Tobacco Smoking Is a Strong Predictor of Failure of Conservative Treatment in Hinchey IIa and IIb Acute Diverticulitis-A Retrospective Single-Center Cohort Study.

Background and Objectives: Therapeutic management of patients with complicated acute diverticulitis remains debatable. The primary objective of this study is to identify predictive factors for the failure of conservative treatment of Hinchey IIa and IIb diverticular abscesses. Materials and Methods: This is a retrospective cohort study that included patients hospitalized from 1 January 2014 to 31 December 2022 at the Emergency Surgery Department of the Cagliari University Hospital (Italy), diagnosed with acute diverticulitis complicated by Hinchey grade IIa and IIb abscesses. The collected variables included the patient's baseline characteristics, clinical variables on hospital admission, abscess characteristics at the contrast-enhanced CT scan, clinical outcomes of the conservative therapy, and follow-up results. Univariable and multivariable logistic regression models were used to identify prognostic factors of conservative treatment failure and success. Results: Two hundred and fifty-two patients diagnosed with acute diverticulitis were identified from the database search, and once the selection criteria were applied, 71 patients were considered eligible. Conservative treatment failed in 25 cases (35.2%). Univariable analysis showed that tobacco smoking was the most significant predictor of failure of conservative treatment (p = 0.007, OR 7.33, 95%CI 1.55; 34.70). Age (p = 0.056, MD 6.96, 95%CI -0.18; 0.99), alcohol drinking (p = 0.071, OR 4.770, 95%CI 0.79; 28.70), platelets level (p = 0.087, MD -32.11, 95%CI -0.93; 0.06), Hinchey stage IIa/IIb (p = 0.081, OR 0.376, 95%CI 0.12; 1.11), the presence of retroperitoneal air bubbles (p = 0.025, OR 13.300, 95%CI 1.61; 291.0), and the presence of extraluminal free air at a distance (p = 0.043, OR 4.480, 95%CI 1.96; 20.91) were the other variables possibly associated with the risk of failure. In the multivariable logistic regression analysis, only tobacco smoking was confirmed to be an independent predictor of conservative treatment failure (p = 0.006; adjusted OR 32.693; 95%CI 2.69; 397.27). Conclusion: The role of tobacco smoking as a predictor of failure of conservative therapy of diverticular abscess scenarios highlights the importance of prevention and the necessity to reduce exposure to modifiable risk factors.

Atti XXIV Convegno Nazionale Tabagismo e SSN - Update on the relationship between smoking and COVID-19

In mid-2021, after more than a year of pandemic, there were still great uncertainties about the role of tobacco smoking or nicotine on COVID-19 incidence, severity and mortality [1]. A large number of case series showed a low prevalence of smokers among patients with COVID-19. However, all these studies had an inadequate design to support any causal conclusion. On the contrary, the number of well-conducted longitudinal studies (i.e., cohort studies) on the issue was limited. This did not allow us to provide robust evidence on the relationship between tobacco smoking and COVID-19. (...)

Knowledge and awareness of Libyan dental patients regarding the adverse effects of tobacco smoking on oral health

Background: Tobacco smoking and periodontitis are still major public health problems. The role of tobacco smoking in the progression and severity of periodontal diseases has been emphasized. The current study aimed to investigate the awareness and knowledge of dental patients regarding the adverse effects of tobacco smoking on “oral and periodontal health” in Benghazi, Libya. Materials and Methods: ‘’A cross-sectional study” was undertaken in several dental practices. The study involved 179 participants which Comprised of 48 smokers and 131 non-smokers. Participants were interviewed and inquired to answer a questionnaire related to awareness and knowledge about the adverse effects of tobacco smoking on oral health. Results: Significantly higher percentages of non-smokers were conscious about the adverse effects of tobacco smoking on oral health (p=0.002), whereas no statistically significant differences were found among male and female participants, although females were more conscious about the adverse effects of tobacco smoking on oral health. Conclusions: The results of the current study reveal that non-smokers have significantly more knowledge about the adverse effects of tobacco smoking on “oral and periodontal health” when compared to smokers. “Smoking cessation” should be an integral part of periodontal treatment and dental professionals can offer “smoking cessation” counseling to their patients and support them to quit tobacco smoking.

The Role of Tobacco Smoking in the Efficacy of Brief Alcohol Intervention: Results from a Randomized Controlled Trial.

This study investigated whether tobacco smoking affected outcomes of brief alcohol interventions (BAIs) in at-risk alcohol-drinking general hospital patients. Between 2011 and 2012 among patients aged 18–64 years, 961 patients were allocated to in-person counseling (PE), computer-based BAI containing computer-generated individual feedback letters (CO), and assessment only. PE and CO included contacts at baseline, 1, and 3 months. After 6, 12, 18, and 24 months, self-reported reduction of alcohol use per day was assessed as an outcome. By using latent growth curve models, self-reported smoking status, and number of cigarettes per day were tested as moderators. In PE and CO, alcohol use was reduced independently of smoking status (IRRs ≤ 0.61, ps < 0.005). At month 24, neither smoking status nor number of cigarettes per day moderated the efficacy of PE (IRR = 0.69, ps > 0.05) and CO (IRR = 0.85, ps > 0.05). Up to month 12, among persons smoking ≤ 19 cigarettes per day, the efficacy of CO increased with an increasing number of cigarettes (ps < 0.05). After 24 months, the efficacy of PE and CO that have been shown to reduce drinking did not differ by smoking status or number of cigarettes per day. Findings indicate that efficacy may differ by the number of cigarettes in the short term.

COVID-19, a syndemic well before a pandemic disease! The role of tobacco smoking

COVID-19, a syndemic well before a pandemic disease! The role of tobacco smoking

The role of tobacco smoking and illicit drug use in adolescent acute alcohol intoxication

BackgroundThis study aims to determine the prevalence of tobacco smoking and illicit drug use among Dutch adolescents admitted to hospital for acute alcohol intoxication treatment. Furthermore, socio-demographic predictors for smoking and illicit drug use in the sample population will be studied. The relationship between illicit drug use and specific characteristics of intoxication, such as blood alcohol concentration (BAC) and duration of reduced consciousness is also investigated.MethodsThe national Dutch Paediatric Surveillance Unit was used to prospectively register cases of acute alcohol intoxication from 2007 through 2017. Cases were included if they met the following inclusion criteria: BAC > 0.0 g/L, aged between 10 to 18 years old and requiring hospital treatment due to reduced consciousness. Questionnaires were sent to paediatricians to obtain clinical information.ResultsDuring the period 2007–2017, 5322 cases that met the inclusion criteria were reported. In this patient group, the prevalence of tobacco smoking was 22.2% (CI 21.0–23.5%), while the prevalence of illicit drug use was 11.8% (CI 10.9–12.7%). The predictors for smoking were the absence of alcohol-specific parental rule-setting, lower educational level, non-traditional family structure and positive drug screening. The predictors for illicit drug use were the absence of alcohol-specific parental rule-setting and smoking. Illicit drug use was also associated with a lower BAC at the time of admission.ConclusionsAssessing smoking and illicit drug use among adolescents admitted for acute alcohol intoxication is important in acute cases of intoxication, for outpatient follow-up and for the purposes of prevention. The relationship between simultaneous illicit drug use and a lower BAC is of relevance for paediatricians’ attempts to diagnose acute intoxication. With respect to outpatient follow-up and preventive measures, it is important to be aware that adolescents’ alcohol consumption, tobacco and illicit drug use are related and, ultimately, increase the odds of using other substances.

Value and Interest Rates: Are Rates to Blame for Value’s Torments?

<h3>Objective</h3> Since conflicting results have been published on the role of tobacco smoking on the risk of endometriosis, we provide an up-to-date summary quantification of this potential association. <h3>Design</h3> We performed a PubMed/MEDLINE search of the relevant publications up to September 2014, considering studies on humans published in English. We searched the reference list of the identified papers to find other relevant publications. Case–control as well as cohort studies have been included reporting risk estimates on the association between tobacco smoking and endometriosis. 38 of the 1758 screened papers met the inclusion criteria. The selected studies included a total of 13 129 women diagnosed with endometriosis. <h3>Setting</h3> Academic hospitals. <h3>Main outcome measure</h3> Risk of endometriosis in tobacco smokers. <h3>Results</h3> We obtained the summary estimates of the relative risk (RR) using the random effect model, and assessed the heterogeneity among studies using the χ² test and quantified it using the I² statistic. As compared to never-smokers, the summary RR were 0.96 (95% CI 0.86 to 1.08) for ever smokers, 0.95 (95% CI 0.81 to 1.11) for former smokers, 0.92 (95% CI 0.82 to 1.04) for current smokers, 0.87 (95% CI 0.70 to 1.07) for moderate smokers and 0.93 (95% CI 0.69 to 1.26) for heavy smokers. <h3>Conclusions</h3> The present meta-analysis provided no evidence for an association between tobacco smoking and the risk of endometriosis. The results were consistent considering ever, former, current, moderate and heavy smokers, and across type of endometriosis and study design.

The role of tobacco smoking in the formation of obstructive disorders of bronchial patency

The role of tobacco smoking in the formation of obstructive disorders of bronchial patency

Determinants of Tobacco Smoking Addiction in Rural Indonesian Communities.

Purpose To analyze the determinants of tobacco smoking addiction in rural areas. Methods A cross-sectional study was conducted on February 2020. The self-administered questionnaire (α = 0.908) and Perceived Stress Scale–10 were used as tobacco smoking determinants and the WHO ASSIST questionnaire V3.0 to determine its addiction risk. Their correlations were analyzed by Spearman's rank-order approach using the SPSS version 23.0. Results Among 75 male respondents that participated in this study, those on low, moderate, and high addiction risk were 45 (60.00%), 23 (30.67%), and 7 (9.33%), respectively, and significantly correlated with the research questionnaire that consisted three parts: 1. awareness toward the health risk; 2. social control; 3. mass media role in tobacco smoking (p=0.014, 0.004, and 0.009 respectively), but there was no significant correlation with the stress level (p=0.287). Conclusion Increased awareness toward the health risk, good social control, and mass media reporting the danger of tobacco smoking is significantly in correlation with the decreased addiction in rural areas. However, the high perceived stress has no correlation with its increase.

Mechanisms of Nicotine Addiction.

Tobacco smoking results in more than five million deaths each year and accounts for ∼90% of all deaths from lung cancer.3 Nicotine, the major reinforcing component of tobacco smoke, acts in the brain through the neuronal nicotinic acetylcholine receptors (nAChRs). The nAChRs are allosterically regulated, ligand-gated ion channels consisting of five membrane-spanning subunits. Twelve mammalian α subunits (α2-α10) and three β subunits (β2-β4) have been cloned. The predominant nAChR subtypes in mammalian brain are those containing α4 and β2 subunits (denoted as α4β2* nAChRs). The α4β2* nAChRs mediate many behaviors related to nicotine addiction and are the primary targets for currently approved smoking cessation agents. Considering the large number of nAChR subunits in the brain, it is likely that nAChRs containing subunits in addition to α4 and β2 also play a role in tobacco smoking. Indeed, genetic variation in the CHRNA5-CHRNA3-CHRNB4 gene cluster, encoding the α5, α3, and β4 nAChR subunits, respectively, has been shown to increase vulnerability to tobacco dependence and smoking-associated diseases including lung cancer. Moreover, mice, in which expression of α5 or β4 subunits has been genetically modified, have profoundly altered patterns of nicotine consumption. In addition to the reinforcing properties of nicotine, the effects of nicotine on appetite, attention, and mood are also thought to contribute to establishment and maintenance of the tobacco smoking habit. Here, we review recent insights into the behavioral actions of nicotine, and the nAChR subtypes involved, which likely contribute to the development of tobacco dependence in smokers.

Abstract SY26-02: Sherlock-Lung: Tracing lung cancer mutational processes in never smokers

Abstract Globally, about 2 million people are diagnosed with lung cancer annually, making it the most common type of cancer in the world. In addition, lung cancer is the leading cause of cancer death among both men and women, accounting for ~25% of all cancer deaths in the United States and ~19% of cancer deaths worldwide. Although tobacco smoking is the most common cause of lung cancer, it is estimated that 10-25% of all patients diagnosed with lung cancer worldwide are never smokers, with higher proportions in Asians and women. Compared to former and current smokers with lung cancer, lung cancers in never smokers tend to present at an earlier age and more frequently have adenocarcinoma histology. Although a few risk factors are known to contribute to the etiology of lung cancer in never smokers, a large fraction of cancer cases cannot be explained by established environmental and genetic risk factors, highlighting the need for research in this area. One promising approach to identify the etiological factors involved in lung tumorigenesis in never smokers is based on the study of the “mutational signatures” that the exogenous and endogenous processes leave on the tumor tissue and surrounding areas. Somatic mutations accumulate throughout individuals’ lifetime, as a result of the balance between DNA damage and DNA repair. Mutational sources can change over time and mutational signatures can provide information on the tumor evolutionary trajectory, tracking activities of mutational processes. We designed “Sherlock-Lung” to identify mutational signatures in lung cancers from never smokers and order them based on their clonal and subclonal localization to have an insight on the factors involved in the initiation of the tumors. Prevention and treatment strategies are likely to be more effective when targeting the tumor initiating factors rather than those responsible for the tumor progression. Here, we present the Sherlock-Lung study design, which includes a combination of lung cancer cases from populations highly exposed to lung cancer risk factors and populations with unknown exposures. We also present preliminary data from this study and what we have learned from whole genome sequencing analysis of the mutational landscape of lung cancers from smokers and nonsmokers and from different histological subtypes. For example, although the mutational signature associated with tobacco smoking is largely clonal in all lung cancers from smokers, consistent with an initiating role of tobacco smoking in lung tumorigenesis, the mutational signatures distribution varies across histological subtypes. Moreover, the frequency of mutations in major cancer driver genes varies dramatically between smokers and never smokers, and mutational signatures distribution appears to differ between tumors with and without specific driver genes. In never smokers, without the dominant mutational source of tobacco smoking, other signatures emerged, e.g., that associated with reactive oxygen species. Although this approach has already revealed important information on the etiological processes involved in tumorigenesis of lung cancer and other cancer types, there is a growing list of open questions and challenges that need to be addressed. In population studies, careful exposure assessment to identify and validate new mutational signatures and the inclusion of study subjects from different geographical locations and ethnicities are critical. Citation Format: Maria Teresa Landi, Tongwu Zhang, Montserrat Garcia-Closas, Yohan Bossé, Jianxin Shi, Bin Zhu, Qing Lan, Nathaniel Rothman, Jiyeon Choi, Neil E. Caporaso, Wei Zhao, Chongyi Chen, Eytan Ruppin, Jennifer Rosenbaum, Dmitry Gordenin, Sai Yendamuri, Chris Amos, Paul Brennan, David C. Christiani, Geoff Liu, Bonnie Gould Rothberg, Matthew Schabath, Han Liang, Ludmil Alexandrov, David Wedge, Stephen Chanock. Sherlock-Lung: Tracing lung cancer mutational processes in never smokers [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr SY26-02.

(330) The Role of Tobacco Smoking in the Transition from Acute to Chronic Pain

Tobacco smoking is highly prevalent among patients with chronic pain. The prevalence of smoking has been found to range between 30-60% among patients with chronic pain, and to be approximately 15% in the general population. To date, however, the degree to which tobacco smoking contributes to the development of chronic pain remains unclear. The main objective of this study was to examine the role of tobacco smoking in the transition from acute pain to chronic pain. The sample consisted of adult patients enrolled in the UK Biobank, a large prospective cohort study involving more than 500,000 patients receiving medical care through the UK National Health Service (NHS). Patients were asked to complete self-report questionnaires at three separate time points (i.e., between 2006 and 2014) that assessed a host of demographic, lifestyle, pain, and psychological variables. Across different types of pain diagnoses, analyses indicated that patients smoking tobacco were significantly more likely to develop chronic pain symptoms after an acute pain episode than patients who never smoked (OR = 1.4, p

Genetic Factors Interact With Tobacco Smoke to Modify Risk for Inflammatory Bowel Disease in Humans and Mice

The role of tobacco smoke in the etiology of inflammatory bowel disease (IBD) is unclear. We investigated interactions between genes and smoking (gene-smoking interactions) that affect risk for Crohn's disease (CD) and ulcerative colitis (UC) in a case-only study of patients and in mouse models of IBD. We used 55 Immunochip-wide datasets that included 19,735 IBD cases (10,856 CD cases and 8879 UC cases) of known smoking status. We performed 3 meta-analyses each for CD, UC, and IBD (CD and UC combined), comparing data for never vs ever smokers, never vs current smokers, and never vs former smokers. We studied the effects of exposure to cigarette smoke in Il10-/- and Nod2-/- mice, as well as in Balb/c mice without disruption of these genes (wild-type mice). Mice were exposed to the smoke of 5 cigarettes per day, 5 days a week, for 8 weeks, in a ventilated smoking chamber, or ambient air (controls). Intestines were collected and analyzed histologically and by reverse transcription polymerase chain reaction. We identified 64 single nucleotide polymorphisms (SNPs) for which the association between the SNP and IBD were modified by smoking behavior (meta-analysis Wald test P < 5.0× 10-5; heterogeneity Cochrane Q test P > .05). Twenty of these variants were located within the HLA region at 6p21. Analysis of classical HLA alleles (imputed from SNP genotypes) revealed an interaction with smoking. We replicated the interaction of a variant in NOD2 with current smoking in relation to the risk for CD (frameshift variant fs1007insC; rs5743293). We identified 2 variants in the same genomic region (rs2270368 and rs17221417) that interact with smoking in relation to CD risk. Approximately 45% of the SNPs that interact with smoking were in close vicinity (≤1 Mb) to SNPs previously associated with IBD; many were located near or within genes that regulate mucosal barrier function and immune tolerance. Smoking modified the disease risk of some variants in opposite directions for CD vs UC. Exposure of Interleukin 10 (il10)-deficient mice to cigarette smoke accelerated development of colitis and increased expression of interferon gamma in the small intestine compared to wild-type mice exposed to smoke. NOD2-deficient mice exposed to cigarette smoke developed ileitis, characterized by increased expression of interferon gamma, compared to wild-type mice exposed to smoke. In an analysis of 55 Immunochip-wide datasets, we identified 64 SNPs whose association with risk for IBD is modified by tobacco smoking. Gene-smoking interactions were confirmed in mice with disruption of Il10 and Nod2-variants of these genes have been associated with risk for IBD. Our findings from mice and humans revealed that the effects of smoking on risk for IBD depend on genetic variants.

Effect of nicotine on the proliferation and chondrogenic differentiation of the human Wharton's jelly mesenchymal stem cells.

Osteoarthritis (OA) is a chronic joint disease characterized by a progressive and irreversible degeneration of articular cartilage. Among the environmental risk factors of OA, tobacco consumption features prominently, although, there is a great controversy regarding the role of tobacco smoking in OA development. Among the numerous chemicals present in cigarette smoke, nicotine is one of the most physiologically active molecules. The aim of the study was (i) to measure the impact of nicotine on the proliferation and chondrogenic differentiation of mesenchymal stem cells from the human Wharton's jelly (hWJ-MSCs) into chondrocytes, (ii) to investigate whether the α7 nicotinic acetylcholine receptors (nAChRs) was expressed in hWJ-MSCs and could play a role in the process. The project benefits from the availability of an umbilical cord bank from which hWJ-MSCs were originated. The hWJ-MSCs were cultured and used up to passage 5. The proliferation of hWJ-MSCs with 5μM nicotine was measured by the MTT assay on the 1st, 2nd, 3rd, and 6th day. Flow cytometry analysis was used to detect cell apoptosis/necrosis by Annexin V/PI double-staining. The chondrogenic differentiation grade of hWJ-MSCs induced by TGFβ3 was assessed by the Sirius red and Alcian blue staining. The expression of markers genes was followed by quantitative real-time PCR. The expression of nAChRs was followed by RT-PCR. The functional activity of α7 nAChR was evaluated by calcium (Ca2+) influx mediated by nicotine using the Fluo-4 NW Calcium assay. The proliferation of hWJ-MSCs was significantly impaired by nicotine (5μM) from the 3rd day of treatment, but nicotine did not significantly induce modifications on the viability of hWJ-MSCs. Alcian blue staining indicated that the amount of proteoglycan was more abundant in control group than in the nicotine group, but no difference was observed on the total collagen amount using Sirius red staining. The mRNA expression of Sox9, type II collagen (Col2a1), aggrecan in control group was higher than in the nicotine group. We found that hWJ-MSCs expressed α7 nAChR. The receptor agonist nicotine caused calcium (Ca2+) influx into hWJ-MSCs suggesting that the calcium ion channel α7 homopolymer could mediate this response. At the concentration used, nicotine had an adverse effect on the proliferation and chondrogenic differentiation of hWJ-MSCs which was probably impaired through a α7 nAChR mediation.

Periodontal disease and smoking: An overview

The role of tobacco smoking as a causative factor in the development of the periodontal disease has long been debated and recently a large number of papers have been published in the literature regarding this symbiosis. Smoking also gives an encouraging environment for microbes in the mouth such as Porphyromonas gingivalis , Prevotella intermedia , and Aggregatibacter actinomycetemcomitans because the by-products of smoking prevent the mechanisms that limit the growth of harmful bacteria in the oral cavity. Thus, smoking promotes early stages of periodontal disease. Smoking in the form of cigars and pipes have similar deleterious effects that cigarettes do on oral health. Much of the literature has also showed that smokers affected with periodontitis respond less favorably to periodontal treatment be it nonsurgical and surgical. In this paper, we have reviewed the effects of smoking on various aspects of the periodontal disease process.

Association of FokI polymorphism of vitamin D receptor with urothelial bladder cancer in Tunisians: role of tobacco smoking and plasma vitamin D concentration.

The aim of the study was to test whether the VDR FokI polymorphism is associated with the risk of urothelial bladder cancer (UBC) in Tunisians. The study included 200 unrelated patients with UBC and 200 healthy controls. Genotyping of the VDR FokI polymorphism was determined by PCR-RFLP method. Plasma 25-hydroxyvitamin D concentrations were measured by immunoassay. Binary logistic regression model was applied to test how the association of VDR FokI polymorphism is independent of potential confounding factors. Genotype distribution (FF, 45 vs. 55%; Ff, 52.1 vs. 47.9%, and ff, 12 vs. 5.5%, respectively) and allele frequencies (F, 66.5 vs. 74.8% and f, 33.5 vs. 25.2%, respectively) were significantly different between UBC patients and controls. The "ff" genotype [OR (95% CI), 2.66 (1.24-5.73); p = 0.012] and "f" allele [1.49 (1.09-2.02); p = 0.010] were associated with increased risk of UBC. The association remained significant in multivariate analysis. Stratified analyses showed that VDR FokI polymorphism is only associated with UBC risk in ever-smokers, subjects exposed to chemical carcinogens and those with plasma 25-hydroxyvitamin D over 12μg/L. The "f" allele of VDR FokI polymorphism is associated with a higher risk of UBC in Tunisians, especially in smokers as well as subjects with occupational exposition and subjects without vitamin D deficiency. These results should be replicated in other ethnic groups and the influence of other genetic factors and environments on this association should be investigated.

Tobacco smoking and risk of endometriosis: a systematic review and meta-analysis

ObjectiveSince conflicting results have been published on the role of tobacco smoking on the risk of endometriosis, we provide an up-to-date summary quantification of this potential association.DesignWe performed a PubMed/MEDLINE...

Factors associated with retreatment tuberculosis in Tshwane, south africa: the role of tobacco smoking

There is evidence from international studies that tobacco smoking increases the risk of tuberculosis recurrence through its effects on the immunological and barrier functions of the airways. In this cross-sectional study, the association between current tobacco smoking and retreatment tuberculosis was studied in a population of 1 926 South African tuberculosis patients with high human immunodeficiency virus (HIV) co-infection rates. Retreatment tuberculosis was more common in male and among HIV-positive participants currently on antiretroviral treatment, or with unknown antiretroviral treatment status. However, we did not find an association between smoking and retreatment tuberculosis. A longitudinal study is needed to confirm these findings.

Quantitative Association of Tobacco Smoking With the Risk of Nasopharyngeal Carcinoma: A Comprehensive Meta-Analysis of Studies Conducted Between 1979 and 2011

Over the years, many studies have attempted to establish a link between tobacco smoking and an increased risk of nasopharyngeal carcinoma (NPC), but their results have been inconsistent. To clarify this link, we first conducted a comprehensive meta-analysis to integrate the findings of epidemiologic studies from the last half-century. The methodology used for this study followed the checklist proposed by the Meta-analysis of Observational Studies in Epidemiology (MOOSE) Group. Pooled risk estimates were generated using a random-effects model. Twenty-eight case-control studies and 4 cohort studies involving a total of 10,274 NPC cases and 415,266 comparison subjects were included. A substantial effect of smoking on the risk of NPC was identified in this study. The results showed that ever smokers had a 60% greater risk of developing the disease than never smokers (95% confidence interval: 1.38, 1.87); this was a robust dose-dependent association. More importantly, stronger associations were observed in low-risk populations and among persons with the predominant histological type of differentiated NPC than in high-risk populations and persons with an undifferentiated type; the odds ratios were 1.76 and 2.20, respectively, versus 1.29 and 1.27. In this comprehensive meta-analysis, well-established statistical evidence was provided about the role of tobacco smoking in the etiology of NPC.