Group Of Heavy Smokers Research Articles

Alcohol Intake More than Doubles the Risk of Early Cardiovascular Events in Young Hypertensive Smokers

PurposeAn interactive effect of tobacco and alcohol use has been described for cancer. The aim of this study was to investigate the joint effect of smoking and alcohol intake on major adverse cardiovascular and renal events (MACE) in young subjects screened for stage 1 hypertension. MethodsA total of 1204 untreated patients aged from 18 to 45 years (mean 33.1) were included in this prospective cohort study. Subjects were classified into 4 categories of cigarette smoking and 3 classes of alcohol use. Main outcome variable was risk for MACE. ResultsDuring a 12.6-year follow-up, there were 74 fatal and nonfatal MACE. In multivariable Cox models, current smoking and alcohol drinking were associated with risk of MACE. In a multivariable model also including follow-up changes in blood pressure and body weight, hazard ratio (HR) was 1.48 (95% confidence interval [CI], 1.20-1.83) for smoking and was 1.82 (95% CI, 1.05-3.15) for alcohol use. In addition, an interactive effect was found between smoking and alcohol on risk of MACE (P <.001). Among the 142 smokers who also drank alcoholic beverages, the risk of MACE (HR 4.02; 95% CI, 1.98-8.15) was more than doubled compared with the 112 smokers who abstained from drinking (HR 1.64; 95% CI, 0.63-4.27). In the group of heavy smokers who also were alcohol drinkers (n = 51), the risk of MACE was even quadrupled (HR 7.79; 95% CI, 4.22-14.37). ConclusionAlcohol use potentiates the deleterious cardiovascular effects of heavy smoking in stage 1 hypertensive subjects younger than 45 years. These results call for prompt intervention addressed to improve unhealthy behaviors in these subjects.

SC17.03 Lung Cancer in India: Challenges and Perspectives

SC17.03 Lung Cancer in India: Challenges and Perspectives

Mineral characteristics, hydroxyapatite crystal, and mesostructure among heavy smoker teeth: a preliminary report

This study aimed to investigate the mineral characteristics, hydroxyapatite crystal, and mesostructure among heavy smoker teeth. Twenty five subjects were divided into two groups including non smoker group (15 subjects) and heavy smoker group (10 subjects). Teeth mineral element was measured using X-Ray Fluorescence. The hydroxyapatite crystal structure was analyzed using X-Ray Diffraction. Mesostructure was determined using Scanning Electron Microscope. The level of Ca, P, Fe, Cu, Zn, S, Si, Cr, Ti, Mn, Ni, In, Re, Ba, K, Mo, V, Sr, Co, Er, Yb, Zr, and Ca/P ratio were not significantly different in the smoker group compared with a non smoker group (P > 0.05). The lattice parameter of smoker was different compared with non smoker group. In addition, the crystal size of the smoker was higher compared with control. We also found that mesostructure of the smoker was different compared with non smoker. In conclusion, smoking activity affect the hydroxyapatite crystal and disrupt the remodeling surface of teeth. Key words: smoking; dental; structure; surface; remodeling

Effect of smoking on risperidone pharmacokinetics – A multifactorial approach to better predict the influence on drug metabolism

PurposeTo disentangle an association between tobacco smoking, smoking habits and pharmacokinetic patterns such as plasma concentrations of risperidone (RIS), its active metabolite 9-hydroxyrisperidone (9-OH-RIS) and the active moiety, AM, (RIS+9-OH-RIS) in a naturalistic sample. MethodsPlasma concentrations, dose adjusted plasma concentrations (C/D) of RIS, 9-OH-RIS and AM in patients out of a therapeutic drug monitoring (TDM) database were compared between smokers (n=401) and non-smokers (n=292). ResultsDaily dosage of risperidone differed significantly with smokers receiving higher doses than patients in the control group (p=0.001). No differences were detected in plasma concentrations of the active moiety, RIS and 9-OH-RIS (p=0.8 for AM, p=0.646 for RIS and p=0.538 for 9-OH-RIS). However, dose corrected concentrations (C/D) of metabolite (C/D 9-OH-RIS) and active moiety (C/D AM) differed between significantly between groups (p=0.002 and p=0.007). After stratifying smokers to a group of moderate smokers (<20cigarettes/day) (RS1, n=109) and a group of heavy smokers (≥20cigarettes/day) (RS2, n=135), the comparison between non-smokers and both groups only showed lower values of C/D for 9-OH-RIS (p=0.011) for the group of moderate smokers while other pharmacokinetic parameters did not differ. ConclusionsApart from the well-known induction of CYP1A2 activity by polycyclic aromatic hydrocarbons, smoking might exert an effect on other CYP isoenzymes as well. A possible interpretation proposes a slight inducing effect of smoking on risperidone metabolism most likely via CYP3A4.

Smoking habits and benign prostatic hyperplasia: A systematic review and meta-analysis of observational studies.

Previous studies have warned against the promoting effects of cigarette smoking on benign prostatic hyperplasia (BPH). In contrast, some have argued that smoking confers a protective effect regarding BPH, while others have observed an aggravated effect. Thus, we performed this meta-analysis to determine whether cigarette use is associated with BPH risk.To identify articles from observational studies of relevance, a search was performed concurrent to March 21, 2016, on PubMed, Web of Science, Cochrane, EBSCO, and EMBASE databases. Random-effect model, according to the heterogeneity, was calculated to reveal the relative risks (RRs) and corresponding 95% confidence intervals (CIs).Eight articles were included in this meta-analysis, representing data for 44,100 subjects, of which 5221 (11.8%) had BPH as defined according to the criteria. Seven reports are concerned with analysis between nonsmokers and ex-smokers, in which no significant difference was observed (RR = 0.99, 95% CI 0.94–1.05). Another meta-analysis of 7 studies indicated an observable trend, but without significant difference between groups of nonsmokers and current smokers (RR = 1.17, 95% CI 0.98–1.41). Between groups of heavy (6 articles; RR = 1.02, 95% CI 0.84–1.24) and light smokers (5 articles; RR = 0.90, 95% CI 0.71–1.15), again no significant difference appears. Finally, we combined individuals as never-smokers and ever-smokers and still found no significant difference between the 2 groups of patients (RR = 1.03, 95% CI 0.92–1.15). Sensitivity analysis was displayed and confirmed the stability of the present results.Combined evidence from observational studies shows no significant association between cigarette smoking and BPH risk, either for ex-smokers or for current smokers. The trend of elevated BPH risk from smoking was observed only in current smokers compared with nonsmokers, while marginal significance was observed in comparing ever-smokers with never-smokers in operative patients with BPH.

Abstract 2765: Asbestos exposure-related DNA methylation markers: a validation study in non-small cell lung tumors

Abstract Introduction. We have earlier explored the epigenome-wide DNA methylation in lung tumors. The study subjects, mostly smokers, consisted of lung cancer patients highly exposed to asbestos and those without exposure. We found methylation markers that associated either with sample type or exposure (asbestos or tobacco smoke) (Kettunen et al submitted). In this validation study, we focused on estimating the prevalence of the distinct methylation markers in a larger material of lung tumor patients with detailed exposure data available. Study design, subjects, and methods. We investigated the DNA methylation of selected markers in a validation set of 69 non-small cell lung cancer cases, tumor (T) and normal lung (N) from each. The patients, given a written informed consent, had been interviewed for detailed data on work and smoking history (as tobacco smoking pack-years, PY), and the pulmonary asbestos fiber counts quantified. Smoking-related methylation was studied in lung cancer groups of heavy-smokers (PYs higher than 36) vs lighter-smokers (PYs 36 or less) whereas methylation in asbestos-exposed lung tumor patients were compared with that in non-exposed lung tumor patients. DNA methylation was studied in tumor (T) and matched peripheral normal (N) lung tissue using pyrosequencing. Results. Numerous CpG positions in T vs N and eleven sites in asbestos-exposed tumors had indicated significant methylation variation (MVPs). Twenty-six differentially methylated positions (DMPs) having mean delta beta of at least 10% had been revealed in T vs N. Tobacco smoking- and asbestos exposure-related methylation sites were distinct, involving different CpG sites. We chose to validate five MVPs and four DMPs, both hypo- and hypermethylated CpG sites that were investigated using two instrumentation PSQ96MA and Pyromark Q24. The validation study set indicated good performance in pyrosequencing and we could demonstrate methylation of selected sites in relation to malignancy and exposure in this larger material. Conclusions. The central observations of the methylation showing distinct changes in relation to sample types and patients’ exposure status could be validated in a larger material. Significant methylation variation was observed in lung tumors. Citation Format: Eeva Kettunen, Kristina Stuopelytė, Hector Hernandez-Vargas, Henrik Wolff, Sisko L. Anttila, Zdenko Herceg, Sonata Jarmalaite, Kirsti Husgafvel-Pursiainen. Asbestos exposure-related DNA methylation markers: a validation study in non-small cell lung tumors. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 2765.

Cytogenetical analysis in blood lymphocytes of cigarette smokers in Tiruchirappalli district, Tamil Nadu, India

BackgroundTobacco smoke causes serious health ill effects to human population. Cancer and cardiovascular diseases are more common in smoking subjects. AimThe present study is focused about the genetical changes in smoking subjects based on their age and pack years. Subjects and methodsBased on a survey report, 160 subjects are selected from Tiruchirappalli district, Tamil Nadu, India. Venous blood and buccal smear samples are collected from each subject. ResultsIncreased CA is observed in heavy smokers compared to light and non smokers which is 8.90±2.58, 4.58±2.36 and 4.31±1.17, respectively. Both medium and light smokers showed significantly increased CA frequencies than control. Comet assay showed increased percentage of abnormalities in smokers (light, medium and heavy) than non-smokers. ConclusionThe frequencies of MN in buccal epithelial and blood lymphocytes are high in smokers; particularly heavy smoker group showed significantly increased results. Among them, the lymphocytic cells showed high MN frequency.

Potential effect of smoking on semen quality through DNA damage and the downregulation of Chk1 in sperm.

Previous studies have found that smoking is associated with decreased male fertility via altering the quality of semen. However, the mechanism by which cigarette smoking affects semen quality remains to be fully elucidated. Heavy smoking-induced DNA damage has been reported to correlate with abnormal spermatozoa and male infertility. It has been reported that, in response to DNA damage, activation of the checkpoint kinase 1 (Chk1) facilitates S and G2 checkpoint arrest. The aim of the present study was to investigate the expression levels of Chk1 in sperm cells of smoking and non-smoking men, and to further examine the correlation between DNA fragmentation rates and the expression levels of Chk1 with smoking. The present study was performed on a cohort of 841 smoking men and 287 non-smoking men. In the investigation, sperm concentration, motility, viability, seminal plasma zinc concentration, acrosin activity and sperm DNA fragmentation were examined. The gene and protein expression levels of Chk1 were detected using reverse transcription quantitative-polymerase chain reaction and western blot analyses, respectively. It was observed that the progressive motility of the sperm was significantly decreased in the moderate and heavy smoking groups, whereas no significant changes were observed in the mild smoking group. The sperm in the medium-term smoking group had significantly decreased progressive motility, and the semen concentration, sperm count and progressive motility vitality were markedly decreased in the long-term smoking group. Compared with the non-smoking group, the abnormal head rates in the heavy smoking group and long-term smoking group were significantly increased. The sperm viability and seminal plasma zinc concentration were markedly increased in the smoking group. Increased DNA fragmentation rates were found in the smoking group. The expression of Chk1 was significantly decreased in the smoking group, compared with the non-smoking group. Progressive motility and sperm concentration showed a nonlinear association with the relative mRNA expression of Chk1. However, an inverse association was found between DNA fragmentation rates and the progressive motility and sperm concentration. These data suggested that the decrease of semen quality caused by cigarette smoking was not only correlated with sperm DNA fragmentation rates, but was also correlated with a decline in the expressive level of Chk1. The expression of Chk1 was associated with DNA damage and apoptosis, the reduction of which may lead to decreased sperm repair and increased sperm apoptosis, with a subsequent effect on semen quality.

Varenicline and Nicotine Patch Therapies in Young Adults Motivated to Quit Smoking: A Randomized, Placebo‐controlled, Prospective Study

This study compares the nicotine patch to placebo in young adult light smokers, and the nicotine patch to varenicline in heavy smokers. Volunteer daily smokers were recruited into a randomized, placebo-controlled study via community media, colleges and the army (aged 18-26 years). Those subjects with light tobacco dependence were randomized to (i) placebo patch (n = 86) and (ii) nicotine patch 10 mg/16 hr for 8 weeks (n = 94), and those with stronger dependence to (iii) nicotine patch 15 mg/16 hr for 8 weeks (n = 51) and (iv) varenicline for 12 weeks (n = 60). The primary outcome variable was self-reported smoking abstinence at week 12. Secondary outcome variables were self-reported smoking abstinence at weeks 4 and 26, and self-reported abstinence verified by saliva cotinine level at week 12. The prevalence of self-reported smoking abstinence did not differ statistically significantly in light smokers during the follow-up (week 4: 19.8% for placebo patch and 26.6% for nicotine patch 10 mg/16 hr; week 12: 17.4% versus 23.4%; week 26: 15.1% versus 20.2%), but the groups of heavy smokers differed significantly for 12 weeks (week 4: 19.6% for nicotine patch 15 mg/16 hr and 73.3% for varenicline, p < 0.001; week 12: 15.7% versus 36.7%, p = 0.018). This statistically significant difference did not endure for the entire follow-up (week 26: 9.8% versus 18.3%, p = 0.280). However, saliva cotinine verified abstinence at week 12 did not support self-reported abstinence. Varenicline may be more effective than the nicotine patch as a smoking cessation pharmacotherapy among young adult heavy smokers in the short-term.

Assessment of depressive symptoms in severe smokers with minimal-mild depressive symptomatology receiving pre-smoking abstinence for integrated treatment: a randomized clinical trial

Abstract Introduction. Smoking and depression have a long-history documented of comorbidity. Objective. The objective of this study was to develop and test a treatment that could simultaneously achieve smoking abstinence and decrease depressive symptoms in a group of heavy smokers with minimal/mild depressive symptomatology. Method. Sixty smokers were randomly assigned to three different treatment settings. Treatment included a pre-abstinence phase, a psychological treatment phase, a pharmacotherapy phase and a follow-up stage. Smokers began the psychological treatment and the pharmacotherapy two weeks before the day they chosen to quit smoking, and monitoring was conducted over a year. Abstinence was confirmed by assessing the levels of urinary cotinine. Results. Using a linear mixed model with individual random effect, baseline data was compared with subsequent assessments; 46% of the patients achieved abstinence. For men, the three treatment settings significantly reduced depressive symptoms and helped smokers to achieve abstinence. For women, only the nicotine patch showed to be effective in the reducing depressive symptoms. Discussion and conclusion. Integral pre-abstinence treatment is effective in aiding smokers to achieve smoking abstinence and improve depressive symptoms.

Evaluation of heart rate recovery index in heavy smokers.

Objective:Cigarette smoking increases the risk of cardiovascular events. The heart rate recovery index (HRRI) is an indicator of autonomous nervous system function and is an independent prognostic risk factor for cardiovascular diseases. In this study, we aimed to evaluate HRRI in heavy smokers.Methods:A total of 179 apparently healthy subjects (67 non-smokers as the control group and 112 heavy smokers) were enrolled into this prospective cross-sectional study. The presence of hypertension, diabetes mellitus, and known cardiac or non-cardiac diseases was specified as the exclusion criteria. Heavy cigarette smoking was defined as the consumption of more than one packet of cigarette per day. All subjects underwent the maximal Bruce treadmill test. HRRIs of the heavy cigarette smoker group at 1, 2, 3, and 5 min after maximal exercise were calculated and compared to those of the control group. Student t-test, chi-square test, and analysis of covariance were used for statistical analysis.Results:The baseline characteristics of the two groups were similar, except for body mass index and high-density lipoprotein level. HRRIs at 1, 2, 3, and 5 min after maximal exercise were found to be significantly lower in the heavy smoker group (HRRI1: 26.78±8.81 vs. 32.82±10.34, p<0.001; HRRI2: 44.37±12.11 vs. 51.72±12.87, p<0.001; HRRI3: 52.73±11.54 vs. 57.22±13.51, p=0.018; and HRRI5: 58.31±10.90 vs. 62.33±13.02, p=0.029).Conclusions:In the present study, we found that HRRI was impaired in heavy smokers. Our results suggest that beside previously known untoward effects on vascular biology, heavy smoking also has deleterious effects on the neuro–cardiovascular system.

Abstract LB-298: The use of lung cancer risk prediction model to stratify heavy smokers: The power of routinely collected lab data

Abstract Background: Previous lung cancer models were mostly based on case control studies and used limited epidemiological risk factors. The clinical utility was hampered due to lack of added value beyond smoking history. In this study, we developed a series of lung cancer risk prediction models using extensive data, including lab testing data, from a large prospective cohort in Taiwan. In particular, we developed a risk prediction model within heavy smokers with ≧30 pack years that could further stratify this group and improve the screening efficiency of Low Dose Computed Tomography (LDCT). Methods: The cohort participants were divided into equal training and validation sets, by using variables from personal history and standard lab tests. Cox proportional hazards regression and goodness of fit were used to generate area under the curve (AUC). Results: A total of 1,774 incident lung cancer cases were identified among 505,030 participants recruited in a 14-year period during 1994-2007. We developed a “History only” model that included smoking status, body mass index (BMI), family history, and personal history; a “lab only” model that included blood in sputum, lung function test and serum biomarkers like carcinoembryonic antigen (CEA), bilirubin, and alpha fetoprotein (AFP); and an integrative model with all these variables. The AUC for “history only” model was 0.837, “lab only” model, 0.839, and integrative model, 0.862. We also developed integrative models for ever-smokers and never-smokers with AUCs of 0.872 and 0.801, respectively. Furthermore, since LDCT is recommended for heavy smokers with ≥ 30 smoking pack-years but with a high false positive rate, we developed a risk model in this group to further stratify this group. A total of 454 incident lung cancer cases were identified among 23,582 heavy smokers. Six variables are significantly associated with lung cancer risk: age, smoking status (current or former), smoking intensity (number of packs smoked in a day), BMI, lung function test and CEA. Current smokers, who smoked &amp;gt;1 pack per day, with BMI &amp;lt;25, lowest lung function and highest CEA, had the highest risk. The number of smokers needed to screen to identify one lung cancer (NNS) could decrease to 13 in this high-risk heavy smokers group from 52 in heavy smokers as a whole, a four-fold increase in risk identification. Highest risks were found among smokers with CEA ≧3.8 ug/L (NNS between 13 and 37) and smokers with lung function MMF&amp;lt;43 ml/sec (NNS between 13 and 25). Conclusion: Routinely collected lab data can significantly improve lung cancer risk prediction models. An integrative lung cancer risk prediction model among heavy smokers with ≧30 pack years can stratify subjects with a 3-4 fold difference in lung cancer risk for LDCT screening. The model found decreased lung function and high CEA values, along with detailed smoking history and low BMI, offered a unique predictive ability to improve the efficiency of LDCT screening. Citation Format: Xifeng Wu, Chi Pang Wen, Yuanqing Ye, MinKwang Tsai, Xia Pu, Wong-Ho Chow, Chad Huff, Sonia Cunningham, Maosheng Huang, Shiuan Bei Wu, Chwen Keng Tsao, Jian Gu. The use of lung cancer risk prediction model to stratify heavy smokers: The power of routinely collected lab data. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr LB-298. doi:10.1158/1538-7445.AM2014-LB-298

Smoking and lipid‐related indices in patients with diabetes mellitus

Lipid-related indices, including the ratio of LDL cholesterol to HDL cholesterol, the ratio of triglycerides to HDL cholesterol and lipid accumulation product, are known to be good discriminators for cardiovascular disease. The aim of this study was to clarify the relationships between smoking and the lipid indices in patients with diabetes. Subjects were those who had been diagnosed as having diabetes mellitus at annual health check-ups at their places of work (n=2563). The subjects were divided into three groups of non-smokers, light smokers (≤20 cigarettes/day) and heavy smokers (>20 cigarettes/day). The relationships between smoking and the lipid indices were investigated. Both in all subjects and in the subjects without a habit of alcohol drinking, the LDL cholesterol:HDL cholesterol ratio and the log-transformed triglyerides:HDL cholesterol ratio tended to be higher with an increase in the amount of smoking, and the log-transformed lipid accumulation product was significantly higher in heavy smokers than in non-smokers. In the non-alcohol drinking subjects, the odds ratios of heavy smokers vs. non-smokers for high LDL cholesterol:HDL cholesterol ratio [2.32 (95%CI 1.40-3.84)], for high triglycerides:HDL cholesterol ratio [1.69 (95%CI 1.06-2.69)] and for high lipid accumulation product [1.65 (95%CI 1.02-2.67)] were significantly higher than a reference level of 1.00. The associations between smoking and the lipid indices were weaker in alcohol drinkers than in non-drinkers. In patients with diabetes, the levels of lipid-related indices were higher in smokers than in non-smokers, and cardiometabolic disorders, reflected by high lipid indices, are thought to be involved in the proneness of smokers to develop atherosclerotic cardiovascular disease.

Influence of Donor Smoking on Midterm Outcomes After Lung Transplantation

Lung transplantation (LTx) is significantly limited by donor organ shortage. Donor smoking history of more than 20 pack-years is considered an extended donor criterion. In this study, we retrospectively evaluated impact of donor smoking history and extent of smoking on midterm outcome after LTx. In all, 237 LTx were performed in our institution between 2007 and 2012. Patients were divided into three groups, receiving lungs from 53% nonsmoking donors, 29% smoking donors with fewer than 20 pack-years, and 18% heavy smokers with more than 20 pack-years. Preoperative donor and recipient characteristics among the groups were comparable. However, donors from the heavy smokers group were significantly older (p < 0.001). The overall presence of abnormal histology (inflammation or metaplasia) in donor main bronchi samples increased with the extent of smoking but did not reach statistical significance (p = 0.211). Although metaplasia was found in significantly more donors from the heavy smokers group (p = 0.037), this did not translate into inferior outcomes for the recipients. There were no statistically significant differences in PaO2/FiO2 ratio after LTx, duration of mechanical ventilation (p = 0.136), intensive care unit stay (p = 0.133), and total postoperative hospital stay (p = 0.322). One-year and three-year survival were comparable across all three groups (log rank p = 0.151). Prevalence of bronchiolitis obliterans syndrome (p = 0.616), as well as bronchiolitis obliterans syndrome free survival (p = 0.898) after LTx were also comparable. In our experience, history and extent of donor smoking do not significantly affect early and midterm outcomes after LTx. Although this finding does not obviate the need for longer-term observation, donor lungs from even heavy smokers may not per se contraindicate LTx and may provide a valuable avenue for expanding donor organ availability.

Effect of smoking on selected blood parameters

Background: Smoking is not only a physical recidivism, but also a psychological inveteracy. Chronic effects of cigarette smoking on haematological parameters, with a good control side by side, were studied by very few. Evectics (including deaddiction) should be based on harm profile. Aims & Objectives: To find out age-wise Hb, BP, leucocyte (total/ differential) count, monocyte count, and eosinophil count in smokers. Materials and Methods: Study was carried out on a group of 108 otherwise healthy subjects from medical college campus –including 36 each in non-smoker, light-smoker and heavy smoker group – further subdivided into 9 each in 4 age ranges of 21-30years, 31-40 years, 41-50 years and 51-60 years. Data regarding age, sex, height, weight and various blood parameters were noted as per standard methods. Results: Chronic effects of smoking on cardiovascular system were found. SBP of both light and heavy smokers were significantly less than control group. DBP of light smokers and non-smokers did not differed very much. TLC and eosinophil count was higher while monocyte count was lower in smokers (insignificantly low in light smokers). Conclusion: The TLC and eosinophil count rise, while BP and monocyte counts fall in smokers. Smoking may lead to isolated systolic hypertension. In Evectics, the improvement/ outcome can be measured by assessing the rate/ extent of normalization of these parameters.

Effect of cigarette smoking on liver function test and some other related parameters

Background and objective: Cigarette smoking is one of the 10 greatest contributors to global death and disease. Cigarette smoke consists of many chemicals, including cytotoxic, carcinogenic and free radicals, therefore it affects many organs if not all.This work is directed to evaluate the effects of dose response patterns of tobacco exposure on liver tissue, through assessing some serum biochemical parameters related with liver efficiency. Methods: This study was done in Kirkuk province. It was conducted on (110) healthy male subjects, their ages ranged from 20 to 40 years. They were divided into three groups; 40 heavy smokers, 30 moderate smokers and 40 non-smokers. Blood was withdrawn for estimation of serum liver function test, lipid profile, protein electrophoresis, and lipid peroxidation test (Serum Malondialdehyde; MAD level). Results: There were statistically significant elevations in serum alkaline phosphatase (ALP), alanine transaminase(GPT) and aspartate aminotransferase(GOT) activities in heavy smokers while serum total bilirubin significantly was lower comparing to non smokers. Serum total protein and albumin were significantly lower in heavy smokers comparing to non smokers. The results of serum protein agarose gel-electrohporesis showed significant changes in serum protein fractions in smoker groups. The mean level of serum total cholesterol, triglyceride, LDL, VLDL and malondialdehyde was significantly higher in heavy smoker group, while serum HDL level had a significantly lower value. Conclusion: Cigarette smoking can affect liver efficiency and functions. These effects are dose exposure depenent.

Periodontal health status of heavy and light smokers and its correlation with salivary superoxide dismutase enzyme (A comparative study)

Background: Periodontal disease is a chronic bacterial infection that affects the gingiva and bone supporting the teeth. Smoking, which is an important risk factor for periodontitis, induce oxidative stress in the body and cause an imbalance between reactive oxygen species (ROS) and antioxidants, such as superoxide dismutase (SOD). This study aimed to evaluate the influence of smoking on periodontal health status by estimating the levels of salivary SOD level in non-smokers (controls) and light and heavy smokers and to test the correlation between the SOD enzyme level and the clinical periodontal parameters in each group. Materials and Methods: The study sample consisted of 75 male, with age ranged from 35 to 50 years. Clinically, the periodontal parameters used in this study were Plaque index (PLI). Gingival index (GI), probing pocket depth (PPD), Bleeding on probing (BOP) and clinical attachment level (CAL), unstimulated saliva sample were collected from all subjects and the levels of superoxide dismutase enzyme was analyzed for each group , and correlate the mean of salivary enzyme levels with the clinical periodontal parameters. Results: Highly significant differences in PLI between (non smokers/heavy smokers) and (light smokers/heavy smokers).On the other hand no significant difference in gingival index between groups. There were a high association between severity of smoking & probing pocket depth and there is association between severity of smoking and clinical attachment loss. There were a significant difference in the level of salivary superoxide dismutase enzyme between the (non smokers/light smokers) groups & between (heavy smokers/light smokers) &there were highly significant differences between (non smokers/heavy smokers) groups. There is no correlation between the activities of the salivary superoxide dismutase enzyme and the clinical periodontal parameters except in SOD with (BOP score 0 and PPD score 1&score 3) in heavy smokers group. Conclusions: Superoxide dismutase enzyme can be used as biomarker for estimating the level of oxidative stress on

Prevalence rate of Metabolic Syndrome in a group of light and heavy smokers

BackgroundSmoking is an important cause of morbidity and mortality worldwide. It is widely accepted as a major risk factor for metabolic and cardiovascular disease. Smoking reduces insulin sensitivity or induces insulin resistance and enhances cardiovascular risk factors such as elevated plasma triglycerides, decreases high-density lipoprotein cholesterol and causes hyperglycemia. Several studies show that smoking is associated with metabolic abnormalities and increases the risk of Metabolic Syndrome. The aim of this study was to estimate the prevalence of the metabolic syndrome in a group of light and heavy smokers, wishing to give up smoking.MethodsIn this cross-sectional study all the enrolled subjects voluntary joined the smoking cessation program held by the Respiratory Pathophysiology Unit of San Matteo Hospital, Pavia, Northern Italy.All the subjects enrolled were former smokers from at least 10 years and had no cancer or psychiatric disorders, nor history of diabetes or CVD or coronary artery disease and were not on any medication.ResultsThe subjects smoke 32.3 ± 16.5 mean Pack Years. The prevalence of the metabolic syndrome is 52.1%: 57.3% and 44.9% for males and females respectively. Analysing the smoking habit influence on the IDF criteria for the metabolic syndrome diagnosis we found that all the variables show an increasing trend from light to heavy smokers, except for HDL cholesterol. A statistical significant correlation among Pack Years and waist circumference (R = 0.48, p < 0.0001), Systolic Blood Pressure (R = 0.18, p < 0.05), fasting plasma glucose (R = 0.19, p < 0.005) and HDL cholesterol (R = −0.26, p = 0.0005) has been observed.ConclusionsCurrently smoking subjects are at high risk of developing the metabolic syndrome.Therapeutic lifestyle changes, including smoking cessation are a desirable Public health goal and should successfully be implemented in clinical practice at any age.

Automatic approach bias towards smoking cues is present in smokers but not in ex-smokers

Drug-addicted individuals show automatic approach tendencies towards drug-related cues, i.e., an approach bias (ApB). Nevertheless, little is known about ApB in tobacco smokers and about the presence of ApB after smoking abstinence. We investigated ApB to smoking cues in heavy tobacco smokers versus never-smokers and studied its relation to smoking characteristics and craving. Second, we compared ApBs of heavy smokers with biases of abstinent heavy smokers. A group of current heavy smokers (n = 24), ex-smokers who were abstinent for at least 5years (n = 20), and never-smokers (n = 20) took part in the experiment. An indirect smoking approach avoidance task was performed, in which participants were required to respond to pictures of smoking and neutral cues by pulling (approach) or pushing (avoid) on a joystick, according to the content-irrelevant format of the picture (landscape or portrait). Craving scores were examined using the Questionnaire of Smoking Urges. Heavy smokers showed an ApB for smoking cues compared to ex-smokers and never-smokers, which correlated positively to craving scores. There were no group differences in ApB scores for ex-smokers and never-smokers. These results suggest that ApBs for smoking cues are present in heavy smokers and decrease after long-term successful smoking cessation.

Smoking as a risk factor for intraoperative hypoxemia during one lung ventilation

Smoking is associated with many intra and postoperative events, especially respiratory complications. Hypoxemia and airway damage are found to aggravate any pre-existing respiratory pathology among smokers. One lung ventilation (OLV) carries a 4-10 % risk of development of hypoxia. The purpose of this study was to predict the incidence of hypoxemia for smokers during OLV for patients undergoing video-assisted thoracoscopic surgery (VATS). Sixty patients undergoing VATS using OLV by double lumen tube were included in this pilot cross-sectional study. These patients were divided into 2 groups, group S which included 30 heavy smoker patients (smoking more than 20 cigarettes per day for more than 20 years) and group NS which included 30 non-smoker patients. Intra and postoperative arterial oxygen tension (PaO(2)), arterial carbon dioxide tension (PaCO(2)), and intraoperative peak airway pressure were compared between the 2 groups. PaO(2) was significantly higher in the non-smoker group than in the smoker group, both at the start and end of OLV. It was 173 ± 68 mmHg for NS compared with 74 ± 10.8 mmHg for S at the start of OLV; at the end of OLV it was 410 ± 78 mmHg for the former and 360 ± 72 mmHg for the latter (P < 0.05). From this study it can be concluded that for heavy smoker patients there was a significant reduction in arterial oxygen tension (PaO(2)) in comparison with non-smokers. However, hypoxemia reported for both groups was comparable.