Impact Of Cigarette Smoking Research Articles

Impact of tobacco smoking upon disease risk, activity and therapeutic response in systemic lupus erythematosus: A systematic review and meta-analysis.

Systemic lupus erythematosus (SLE) is a complex disease with variable presentations, course and prognosis. Published studies present conflicting data regarding the impact of cigarette smoking on SLE risk, disease activity, clinical manifestations and treatment response. We performed a comprehensive literature search using Medline, EMBASE and the Cochrane Collaboration database, and hand searches of relevant bibliographies. All original studies investigating the relationship between smoking and SLE were included in TABALUP. Two investigators systematically extracted data from the relevant studies. When possible, meta-analyses were performed. The meta-analysis of 9 case-controls studies show an increased risk of SLE in current-smokers compared to never-smokers (OR: 1.49 [95%CI: 1.06-2.08]), while former-smokers were not at increased risk of SLE. Data on passive smoking remains scarce and controversial. Pooled analysis studies did not find an over-risk of anti-dsDNA, anti-Sm or anti-SSA positivity according to smoking status. Tobacco smoking significantly reduced the therapeutic effectiveness of hydroxychloroquine in cutaneous lesions (pooled OR 0.53; 95%CI: 0.305-0.927) and belimumab in systemic manifestations (HR 0.10; 95% CI 0.02-0.43). In addition to its usual adverse effects, cigarette smoking is a risk factor of SLE and negatively influences the course of the disease and its treatment. We believe that smoking cessation should be one of the main target of physicians treating SLE patients.

Impact of Cigarette Smoking and Head and Neck Squamous Cell Carcinoma on Circulating Inflammatory Biomarkers

Introduction: Smoking induces inflammation and an immune response. A cancer-related inflammatory response has been seen in smoking and nonsmoking head and neck squamous cell carcinoma (HNSCC) patients. Objectives: The aim of this study was to analyze the possible separated effects of smoking or HNSCC on 18 inflammatory or immune regulatory biomarkers. Methods: Fifty-one nonsmoking and 36 smoking pretreated HNSCC patients and 101 nonsmoking and 39 smoking controls were included in this study. The levels of 18 inflammatory or immune regulatory biomarkers were analyzed. A multivariable linear regression model was used to predict the impact of smoking and HNSCC on the levels of the biomarkers. Results: Smoking had the highest impact on total WBC, IFN-γ, and MCP-1 levels. The highest impact of HNSCC was found on neutrophils, neutrophil-to-lymphocyte ratio, HsCRP, MIP-1b, and TNF-α levels. Conclusion: IdentifyingHNSCC or smoking-related inflammatory biomarkers might contribute to the understanding of the immune response in HNSCC patients. This study could provide information of inflammatory biomarkers in HNSCC patients.

Shared epitope defines distinct associations of cigarette smoking with levels of anticitrullinated protein antibody and rheumatoid factor

ObjectsAlthough the association of cigarette smoking (CS) with susceptibility to rheumatoid arthritis (RA) has been established, the impact of CS on anticitrullinated cyclic peptide/protein antibody (ACPA) and rheumatoid factor (RF)...

A Novel Risk-based Approach Simulating Oncological Surveillance After Radical Nephroureterectomy in Patients with Upper Tract Urothelial Carcinoma

BackgroundThe current guideline lacks evidence for creating individualized surveillance strategies for upper tract urothelial carcinoma (UTUC) patients after radical nephroureterectomy (RNU). ObjectiveTo create a novel risk model and to simulate individualized surveillance duration that dynamically illustrates the changing risk relationship of UTUC-related death and non-UTUC death, considering the impact of cigarette smoking. Design, setting, and participantsThis multicenter cohort study comprised 714 pTa-T4N0M0 UTUC patients, with a median follow-up duration of 65mo. There were 279 (39.1%) nonsmokers, 260 (36.4%) current smokers, and 175 (24.5%) ex-smokers. InterventionAll patients underwent RNU. Outcome measurements and statistical analysisThe risks of UTUC death and non-UTUC death over time were estimated using parametric models for time to failure with Weibull distributions. Age-specific, stage-specific, and smoking status-specific surveillance durations were simulated based upon Weibull estimates. Results and limitationsThe hazard rate (HR) of non-UTUC death gradually increased over time in all age groups regardless of the smoking status, whereas that of UTUC-related death decreased markedly according to the pathological T (pT) stage and was affected by the smoking status. Among current smokers, the baseline HR of UTUC-related death in pT3/4 was higher than that of pT ≤2 and remained high even 10yr after RNU. Among heavy smokers, the HR of UTUC-related death in all pT stages was highest at baseline and remained high after RNU, compared with nonsmokers, current smokers, or ex-smokers. We simulated specific time points when the risk of non-UTUC death was greater than that of UTUC-related death. Among patients ≥80yr of with pT3N0M0, the risk of non-UTUC death was greater than that of UTUC-related death 1yr after RNU in nonsmokers, but 7yr for heavy smokers. ConclusionsOur result revealed that smokers bear a long-term risk burden of UTUC-related death more than the risk of non-UTUC death. For UTUC smokers, longer-term surveillance duration is recommended even in elderly stage. Patient summaryIn the present study, we evaluated the risk transition of upper tract urothelial carcinoma (UTUC)-related death and non-cancer-related death over time. We found that smoking weighed a huge impact upon UTUC-related death compared with death from other cause, and therefore, we created a more individualized surveillance duration model.

The impact of cigarette smoking on metabolic syndrome in diabetic patients type 2: about 322 cases

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Altered fibrin clot properties in advanced lung cancer: strong impact of cigarette smoking

BackgroundDense fibrin networks resistant to lysis have been reported in patients at high risk of thromboembolism. Little is known about fibrin clot properties in cancer. We investigated fibrin clot properties and their determinants in patients with inoperable lung cancer.MethodsWe enrolled 150 patients with advanced lung cancer prior to therapy and 90 control subjects matched by age, sex, cardiovascular disease, and diabetes. Plasma clot permeability (Ks), turbidimetric analysis of clot formation, clot lysis time (CLT), microparticle-associated tissue factor (MP-TF) activity, thrombin generation, and serum cotinine levels were determined.ResultsLung cancer patients, compared with controls, formed at a faster rate (− 8.1% lag phase) denser plasma fibrin networks (− 27.2% Ks) that displayed impaired lysis (+ 26.5% CLT), along with 19.5% higher MP-TF activity and 100% higher peak thrombin generated, also after adjustment for potential confounders. Cotinine levels were associated with fibrin maximum absorbance (r = 0.20, p = 0.016) and Ks (r = − 0.50, p < 0.0001) in cancer patients. On multivariate regression analysis, an increase in cotinine levels was a predictor of low Ks (the lower quartile, < 5.8 × 10−9 cm2; odds ratio = 1.21 per 10 ng/ml, 95% confidence interval 1.02–1.46), but not CLT.ConclusionAdvanced lung cancer is associated with the prothrombotic plasma clot phenotype largely driven by smoking.

Impact of cigarette smoking on kidney inflammation and fibrosis in diabetic rats

Background: Cigarette smoking is a very common habit worldwide contributing to risk of kidney dysfunction and diabetes (DM). However, the mechanisms are unclear.Aim: The goal of the present study was to assess the effects of cigarette smoking on kidney oxidative stress, inflammation, and remodeling in streptozotocin (STZ) rat model of diabetes.Methods: Rats were randomized into control (intraperitoneal (i.p.) citrate buffer injection and exposure to fresh air), cigarette smoking (1 h daily for 6 d/week, citrate buffer), DM (single dose STZ 35 mg/kg i.p. and exposure to fresh air), and DM + smoking groups for a period of 4 weeks. Kidney biomarkers of inflammation, oxidative stress, and remodeling were measured.Results: A significant increase in kidney to body weight ratio was observed in diabetic groups. Diabetes but not smoking increased blood urea nitrogen levels without changes in creatinine levels. Kidney levels of thiobarbituric acid substances, nitrite, endothelin-1, and C-reactive protein were increased significantly in the DM + smoking groups. Smoking induced GSH expression and activity of superoxide dismutase. A significant increase in kidney fibrosis was observed in the DM + smoking group coupled with a similar increase in transforming growth factor beta. Protein levels of matrix metalloproteinase-2, (MMP-2), mitogen-activated protein kinases, and c-Jun N terminal kinase were elevated in Smoking and DM + smoking groups.Conclusion: Cigarette smoke might promote risk of kidney dysfunction in DM by augmentation of renal inflammation, oxidant radicals and fibrosis. The kidney promotes compensatory increase in MMP-2 in response to smoking probably to prevent pro-fibrotic factors induced-fibrosis.

The effect of cigarette smoking on lung cancer evolution.

The aim of this paper is to elucidate the risk of lung carcinogenesis from cigarette smoking among current and former smokers. To achieve this goal, we have set up a stochastic three-stage model to fit the data of Surveillance, Epidemiology, and End Results (SEER) program besides the data set of smoking derived from the Nurses' Health Study cohort of females (NHS) and the Health Professionals Follow up Study cohort of men (HPFS). The calculations are performed by considering both mutation and clonal expansion rates as parameters in each compartment. For current smokers, our findings show that cigarette smoking has more significant impact on the mutation rates of cells than the clonal expansion rates of premalignant cells among men and women. In particular, for male patients, cigarette smoking affects the mutation in normal cells and the transformation from premalignant cells to malignant ones in the optimal model. In addition, cigarette smoking induces only the initial mutation rates in normal cells among American women. For current and former smokers, cigarette smoking stimulates only the clonal expansion rate of the first premalignant cells in both sexes. However, we find that the impact of cigarette smoking is minimal in former smokers who have stopped smoking for over ten years among men and women in US.

The impact of cigarette smoking on infarct location and in-hospital outcome following acute ST-elevation myocardial infarction.

Introduction: Smoking, which is a major modifiable risk factor for coronary artery diseases, affects cardiovascular system with different mechanisms. We designed this study to investigate the association of smoking with location of ST-segment elevation myocardial infarction (STEMI), and short-term outcomes during hospitalization. Methods: In 1017 consecutive patients with anterior/inferior STEMI, comprehensive demographic, biochemical data, as well as clinical complications and mortality rate, were recorded. Patients were allocated into two groups based on smoking status and compared regarding the location of myocardial infarction, the emergence of clinical complications and in-hospital mortality in univariate and multivariate logistic regression analysis. Results: Among 1017 patients, 300 patients (29.5%) were smoker and 717 patients (70.5 %) were non-smoker. Smokers were significantly younger and had lower prevalence of diabetes, hyperlipidemia and hypertension. Inferior myocardial infarction was considerably more common in smokers than in non-smokers (45.7% vs. 36%, P = 0.001). Heart failure was developed more commonly in non-smokers (33.9% vs. 20%, P = 0.001). In-hospital mortality was significantly lower in smokers (6.7% vs. 17.3%, P = 0.001). After adjustment for confounding variables, smoking was independently associated with inferior myocardial infarction and lower heart failure [odds ratio: 1.44 (1.06-1.96), P = 0.01 and odds ratio: 0.61 (0.40-0.92), P = 0.02, respectively]. However, in-hospital mortality was not associated with smoking after adjustment for other factors [odds ratio: 0.69 (0.36-1.31), P = 0.2]. Conclusion: Smoking is independently associated with inferior myocardial infarction. Although smokers had lower incidence of heart failure, in-hospital mortality was not different after adjustment for other factors.

Impact of smoking on patient outcomes after arthroscopic rotator cuff repair

BackgroundCigarette smoking may adversely affect rotator cuff tear pathogenesis and healing. However, the impact of cigarette smoking on outcomes after arthroscopic rotator cuff repair is relatively unknown.Patients and methodsA cohort...

The impact of cigarette smoking on healthcare utilization among rural residents in China

ABSTRACTObjectives: To assess how cigarette smoking affects health care utilization among rural residents in China and to analyze the choice of health facility among current and former smokers in rural China.Methods: This study employed three waves (2010–2014) of the China Family Panel Studies. The data set included 10,330 adults in each wave. Fixed effect and random effect logistic models and multinomial logistic model were used for data analysis.Results: First, according to the fixed effect logistic model, the results showed that current and former smokers are positively (ORs > 1) and significantly associated with outpatient care. Moreover, former smokers are positively (ORs > 1) and significantly associated with inpatient utilization. Second, based on the random effect logistic model, the results illustrated that heavy smokers and long-term quitters are positively (ORs > 1) and significantly related to outpatient care, and former smokers are positively (ORs > 1) and significantly associated with inpatient utilization.Conclusions: Firstly, the present study found that current and former smokers use more outpatient care than non-smokers. Moreover, former smokers use more inpatient care than non-smokers. Secondly, former smokers use more inpatient care than non-smokers, long-term quitters decrease the probability of using inpatient care compared with recent and moderate-term quitters.

Influence of Cigarette Smoking on Myocardial Infarction Induced Renal Damage

Both, cigarette smoking (CS) and myocardial infarction (MI) remain a major public health concern and a leading cause of cardio‐renal morbidity in both males and females. In addition to nicotine, cigarette smoke contains thousands of carcinogenic and non‐carcinogenic chemicals that play a key role in reducing cell viability in renal proximal tubular epithelial cells through acute or chronic pathological mechanisms. In this study, the impact of CS on renal remodeling in both genders was investigated in a mouse model of MI using 2 groups: MI as a control, and MI + CS. Histological analysis of MI group showed alterations in the kidney structure including patchy glomerular retraction which was heightened by two‐fold post‐CS in both genders. As well, molecular analysis revealed that reactive oxygen species production was significantly accentuated in MI+CS compared to MI group similarly in both genders. These findings indicate that CS aggravates MI‐induced renal damage without an exhibition of gender based differences. In order to get more conclusive results, further molecular analysis is under way to study the role of inflammation, and fibrosis on the observed renal changesSupport or Funding InformationSupported by AUB Seed fund #10041This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Impact of cigarette smoking on the relationship between body mass index and insulin: Longitudinal observation from the Bogalusa Heart Study.

Despite the inverse association between cigarette smoking and body mass index (BMI), it is unknown whether the effect of smoking on insulin is mediated through decreased BMI. This study aims to examine the temporal relationship between BMI and insulin, the impact of smoking on this relationship and the mediation effect of BMI on the association between smoking and insulin levels. The longitudinal cohort consisted of 1121 adults (807 white and 314 black participants, mean age, 42.0 years at follow-up) for whom BMI and fasting insulin were measured twice, with an average follow-up period of 17.1 years. Cross-lagged panel and mediation analysis models were used to examine the temporal relationship between BMI and insulin, and the mediation effect of BMI on the smoking-insulin association. Smoking was inversely associated with insulin (regression coefficient, -0.073; P = .015 at baseline and -0.121; P < .001 at follow-up), adjusting for age, race and gender. After additional adjustment for follow-up periods, the cross-lagged path coefficient from BMI to insulin (β, 0.226; P < .001) was significantly greater than that from insulin to BMI (β, -0.029; P = .208), with P < .001 for the difference. The path coefficient from BMI to insulin was significantly greater in non-smokers (β, 0.273; P < .001) than in smokers (β, 0.122; P = .046), with P = .013 for the difference. The mediation effect of BMI on the smoking-insulin association was estimated at 53.4% (P = .030) at baseline and 58.7% (P < .001) at follow-up. These findings suggest that cigarette smoking has a significant impact on the one-directional relationship from BMI to insulin. The insulin-lowering effect of smoking is predominantly mediated through decreased BMI as the result of smoking.

714 - The impact of cigarette smoking on adverse pathological features and survival in patients undergoing radical cystectomy for urinary bladder cancer - a prospective, European multicenter study of the EAU young academic urologists urothelial carcinoma group

714 - The impact of cigarette smoking on adverse pathological features and survival in patients undergoing radical cystectomy for urinary bladder cancer - a prospective, European multicenter study of the EAU young academic urologists urothelial carcinoma group

Impact of Cigarette Smoking on the Gastrointestinal Tract Inflammation: Opposing Effects in Crohn's Disease and Ulcerative Colitis.

Cigarette smoking is a major risk factor for gastrointestinal disorders, such as peptic ulcer, Crohn’s disease (CD), and several cancers. The mechanisms proposed to explain the role of smoking in these disorders include mucosal damage, changes in gut irrigation, and impaired mucosal immune response. Paradoxically, cigarette smoking is a protective factor for the development and progression of ulcerative colitis (UC). UC and CD represent the two most important conditions of inflammatory bowel diseases, and share several clinical features. The opposite effects of smoking on these two conditions have been a topic of great interest in the last 30 years, and has not yet been clarified. In this review, we summarize the most important and well-understood effects of smoking in the gastrointestinal tract; and particularly, in intestinal inflammation, discussing available studies that have addressed the causes that would explain the opposite effects of smoking in CD and UC.

Impact of cigarette smoking on decline in forced expiratory volume in 1s relative to severity of airflow obstruction in a Japanese general population: The Yamagata-Takahata study.

Few studies are available regarding the annual decline of forced expiratory volume in 1s (FEV1) in chronic obstructive pulmonary disease patients with mild airflow obstruction. This study sought to clarify to what extent cigarette-smoking individuals with mild airflow obstruction lose pulmonary function annually. From 2004 to 2006, pulmonary function tests were performed on people >40 years of age, during the annual health checkup held in Takahata, Yamagata, Japan (initial study population, n=3253). In 2011, pulmonary function tests were performed again on participants who agreed to undergo reexamination (follow-up study population, n=838). Smokers have decreased pulmonary function in terms of percent forced vital capacity (FVC), %FEV1, and FEV1/FVC; the stages of airflow obstruction were also more severe in smokers than never-smokers. The annual decline in FEV1 was significantly greater in smokers than in never-smokers. The median annual decline in FEV1 was most significant in individuals with mild airflow obstruction. The annual decline in FEV1 was greater in smokers with mild airflow obstruction than in smokers with moderate airflow obstruction. In analyzing the decline in %FEV1, the annual change in smokers with mild airflow obstruction was greater than that in smokers with normal spirometric values. The annual decline in FEV1 was most significant in smokers with mild airflow obstruction in a Japanese general population. This highlights the importance of early detection of chronic obstructive pulmonary disease patients among the general population in order to prevent disease progression in undiagnosed patients.

Cigarette smoking reduces platelet reactivity independently of clopidogrel treatment in patients with non-ST elevation acute coronary syndromes

Smokers receiving clopidogrel show a lower residual platelet reactivity than non-smokers, a phenomenon generally ascribed to smoking-induced increased production of clopidogrel active metabolite, but also associated with the high hemoglobin levels of smokers, which decreases platelet reactivity in tests that measure platelet function in whole blood. We evaluated the impact of cigarette smoking and of hemoglobin levels on platelet reactivity index (PRI) measured by the vasodilator-stimulated phosphoprotein phosphorylation (VASP-P) assay in whole blood samples from patients with non-ST elevation acute coronary syndrome (NSTE-ACS) undergoing percutaneous coronary interventions, both before and after clopidogrel administration.PRI was measured in 718 clopidogrel-naïve NSTE-ACS patients, both before and 1 month after treatment with clopidogrel (75 mg daily). Smokers (n = 347, 48%) had significantly lower mean PRI levels at both baseline (57.7 ± 24.1 vs. 64.8 ± 19.8, p < 0.001) and 1 month (43.4 ± 20.3% vs. 46.8 ± 18.0%, p = 0.017) than non-smokers. After adjusting for potential confounders (age, sex, diabetes, chronic kidney disease, Syntax score>15), the β coefficient of smoke on PRI was −8.51 [−11.90 to −5.11, p < 0.001] at baseline and −3.41 [−6.30 to −0.51, p = 0.02] after 1 month. Hemoglobin was higher in smokers (13.8 ± 1.5 g/dL) than non-smokers (13.1 ± 1.7 g/dL, p < 0.001), but was not significantly correlated with PRI both at baseline (Rho = 0.02, p = 0.60) and at 1 month (Rho = 0.01, p = 0.80).Our analysis confirms that clopidogrel-treated smokers have lower platelet reactivity, measured by the VASP-P assay, compared to clopidogrel-treated non-smokers. However, smokers had lower platelet reactivity already before receiving clopidogrel treatment, suggesting that smoke affects platelet reactivity independently of its potential effect on the pharmacokinetics of clopidogrel. Our data also indicate that such an effect is not mediated by increased hemoglobin levels.

Meta-analysis of Cigarette Smoking and Musculoskeletal Injuries in Military Training.

Tobacco use is common among military personnel, as is musculoskeletal injury during training. In a review of the literature on musculoskeletal injuries, there was mixed evidence on the role of smoking as a risk factor. The purpose of this study is to review and analyze the literature on the impact of cigarette smoking on lower-extremity overuse injuries in military training. We performed a literature search on articles published through October 2016. Search terms focused on lower-extremity overuse musculoskeletal injuries and cigarette smoking in military populations. We conducted a meta-analysis overall and by sex, including smoking intensity. We identified 129 potential studies and selected 18 based on quality. The overall rate ratio for smoking was 1.31, 1.31 for men, and 1.23 for women. Overall and for each sex, rate ratios were significantly greater than 1.0 for each intensity level of smoking. Smoking is a moderate risk factor for musculoskeletal injury and may account for a meaningful proportion of injuries among men and women due to the high prevalence of smoking and injury in this population. Although enlistees are not allowed to smoke during basic training, their risk of injury remains high, indicating that smokers may remain at increased risk for medium- to long-term duration.

The impact of cigarette smoking on protamines 1 and 2 transcripts in human spermatozoa

This study was conducted to evaluate the relation between cigarette smoking, semen quality and ratios of protamine mRNAs in smokers and non-smokers. Spermatozoa from 123 men and 64 smokers and 59 non-smokers whose female partners attended an assisted reproduction and andrology laboratory were evaluated. Protamine mRNA was extracted from purified sperm, reverse-transcribed and subjected to real-time quantitative PCR using specific primer pairs for protamine 1 (PRM1) and protamine 2 (PRM2). The main outcomes showed that PRM1 mRNA levels in smokers were significantly lower (p = 0.05) than that of non-smokers. Additionally, PRM2 mRNA levels in smokers were significantly lower (p = 0.001) than that of non-smokers. PRM1/PRM2 mRNA ratios in non-smokers samples show significant differences (p = 0.001) compared with those in smokers. PRM1/PRM2 mRNA ratios were negatively and significantly correlated (p = 0.001) with semen volume, sperm count and normal sperm morphology. We concluded that sperm quality and sperm protamine mRNAs were negatively affected by smoking, and these data will serve as new evidence for the hazardous effect of smoking on male fertility. Additionally, protamine transcripts ratios may serve as a marker for male fertility.

A Retrospective Study Evaluating the Impact of Cigarette Smoking on Right- versus Left-Sided Polyps and Colorectal Cancer in an Afro-Caribbean Population

A Retrospective Study Evaluating the Impact of Cigarette Smoking on Right- versus Left-Sided Polyps and Colorectal Cancer in an Afro-Caribbean Population