Impact Of Cigarette Smoking Research Articles

Impact of cigarette smoking on impaired insulin secretion and insulin resistance in Japanese men: The Saku Study.

To assess the impact of smoking on impaired insulin secretion and insulin resistance in Japanese men. This study included 1,199 men aged 30-79years without diabetes, impaired insulin secretion and insulin resistance at baseline who underwent a comprehensive medical check-up between April 2006 and March 2007 at Saku Central Hospital. Smoking status was categorized as current, ex-smoker and never-smoker. Insulinogenic index and homeostasis model assessment-insulin resistance were determined using a standard 75-g oral glucose tolerance test. The Japan Diabetes Society criteria were used to define impaired insulin secretion and insulin resistance. Participants were followed up until March 2011. A total of 449 and 99 men developed impaired insulin secretion and insulin resistance during 3,403 and 4,092 person-years follow up, respectively. The multivariable-adjusted hazard ratios (HRs) for impaired insulin secretion were 1.06 (95% confidence interval [CI] 0.84-1.33) in ex-smokers and 1.95 (95% CI 1.44-2.63) in current smokers compared with never-smokers after adjustment for age, familial history of diabetes, alcohol consumption, exercise, systolic blood pressure, triglyceride, γ-glutamyltransferase, waist circumference, leukocyte count, changes in smoking status and changes in waist circumference. The number of pack-years was positively associated with the risk for impaired insulin secretion in a dose-dependent manner (P-values for trend <0.001). The multivariable-adjusted HRs for insulin resistance were 0.95 (95% CI 0.56-1.61) in ex-smokers and 1.11 (95% CI 0.67-1.79) in current smokers compared with never-smokers. Cigarette smoking is a modifiable risk factor for impaired insulin secretion. The findings might also be important for other Asian populations, which have low insulin secreting ability.

The Impact of Cigarette Smoking On Overall Survival in Non-Hodgkin Lymphoma

AbstractAbstract 5100 Introduction:Smoking has been suggested as a potential risk factor for the development of non-Hodgkin lymphoma (NHL). However, the prognostic impact of smoking in patients with NHL has not been well studied and may have important implications regarding outcome. Methods:In a population-based cohort of 308 NHL patients diagnosed between 1999 and 2002, we examined the association between cigarette smoking habits prior to NHL diagnosis and overall survival (OS). Multivariable Cox proportional hazards models adjusted for age, gender, and education were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) for all NHL, and for follicular lymphoma (FL) and diffuse large B-cell lymphoma (DLBCL). Measurements of smoking included categories for smoking status, pack-years of smoking, years of smoking, daily number of cigarettes smoked, and years since quitting smoking. Continuous exposures for cigarette smoking were also examined with potential non-linear relations tested using restricted cubic splines. We conducted subgroup analyses adjusting for established clinical and prognostic variables. Results:In the patient cohort, a total of 96 deaths occurred over a median follow-up period of 8. 2 years. For all NHL cases, current smokers had worse survival (HR=1. 8 [1. 0–3. 1], ptrend=0. 07, for risk of all-cause mortality) when compared to never smokers. The inferior survival was also associated with pack-years of smoking (HR=1. 5 [0. 9–2. 4], ptrend=0. 12, for >30 pack-years) and smoking duration (HR=1. 5 [0. 9–2. 3], ptrend=0. 13, for >30 years). Smoking remained an independent predictor of OS after adjustment for initial treatment, stage at diagnosis and the presence of B symptoms: HR=2. 6 [1. 1–6. 3], ptrend=0. 03, for current smokers; HR=2. 4 [1. 1–5. 6], ptrend=0. 03, for patients with >30 pack-years of cigarette smoking; and HR=2. 5 [1. 2–5. 5], ptrend=0. 02, for patients smoking longer than 30 years. Among former smokers, a shorter interval from quitting to diagnosis was associated with worse survival (per 5 years of quitting cigarette smoking, HR=0. 9 [0. 8–1. 0], ptrend=0. 06). The associations with cigarette smoking and OS were stronger for FL than for DLBCL. In analyses stratified by age at diagnosis, the associations for current smokers (HR=3. 7 [1. 5–9. 2], ptrend=0. 01), daily number of cigarettes smoked (HR=2. 8 [1. 0–7. 5], ptrend=0. 04), and years of cigarette smoking (HR=3. 0 [1. 1–8. 3], ptrend=0. 04) were stronger for patients diagnosed at <60 years of age. The risk estimates for smoking with OS did not depart from unity among those diagnosed at ≥ 60 years of age. The associations between cigarette smoking and OS were similar for men and women. Conclusion:Our data suggest that cigarette smoking prior to diagnosis is associated with inferior OS in NHL patients. The reduction in survival is most prominent for patients diagnosed at <60 years of age and for those with FL. Among former smokers, greater time from cessation of smoking to diagnosis may improve OS. Further research examining the impact of smoking cession on OS among NHL patients is warranted. [Display omitted] [Display omitted] Disclosures:No relevant conflicts of interest to declare.

Impact of cigarette smoking on rates and clinical prognosis of pulmonary tuberculosis in Southern Mexico

To examine the relationship between cigarette smoking and incidence and mortality rates of pulmonary tuberculosis (TB) and treatment outcomes. From 1995 to 2010, we analyzed data from 1062 patients with TB and from 2001 to 2004, 2951 contacts in Southern Mexico. Patients with acid-fast bacilli or Mycobacterium tuberculosis in sputum samples underwent epidemiological, clinical and mycobacteriological evaluation and received treatment by the local DOTS program. Consumers of 1-10 (LS) or 11 or more (HS) cigarettes per day incidence (1.75 and 11.79) and mortality (HS, 17.74) smoker-non-smoker rate ratios were significantly higher for smokers. Smoker population was more likely to experience unfavorable treatment outcomes (HS, adjusted OR 2.36) and retreatment (LS and HS, adjusted hazard ratio (HR) 2.14 and 2.37). Contacts that smoked had a higher probability of developing active TB (HR 2.38) during follow up. Results indicate the need of incorporating smoking prevention and cessation, especially among men, into international TB control strategies.

The effect of smoking on the kidneys

Graham Cope outlines the ways in which smoking impairs both kidney function and prognosis in kidney disease. Knowledge of the negative impact of cigarette smoking in renal disease can assist the nurse in educating and supporting patients in smoking cessation.

Cigarette smoking behaviors and time since quitting are associated with differential DNA methylation across the human genome

The impact of cigarette smoking can persist for extended periods following smoking cessation and may involve epigenetic reprogramming. Changes in DNA methylation associated with smoking may help to identify molecular pathways that contribute to the latency between exposure and disease onset. Cross-sectional cohort data from subjects in the International COPD Genetics Network (n = 1085) and the Boston Early-Onset COPD study (n = 369) were analyzed as the discovery and replication cohorts, respectively. Genome-wide methylation data on 27 578 CpG sites in 14 475 genes were obtained on DNA from peripheral blood leukocytes using the Illumina HumanMethylation27K Beadchip in both cohorts. We identified 15 sites significantly associated with current smoking, 2 sites associated with cumulative smoke exposure, and, within the subset of former smokers, 3 sites associated with time since quitting cigarettes. Two loci, factor II receptor-like 3 (F2RL3) and G-protein-coupled receptor 15 (GPR15), were significantly associated in all three analyses and were validated by pyrosequencing. These findings (i) identify a novel locus (GPR15) associated with cigarette smoking and (ii) suggest the existence of dynamic, site-specific methylation changes in response to smoking which may contribute to the extended risks associated with cigarette smoking that persist after cessation.

The impact of cigarette smoking on the health of descendants

This paper presents a review of the literature on the effects of cigarette smoking on the health of descendants and the possible mechanisms that lead to them. The evidence of the effects of prenatal cigarette smoke exposure on neonatal morbidity is clear. A number of birth defects have their incidence raised by maternal cigarette smoking during pregnancy. Prenatal smoke exposure also increases the risk of infant irritability, inattention, decreased response to inanimate auditory stimuli and hypertonia. In addition, the prevalence of obesity in preschool children is higher if the mother smoked during pregnancy, as well as the presence of male or female subfertility/infertility in adult life. Studies on the association between parental smoking and childhood cancer correlate paternal smoking to a higher risk of neoplasm in early life, especially of hematopoietic origin.

Impact of cigarette smoking on symptoms and quality of life of adults with asthma managed in public primary care clinics in Singapore: a questionnaire study

Cigarette smoking aggravates asthma exacerbations, yet some patients with asthma continue to smoke. To compare the quality of life of adult smokers and non-smokers with asthma. Asthma Quality of Life (AQLQ) questionnaires were administered to adult patients with asthma managed in primary care in Singapore. The survey also included data of their asthma status including symptom profiles. Independent two-sample t-test, ANCOVA model, χ2 test and ordinal logistic regression were used to compare the mean domain scores and the effect of smoking on nocturnal symptoms and awakening, respectively. 357 adult asthma patients (183 non-smokers and 174 smokers) were recruited. Smokers were mainly male (p<0.001), single (p=0.008), and younger (mean age 30 years) (p=0.007). They were more affected by nocturnal cough and wheezing (p=0.016). After adjustment for age, gender, and asthma medications, the mean scores of the AQLQ 'symptoms' and 'emotional function' domains of smokers were 0.41 (95% CI 0.10 to 0.72) and 0.50 (95% CI 0.16 to 0.84) points lower than for non-smokers, with no statistical differences in the 'activity limitations' and 'exposure to environmental stimuli' domains. Adult patients with asthma who smoke are more affected by nocturnal symptoms, with lower 'emotional function' scores in the AQLQ.

Effect of Smoking Status on Seminal Parameters and Apoptotic Markers in Infertile Men

We assessed semen parameters, sperm apoptotic markers and seminal plasma cotinine in infertile smokers. A total of 160 men were divided into 4 equal groups, including fertile smokers, fertile nonsmokers, infertile smokers and infertile nonsmokers. Smoking was classified as mild--fewer than 10, moderate--10 to 20 or heavy--more than 20 cigarettes daily. All men underwent semen analysis, and assessment of sperm caspase-9, Smac/DIABLO, DNA fragmentation and seminal plasma cotinine. Infertile men, particularly smokers, have significantly lower semen variables and significantly higher sperm Smac/DIABLO, caspase-9 activity, the percent of DNA fragmentation and seminal plasma cotinine. The mean number of cigarettes smoked daily and smoking duration significantly correlated positively with sperm Smac/DIABLO, caspase-9 activity, the percent of DNA fragmentation and seminal plasma cotinine, and significantly correlated negatively with tested semen variables. Heavy smoking was associated with a significant increase in sperm Smac/DIABLO, caspase-9 activity and seminal plasma cotinine, and with a significant decrease in tested semen variables compared with those in moderate or mild smokers. Smoking has a negative impact on semen variables. It is associated with increased sperm caspase-9, Smac/DIABLO and the percent of DNA fragmentation, especially in infertile heavy smokers.

Impact of cigarette smoking on Volatile Organic Compound (VOC) blood levels in the U.S. Population: NHANES 2003–2004

The impact of cigarette smoking on volatile organic compound (VOC) blood levels is studied using 2003–2004 National Health and Nutrition Examination Survey (NHANES) data. Cigarette smoke exposure is shown to be a predominant source of benzene, toluene, ethylbenzene, xylenes and styrene (BTEXS) measured in blood as determined by (1) differences in central tendency and interquartile VOC blood levels between daily smokers [≥ 1 cigarette per day (CPD)] and less-than-daily smokers, (2) correlation among BTEXS and the 2,5-dimethylfuran (2,5-DMF) smoking biomarker in the blood of daily smokers, and (3) regression modeling of BTEXS blood levels versus categorized CPD. Smoking status was determined by 2,5-DMF blood level using a cutpoint of 0.014 ng/ml estimated by regression modeling of the weighted data and confirmed with receiver operator curve (ROC) analysis. The BTEXS blood levels among daily smokers were moderately-to-strongly correlated with 2,5-DMF blood levels (correlation coefficient, r, ranging from 0.46 to 0.92). Linear regression of the geometric mean BTEXS blood levels versus categorized CPD showed clear dose–response relationship (correlation of determination, R 2, ranging from 0.81 to 0.98). Furthermore, the pattern of VOCs in blood of smokers is similar to that reported in mainstream cigarette smoke. These results show that cigarette smoking is a primary source of benzene, toluene and styrene and an important source of ethylbenzene and xylene exposure for the U.S. population, as well as the necessity of determining smoking status and factors affecting dose (e.g., CPD, time since last cigarette) in assessments involving BTEXS exposure.

Cigarette Smoke Inhibits Brain Mitochondrial Adaptations of Exercised Mice

Physical exercise and smoking are environmental factors that generally cause opposite health-promoting adaptations. Both physical exercise and smoking converge on mitochondrial adaptations in various tissues, including the pro-oxidant nervous system. Here, we analyzed the impact of cigarette smoking on exercise-induced brain mitochondrial adaptations in the hippocampus and pre-frontal cortex of adult mice. The animals were exposed to chronic cigarette smoke followed by 8 weeks of moderate-intensity physical exercise that increased mitochondrial activity in the hippocampus and pre-frontal cortex in the non-smoker mice. However, mice previously exposed to cigarette smoke did not present these exercise-induced mitochondrial adaptations. Our results suggest that smoking can inhibit some brain health-promoting changes induced by physical exercise.

Effects of cigarette smoking on reproduction

BACKGROUND Cigarette smoking is associated with lower fecundity rates, adverse reproductive outcomes and a higher risk of IVF failures. Over the last few decades, prevalence of smoking among women of reproductive age has increased. This review focuses on current knowledge of the potential effects of smoke toxicants on all reproductive stages and the consequences of smoke exposure on reproductive functions. METHODS We conducted a systematic review of the scientific literature on the impact of cigarette smoking and smoke constituents on the different stages of reproductive function, including epidemiological, clinical and experimental studies. We attempted to create hypotheses and find explanations for the deleterious effects of cigarette smoke observed in experimental studies. RESULTS Cigarette smoke contains several thousand components (e.g. nicotine, polycyclic aromatic hydrocarbons and cadmium) with diverse effects. Each stage of reproductive function, folliculogenesis, steroidogenesis, embryo transport, endometrial receptivity, endometrial angiogenesis, uterine blood flow and uterine myometrium is a target for cigarette smoke components. The effects of cigarette smoke are dose-dependent and are influenced by the presence of other toxic substances and hormonal status. Individual sensitivity, dose, time and type of exposure also play a role in the impact of smoke constituents on human fertility. CONCLUSIONS All stages of reproductive functions are targets of cigarette smoke toxicants. Further studies are necessary to better understand the deleterious effects of cigarette smoke compounds on the reproductive system in order to improve health care, help to reduce cigarette smoking and provide a better knowledge of the molecular mechanisms involved in reproductive toxicology.

The impact of cigarette smoking on arterial stiffness in Korea

The impact of cigarette smoking on arterial stiffness in Korea

Cigarette Smoking and Fertility

A strong body of evidence indicates that the negative effect of cigarette smoking on fertility comprises fairly every system involved in the reproductive process. The impact of cigarette smoking on ovarian reserve is clearly evidenced by younger age at menopause of smokers. Tobacco compounds’ impairment of the process of ovarian follicle maturation is expressed by worse in-vitro fertilization parameters in cycles performed on women with smoking habits. Also, uterine receptiveness and tubal function are significantly altered by the smoking habit. In men, cigarette smoking reduces sperm production, increases oxidative stress, and DNA damage. Spermatozoa from smokers have reduced fertilizing capacity, and embryos display lower implantation rates. Couples at reproductive age should be strongly discouraged to smoke.

Impact of cigarette smoking on the relationship between body mass index and coronary heart disease: a pooled analysis of 3264 stroke and 2706 CHD events in 378579 individuals in the Asia Pacific region.

BackgroundElevated levels of body mass index (BMI) and smoking are well established lifestyle risk factors for coronary heart disease (CHD) and stroke. If these two risk factors have a synergistic relationship, rigorous lifestyle modification may contribute to greater reduction in cardiovascular burden than previously expected.MethodsA pooled analysis of individual participant data from 38 cohorts, involving 378,579 participants. Hazards ratios (HRs) and 95% confidence intervals (CIs) for BMI by cigarette smoking status were estimated using Cox proportional hazard models.ResultsDuring a mean follow-up of 3.8 years, 2706 CHD and 3264 strokes were recorded. There was a log-linear, positive relationship of BMI with CHD and stroke in both smokers and non-smokers with evidence of a synergistic effect of smoking on the association between BMI and CHD only: HRs (95% CIs) associated with a 2 kg/m2 higher BMI were 1.13 (1.10 – 1.17) in current smokers and 1.09 (1.06 – 1.11) in non-smokers (p-value for interaction = 0.04).ConclusionSmoking amplifies the positive association between BMI and CHD but not stroke. If confirmed, these results suggest that effective strategies that target smoking cessation and weight loss are likely to have a greater impact than anticipated on reducing the burden of CHD.

The Impact of Cigarette Smoking on HIV/AIDS: Urgent Need for Research and Cessation Treatment

This special issue on the impact of cigarette smoking on HIV/AIDS is the culmination of an effort that began over 2 years ago. In June of 2006, the National Institutes of Health (NIH) convened a State-of-the-Science conference on Tobacco Use: Prevention, Cessation and Control, with the goal of providing health care providers, scientists, health policy experts, patients, and the general public a responsible assessment of currently available data. During this conference, presentations by experts were combined with a systematic review of the literature to develop a final statement on the current available research knowledge.1 An invited expert, Dr. Ellen R. Gritz, gave a presentation on chronic disease and co-occurring risk, which included a topic on smoking and HIV/AIDS. The presentation emphasized the extremely high smoking prevalence rates in the HIV-positive population (50%-65%), and the disturbing association of smoking with several AIDS-related diseases, such as pulmonary infections, oral diseases and malignancies (as well as the proven risk for lung cancer, in general). Further, the increased risk for cardiovascular disease (CVD) among smokers and among persons on prolonged HAART regimens underscores the need for targeting smoking as a modifiable risk factor for CVD. Dr. Gritz summarized the extant literature on smoking cessation in this population and described several intervention trials currently underway, as well as indicating the urgent need for further research. After discussions of the current research on smoking and HIV/AIDS health outcomes, Dr. Allison Chausmer Hoffman was inspired to explore this topic in greater depth. Using the NIH Tobacco and Nicotine Research Interest Group as a platform, several NIH Institutes and Centers2 worked cooperatively to sponsor an invitationonly workshop entitled “Current Issues in Cigarette Smoking and HIV/AIDS.” On Oct 8, 2007, NIH held a workshop featuring presentations from leaders in the field of tobacco research and HIV/AIDS, including basic neuroscientists to clinicians, epidemiologists, and behavioral scientists. The goal of the workshop was to highlight understudied research related to cigarette smoking and HIV-infected persons. The program was divided into four sessions, including “Smoking, Progression to AIDS-related Complications and Host Defense Against Opportunistic Infection”; “Interactions Between Smoking and Pharmacotherapy for People with HIV/AIDS”;

Impact of Cigarette Smoking on Mortality in HIV-Positive and HIV-Negative Veterans

It is unknown whether smoking confers similar mortality risk in HIV-positive as in HIV-negative patients. We compared overall mortality stratified by HIV and smoking of 1,034 HIV-positive block-matched to 739 HIV-negative veterans, enrolled 2001-2002 in the Veterans Aging Cohort 5 Site Study. Adjusted incidence rate ratios (IRR) for mortality were calculated using Poisson regression. Mortality was significantly increased in HIV-positive veterans according to both smoking status and pack-years in unadjusted and adjusted analyses (adjusted IRR 2.31, 95% confidence interval [CI] 1.53-3.49 for HIV-positive current smokers and IRR 1.32, 95% CI 0.67-2.61 for HIV-negative current smokers). Comorbid diseases were also significantly increased according to smoking status and pack-years. Current smoking is associated with poor outcomes; even lower levels of exposure appear to be detrimental in HIV-infected veterans. These findings support the need for improvements in smoking cessation and for studies of mechanisms and diseases underlying increased mortality in smokers with HIV.

Impact of cigarette smoking in type 2 diabetes development.

Many patients with type 2 diabetes mellitus (DM2) are at risk for micro and macro vascular complications, which could be observed in heavy smokers. Cigarette smoking increases the risk for type 2 diabetes incidence. Nicotine, acknowledged as the major pharmacologically active chemical in tobacco, is responsible for the association between cigarette smoking and development of diabetes. This minireview summarized recent studies on nicotine effects on insulin action and insulin secretion, indicating the impact of nicotine on type 2 diabetes development.

The Impact of Cigarette Smoking, Alcohol Drinking and Betel Quid Chewing on the Risk of Calcium Urolithiasis

To evaluate the independent and combined effects of alcohol drinking, cigarette smoking and betel quid chewing on the risk of calcium urolithiasis. A total of 354 cases diagnosed with calcium urolithiasis and 354 age- and sex-matched healthy controls were recruited from Kaohsiung Medical University Hospital between June 2003 and February 2007. All subjects completed a detailed questionnaire survey and provided blood and urine samples for biochemical evaluation. Current cigarette smoking (odds ratio [OR], 1.66; 95% confidence interval [95%CI], 1.11-2.50; p=0.014) and current betel quid chewing (OR, 1.97; 95%CI, 1.06-3.64; p=0.032), but not current alcohol drinking, were found to be independent risk factors for the development of calcium urolithiasis. The joint risk of current cigarette smoking and current betel quid chewing was increased 3.73-fold (OR, 3.73; 95%CI, 1.81-7.70, p<0.001) compared to those who had neither habit. Both cigarette smoking and betel quid chewing are independent risk factors for the development of calcium urolithiasis. The risk effect is even strengthened when subjects have both habits. These findings suggest users can greatly reduce the risk of calcium urolithiasis if they quit these two habits.

The Impact of Cigarette Smoking on Prognosis in Small Adenocarcinomas of the Lung: The Association Between Histologic Subtype and Smoking Status

In this retrospective study, we clarified the impact of smoking on prognosis and the association of clinicopathological factors, particularly histologic subtype, in patients with small adenocarcinoma of the lung. Between 1996 and December 2006, 121 patients presenting with adenocarcinomas that had a diameter </=2 cm were analyzed. The clinicopathological records of the patients were examined for age, gender, nodal status (c-N and p-N), tumor size, serum carcinoembryonic antigen level, histologic subtype, and smoking history. A histologic subtype was defined using a modified World Health Organization classification. These subtypes are bronchioloalveolar carcinoma (BAC), adenocarcinoma with little or no BAC component (Non or min BAC), and mixed bronchioloalveolar carcinoma with other adenocarcinoma components. The overall 5-year survival rates were 94.4% for never-smokers (N = 55) and 79.2% for smokers (N = 66) (p = 0.05). Cancer-specific 5-year survival rates were 98.0% for never-smokers and 80.4% for smokers (p = 0.03). Gender, serum carcinoembryonic antigen level, and histologic subtype were significantly associated with smoking status. Histologic subtype (Non or min BAC) was the only significant prognostic factor in multivariate analyses. The prevalence of smoking by histologic subtype was 27.3% for BAC, 43.2% for mixed bronchioloalveolar carcinoma, and 74.6% for Non or min BAC. The prevalence was significantly higher in Non or min BAC than in the others. Furthermore, the smoking index (daily cigarette consumption times years of smoking) was significantly higher in Non or min BAC than in the other two subtypes. In addition, patients with a high smoking index showed a greater percentage of Non or min BAC subtypes. Finally, male gender was associated with Non or min BAC independent of smoking status (p = 0.03). When adenocarcinomas were small (diameter </=2 cm) cigarette smoking and male gender were associated with Non or min BAC histologic subtypes, which are thought to have more aggressive biologic features resulting in poorer outcome compared with other subtypes.

Behavioural interventions for smoking cessation in patients hospitalised for a major cardiovascular event

The impact of cigarette smoking on progression of atherosclerosis in patients with known cardiovascular disease suggests a strong need for effective cessation interventions in this group. This letter compares and discusses smoking cessation outcomes following behavioural smoking cessation interventions versus usual care in hospitalised cardiovascular patients using meta-analysis of randomised controlled peer-reviewed publications. It particularly focuses on the impact of intensity and duration of intervention on outcome.