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CORK Bibliography: Nicotine, Chronic Effects

76 citations. January 2019 to present

Prepared: March 2011

Airoldi L; Magagnotti C; Iannuzzi AR; Marelli C; Bagnati R; Pastorelli R et al. Effects of cigarette smoking on the human urinary proteome. Biochemical and Biophysical Research Communications 381(3): 397-402, 2009. (25 refs.)

In this pilot study we used a proteomic approach to compare the urinary protein patterns of healthy smokers and non-smokers. Proteins were resolved by two-dimensional gel electrophoresis and identified by mass spectrometry. The relative abundance of three inflammatory proteins (S100A8, inter-alpha-trypsin inhibitor heavy chain 4, CD59) and that of two isoforms of pancreatic alpha amylase was significantly higher in smokers. Zinc-alpha-2-glycoprotein was the only protein clown-regulated in smokers. Its abundance was significantly correlated with urinary glucocorticoids. Most of the proteins identified may be non-specific biomarkers of tobacco effects, since they are involved in inflammatory responses associated with several diseases. Of greater interest are the changes in abundance of pancreatic alpha amylase and zinc alpha 2 glycoprotein, which after proper validation, might be candidate biomarkers of diseases resulting from exposure to tobacco smoke. The data also show for the first time that smoking can affect the expression profile Of urinary proteins.

Armstrong AW; Armstrong EJ; Fuller EN; Sockolov ME; Voyles SV. Smoking and pathogenesis of psoriasis: A review of oxidative, inflammatory and genetic mechanisms. (review). British Journal of Dermatology 165(6): 1162-1168, 2011. (79 refs.)

Recent studies suggest that cigarette smoking may trigger the development of psoriasis through oxidative, inflammatory and genetic mechanisms. Smoking initiates formation of free radicals that stimulate cell signalling pathways active in psoriasis including mitogenactivated protein kinase (MAPK), nuclear factor?B (NF?B) and Janus kinase/signal transducers and activators of transcription (JAKSTAT). Smoking damages the skin by increasing formation of reactive oxygen species and decreasing the gene expression of antioxidants. Nicotine also stimulates innate immune cells integral to the pathogenesis of psoriasis including dendritic cells, macrophages and keratinocytes. These cells release cytokines that activate T lymphocytes and perpetuate a cycle of chronic inflammation. Smoking also enhances expression of genes known to confer an increased risk of psoriasis, including HLACw6, HLADQA1*0201 and CYP1A1. Improved understanding of the possible link between smoking and psoriasis pathogenesis may provide further insight into mechanisms underlying smoking, psoriasis and risk of subsequent cardiovascular disease.

Awan SN. The effect of smoking on the Dysphonia Severity Index in females. Folia Phoniatrica et Logopaedica 63(2): 65-71, 2011. (45 refs.)

Objective: This study investigated the capability of the Dysphonia Severity Index (DSI) and its component measures to reveal differences in vocal capability between groups of young adult female smokers and nonsmokers. Patients and Methods: The subjects were 30 female nonsmokers and 30 female smokers between the ages of 18 and 24 years. Data on the DSI components (maximum phonation time, MPT; highest phonational frequency, F(0) (high); lowest intensity, I(low), and jitter) were collected, followed by calculation of the DSI. Results: Significant differences between groups were observed on the DSI, with reduced DSI scores in smokers primarily due to reductions in F(0) (high) and increases in I(low). A strong partial correlation between MPT and the DSI in smokers may be indicative of reductions in respiratory support and/or phonatory control. Conclusions: Significant group differences in the DSI and component measures may be indicative of early changes in vocal function secondary to smoking. Reductions in frequency and dynamic range are consistent with the possibility of increased vocal fold mass in smokers. The results indicate that significant differences in the DSI between groups may be observed in subjects with perceptually normal vocal quality and with normal levels of vocal perturbation.

Babizhayev MA; Savel'yeva EL; Moskvina SN; Yegorov YE. Telomere length is a biomarker of cumulative oxidative stress, biologic age, and an independent predictor of survival and therapeutic treatment requirement associated with smoking behavior. American Journal of Therapeutics 18(6): E209-E226, 2011. (148 refs.)

Globally, tobacco use is associated with 5 million deaths per annum and is regarded as one of the leading causes of premature death. Major chronic disorders associated with smoking include cardiovascular diseases, several types of cancer, and chronic obstructive pulmonary disease (lung problems). Cigarette smoking (CS) generates a cumulative oxidative stress, which may contribute to the pathogenesis of chronic diseases. Mainstream and side stream gas-phase smoke each have about the same concentration of reactive free radical species, about 1 x 10(16) radicals per cigarette (or 5 x 10(14) per puff). This effect is critical in understanding the biologic effects of smoke. Several lines of evidence suggest that cigarette smoke constituents can directly activate vascular reactive oxygen species production. In this work we present multiple evidence that CS provide the important risk factors in many age-related diseases, and is associated with increased cumulative and systemic oxidative stress and inflammation. The cited processes are marked by increased white blood cell (leucocytes, WBCs) turnover. The data suggest an alteration of the circulating WBCs by CS, resulting in increased adherence to endothelial cells. Telomeres are complex DNA-protein structures located at the end of eukaryotic chromosomes. Telomere length shortens with biologic age in all replicating somatic cells. It has been shown that tobacco smoking enhances telomere shortening in circulating human WBCs. Telomere attrition (expressed in WBCs) can serve as a biomarker of the cumulative oxidative stress and inflammation induced by smoking and, consequently, show the pace of biologic aging. We originally propose that patented specific oral formulations of nonhydrolized carnosine and carcinine provide a powerful tool for targeted therapeutic inhibition of cumulative oxidative stress and inflammation and protection of telomere attrition associated with smoking. The longitudinal studies of the clinical population groups described in this study including elderly support the hypothesis that telomere length is a predictor of survival and therapeutic treatment requirement associated with smoking behavior.

Baka Z; Buzas E; Nagy G. Rheumatoid arthritis and smoking: Putting the pieces together. (review). Arthritis Research & Therapy 11(4): e-238, 2009. (94 refs.)

Besides atherosclerosis and lung cancer, smoking is considered to play a major role in the pathogenesis of autoimmune diseases. It has long been known that there is a connection between rheumatoid factor-positive rheumatoid arthritis and cigarette smoking. Recently, an important gene-environment interaction has been revealed; that is, carrying specific HLA-DRB1 alleles encoding the shared epitope and smoking establish a significant risk for anti-citrullinated protein antibody-positive rheumatoid arthritis. We summarize how smoking-related alteration of the cytokine balance, the increased risk of infections (the possibility of cross-reactivity) and modifications of autoantigens by citrullination may contribute to the development of rheumatoid arthritis.

Balakumar P; Kaur J. Is nicotine a key player or spectator in the induction and progression of cardiovascular disorders? (review). Pharmacological Research 60(5): 361-368, 2009. (141 refs.)

Cigarette smoking is common in societies worldwide and a growing body of evidence suggests that chronic cigarette smoking may affect the structure and function of cardiovascular system. The chronic exposure to high levels of nicotine, a major component of cigarette smoking, has been observed to play a pathogenic role in the induction and progression of cardiovascular disorders including cardiomyopathy and peripheral vascular disease. Nicotine alters the function of vascular endothelium, initiates the adhesion cascade and stimulates the vascular inflammatory events to induce atherosclerosis and hypertension. Moreover, nicotine has been noted to induce direct coronary spasm and ischemia, which develop coronary artery disease and myocardial infarction. In addition, nicotine stimulates the excessive release of impulses from sinoatrial node that may account for the induction of cardiac arrhythmia. The present review critically discussed the possible detrimental role of chronic nicotine exposure in cardiac and vascular endothelial dysfunction. Moreover, the signaling mechanisms involved in the pathogenesis of nicotine exposure-induced cardiovascular dysfunction have been discussed. In addition, the pharmacological interventions to ameliorate chronic nicotine exposure-induced cardiovascular abnormalities have been delineated.

Balbi B; Cottin V; Singh S; De Wever W; Herth FJF; Cordeiro CR. Smoking-related lung diseases: A clinical perspective. (editorial). European Respiratory Journal 35(2): 231-233, 2010. (22 refs.)

Bellomi M; Rampinelli C; Veronesi G; Harari S; Lanfranchi F; Raimondi S et al. Evolution of emphysema in relation to smoking. European Radiology 20(2): 286-292, 2010. (26 refs.)

We have little knowledge about the evolution of emphysema, and relatively little is understood about its evolution in relation to smoking habits. This study aims to assess the evolution of emphysema in asymptomatic current and former smokers over 2 years and to investigate the association with subjects' characteristics. The study was approved by our Ethics Committee and all participants provided written informed consent. We measured emphysema by automatic low-dose computed tomography densitometry in 254 current and 282 former smokers enrolled in a lung-cancer screening. The measures were repeated after 2 years. The association between subjects' characteristics, smoking habits and emphysema were assessed by chi-squared and Wilcoxon tests. Univariate and multivariate odds ratios (OR) with 95% confidence intervals (CI) were calculated for the risk of emphysema worsening according to subjects' characteristics. We assessed the trend of increasing risk of emphysema progression by smoking habits using the Mantel-Haenszel chi-squared test. The median percentage increase in emphysema over a 2-year period was significantly higher in current than in former smokers (OR 1.8; 95% CI 1.3-2.6; p < 0.0001). The risk of worsening emphysema (by 30% in 2 years) in current smokers increased with smoking duration (p for trend < 0.02). As emphysema is a known risk factor for lung cancer, its evaluation could be used as a potential factor for identification of a high-risk population. The evaluation of emphysema progression can be added to low-dose CT screening programmes to inform and incite participants to stop smoking.

Blanc FX; Macedo P; Hew M; Chung KF. Capsaicin cough sensitivity in smokers with and without airflow obstruction. Respiratory Medicine 103(5): 786-790, 2009. (16 refs.)

Background: Cough is a frequent symptom of cigarette smokers that often precedes the development of airflow obstruction. We determined whether chronic cigarette smoking is associated with an increase in capsaicin cough response in the absence of cough. Methods: We examined this in asymptomatic smokers with normal lung function (n = 68, FEV1 99.3 +/- 2.1 % predicted) and in patients with established COPD without cough symptoms (n = 42; FEV1 57.0 +/- 2.6% predicted), using healthy non-smoking volunteers as control (n = 92; FEV1 100.6 +/- 1.7% predicted). Using an incremental capsaicin concentration challenge protocol, we recorded the concentrations that induced 2 (C2) and 5 or more coughs (C5). Results: Because females have a lower C2 and C5 than mates in the control group, we analysed the data in each group according to gender. Log C5 was decreased both in asymptomatic smokers (1.56 +/- 0.11 mu mol/L, p < 0.05) and in COPD patients (1.44 +/- 0.14 mu mol/L, p < 0.01) when compared to non-smokers (1.90 +/- 0.09 mu mol/L). Log C2 did not differ between groups. Log C2 and log C5 were decreased in women (0.772 +/- 0.071 mu mol/L and 1.481 +/- 0.094 mu mol/L, respectively) when compared to men (1.045 +/- 0.088 mu mol/L and 1.923 +/- 0.087 mu mol/L, respectively) (p < 0.05 for log C2; p < 0.001 for log C5). Conclusion: We conclude that chronic cigarette smoking increases capsaicin cough reflex and that this remains so with the development of COPD.

Brizer D; Castandea R, eds. Clinical Addiction Psychiatry. New York: Cambridge University Press, 2011. (Chapter refs.)

This book is described as an anthology of essays setting forth the most current and authoritative information on addiction theory, practice and research. Each chapter is authored by a recognized authority in the field. The volume covers diverse material, from the environment, to genetics, culture and spirituality, treatment and pharmacology. The book, with 24 essays, is organized in three parts. Part I sets forth basic constructs of addiction medicine. This includes discusssion of the disease concept, abstinence as a treatment goal, medical sequelae of addiction, the relationship of substance use and suicide. psychotherapic paradigms, and drug therapies. Part II focuses upon "the real world." It includes twelve step approaches; nicotine addiction and smokng cessation; managing alcoholism in primary care; methadone treatment; prescription drug abuse. Part III considers special topics, such as pain management and addiction treatment; neurofeedback; drug therapies for alcohol dependence; emergency medical presentation; acupuncture; and and EEG neurofeedback therapy.

Calabro KS; Prokhorov AV. Respiratory symptoms after smoking cessation among college students. Pediatric Allergy, Immunology and Pulmonology 24(4): 215-219, 2011. (11 refs.)

Data on respiratory symptoms after smoking cessation are available for mature adults, but for young adults these data are limited to observational studies. This retrospective analysis of smoking cessation trials addresses the gap. A cohort of 18- to 24-year-olds without chronic respiratory illness was developed from 2 randomized trials of behavioral interventions versus standard care to promote smoking cessation. This secondary analysis was performed to determine whether short-term respiratory health improvements occurred among those who achieved smoking cessation for 2 weeks or more. Self-reported respiratory symptoms were assessed at baseline and last follow-up. The sample numbered 327, 60% smoked 5-10 cigarettes a day and 56% smoked for 1-5 years. Abstinence periods among those achieving cessation ranged from 2 to 78 weeks. The mean overall baseline respiratory symptom score was 14.3, standard deviation (SD) = 11.5. Respiratory symptoms for those achieving cessation were mean = 13.3, SD = 11.2, decreasing to mean = 3.8, SD = 5.9 symptom days at the last follow-up. Baseline symptoms for those who continued smoking were mean = 14.6, SD = 11.6, decreasing to mean = 10.3, SD = 10.3 at follow-up. Five fewer respiratory symptom days per week were noted for those who stopped smoking (mean = 5.2, SD = 1.5, P < 0.0001). Smoking cessation is associated with reduced respiratory symptoms. Feedback of short-term health consequences may be relevant to younger populations who may perceive smoking hazards as in the distant future.

Calapai G; Caputi AP; Mannucci C; Gregg EO; Pieratti A; Russo GA et al. A cross-sectional investigation of biomarkers of risk after a decade of smoking. Inhalation Toxicology 21(13): 1138-1143, 2009. (24 refs.)

Two groups of 20 healthy volunteers with cigarettes of different tar yield were compared with a group of 20 never smokers over 24 h for several biomarkers. All groups were of similar mean ages and the smokers had smoked for a homogeneous period of approximately 10 yr. The groups were assessed using routine medical parameters as well as biomarkers of recent smoke exposure and other biomarkers that were under evaluation as possible markers of risk for smoking-associated diseases. All biomarkers of exposure-carbon monoxide, nicotine plus its five major metabolites, and 4-(methylnitrosamine)-1-(3-pyridyl)-1-butanol (NNAL)-were significantly elevated in smokers. For biomarkers of potential risk evaluated in the blood, white cells and immunoglobulin (Ig) G showed a decrease related to smoking status (p < .01). Interleukin 6 levels were higher in smoker groups compared to never smokers, with a significant increasing trend across the groups (p < .05). Among the urinary biomarkers studied, 11-deydrothromboxane B2, 2,3-dinor-thromboxane B2, and thymidine glycol showed significant increasing trends across the groups (p < .01). The results suggest that after the first decade or less of smoking, changes in inflammatory, immunological, and cardiovascular function can be observed. However, further studies on larger groups will be required to better understand the kinetics of these subtle effects observed early in smokers and their relationship with the potential risk of subsequent smoking-associated disease.

Chua HF; Liberzon I; Welsh RC; Strecher VJ. Neural correlates of message tailoring and self-relatedness in smoking cessation programming. Biological Psychiatry 65(2): 165-168, 2009. (19 refs.)

Background: Smoking leads to illnesses including addiction, cancer, and cardiovascular and respiratory diseases. Different intervention programs have become available. In the past decade, providing tailored smoking cessation messages has been shown to be more effective in inducing smoking cessation than one-size-fits-all interventions. However, little is known about the brain responses of smokers when they receive tailored smoking cessation messages. Methods: A neuroimaging study using blocked and event-related designs examined neural activity in 24 smokers exposed to high-tailored and low-tailored smoking cessation messages. Results: In both blocked and event-related conditions, rostral medial prefrontal cortex and precuneus/posterior cingulate were engaged more during the processing of high-tailored smoking cessation messages than low-tailored smoking cessation messages. Conclusions: The activation patterns of smokers to tailored cessation messages show involvement of brain areas commonly implicated in self-related processing. Results seem to add support to the suggested role of self-relevance in tailored cessation programs, where previous studies have shown a potential mediating role of self-relevance on smoking abstinence. The findings are relevant to understanding the cognitive mechanisms underlying tailored message processing and might point to new directions for testing response to health communications programming.

Claessen H; Arndt V; Drath C; Brenner H. Smoking habits and occupational disability: A cohort study of 14,483 construction workers. Occupational and Environmental Medicine 67(2): 84-90, 2010. (39 refs.)

Objectives Although smoking causes a variety of diseases and both, a high smoking prevalence and permanent occupational disability are a great burden on the population level, data about the impact of smoking habits on occupational disability are sparse. The objective of this study was to examine the influence of smoking habits on occupational disability among construction workers, an occupational group with particularly high smoking prevalence. Methods The association between smoking and occupational disability was examined during a mean follow-up of 10.8 years in a cohort of 14,483 male construction workers in Wurttemberg, Germany. The cohort was linked to the regional pension register of the German pension fund to identify workers who were granted a disability pension during the follow-up. HRs (Hazard Ratios) were calculated with non-smokers as reference by the Cox proportional hazards model adjusting for potential confounding factors such as age, nationality, type of occupation, alcohol consumption and body mass index. Results Overall, 2643 cases of occupational disability were observed, with dorsopathy (21%) being the most common cause. Clear dose-response relationships were seen between smoking and occupational disability due to all causes, as well as occupational disability due to respiratory, cardiovascular and mental diseases, cancer and dorsopathy. Particularly strong associations were seen between heavy smoking (>= 20 cigarettes/day) and occupational disability due to mental and respiratory diseases (HR 3.25, 95% CL 1.93 to 5.46 and HR 3.26, 95% CL 1.69 to 6.27, respectively). Conclusion: Smoking is associated with increased risk of occupational disability among construction workers, in particular occupational disability due to respiratory, cardiovascular and mental diseases, cancer and dorsopathy.

Costello MR; Mandelkern MA; Shoptaw S; Shulenberger S; Baker SK; Abrams AL et al. Effects of treatment for tobacco dependence on resting cerebral glucose Metabolism. Neuropsychopharmacology 35(3): 605-612, 2010. (54 refs.)

While bupropion HCl and practical group counseling (PGC) are commonly used treatments for tobacco dependence, the effects of these treatments on brain function are not well established. For this study, 54 tobacco-dependent cigarette smokers underwent resting F-18-fluorodeoxyglucose-positron emission tomography (FDG-PET) scanning before and after 8 weeks of treatment with bupropion HCl, PGC, or pill placebo. Using Statistical Parametric Mapping (SPM 2), changes in cerebral glucose metabolism from before to after treatment were compared between treatment groups and correlations were determined between amount of daily cigarette usage and cerebral glucose metabolism. Compared with placebo, the two active treatments (bupropion HCl and PGC) had reductions in glucose metabolism in the posterior cingulate gyrus. Further analysis suggested that PGC had a greater effect than bupropion HCl on glucose metabolism in this region. We also found positive correlations between daily cigarette use and glucose metabolism in the left occipital gyrus and parietal-temporal junction. There were no significant negative correlations between daily cigarette use and glucose metabolism. Our findings suggest that bupropion HCl and PGC reduce neural activity much as the performance of a goal-oriented task does in the default mode network of the brain, including the posterior cingulate gyrus. Thus, this study supports the theory that active treatments for tobacco dependence move the brain into a more goal-oriented state.

Cox DR. Commentary: Smoking and lung cancer: Reflections on a pioneering paper. (editorial). International Journal of Epidemiology 38(5): 1192-1193, 2009. (2 refs.)

Crow P; Bayley J; Keeley F. Smoking and urological disease. (editorial). BJU International 103(10): 1317-1319, 2009. (17 refs.)

Dar-Odeh NS; Abu-Hammad OA. The changing trends in tobacco smoking for young Arab women: Narghile, an old habit with a liberal attitude. Harm Reduction Journal 8: article 24, 2011. (28 refs.)

Narghile smoking by young females is becoming more acceptable than cigarettes in the conservative societies of Arab countries. Lack of social constraints on narghile smoking has resulted in an increased prevalence of narghile smoking among young Arab females and an earlier age of onset of this habit when compared to cigarette smoking. Documented health hazards of narghile smoking including pulmonary, cardiovascular and neoplastic ailments are consequently expected to affect this vulnerable sector of the population together with their offspring. In this commentary, we shed some light on the changing trend of tobacco use among young Arabic women as shown by an increasing number of studies investigating habits of tobacco use in young people.

Durazzo TC; Meyerhoff DJ; Nixon SJ. Chronic cigarette smoking: Implications for neurocognition and brain neurobiology. International Journal of Environmental Research and Public Health 7(10): 3760-3791, 2010. (196 refs.)

Compared to the substantial volume of research on the general health consequences associated with chronic smoking, little research has been specifically devoted to the investigation of its effects on human neurobiology and neurocognition. This review summarizes the peer-reviewed literature on the neurocognitive and neurobiological implications of chronic cigarette smoking in cohorts that were not seeking treatment for substance use or psychiatric disorders. Studies that specifically assessed the neurocognitive or neurobiological (with emphasis on computed tomography and magnetic resonance-based neuroimaging studies) consequences of chronic smoking are highlighted. Chronic cigarette smoking appears to be associated with deficiencies in executive functions, cognitive flexibility, general intellectual abilities, learning and/or memory processing speed, and working memory. Chronic smoking is related to global brain atrophy and to structural and biochemical abnormalities in anterior frontal regions, subcortical nuclei and commissural white matter. Chronic smoking may also be associated with an increased risk for various forms of neurodegenerative diseases. The existing literature is limited by inconsistent accounting for potentially confounding biomedical and psychiatric conditions, focus on cross-sectional studies with middle aged and older adults and the absence of studies concurrently assessing neurocognitive, neurobiological and genetic factors in the same cohort. Consequently, the mechanisms promoting the neurocognitive and neurobiological abnormalities reported in chronic smokers are unclear. Longitudinal studies are needed to determine if the smoking-related neurobiological and neurocognitive abnormalities increase over time and/or show recovery with sustained smoking cessation.

Edwards D. Immunological effects of tobacco smoking in "Healthy" smokers. (review). COPD: Journal of Chronic Obstetric Pulmonary Disease 6(1): 48-58, 2009. (80 refs.)

The history of tobacco smoking is quite extensive having existed for many years. Over the past 10-15 years significant gains have been made in curbing exposure to tobacco smoke, but tobacco smoke continues to contribute to significant disease. The immunological effects of cigarette smoking have been evaluated and can provide important insight into mechanism of disease. With the extensive growth in elucidation of basic immune processes within healthy host, further research is possible to aide understanding of immune alterations associated with smoking. Specifically, in the area of cellular immunity in which over 30 different cytokines contributing various regulatory functions in immunity, there are many proteins and mechanisms that may be altered. This review will cover the current state of knowledge in the areas of humoral, cellular immunity including results of cytokine studies in healthy smokers.

Edwards G. Matters of Substance: Drugs and Why Everyone's a User. New York: Thomas Dunne Books, 2005

This book examines the relationship between humankind and addictive substances. The author does not use the common approach, that underpins control laws, that a given drug produces similar effects in all humans under all circumstances. Rather the effects of drug use are presented as tied to the social milieu as well as within the individual's biologic and psychological constitution. Individual chapters cover the major drug categories, icit and illicit, and provides a straightforward descriptions of each drug's physiologic effects. However, the chapter then preceds with carefully selected examples, many dating back to previous centuries. These illustrate how a drug's action is mediated by the culture in which it is consumed, including factors such as the socioeconomic status of the user, advertising and other vehicles to encourage consumption, peer-group expectations, tax and trade policies, informal (but nevertheless powerful) customs, and formal control regulations. The book also considers the importance of the technology of administration - how the introduction of intravenous injection or innovations that facilitate inhalation (mass-produced cigarettes, heroin, "crack" cocaine) can increase drug-abuse problems exponentially. The illustrations also point out how tightening or loosening of availability, a breakdown in deterrence, the effect of medical prescribing patterns, government interest in revenue collection, changes in the symbolic meaning of a specific drug's consumption, and the drive for corporate profits all contribute to the environment of substance use and abuse. The concluding chapter is drected to considering the pros and cons that are associated with discussion of legalization. For alcohol, he advocates reducing usage to a "national consumption benchmark" by limiting access, restricting advertising, establishing government-operated retail outlets, designing tax and trade policies to discourage consumption without creating a revenue-dependent state, and increasing treatment opportunities. He prescribes much the same program for tobacco, but with a goal of reducing use as much as possible. He suggests that the jury is still out concerning the effects of "mass recreationals" such as marijuana and hallucinogenic drugs, and thus major research is required before proceeding with decriminalization. In the concluding pages of his book, when considering substances in the most restrictive regulatory categories (e.g., "hard drugs" such as opiates and central nervous system stimulants and depressants), the author notes the common pleas for more treatment resources and efforts to reduce the damage resulting from the enforcement of harsh drug laws. He then suggests that considerable research has shown that the key environmental factor associated with drug abuse is "social deprivation" - a combination of economic, political, and social disenfranchisement that causes primary producers, illicit distributors, and users to conclude that they have no viable alternative to participation in the drug-abuse-industrial complex. While not offering any specific plan, he makes a general plea for improving the material lives of the poor.

Freedman LS; Oberman B; Sadetzki S. Using time-dependent covariate analysis to elucidate the relation of smoking history to Warthin's tumor risk. American Journal of Epidemiology 170(9): 1178-1185, 2009. (25 refs.)

The authors aimed to elucidate the relation of the time-dependent smoking history parameters -- age at smoking initiation and smoking intensity, duration, and latency -- to the risk of Warthin's tumor, a benign tumor of the salivary gland for which cigarette smoking is a strong risk factor. They studied 117 cases of Warthin's tumor and 336 matched controls included in an Israeli nationwide case-control study of parotid gland tumors conducted from 2002 to 2003 by using the Cox regression model with time-dependent covariates, with age as the time axis. When current age and smoking duration were included in the statistical model, the authors show that the coefficient of a latency variable does not represent latency as such, but a balancing of the effects of age at initiation and time since cessation. They found a strong positive linear effect of duration of smoking, together with a positive nonlinear effect of intensity that levels off at higher intensities, and a negative effect of latency from 25 years onward. The latter finding implies that the effect of time since cessation dominates the effect of age at initiation, with risk decreasing sharply after smoking cessation. The relation of smoking variables to Warthin's tumor agrees with the patterns reported for lung cancer.

Gangl K; Reininger R; Bernhard D; Campana R; Pree I; Reisinger J et al. Cigarette smoke facilitates allergen penetration across respiratory epithelium. Allergy 64(3): 398-405, 2009. (41 refs.)

The association between cigarette smoke exposure and allergic airway disease is a matter for debate. We sought to investigate in an in vitro system whether active smoking reduces the integrity and barrier function of the respiratory epithelium and thus facilitates allergen penetration. We cultured the human bronchial epithelial cell line 16HBE14o- in a transwell culture system as a surrogate for the intact respiratory epithelium. The cell monolayer was exposed to standardized cigarette smoke extract (CSE). The extent and effects of trans-epithelial allergen penetration were measured using I-125-labelled purified major respiratory allergens (rBet v 1, rPhl p 5 and rDer p 2) and histamine release experiments. Exposure of cells to concentrations of CSE similar to those found in smokers induced the development of para-cellular gaps and a decrease in trans-epithelial resistance. CSE exposure induced a more than threefold increase in allergen penetration. Increased subepithelial allergen concentrations provoked a substantial augmentation of histamine release from sensitized basophils. Our results indicate that cigarette smoke is a potent factor capable of reducing the barrier function of the respiratory epithelium for allergens and may contribute to increased allergic inflammation, exacerbation of allergic disease and boosting of IgE memory.

Gepner AD; Piper ME; Johnson HM; Fiore MC; Baker TB; Stein JH. Effects of smoking and smoking cessation on lipids and lipoproteins: Outcomes from a randomized clinical trial. American Heart Journal 161(1): problem ?, 2011. (40 refs.)

Background: The effects of smoking and smoking cessation on lipoproteins have not been studied in a large contemporary group of smokers. This study was designed to determine the effects of smoking cessation on lipoproteins. Methods: This was a 1-year, prospective, double-blind, randomized, placebo-controlled clinical trial of the effects of 5 smoking cessation pharmacotherapies. Fasting nuclear magnetic resonance spectroscopy lipoprotein profiles were obtained before and 1 year after the target smoking cessation date. The effects of smoking cessation and predictors of changes in lipoproteins after 1 year were identified by multivariable regression. Results: The 1,504 current smokers were (mean [SD]) 45.4 (11.3) years old and smoked 21.4 (8.9) cigarettes per day at baseline. Of the 923 adult smokers who returned at 1 year, 334 (36.2%) had quit smoking. Despite gaining more weight (4.6 kg [5.7] vs 0.7 kg [5.1], P < .001], abstainers had increases in high-density lipoprotein cholesterol (HDL-C) (2.4 [8.3] vs 0.1 [8.8] mg/dL, P < .001), total HDL (1.0 [4.6] vs -0.3 mu mol/L [5.0], P < .001), and large HDL (0.6 [2.2] vs 0.1 [2.1] mu mol/L, P = .003) particles compared with continuing smokers. Significant changes in low-density lipoprotein (LDL) cholesterol and particles were not observed. After adjustment, abstinence from smoking (P < .001) was independently associated with increases in HDL-C and total HDL particles. These effects were stronger in women. Conclusions: Despite weight gain, smoking cessation improved HDL-C, total HDL, and large HDL particles, especially in women. Smoking cessation did not affect LDL or LDL size. Increases in HDL may mediate part of the reduced cardiovascular disease risk observed after smoking cessation.

Gossett LK; Johnson HM; Piper ME; Fiore MC; Baker TB; Stein JH. Smoking intensity and lipoprotein abnormalities in active smokers. Journal of Clinical Lipidology 3(6): 372-378, 2009. (31 refs.)

BACKGROUND: Smoking is associated with decreased high-density lipoprotein cholesterol (HDL-C) and increased levels of triglycerides. OBJECTIVE: We sought to evaluate the effects of five markers of smoking intensity on lipoprotein concentrations and particle sizes in a large, modern cohort of current smokers. METHODS: Fasting nuclear magnetic resonance spectroscopy lipoprotein profiles were obtained in a large cohort of current smokers enrolled in a smoking-cessation trial. Multivariate linear regression models were constructed to determine predictors of lipoprotein fractions. Models included age, sex, race, waist circumference, level of physical activity, and alcohol consumption. Smoking intensity parameters included current cigarettes smoked/day, pack-years, the Fagerstrom Test of Nicotine Dependence score, and carbon monoxide (CO) levels. RESULTS: The 1504 subjects (58% women, 84% white) had a mean (standard deviation) age of 45 (11.0) years. They smoked 21.4 (8.9) cigarettes/day (29.4 [20.4] pack-years). HDL-C (42.0 [13.5] mg/dL) and total HDL particles (30.3 [5.9] mu mol/L) were low. Cigarettes smoked/day independently predicted greater total cholesterol (P = .009), low-density lipoprotein cholesterol (P = .023), and triglycerides (P = .002). CO levels predicted lower HDL-C (P = .027) and total HDL particles (P = .009). However, the incremental R-2 for each marker of smoking intensity on each lipoprotein was small. Relationships between the Fagerstrom Test of Nicotine Dependence score and lipoproteins were weak and inconsistent. Participants in the lowest quintiles of current smoking, pack-years, and CO had more favorable lipoproteins (all P < .04). CONCLUSIONS: Among current smokers, increased smoking burden is associated with small increases in total cholesterol, low-density lipoprotein cholesterol, and triglycerides. Increased recent smoke exposure is associated with small decreases in HDL-C and HDL particles.

Gould NS; Min E; Gauthier S; Martin RJ; Day BJ. Lung glutathione adaptive responses to cigarette smoke exposure. Respiratory Research 12: 133, 2011. (44 refs.)

Background: Smoking tobacco is a leading cause of chronic obstructive pulmonary disease (COPD), but although the majority of COPD cases can be directly related to smoking, only a quarter of smokers actually develop the disease. A potential reason for the disparity between smoking and COPD may involve an individual's ability to mount a protective adaptive response to cigarette smoke (CS). Glutathione (GSH) is highly concentrated in the lung epithelial lining fluid (ELF) and protects against many inhaled oxidants. The changes in GSH that occur with CS are not well investigated; therefore the GSH adaptive response that occurs with a commonly utilized CS exposure was examined in mice. Methods: Mice were exposed to CS for 5 h after which they were rested in filtered air for up to 16 h. GSH levels were measured in the ELF, bronchoalveolar lavage cells, plasma, and tissues. GSH synthesis was assessed by measuring gamma-glutamylcysteine ligase (GCL) activity in lung and liver tissue. Results: GSH levels in the ELF, plasma, and liver were decreased by as much as 50% during the 5 h CS exposure period whereas the lung GSH levels were unchanged. Next, the time course of rebound in GSH levels after the CS exposure was examined. CS exposure initially decreased ELF GSH levels by 50% but within 2 h GSH levels rebound to about 3 times basal levels and peaked at 16 h with a 6-fold increase and over repeat exposures were maintained at a 3-fold elevation for up to 2 months. Similar changes were observed in tissue GCL activity which is the rate limiting step in GSH synthesis. Furthermore, elevation in ELF GSH levels was not arbitrary since the CS induced GSH adaptive response after a 3d exposure period prevented GSH levels from dropping below basal levels. Conclusions: CS exposures evoke a powerful GSH adaptive response in the lung and systemically. These data suggests there may be a sensor that sets the ELF GSH adaptive response to prevent GSH levels from dipping below basal levels. Factors that disrupt GSH adaptive responses may contribute to the pathophysiology of COPD.

Grundtvig M; Hagen TR; German M; Reikvam A. Sex-based differences in premature first myocardial infarction caused by smoking: Twice as many years lost by women as by men. European Journal of Cardiovascular Prevention & Rehabilitation 16(2): 174-179, 2009. (18 refs.)

Background: It has been debated whether smoking increases the risk of heart disease relatively more in women than in men. It is not known whether there are sex differences with regard to how many years prematurely smoking causes acute myocardial infarction (AMI) to occur. We aimed to determine how smoking affects the age of onset of first myocardial infarction in both the sexes. Design: Clinical data were consecutively entered into a database and were analysed with a multivariate regression technique. Methods In the years 1998-2005, data on 1784 consecutive patients (38.3% women) who were discharged from or died in a district general hospital with a diagnosis of first myocardial infarction were included in the study. Age at first AMI was analysed. Results: Unadjusted mean ages were 76.2 years for women and 69.8 years for men, a difference of 6.4 years (P<0.001). Mean age within the various groups was: women nonsmokers 80.7 years, women smokers 66.2 years, difference 14.4 years (P<0.001); men nonsmokers 72.2 years, men smokers 63.9 years, difference 8.3 years (P<0.001). After adjustment for risk factors (hypertension, cholesterol levels, diabetes) and patient characteristics (history of angina, history of stroke) 13.7 years of the age difference in women were attributed to smoking; the corresponding figure in men was 6.2 years (P<0.001). Conclusion: First AMI occurred significantly more prematurely in women than in men smokers, implying that twice as many years were lost by women as by men smokers.

Guarisi R; Sarian LO; Hammes LS; Longatto A; Derchain SFM; Roteli-Martins C et al. Smoking worsens the prognosis of mild abnormalities in cervical cytology. Acta Obstetricia et Gynecologica Scandinavica 88(5): 514-520, 2009. (27 refs.)

Objective. To examine the effect of smoking on the incidence of low- and high-grade cervical intraepithelial neoplasia (CIN) in women with a baseline Pap smear of atypical squamous cells (ASC) or a low-grade squamous intraepithelial lesion (LSIL). Design. Prospective study in which a cohort of women with normal colposcopy and ASC/LSIL at baseline were followed at 6-month intervals of up to 36 months. Women were grouped in post-hoc analysis according to their smoking behavior: never (or past) smokers and current smokers. Setting. This report was based on data from the Latin American Screening Study, conducted in Sao Paulo, Campinas, Porto Alegre (Brazil) and Buenos Aires (Argentina). Population. A subset of 150 women derived from a cohort of 1,011 women. Methods. Multivariate Cox analysis and Kaplan-Meier curves were used. Main outcome measures. Low- and high-grade CIN during follow-up. Results. The only factor related to an increased risk of developing CIN was the positive high-risk (hr) HPV status (hazard ratio (HR) = 3.42; 95% CI: 1.11-9.43). A total of 21 cases of incident CIN were detected during follow-up. Of these, 11 appeared in the group of 67 smokers and 10 among the 83 non-smoker women (log-rank, p=0.33). Smoking status was not associated with the risk of developing CIN (HR = 0.73; 95% CI: 0.40-1.33). However, when restricting the analysis to high-grade CIN only (11 cases), the probability of developing the disease was significantly higher among smokers. Conclusions. Smoking contributes additional risk for developing high-grade CIN in women with ASC or LSIL cytology but normal colposcopy.

Guyuron B; Rowe DJ; Weinfeld AB; Eshraghi Y; Fathi A; Iamphongsai S. Factors contributing to the facial aging of identical twins. Plastic and Reconstructive Surgery 123(4): 1321-1331, 2009. (10 refs.)

Background: The purpose of this study was to identify the environmental factors that contribute to facial aging in identical twins. Methods: During the Twins Day Festival in Twinsburg, Ohio, 186 pairs of identical twins completed a comprehensive questionnaire, and digital images were obtained. A panel reviewed the images independently and recorded the differences in the perceived twins' ages and their facial features. The perceived age differences were then correlated with multiple factors. Results: Four-point higher body mass index was associated with an older appearance in twins younger than age 40 but resulted in a younger appearance after age 40 (p = 0.0001). Eight-point higher body mass index was associated with an older appearance in twins younger than age 55 but was associated with a younger appearance after age 55 (p = 0.0001). The longer the twins smoked, the older they appeared (p < 0.0001). Increased sun exposure was associated with an older appearance and accelerated with age (p = 0.015), as was a history of outdoor activities and lack of sunscreen use. Twins who used hormone replacement had a younger appearance (p = 0.002). Facial rhytids were more evident in twins with a history of skin cancer (p = 0.05) and in those who smoked (p = 0.005). Dark and patchy skin discoloration was less prevalent in twins with a higher body mass index (p = 0.01) and more common in twins with a history of smoking (p = 0.005) and those with sun exposure (p = 0.005). Hair quantity was better with a higher body mass index (p = 0.01) although worse with a history of skin cancer (p = 0.005) and better with the use of hormones (p = 0.05). Conclusion: This study offers strong statistical evidence to support the role of some of the known factors that govern facial aging.

Hadar T; Yaniv E; Shvili Y; Koren R; Shvero J. Histopathological changes of the nasal mucosa induced by smoking. Inhalation Toxicology 21(13): 1119-1122, 2009. (33 refs.)

Changes in the histopathology of the respiratory epithelium in response to cigarette smoking have been studied in depth in the lungs, but data on the nasal lining are lacking. The aim of the present retrospective study was to investigate the histological changes that occur in the nasal mucosa of smokers compared with non-smokers. The study group included 47 patients who underwent partial resection of the inferior turbinates. Archival nasal tissue samples were collected and examined by light microscopy: the number of goblet cells was counted, and the degree of inflammation, congestion, and edema was graded as mild, moderate, or severe. Epithelial thickness was measured as well. Findings were compared between smokers (n = 21) and non-smokers (n = 26). On statistical analysis, significant differences were found between the smokers and non-smokers in mean number of goblet cells in the nasal epithelium, 43.43 +/- 16.80 vs. 16.23 +/- 5.65 respectively (p < 0.0001), mean edema grade, 2.43 +/- 0.75 vs. 1.12 +/- 0.33 respectively (p < 0.0001), and mean epithelial thickness, 111.9 +/- 25.8 mu m vs. 60.4 +/- 18.4 mu m respectively (p < 0.0001). The corresponding mean values of congestion were 2 +/- 0.71 and 1.27 +/- 0.67 (p < 0.001), and of inflammation, 1.81 +/- 0.60 and 1.81 +/- 0.85 (NS). In conclusion, the histopathological findings in the nasal mucosa of smokers resemble reported findings in the bronchial respiratory epithelium. The main differences from nonsmokers are greater goblet cell hyperplasia and thicker epithelium.

Hahn C; Pogun S; Gunturkun O. Smoking modulates language lateralization in a sex-specific way. Neuropsychologia 48(14): 3993-4002, 2010. (119 refs.)

Smoking affects a widespread network of neuronal functions by altering the properties of acetylcholinergic transmission. Recent studies show that nicotine consumption affects ascending auditory pathways and alters auditory attention, particularly in men. Here we show that smoking affects language lateralization in a sex-specific way. We assessed brain asymmetries of 90 healthy, right-handed participants using a classic consonant-vowel syllable dichotic listening paradigm in a 2 x 3 experimental design with sex (male, female) and smoking status (non-smoker, light smoker, heavy smoker) as between-subject factors. Our results revealed that male smokers had a significantly less lateralized response pattern compared to the other groups due to a decreased response rate of their right ear. This finding suggests a group-specific impairment of the speech dominant left hemisphere. In addition, decreased overall response accuracy was observed in male smokers compared to the other experimental groups. Similar adverse effects of smoking were not detected in women. Further, a significant negative correlation was detected between the severity of nicotine dependency and response accuracy in male bur not in female smokers. Taken together, these results show that smoking modulates functional brain lateralization significantly and in a sexually dimorphic manner. Given that some psychiatric disorders have been associated with altered brain asymmetries and increased smoking prevalence, nicotinergic effects need to be specifically investigated in this context in future studies.

Halmenschlager G; Rossetto S; Lara GM; Rhoden EL. Evaluationion of the effects of cigarette smoking on testosterone levels in adult men. Journal of Sexual Medicine 6(6): 1763-1772, 2009. (50 refs.)

Cigarette smoking is highly prevalent among men. Many studies have evaluated the effect of cigarette smoking on levels of male reproductive hormones; however, the findings still remain controversial. To evaluate the influence of cigarette smoking on serum levels of total testosterone (TT), free testosterone (FT), bioavailable testosterone (BT), sex hormone-binding globulin (SHBG), luteinizing hormone (LH), and follicle-stimulating hormone (FSH). A total of 255 men (90 smokers and 165 nonsmokers), aged 30 to 70 years, were investigated. Weight and height were obtained and body mass index (BMI) was calculated. Also, waist circumference and hip circumference were measured and waist-to-hip ratio was obtained. Fasting blood samples were drawn for determination of plasmatic glucose levels and serum levels of total cholesterol, high-density lipoprotein cholesterol (HDL-c), triglycerides, albumin, prolactin, TT, SHBG, LH, and FSH. The values of low-density lipoprotein cholesterol (LDL-c) were determined by Friedwald equation and the values of FT and BT were calculated from TT, SHBG, and albumin. Statistical significance was set at P <= 0.05. The influence of smoking on levels of TT, FT, and BT. No significant difference was observed in the mean values of TT (P = 0.580), FT (P = 0.869), BT (P = 0.933), SHBG (P = 0.279), LH (P = 0.573), and FSH (P = 0.693) in the different levels of pack-years when compared to nonsmokers. Moreover, after multivariate logistic regression, no association between increased pack-years of smoking and increased odds ratio for occurrence of low hormones and SHBG levels was observed. In this study, smokers and nonsmokers had similar mean values of androgens, gonadotropins and SHBG. However, it is necessary to standardize pack-years of smoking in order to elucidate the influence of cigarette smoking on sex hormone levels, as well as to minimize differences among studies and to confirm our results.

Heffernan T; O'Neill T; Moss M. Smoking and everyday prospective memory: A comparison of self-report and objective methodologies. Drug and Alcohol Dependence 112(3): 234-238, 2010. (30 refs.)

Aims: To examine whether persistent smoking leads to impairments in self-reported and objective measures of prospective memory (PM the cognitive ability to remember to carry out activities at some future point in time). Methods: An opportunity sample of 18 existing smokers and 22 who had never smoked were compared An existing-groups design was utilised comparing a smoking group with a never-smoked control group as the independent factor Scores on the sub-scales of the Prospective and Retrospective Memory Questionnaire (PRMQ) and scores on the Cambridge Prospective Memory Test (CAMPROMPT) constituted the dependent factors. Age, mood, other drug use strategy scores and IQ were also measured. Each participant was tested in a laboratory setting. Self-reported PM lapses were measured using the PRMQ. The CAMPROMPT was used as an objective measure of PM. Alcohol and other drug use were assessed by a Recreational Drug Use Questionnaire, The Hospital Anxiety and Depression Scale gauged levels of anxiety and depression. A strategy scale measured the number of strategies used to aid memory. The National Adult Reading Test measured IQ. Results: After observing no between-group differences on age mood alcohol use strategy use and IQ, smokers and the never-smoked did not differ on the self-reported lapses measured on the PRMQ. However smokers recalled significantly fewer items on the CAMPROMPT than the never-smoked group. Conclusion The results of the present study suggest that persistent smoking leads to impairments in everyday PM.

Horvathova M; Jahnova E; Szabova M; Tulinska M; Kuricova M; Liskova A et al. The relationship between cell surface markers, cytokines, ageing, and cigarette smoking. Bratislava Medical Journal 110(7): 394-400, 2009. (81 refs.)

The purpose of this study was to investigate the modulation of selected cell surface markers and proinflammatory cytokines production in relation to ageing, and cigarette smoking. The analysis of cell surface receptors was performed by the flow cytometry and cytokines levels were evaluated by the sandwich enzyme immunoassays. We found a decreased expression of CD69, CD28, CD11b, CD95 markers in old population compared to young people (p<0.05; p<0.001). The memory CD45RO lymphocytes were markedly expanded in older population in comparison to young donors (12.93 +/- 5.92%, p<0.001) and the selectin CD62L was significantly increased on granulocytes in aged people (p<0.05). Our findings demonstrated an augmented level of CD3 and CD28 on lymphocytes in smokers (p<0.05; p<0.005). The significant depression of CD16+56 molecule was recorded in smokers (10.86 +/- 0.80%) when compared to non-smokers (14.44 +/- 0.46; p<0.05). Our results showed a significantly diminished levels of interleukin (IL)-1 beta (1.93 +/- 0.48 pg/ml), and increased levels of IL-6 and tumor necrosis factor (TNF)-alpha in elderly population compared to young people (p<0.05; p<0.001). The present data support previous suggestions that senescence and cigarette smoking may contribute to changes in the immune system activity, resulting in altered cell surface marker expression and cytokine levels (Tab. 1, Fig. 3, Ref. 81). Full Text (Free, PDF) www.bmj.sk.

Hossain M; Sathe T; Fazio V; Mazzone P; Weksler B; Janigro D et al. Tobacco smoke: A critical etiological factor for vascular impairment at the blood-brain barrier. Brain Research 1287: 192-205, 2009. (62 refs.)

Active and passive tobacco smoke are associated with the dysfunction of endothelial physiology and vascular impairment. Studies correlating the effects of smoking and the brain microvasculature at the blood-brain barrier (BBB) level have been largely limited to few selective compounds that are present in the tobacco smoke (TS) yet the pathophysiology of smoking has not been unveiled. For this purpose, we characterized the physiological response of isolated human brain microvascular endothelial cells (HBMEC) and monocytes to the exposure of whole soluble TS extract. With the use of a well established humanized flow-based in vitro blood-brain barrier model (DIV-BBB) we have also investigated the BBB physiological response to TS under both normal and impaired hemodynamic conditions simulating ischemia. Our results showed that TS selectively decreased endothelial viability only at very high concentrations while not significantly affecting that of astrocytes and monocytes. At lower concentrations, despite the absence of cytotoxicity, TS induced a strong vascular pro-inflammatory response. This included the upregulation of endothelial pro-inflammatory genes, a significant increase of the levels of pro-inflammatory cytokines, activated matrix metalloproteinase, and the differentiation of monocytes into macrophages. When flow-cessation/reperfusion was paired with TS exposure, the inflammatory response and the loss of BBB viability were significantly increased in comparison to sham-smoke condition. in conclusion, TS is a strong vascular inflammatory primer that can facilitate the loss of BBB function and viability in pathological settings involving a local transient loss of cerebral blood flow such as during ischemic insults.

Hukkinen M; Korhonen T; Broms U; Koskenvuo M; Kaprio J. Long-term smoking behavior patterns predicting self-reported chronic bronchitis. COPD: Journal of Chronic Obstructive Pulmonary Disease 6(4): 242-249, 2009. (42 refs.)

We examined the effects of long-term smoking patterns on self-reported symptoms of chronic bronchitis within the Finnish adult twin cohort including 21, 609 individuals responding to questionnaires in 1975 and 1981, of which 11,015 respondents participated also in 1990. We also explored the association between smoking and bronchitis among discordant twin pairs. Among those without chronic bronchitis at baseline we examined incidence of chronic bronchitis in 1981 both by 1975 smoking status, but also based on subgroups formed according to change in smoking behaviors between 1975 and 1981. We conducted similar analyses in the longitudinal data including three consecutive measurements of smoking status. Logistic regressions demonstrated that among current smokers, the risk of chronic bronchitis increased about 1.5-fold by each amount category of daily cigarettes. When analyzing change of smoking status between 1975 and 1981, daily moderate and heavy smokers, smoking increasers and decreasers, as well as re-current smokers demonstrated elevated risks. In the analysis among discordant twin pairs the smoking co-twins had a 14-fold likelihood for chronic bronchitis compared to their never-smoking co-twins. Panel analyses showed that, not only moderate and heavy, but also former and light smokers, had significant risks for chronic bronchitis. Those with late smoking initiation, leisure time physical activity or over 10 years of smoking cessation were less likely to have chronic bronchitis. We conclude that in long term evaluation no safe level of smoking exists. Abstinence from tobacco seems to be the public health message justified by these results in prevention of chronic bronchitis.

Jacob P; Abu Raddaha AH; Dempsey D; Havel C; Peng M; Yu L et al. Nicotine, carbon monoxide, and carcinogen exposure after a single use of a water pipe. Cancer Epidemiology, Biomarkers & Prevention 20(11): 2345-2353, 2011. (23 refs.)

Background: Smoking tobacco preparations in a water pipe (hookah) is widespread in many places of the world, including the United States, where it is especially popular among young people. Many perceive water pipe smoking to be less hazardous than cigarette smoking. We studied systemic absorption of nicotine, carbon monoxide, and carcinogens from one water pipe smoking session. Methods: Sixteen subjects smoked a water pipe on a clinical research ward. Expired carbon monoxide and carboxyhemoglobin were measured, plasma samples were analyzed for nicotine concentrations, and urine samples were analyzed for the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and polycyclic aromatic hydrocarbon (PAH) metabolite biomarker concentrations. Results: We found substantial increases in plasma nicotine concentrations, comparable to cigarette smoking, and increases in carbon monoxide levels that are much higher than those typically observed from cigarette smoking, as previously published. Urinary excretion of NNAL and PAH biomarkers increased significantly following water pipe smoking. Conclusions: Absorption of nicotine in amounts comparable to cigarette smoking indicates a potential for addiction, and absorption of significant amounts of carcinogens raise concerns of cancer risk in people who smoke tobacco products in water pipes. Impact: Our data contribute to an understanding of the health impact of water pipe use.

Jacobsen LK; Picciotto MR; Heath CJ; Mencl WE; Gelernter J. Allelic variation of calsyntenin 2 (CLSTN2) modulates the impact of developmental tobacco smoke exposure on mnemonic processing in adolescents. Biological Psychiatry 65(8): 671-679, 2009. (63 refs.)

Background: Exposure to nicotine in tobacco smoke during development has been linked to subsequent deficits inattention and memory. The present study tested for evidence that genetic variation may contribute to individual differences in vulnerability to the effects of developmental exposure to tobacco smoke on memory and medial temporal lobe function in adolescents. Methods: Verbal and visuospatial memory were assessed and functional magnetic resonance imaging (fMRI) data were acquired in 101 adolescents systematically characterized for prenatal and adolescent exposure to tobacco smoke, while they performed an encoding and recognition memory task. The impact of allelic variation at loci within CLSTN2 (encoding synaptic protein calsyntenin 2) and KIBRA, shown previously to modulate early and delayed recall of words, on the dependent measures was examined. Results: KIBRA genotype did not exert significant main or interacting effects with prenatal or adolescent exposure to tobacco smoke on verbal or visuospatial memory. Previous observations of a beneficial effect of the CLSTN2 C allele on verbal recall were replicated. Adolescent exposure to tobacco smoke reversed this beneficial effect and was associated with increased activation of parahippocampal gyrus during early and delayed recognition in CLTSN2 C allele carriers. While the CLSTN2 C allele conferred enhanced functional connectivity between brain regions subserving accurate verbal recognition, adolescent exposure to tobacco smoke reversed this effect. Conclusions: These findings extend previous work demonstrating that calsyntenins play an essential role in learning and indicate that this role is modulated both by CLSTN2 genotype and, during adolescent development, by exposure to tobacco smoke.

Jang AS; Park JS; Lee JH; Park SW; Kim DJ; Uh ST et al. The impact of smoking on clinical and therapeutic effects in asthmatics. Journal of Korean Medical Science 24(2): 209-214, 2009. (30 refs.)

Smoking is associated with poor symptom control and impaired therapeutic responses in asthma. A total of 843 patients with asthma were recruited. The patients received treatment for 1 yr according to the severity of their asthma. We compared the forced expiratory volume in 1 sec (FEV1), the ratio of FEV1 to forced vital capaity (FVC), atopy, total IgE, emphysema on high-resolution computed tomography (HRCT), the number of near-fatal asthma attacks, and physiological fixed airway obstruction between the smoking and nonsmoking groups. The study population consisted of 159 (18.8%) current smokers, 157 (18.7%) ex-smokers, and 525 (62.5%) nonsmokers. Although the prevalence of atopy was not different between the smoking and nonsmoking groups, the total IgE was higher among the smokers than the nonsmokers. Compared with the nonsmoking group, the smokers had a lower FEV1 % predicted and forced expiratory flow between 25 and 75% of FVC. A greater prevalence of emphysema and a significantly higher number of asthmatic patients with fixed airway obstruction were detected in the smoking versus nonsmoking group. The 37.5% of asthmatic patients who were former or current smokers showed decreased pulmonary function and increased IgE, emphysema on HRCT, and fixed airway obstruction, indicating that smoking can modulate the clinical and therapeutic responses in asthma.

Jochmann N; Mueller S; Kuhn C; Gericke C; Baumann G; Stangl K et al. Chronic smoking prevents amelioration of endothelial function in the course of the menstrual cycle. Circulation Journal 73(3): 568-572, 2009. (28 refs.)

Background: Smoking is the most important modifiable cardiovascular risk factor in young women. The aim of this study was to investigate whether tobacco use influences physiological changes in endothelial function during the menstrual cycle. Methods and Results: Flow-mediated dilation (FMD) and nitro-mediated dilation (NMD) were assessed in healthy smoking and non-smoking women, by high-resolution ultrasound at 3 time points during the menstrual cycle: at menstruation, in the mid-follicular phase, and in the mid-luteal phase. A total of 25 women (12 nonsmokers, 13 smokers) completed the study protocol. FMD did not show differences between smoking and nonsmoking women at menstruation and the mid-follicular phase. At the mid-luteal phase, however, FMD was significantly reduced in smoking when compared with non-smoking women. NMD did not differ between smoking and non-smoking women, nor between the different cycle phases. Conclusions: In healthy women, smoking eliminates the physiological amelioration of endothelial function during the menstrual cycle. This study underlines the importance of an exact description of menstrual cycle phase and smoking status in studies investigating endothelial function in premenopausal women.

Jonas JB; Xu L. Smoking and age-related macular degeneration. (editorial). Archives of Ophthalmology 127(6): 826-827, 2009. (5 refs.)

Karaman M; Tek A. Deleterious effect of smoking and nasal septal deviation on mucociliary clearance and improvement after septoplasty. American Journal of Phonology & Allergy 23(1): 2-7, 2009. (45 refs.)

Objectives: To investigate the effect of septal deviation, septoplasty, and smoking upon nasal mucociliary clearance by using saccharine test. Methods: Included in this study. were 40 patients (15 women and 25 men) who had septal deviation and septoplasty surgery performed between March and June 2006. Patients are classified into three groups: group I (n = 20) nonsmoking patients Who had septoplasty surgery, group II (n = 20) smoking patients who had septoplasty surgery, and the control (n = 20) group. None of the control group has nasal breathing problem or smoking history. For determining preoperative and postoperative nasal mucociliary clearance (MCC) time, a saccharine test was performed on the patients I day before surgery and at the third month of postoperative control. Results: Preoperative and postoperative nasal MCC time in patients of group I are statistically significantly lower than the group II (p < 0.01). Postoperative MCC time in group I and II is significantly decreased compared with preoperative MCC time, statistically (p < 0.01). Preoperative and postoperative MCC time of group I and group If is significantly higher than MCC time of the control group (p < 0.01). Conclusion: Nasal septal deviation and smoking deteriorates nasal MCC time and this result can be shown easily With the saccharine test. Properly performed septoplasty surgery decreases nasal MCC time during the late postoperative period but MCC times are still longer than normal. The saccharine test can be used for following up the effect of septoplasty upon nasal mucosa.

Kinnula VL; Crapo JD. Smoking and COPD: Mechanisms and prevention. (editorial). COPD: Journal of Chronic Obstructive Pulmonary Disease 6(4): 231-233, 2009. (18 refs.)

Kirby ML; Beatty S; Loane E; Akkali MC; Connolly EE; Stack J et al. A central dip in the macular pigment spatial profile is associated with age and smoking. Investigative Ophthalmology & Visual Science 51(12): 6722-6728, 2010. (34 refs.)

PURPOSE. To investigate the relationship between specific macular pigment (MP) spatial profiles and risk factors for age-related macular degeneration (AMD). METHODS. The MP spatial profile of 484 healthy subjects was measured with customized heterochromatic flicker photometry (cHFP) and categorized into one of two profile types: typical exponential or atypical "central dip." Data on risk factors for AMD were obtained with a general health and lifestyle questionnaire. Dietary and serum concentrations of lutein (L) and zeaxanthin (Z) were also assessed. RESULTS. The presence of the central dip MP spatial profile was significantly more common in older subjects (the mean +/- SD age of subjects with a central dip MP spatial profile was 46.9 +/- 12 years, whereas the mean age of subjects with a typical MP spatial profile was 41.8 +/- 12 years; P = 0.004) and in current cigarette smokers (P = 0.031). Also, there was a significant age-related decline in central MP optical density (MPOD; 0.25 degrees retinal eccentricity), but in the men only (r = -0.146, P = 0.049). CONCLUSIONS. A central dip in the MP spatial profile, seen in older subjects and in cigarette smokers, may represent an undesirable feature of macular pigmentation. Further research is needed in this area.

Koczulla AR; Noeske S; Herr C; Jorres RA; Rommelt H; Vogelmeier C et al. Acute and chronic effects of smoking on inflammation markers in exhaled breath condensate in current smokers. Respiration 79(1): 61-67, 2010. (32 refs.)

Background: Long-term cigarette smoking is associated with pulmonary inflammation, but the acute effects of smoking have been less well studied. Analysis of the exhaled breath condensate (EBC) can provide noninvasive markers that might be indicative of inflammation. Objectives: The aim of the study was to determine whether the pH, electrical conductivity and the levels of ammonium and interleukin 8 (IL-8) of EBC were altered in smokers and whether they changed after smoking a single cigarette. Methods: We included 19 healthy nonsmokers (controls), 29 asymptomatic smokers, 10 patients with stable chronic obstructive pulmonary disease (COPD) [Global Initiative for Chronic Obstructive Lung Disease stages (GOLD) stages II-III], and 10 patients with exacerbated COPD. In 13 smokers, EBC was also analyzed before and after smoking. EBC was obtained during 10 min tidal breathing with a cooled RTube (TM). pH was determined after deaeration with argon. Results: Acute smoking did not alter the pH or ammonium and IL-8 levels, but raised conductivity. As in COPD patients, the pH was significantly decreased in chronic smokers with a history of at least 10 pack-years compared to controls. Conclusions: EBC can be used to detect the acute and chronic effects of smoking. The increased conductivity of EBC after smoking suggests acute inflammatory effects. The reduced pH in chronic smokers shows cigarette-induced inflammation.

Koskenvuo K; Broms U; Korhonen T; Laitinen LA; Huunan-Seppala A; Keistinen T et al. Smoking strongly predicts disability retirement due to COPD: the Finnish Twin Cohort Study. European Respiratory Journal 37(1): 26-31, 2011. (34 refs.)

No previous studies on the association of smoking behaviour with disability retirement due to register verified chronic obstructive pulmonary disease (COPD) exist. This 30-yr follow-up study examined how strongly aspects of cigarette smoking predict disability retirement due to COPD. The study population consisted of 24,043 adult Finnish twins (49.7% females) followed from 1975 to 2004. At baseline the participants had responded to a questionnaire. Information on retirement was obtained from the Finnish pension registers. Smoking strongly predicted disability retirement due to COPD. In comparison to never-smokers, age adjusted hazard ratio (HR) for current smokers was 22.0 (95% CI 10.0-48.5) and for smokers with >= 12 pack-yrs was 27.3 (95% CI 12.6-59.5). Similar estimates of risk were observed in within-pair analyses of twin pairs discordant for disability retirement due to COPD. Among discordant monozygotic pairs those with disability pension due to COPD were more often current smokers. The effect of early smoking onset (<18 yrs) on the risk of disability retirement due to COPD remained after adjustment for the amount smoked (HR 1.70, 95% CI 1.08-2.68). Smoking strongly predicts disability retirement due to COPD. Preventive measures against disability retirement and other harmful consequences of tobacco smoking should receive greater emphasis.

Lai HK; Ho SY; Wang MP; Lam TH. Secondhand smoke and respiratory symptoms among adolescent current smokers. Pediatrics 124(5): 1306-1310, 2009. (13 refs.)

OBJECTIVE: No study has ever reported the association between persistent respiratory symptoms and exposure to secondhand smoke (SHS) in adolescent smokers. The impact of SHS exposure on child health could be largely underestimated by not taking into account such effects. We investigated the association between exposure to SHS and respiratory symptoms among adolescent current smokers. METHODS: A total of 32 506 students aged 11 to 20 years from 85 randomly selected secondary schools in Hong Kong completed a self-administered questionnaire that included persistent respiratory symptoms (for 3 consecutive months in the past 12 months), number of days of SHS exposure per week at home and outside home, smoking status, amount of active smoking, and other basic demographic characteristics and socioeconomic status. RESULTS: Adolescent current smokers who were exposed to SHS at home 1 to 4 and 5 to 7 days/wk were 50% (95% confidence interval [CI]: 3%-121%) and 77% (95% CI: 5%-199%) more likely, respectively, to report respiratory symptoms compared with those who were unexposed (P = .01 for trend). The corresponding figures for exposure outside home were 41% (95% CI: 3%-94%) and 85% (95% CI: 31%-161%; P = .004 for trend). Such associations were also observed among never-smokers, but they were weaker than those among current smokers (P = .01 for interaction). CONCLUSIONS: This is the first evidence that SHS exposure is associated with increased risks for persistent respiratory symptoms among adolescent current smokers. Health promotion programs should aim at SHS reduction as well as smoking cessation among adolescent smokers.

Lao XQ; Jiang CQ; Sen Zhang W; Adab P; Lam TH; Cheng KK et al. Smoking, smoking cessation and inflammatory markers in older Chinese men: The Guangzhou Biobank Cohort Study. Atherosclerosis 203(1): 304-310, 2009. (30 refs.)

Aims: Smoking increases the risk of cardiovascular disease and inflammation plays a key role in the process of atherosclerosis. We therefore study the role of smoking and smoking cessation on the levels of inflammatory markers, C-reactive protein (CRP) and white blood cell (WBC) count, in older Chinese men. Methods: This cross-sectional analysis included 2999 men aged 50-85 years who received a medical check-up including measurement of fasting plasma vascular risk factors. Information on smoking status, socioeconomic and lifestyle factors was collected by standardized interview. Results: After adjustment for potential confounders, both CRP and WBC increased linearly across never. former and current smokers (both p < 0.01). The odds ratios of elevated CRP and WBC (upper tertiles) were also increased across never, former and current smokers (both p < 0.01). Dose-response relationships were observed among current smokers. Compared to current smokers, the odds ratios of elevated CRP and WBC and means of CRP and WBC declined with longer duration of smoking cessation (all p < 0.01). Conclusions: Smoking is associated with increased CRP and WBC levels, and smoking cessation is associated with the reduction of the increase, confirming the benefits of quitting. Inflammation may be a potential mechanism by which smoking promotes atherosclerotic disease.

Lee CH; Chuang HY; Hong CH; Huang SK; Chang YC; Ko YC et al. Lifetime exposure to cigarette smoking and the development of adult-onset atopic dermatitis. British Journal of Dermatology 164(3): 483-489, 2011. (38 refs.)

Background: Adult-onset atopic dermatitis (AD) has recently been recognized as a distinct disease entity, but its risk factors have not yet been clearly defined. Although gestational and perinatal exposure to tobacco smoking may be associated with the development of classic AD, the association between active/passive smoking and adult-onset AD remains controversial. Objectives: To determine if exposure to smoking, including environmental tobacco smoke (ETS), is associated with the risk of adult-onset AD. Methods: Tobacco smoking and exposure to ETS were measured in a case-control association analysis in 83 patients with physician-diagnosed adult-onset AD and 142 age- and sex-matched controls. Results: Multiple logistic regression analyses showed that, among the potential environmental risk factors, both current and ever smoking were significant risk factors for adult-onset AD [odds ratio (OR) 4:994 and 3:619, respectively], compared with never smoking. Also, packs per year was significantly associated with adult-onset AD (OR 1. 058, 95% confidence interval 1:028-1:089), suggesting a lifelong cumulative risk in current smokers. Moreover, nonsmokers with adult-onset AD reported significantly more exposure to ETS. Conclusions: Early and/or current exposure to cigarette smoking may contribute cumulatively to the development of adult-onset AD. Exposure to ETS in childhood is associated with the development of adult-onset AD. Adults should be discouraged from smoking to prevent adult-onset AD in themselves and their family members.

Lee PN; Fry JS. Systematic review of the evidence relating FEV1 decline to giving up smoking. (review). BMC Medicine 8: e-article 84, 2010. (264 refs.)

Background: The rate of forced expiratory volume in 1 second (FEV1) decline ("beta") is a marker of chronic obstructive pulmonary disease risk. The reduction in beta after quitting smoking is an upper limit for the reduction achievable from switching to novel nicotine delivery products. We review available evidence to estimate this reduction and quantify the relationship of smoking to beta. Methods: Studies were identified, in healthy individuals or patients with respiratory disease, that provided data on beta over at least 2 years of follow-up, separately for those who gave up smoking and other smoking groups. Publications to June 2010 were considered. Independent beta estimates were derived for four main smoking groups: never smokers, ex-smokers (before baseline), quitters (during follow-up) and continuing smokers. Unweighted and inverse variance-weighted regression analyses compared betas in the smoking groups, and in continuing smokers by amount smoked, and estimated whether beta or beta differences between smoking groups varied by age, sex and other factors. Results: Forty-seven studies had relevant data, 28 for both sexes and 19 for males. Sixteen studies started before 1970. Mean follow-up was 11 years. On the basis of weighted analysis of 303 betas for the four smoking groups, never smokers had a beta 10.8 mL/yr (95% confidence interval (CI), 8.9 to 12.8) less than continuing smokers. Betas for ex-smokers were 12.4 mL/yr (95% CI, 10.1 to 14.7) less than for continuing smokers, and for quitters, 8.5 mL/yr (95% CI, 5.6 to 11.4) less. These betas were similar to that for never smokers. In continuing smokers, beta increased 0.33 mL/yr per cigarette/day. Beta differences between continuing smokers and those who gave up were greater in patients with respiratory disease or with reduced baseline lung function, but were not clearly related to age or sex. Conclusion: The available data have numerous limitations, but clearly show that continuing smokers have a beta that is dose-related and over 10 mL/yr greater than in never smokers, ex-smokers or quitters. The greater decline in those with respiratory disease or reduced lung function is consistent with some smokers having a more rapid rate of FEV1 decline. These results help in designing studies comparing continuing smokers of conventional cigarettes and switchers to novel products.

Lovasi GS; Roux AVD; Hoffman EA; Kawut SM; Jacobs DR; Barr RG. Association of environmental tobacco smoke exposure in childhood with early emphysema in adulthood among nonsmokers. American Journal of Epidemiology 171(1): 54-62, 2010. (39 refs.)

Mechanical stress to alveolar walls may cause progressive damage after an early-life insult such as exposure to environmental tobacco smoke (ETS). This hypothesis was examined by using data from the Multi-Ethnic Study of Atherosclerosis (MESA), a population-based cohort aged 45-84 years, free of clinical cardiovascular disease, recruited from 6 US sites in 2000-2002. The MESA-Lung Study assessed a fractal, structural measure of early emphysema ("alpha," lower values indicate more emphysema) and a standard quantitative measure ("percent emphysema") from cardiac computed tomography scans. Childhood ETS exposure was assessed retrospectively as a report of living with one or more regular indoor smokers. Analyses included 1,781 nonsmokers (< 100 cigarettes, 20 cigars, or 20 pipefulls in their lifetime and urinary cotinine levels < 100 ng/mL); mean age was 61 years (standard deviation, 10), and 65% were women. Childhood ETS exposure from 2 or more smokers (17%) compared with none (52%) was associated with 0.05 lower alpha and 2.8 higher percent emphysema (P for trend = 0.04 and 0.01, respectively) after adjustment for demographic, anthropometric, parental, and participant characteristics, as well as adult exposures (e.g., cumulative residential air pollution exposure, exposure to ETS as an adult). Childhood ETS exposure was associated with detectable differences on computed tomography scans of adult lungs of nonsmokers.

Mon A; Durazzo TC; Gazdzinski S; Meyerhoff DJ. The impact of chronic cigarette smoking on recovery from cortical gray matter perfusion deficits in alcohol dependence: Longitudinal arterial spin labeling MRI. Alcoholism: Clinical and Experimental Research 33(8): 1314-1321, 2009. (54 refs.)

Background: Neuroimaging studies reported cerebral perfusion abnormalities in individuals with alcohol use disorders. However, no longitudinal magnetic resonance imaging (MRI) studies of cerebral perfusion changes during abstinence from alcohol have been reported. Methods: Arterial spin labeling MRI was used to evaluate cortical gray matter perfusion changes in short-term abstinent alcohol dependent individuals in treatment and to assess the impact of chronic cigarette smoking on perfusion changes during abstinence. Seventy-six patients were scanned at least once. Data from 19 non-smoking (17 males, 2 females) and 22 smoking (21 males, 1 female) patients scanned at 1 and 5 weeks of abstinence were used to assess perfusion changes over time. Twenty-eight age-equated healthy controls (25 males, 3 females) were scanned for cross-sectional comparison, 13 of them were scanned twice. Given the age range of the cohort (28 to 68 years), age was used as a covariate in the analyses. Mean perfusion was measured in voxels of at least 80% gray matter in the frontal and parietal lobes and related to neurocognitive and substance use measures. Results: At 1 week of abstinence, frontal and parietal gray matter perfusion in smoking alcoholics was not significantly different from that in non-smoking alcoholics, but each group's perfusion values were significantly lower than in controls. After 5 weeks of abstinence, perfusion of frontal and parietal gray matter in non-smoking alcoholics was significantly higher than that at baseline. However, in smoking alcoholics, perfusion was not significantly different between the time-points in either region. The total number of cigarettes smoked per day was negatively correlated with frontal gray matter perfusion measured at 5 weeks of abstinence. Lobar perfusion measures did not correlate significantly with drinking severity or cognitive domain measures at either time-point. Conclusion: Although cerebral perfusion in alcohol dependent individuals shows improvement with abstinence from alcohol, cigarette smoking appears to hinder perfusion improvement.

Moraros J; Bird Y; Chen S; Buckingham R; Meltzer RS; Prapasiri S et al. The impact of the 2002 Delaware smoking ordinance on heart attack and asthma. International Journal of Environmental Research and Public Health 7(12): 4169-4178, 2010. (22 refs.)

In the United States, smoking is the leading cause of death - having a mortality rate of approximately 435,000 people in 2000-accounting for 8.1% of all US deaths recorded that year. Consequently, we analyzed the Delaware Hospital Discharge Database, and identified state and non-state residents discharged with AMI or asthma for the years 1999 to 2004. Statistical data analysis compared the incidence of AMI or asthma for each group before (1999-2002) and after (2003-2004) the amendment. As a result, we found that pre-ordinance and post-ordinance quarterly rates of AMI for Delaware residents were 451 (se = 21) and 430 (se = 21) respectively, representing a 4.7% reduction. Over the same time period, there was negligible change in the incidence of AMI for non-Delaware residents. After adjusting for population growth, the Risk Ratio (RR) for asthma in Delaware residents post-ordinance was 0.95 (95% CI, 0.90 to 0.999), which represented a significant reduction (P = 0.046). By comparison, non-Delaware residents had an increased RR for asthma post-ordinance of 1.62 (95% CI, 1.46 to 1.86; P < 0.0001). The results suggest that Delaware's comprehensive non-smoking ordinance effectively was associated with a statistically significant decrease in the incidence of AMI and asthma in Delaware residents when compared to non-Delaware residents.

Nardini S; Baghiris C. Inflammation in COPD and tobacco smoking. (commentary). Multidisciplinary & Respiratory Medicine 4(1): 71-72, 2009. (11 refs.)

Pan WC; Chen RM; Shen YC; Chen CC; Ueng YF. Suppressive effect of tobacco smoke extracts on oral P-glycoprotein function and its impact in smoke-induced insult to oral epidermal cells. Toxicology Letters 185(2): 116-123, 2009. (39 refs.)

P-glycoprotein (Pgp) participates in the export of numerous toxins, drugs, and physiological compounds. To examine the involvement of Pgp in smoke-induced oral cell insult, the effects of extracts of the mainstream tobacco smoke (TS) on Pgp were studied in an oral epidermal carcinoma cell line, OECM-1. TS was first extracted with cyclohexane (CTS) and the residues were further extracted with isopropanol (ITS). For comparison, cells were exposed to CTS and ITS at the concentrations according to their relative extraction yield. ITS but not CTS decreased the efflux of a Pgp substrate. rhodamine (Rh) 123, in a concentration-and time-dependent manner. The efflux was also decreased by co-exposure to CTS and ITS. However, immunoblot analysis revealed that the protein level of Pgp was not affected by ITS. Naphthalene, mainly detected in the ITS, decreased Rh 123 efflux. However, the efflux activity was not affected by benzo(a)pyrene and nicotine, which were present in the CTS and both extracts, respectively. Co-exposure to CTS in combination with ITS, naphthalene, or verapamil enhanced cell insult compared to single exposure. These results demonstrated that smoke and its constituent, naphthalene, diminished Pgp-mediated efflux. The reduction in Pgp function could be a stimulatory factor of TS-induced oral cell insult.

Radzeviciene L; Ostrauskas R. Smoking habits and the risk of type 2 diabetes: A case-control study. Diabetes & Metabolism 35(3): 192-197, 2009. (38 refs.)

Aim. - The objective of the study was to assess the relationship between smoking and the risk of type 2 diabetes. Subject and methods. - This case-control study included 234 cases with newly confirmed diagnoses of type 2 diabetes and 468 controls who were free of the disease in 2001. Cases and controls were matched by gender and age (+/-5 years). A questionnaire was used to collect information on the possible risk factors of type 2 diabetes. Clinical measurements were taken in accordance with the recommendations of the WHO. Fasting plasma glucose and triglycerides were also measured, and the glucose tolerance test was performed in the controls. The odds ratios (OR) and 95% confidence intervals (CI) for type 2 diabetes were calculated using conditional logistic regression. Results. - The diabetes cases had significantly less education, more first-degree relatives with a positive family history of diabetes and higher body mass index (BMI) scores compared with the controls. Also, after adjusting for possible confounders, an increased risk of type 2 diabetes was determined for current smokers (OR = 2.4 1; 95% Cl 1.07-5.44) vs. non-smokers. In addition, there was an association between the disease and duration of smoking (OR = 2.47; 95% CI 1.03-5.93 for 40 years or more) vs. non-smokers, and those who had been smokers for 10 or more pack-years had twice the risk of diabetes (OR = 2.17; 95% CI 1.07-4.40) vs. non-smokers. There were no significant associations found between the risk of type 2 diabetes and number of cigarettes smoked per day or stopping smoking. Conclusion. - Our data confirms that smoking may be an independent risk factor for type 2 diabetes.

Sanders AE; Slade GD; Beck JD; Agustsdottir H. Secondhand smoke and periodontal disease: Atherosclerosis Risk in Communities Study. American Journal of Public Health 101(1, supplement): S339-S346, 2011. (37 refs.)

Objectives. We investigated the relationship between secondhand smoke and periodontal disease in nonsmokers. Methods. We undertook a cross-sectional analysis of the Atherosclerosis Risk in Communities study with 2739 lifetime nonsmokers aged 53-74 years, unexposed to other sources of tobacco, who received a complete periodontal examination at visit 4. Exposure was reported as average hours per week in close contact with a smoker in the preceding year. We defined severe periodontitis as 5 or more periodontal sites with probing pocket depth of 5 millimeters or more and clinical attachment levels of 3 millimeters or more in those sites. Other outcomes were extent of periodontal probing depths of 4 millimeters or more and extent of clinical attachment levels of 3 millimeters or more. Results. In a binary logistic regression model, adjusted odds of severe periodontitis for those exposed to secondhand smoke 1 to 25 hours per week increased 29% (95% confidence interval = 1.0, 1.7); for those exposed to secondhand smoke 26 hours per week, the odds were twice as high (95% confidence interval = 1.2, 3.4) as for those who were unexposed. Conclusions. Exposure to secondhand smoke and severe periodontitis among nonsmokers had a dose-dependent relationship.

Sarma AV; Jacobson DJ; Sauver JLS; Lieber MM; Girman CJ; Nehra A et al. Smoking and acute urinary retention: The Olmsted County Study of urinary symptoms and health status among men. Prostate 69(7): 699-705, 2009. (20 refs.)

BACKGROUND. Previous reports have suggested an inverse relationship between smoking and surgery for benign prostatic hyperplasia (BPH). We hypothesized that acute urinary retention (AUR), an adverse outcome of this disease and indication for surgical treatment, may be related to smoking. METHODS. Study subjects were randomly selected from Olmsted County men aged 40-79 identified through the Rochester Epidemiology Project. Of the 3,854 eligible men, 2,089 (54%) completed a questionnaire that included the American Urological Association Symptom Score and assessed smoking status. Community medical records were examined for occurrence of AUR with documented catheterization in the subsequent 10 years and occurrence of BPH surgery. Proportional hazard models were used to assess the relationship between baseline smoking status and subsequent retention. RESULTS. In the 18,307 person-years of follow-up, 114 men had AUR. When compared to 727 never-smokers, there was a trend among the 336 current smokers to be at lower risk (Relative risk (RR) = 0.62, 95% Confidence Interval (CI) = 0.33, 1.18) whereas the 1,026 former smokers were at similar risk to non-smokers (RR = 1.0, 95%CI = 0.67,1.46). Among men with moderate-severe symptoms at baseline, current smokers were at lower risk of retention compared to nonsmokers (RR = 0.65, 95%CI = 0.22, 1.91) but the association approached the null among those with none-mild symptoms (RR = 0.91, 95% CI = 0.40, 2.06). CONCLUSIONS. Community-dwelling men who currently smoke may be at a modestly reduced risk of AUR. The magnitude of this association is sufficiently small that it seems unlikely that this explains a sizable proportion of the inverse association between smoking and surgically treated BPH.

Self TH; Wallace JL; Gray LA; Usery JB; Finch CK; Deaton PR. Are we failing to document adequate smoking histories? A brief review 1999-2009. (review). Current Medical Research and Opinion 26(7): 1691-1696, 2010. (25 refs.)

Background: Documenting a detailed smoking history is of obvious importance. Failure to adequately document the smoking history may result in the misdiagnosis and management of asthma, and may be associated with a deficiency of care in patients with cardiovascular disease and several other common diseases. Scope: The purpose of this article is to review the evidence over the past decade that demonstrates inadequate documentation of smoking history. A literature search of English language journals from 1999 to 2009 was completed using several databases, including PubMed, MEDLINE, EMBASE, and SCOPUS. Findings: Fourteen studies demonstrated inadequate documentation of smoking histories by primary care clinicians, specialists, residents, and medical students. Failure to document smoking histories was observed in patients with conditions such as heart failure, coronary artery disease, and asthma. Electronic decision support systems and simple medical record reminders were effective in improving the documentation of smoking histories. Conclusions: Failure to adequately document the smoking history appears to be common. Strategies such as electronic decision support systems are needed to correct this problem in order for patients to receive optimal therapy for their appropriate diagnoses.

Shimada S; Hasegawa K; Wada H; Terashima S; Satoh-Asahara N; Yamakage H et al. High blood viscosity is closely associated with cigarette smoking and markedly reduced by smoking cessation. Circulation Journal 75(1): 185-189, 2011. (14 refs.)

Background: Cigarette smoking is an independent risk factor for cardiovascular events such as myocardial infarction and stroke. To date, a useful and convenient method of predicting such events in smokers has not been established. The rheological properties of blood assessed by the microchannel method reflect the blood's viscosity and the state of microthrombus formation, which may predict cardiovascular thrombotic events. Methods and Results: Blood fluidity was assessed in 74 smoking patients (54 men, 20 women, mean age 57.9 years) by measuring the blood passage time (BPT) in an aliquot (100 mu l) of blood using the Micro Channel Array Flow Analyzer. BPT was significantly related with smoking variables such as daily consumption of tobacco (r=0.236, P=0.044), Brinkman's index (r=0.252, P=0.033), the Fagerstrom Test for Nicotine Dependence (r=0.257, P=0.029), and the score of a self-rating depression scale (r=0.236, P<0.05). Multivariate regression analysis revealed that an independent BPT determinant was daily consumption of tobacco (r=0.326, P=0.045). Furthermore, smoking cessation markedly decreased BPT from 63.0 s to 49.7 s (P=0.002) at 3 months after the start of therapy. Conclusions: Unfavorable blood rheology is closely associated with cigarette smoking and may reflect increased cardiovascular risk in smokers. The study results also suggest that such risk can be reduced after only 3 months of smoking cessation.

Smith K; Flicker L; Dwyer A; Atkinson D; Almeida OP; Lautenschlager NT et al. Factors associated with dementia in Aboriginal Australians. Australian and New Zealand Journal of Psychiatry 44(10): 888-893, 2010. (22 refs.)

Objective: Although the prevalence of dementia in remote living Aboriginal Australians is one of the highest in the world, the factors associated with dementia in this population are yet to be examined. This study was designed to determine the demographic, lifestyle and clinical factors associated with dementia in Aboriginal Australians living in the Kimberley region of Western Australia. Method: A total of 363 Aboriginal Australians aged over 45 years from the Kimberley region were selected by semi-purposeful sampling. The factors analysed for association with dementia were age, sex, education, smoking, chewing tobacco, alcohol, head injury, heart disease, hypertension, diabetes, previous stroke, epilepsy, falls, mobility, incontinence, urinary problems, vision and hearing. This exposure data was collected from participants' and informants' reports using the Kimberley Indigenous Cognitive Assessment and specialist review, and medical records. Results: Factors associated with dementia included older age, male gender (OR 3.1, 95% 1.4, 6.8) and no formal education (OR 2.7, 95%CI 1.1, 6.7) and after adjusting for age, sex and education, dementia was associated with current smoking (OR 4.5, 95%CI 1.1, 18.6), previous stroke (OR 17.9, 95%CI 5.9, 49.7), epilepsy (OR 33.5, 95%CI 4.8, 232.3), head injury (OR 4.0, 95%CI 1.7, 9.4), and poor mobility, incontinence and falls. Conclusions: Interventions aimed at better management or prevention of the modifiable factors identified could reduce dementia risk in Aboriginal populations.

Tamaki J; Iki M; Fujita Y; Kouda K; Yura A; Kadowaki E et al. Impact of smoking on bone mineral density and bone metabolism in elderly men: the Fujiwara-kyo Osteoporosis Risk in Men (FORMEN) study. Osteoporosis International 22(1): 133-141, 2011. (40 refs.)

Our cross-sectional analysis of 1,576 men aged a parts per thousand yen65 years examined smoking effects on bone status. Number of smoking years was associated with decreased bone mineral density (BMD), after adjusting for age, height, weight, and number of cigarettes smoked daily. Smoking did not affect biochemical marker serum values for bone turnover. The impact of smoking on bone status in men has not been conclusively established. We examined how smoking and its cessation influence bone status and metabolism in men. We analyzed 1,576 men among a baseline survey of Japanese men aged a parts per thousand yen65 years, the Fujiwara-kyo Osteoporosis Risk in Men study, conducted during 2007-2008. Lumbar spine (LS) BMD values among never, former, and current smokers were 1.045 +/- 0.194, 1.030 +/- 0.189, and 1.001 +/- 0.182 g/cm(2) (P = 0.005), respectively, while total hip (TH) BMD values were 0.888 +/- 0.120, 0.885 +/- 0.127, and 0.870 +/- 0.124 (P = 0.078), respectively. The significant trend for LS BMD remained after adjusting for the covariates; age, height, weight, physical activity, milk consumption, and drinking habit (P = 0.036). Among never and ever (current and former) smokers, LS and TH BMD decreased with the number of pack years or the number of smoking years, respectively, adjusted for those covariates. Among ever smokers, LS and TH BMD decreased with the number of smoking years after adjusting for age, height, weight, and number of cigarettes smoked daily. Smoking did not reveal significant effect for serum osteocalcin or tartrate resistant acid phosphatase isoenzyme 5b. The impact of smoking on bone status is mainly associated with the number of smoking years in elderly men.

Toljamo T; Kaukonen M; Nieminen P; Kinnula VL. Early detection of COPD combined with individualized counselling for smoking cessation: A two-year prospective study. Scandinavian Journal of Primary Health Care 28(1): 41-46, 2010. (38 refs.)

Objective. Though the prevalence of COPD is related to the definition, even with this proviso COPD remains under-diagnosed. Screening can detect many new COPD cases, but its effects on smoking cessation remain unknown. Design. To evaluate symptoms in "healthy" cigarette smokers, to screen new COPD cases using international and national guidelines, and to assess the success of a smoking cessation. Subjects. Healthy asymptomatic smokers with a > 20 pack-years smoking history were recruited. The first visit included a standardized personal interview, Fagerstom nicotine dependence test (FNDT) and individualized smoking counselling by Motivational Interviewing. At the follow-up visit two years later, the same analyses were repeated and smoking status assessed. To avoid bias in the counselling attributable to spirometry, the test was evaluated at the two-year follow-up assessment. Results. Almost all, 93.2%, of 584 participants attended the second visit. Spirometry revealed COPD by GOLD criteria in 11.0% and by national guidelines in 15.3%, mid-expiratory flow (MEF50) had significantly declined in 19.5%, chronic cough or sputum production was detected in 62% of the subjects. After two years, 23.3% had succeeded in giving up smoking. There were four predictors of successful quitting, i.e. positive attitude to the intervention, pharmacotherapy, older age, and higher BMI, whereas other factors such as cough, obstruction, gender, pack-years, or nicotine dependence showed no association with ability to achieve successful cessation. Conclusion. Significant numbers of "healthy" smokers experience symptoms, according to detailed questionnaires, and have COPD. Motivation is the most significant factor in determining the chance of stopping smoking.

Tsuang D; Larson EB; Li G; Shofer JB; Montine KS; Thompson ML et al. Association between lifetime cigarette smoking and Lewy body accumulation. Brain Pathology 20(2): 412-418, 2010. (24 refs.)

Cigarette smoking has been associated repeatedly in observational studies with decreased risk of Parkinson's disease (PD), but its relationship to the risk of dementia or Alzheimer's disease (AD) is inconsistent. All of these studies have used clinical diagnoses of disease. We tested the hypothesis that lifetime cigarette use might be associated with reduced risk of neuropathologic changes of Lewy-related pathology (LRP) in multiple brain regions or with reduced risk of consensus neuropathologic changes of AD in a prospective community-based study of brain aging and dementia, the Adult Changes in Thought (ACT) study. We observed that heavy lifetime cigarette smoking (> 50 pack years) was associated with significantly reduced relative risk (RR) for LRP, but not AD-type pathologic changes, after correcting for selection bias, and with significantly reduced frequency of LRP in the substantia nigra. These findings are the first of which we are aware to associate reduced LRP in human brain with any exposure, and substantiate observational studies that have associated cigarette smoking with reduced risk of PD. Although cigarette smoking is too toxic to suggest as a treatment, if confirmed, these findings may guide future therapeutic strategies that attempt to suppress LRP in human brain by other means.

Unverdorben M; Mostert A; Munjal S; van der Bijl A; Potgieter L; Venter C et al. Acute effects of cigarette smoking on pulmonary function. Regulatory Toxicology and Pharmacology 57(2-3): 241-246, 2010. (42 refs.)

Introduction: Chronic smoking related changes in pulmonary function are reflected as accelerated decrease in FEV1 although histologic changes occur in the peripheral bronchi earlier. More sensitive pulmonary function parameters might mirror those early changes and might show a dose response. Methods: In a randomized three-period cross-over design 57 male adult conventional cigarette (CC)smokers (age: 45.1 +/- 7.1 years) smoked either CC (tar:11 mg, nicotine:0.8 mg, carbon monoxide:11 mg [Federal Trade Commission (FTC)]), or used as a potential reduced-exposure product the electrically heated smoking system (EHCSS) (tar:5 mg, nicotine:0.3 mg, carbon monoxide:0.45 mg (FTC)) or did not smoke (NS). After each 3-day exposure period, hematology and exposure parameters were determined preceding body plethysmography. Results: Cigarette smoke exposure was significantly (p < 0.0001) higher in CC than in EHCSS and in NS: (carboxyhemoglobin: CC: 6.4 +/- 1.9%; EHCSS: 1.3 +/- 0.6%; NS: 0.5 +/- 0.3%; serum nicotine: CC: 18.9 +/- 7.4 ng/ml; EHCSS: 8.4 +/- 4.3 ng/ml; NS: 1.2 +/- 1.6 ng/ml). Significantly lower in CC than in EHCSS and NS were specific airway conductance (0.22 +/- 0.09; 0.25 +/- 0.12; 0.25 +/- 0.1 1/cmH(2)O x s; CC vs EHCSS: p < 0.05; CC vs NS: p < 0.01), forced expiratory flow 25% (7.6 +/- 1.7; 7.8 +/- 1.7; 7.9 +/- 1.7 L/s; CC vs EHCSS or NS: p < 0.01). Thoracic gas volume (5.1 +/- 1; 5 +/- 1.1; 5 +/- 1.1 L/min) changed insignificantly. Conclusion: The data indicate acute and reversible effects of cigarette smoke exposures and no-smoking on mid to small size pulmonary airways in a dose dependent manner.

van der Heide F; Dijkstra A; Albersnagel FA; Kleibeuker JH; Dijkstra G. Active and passive smoking behaviour and cessation plans of patients with Crohn's disease and ulcerative colitis. Journal of Crohn's & Colitis 4(2): 125-131, 2010. (37 refs.)

Background: Smoking is a remarkable risk factor in inflammatory bowel disease (IBD), with negative effects on Crohn's disease (CD) and positive effects on ulcerative colitis (UC). This makes different changes in smoking behaviour after diagnosis between CD and UC likely. Changes in active smoking, cessation plans and passive smoking were studied in IBD patients. Methods: 820 IBD patients were sent a questionnaire on active and passive smoking, and cessation plans. A total of 675 (82%) patients (380 CD and 295 UC) responded. Results: More ever smoking UC patients stopped smoking before diagnosis than CD patients (63% vs 22%; p<0.001), resulting in 30% former smokers at diagnosis in UC and 13% in CD (p<0.001). The smoking cessation rates at and after diagnosis are equal between CD and UC. Half of the CD patients stopped smoking after diagnosis leading to less present smokers in CD than in a control population (26% (95% confidence interval: 21.1%-29.9%) vs 33%). For both CD (22% vs 35%; p = 0.044) and UC (24% vs 53%; p = 0.024) continuing smokers after diagnosis were less often higher educated than quitters. Cessation plans (89%), passive smoking in childhood and present passive smoking were not different between CD and UC patients. Conclusion: There are no differences in changes in smoking behaviour at and after diagnosis between CD and UC patients, suggesting a lack of knowledge in these patients about the link between their disease and smoking behaviour. However, CD patients seem less refractory to smoking cessation than the general population. Therefore it is worthwhile putting energy in helping CD patients stop smoking.

Virdis A; Giannarelli C; Neves MF; Taddei S; Ghiadoni L. Cigarette smoking and hypertension. (review). Current Pharmaceutical Design 16(23): 2518-2525, 2010. (99 refs.)

Cigarette smoking is a powerful cardiovascular risk factor and smoking cessation is the single most effective lifestyle measure for the prevention of a large number of cardiovascular diseases. Impairment of endothelial function, arterial stiffness, inflammation, lipid modification as well as an alteration of antithrombotic and prothrombotic factors are smoking-related major determinants of initiation, and acceleration of the atherothrombotic process, leading to cardiovascular events. Cigarette smoking acutely exerts an hypertensive effect, mainly through the stimulation of the sympathetic nervous system. As concern the impact of chronic smoking on blood pressure, available data do not put clearly in evidence a direct causal relationship between these two cardiovascular risk factors, a concept supported by the evidence that no lower blood pressure values have been observed after chronic smoking cessation. Nevertheless, smoking, affecting arterial stiffness and wave reflection might have greater detrimental effect on central blood pressure, which is more closely related to target organ damage than brachial blood pressure. Hypertensive smokers are more likely to develop severe forms of hypertension, including malignant and renovascular hypertension, an effect likely due to an accelerated atherosclerosis.

Walker SL; Saltman DL; Colucci R; Martin L. Awareness of risk factors among persons at risk for lung cancer, chronic obstructive pulmonary disease and sleep apnea: A Canadian population-based study. Canadian Respiratory Journal 17(6): 287-294, 2010. (33 refs.)

OBJECTIVE: To assess awareness among persons at risk for lung cancer, chronic obstructive pulmonary disease (COPD) and sleep apnea regarding symptoms and risk factors of the disease, and their attitudes regarding the disease and toward those who are affected. METHODS: A quantitative hybrid telephone and Internet survey of a representative population of Canadian adults at risk for at least one of the three diseases was conducted. To measure the awareness and attitudes of First Nations, Inuit and Metis people to these diseases, a proportionate number were also surveyed. RESULTS: A total of 3626 individuals were contacted. Of these, 3036 (84%) were eligible to participate. Of those at risk for lung cancer and COPD, 65% and 69%, respectively, were due to tobacco smoke exposure. Among those at risk, 72% believed that they were informed about lung cancer compared with 36% for COPD and 56% for sleep apnea. Most respondents were knowledgeable about the common symptoms of lung cancer, COPD and sleep apnea, but were less aware of the impact lifestyle choices could have on the development of these disorders and the availability of treatment. Most of the participants (77%) believed that smoking was an addiction rather than a habit (19%). There were no significant differences in the awareness of risk factors, symptoms and attitudes toward all three lung diseases between First Nations, Inuit and Metis people and the general population. CONCLUSIONS: Canadians are reasonably aware of risk factors and symptoms for lung cancer and sleep apnea. However, there is poor awareness of COPD as a disease entity. There is a lack of appreciation for the impact lifestyle choices and changes can have on lung diseases.

Weakley J; Webber MP; Gustave J; Kelly K; Cohen HW; Hall CB et al. Trends in respiratory diagnoses and symptoms of firefighters exposed to the World Trade Center disaster: 2005-2010. Preventive Medicine 53(6): 364-369, 2011. (14 refs.)

Objectives. To compare the prevalence of self-reported respiratory diagnoses in World Trade Center-exposed Fire Department of New York City firefighters to the prevalence in demographically similar National Health Interview Survey participants by year; and, 2) to describe the prevalence of World Trade Center-related symptoms up to 9 years post-9/11. Methods. We analyzed 45,988 questionnaires completed by 10.999 firefighters from 10/2/2001 to 9/11/2010. For comparison of diagnosis rates, we calculated 95% confidence intervals around yearly firefighter prevalence estimates and generated odds ratios and confidence intervals to compare the odds of diagnoses in firefighters to the National Health Interview Survey prevalence, by smoking status. Results. Overall. World Trade Center-exposed firefighters had higher respiratory diagnosis rates than the National Health Interview Survey; Fire Department of New York City rates also varied less by smoking status. In 2009, bronchitis rates in firefighters aged 45-65 were 13.3 in smokers versus 13.1 in never-smokers while in the National Health Interview Survey, bronchitis rates were doubled for smokers: 4.3 vs. 2.1. In serial cross-sectional analyses, the prevalence of most symptoms stabilized by 2005. at similar to 10% for cough to similar to 48% for sinus. Conclusions. We found generally higher rates of respiratory diagnoses in World Trade Center-exposed firefighters compared to US males, regardless of smoking status. This underscores the impact of World Trade Center exposure and the need for continued monitoring and treatment of this population.

Wust RCI; Winwood K; Wilks DEC; Morse CI; Degens H; Rittweger J. Effects of smoking on tibial and radial bone mass and strength may diminish with age. Journal of Clinical Endocrinology and Metabolism 95(6): 2763-2771, 2010. (38 refs.)

Purpose: The purpose of the study was to assess the effect of cigarette smoking on indicators of bone strength across a wide age range, controlling for physical activity and neuromuscular performance. Methods: We conducted a cross-sectional study with 41 smokers (mean age +/- SD, 41.0 +/- 16.1 yr) and 53 nonsmokers (47.5 +/- 18.2 yr) of both sexes. Bone strength indicators (BSI) were assessed in the lower leg and forearm by peripheral quantitative computed tomography along with physical activity, muscle cross-sectional area, and maximal voluntary muscle force. Results: Physical activity level and muscle cross-sectional area of the leg and arm were similar in smokers and nonsmokers. Although trabecular volumetric bone mineral density and epiphyseal bone mineral content, both indicators of BSI, decreased with age in the nonsmokers' tibia (P < 0.001), this was not observed in the smokers (interaction age x smoking: P = 0.014 and P = 0.032 for density and content, respectively). Regression coefficients were nonsignificant in nonsmokers, whereas coefficients in smokers were -1.24 mg/cm . yr [95% confidence interval (CI) = -2.16-0.33; P = 0.01] for content and -1.20 mg/cm(3) . yr (95% CI = -1.76-0.62; P < 0.001) for trabecular density. The BSI values in the smokers were independent of their smoking history (r(2) = 0.000-0.021), and no effects of sex were observed in the smoking-related differences in BSI. Conclusions: Smoking compromises bone strength by diaphyseal marrow cavity expansion and epiphyseal trabecular bone content reductions. These effects seem to wane with age. The causes of the attenuated effect of smoking on bone at old age remain enigmatic but might be linked to an interaction between the smoke-related factors and senescence processes affecting bone.

Yacoub R; Habib H; Lahdo A; Al Ali R; Varjabedian L; Atalla G et al. Association between smoking and chronic kidney disease: A case control study. BMC Public Health 10: e-article 731, 2010. (42 refs.)

Background: The progression of chronic kidney disease (CKD) remains one of the main challenges in clinical nephrology. Therefore, identifying the pathophysiological mechanisms and the independent preventable risk factors helps in decreasing the number of patients suffering end stage renal disease and slowing its progression. Methods: Smoking data was analyzed in patients with CKD throughout 2005-2009. One hundred and ninety-eight patients who had recently been diagnosed with stage three CKD or higher according to the National Kidney Foundation (NKF) 2002 Classification were studied. The control group was randomly selected and then matched with the case subjects using a computerized randomization technique. The relative risk was estimated by computing odds ratio (OR) by using multinomial logistic regression in SPSS (R) for Windows between the two groups. Results: Smoking significantly increases the risk of CKD (OR = 1.6, p = 0.009, 95% CI = 1.12-2.29). When compared to nonsmokers, current smokers have an increased risk of having CKD (OR = 1.63 p = 0.02, 95% CI = 1.08-2.45), while former smokers did not have a statistically significant difference. The risk increased with high cumulative quantity (OR among smokers with > 30 pack-years was 2.6, p = 0.00, 95% CI = 1.53-4.41). Smoking increased the risk of CKD the most for those classified as hypertensive nephropathy (OR = 2.85, p = 0.01, 95% CI = 1.27-6.39) and diabetic nephropathy (2.24, p = 0.005, 95% CI = 1.27-3.96). No statistically significant difference in risk was found for glomerulonephritis patients or any other causes. Conclusion: This study suggests that heavy cigarette smoking increases the risk of CKD overall and particularly for CKD classified as hypertensive nephropathy and diabetic nephropathy.

Yang JL; Hammond D; Driezen P; Fong GT; Jiang YA. Health knowledge and perception of risks among Chinese smokers and non-smokers: Findings from the Wave 1 ITC China Survey. Tobacco Control 19(Supplement 2): i18, 2010. (25 refs.)

Background Awareness of health risks of smoking is strongly associated with smoking behaviour. However, there are no population-based studies of smoking-related health knowledge in China. Objective The aim of current study was to use a population-based sample from the International Tobacco Control China Wave 1 survey to examine variations between current, former and never smokers' health knowledge about smoking and the impact of health knowledge awareness on smokers' intention to quit. Methods A face-to-face interview was conducted with 5986 adult smokers and non-smokers from six cities in China. Respondents were asked whether they believed smoking causes heart disease, stroke, impotence, lung cancer, emphysema, stained teeth, premature ageing in smokers and lung cancer in non-smokers. Current smokers were also asked additional questions on how smoking affects their current and future health as well as whether they had plans to quit smoking and if they believe they would have health benefit from quitting. Findings The overall awareness of health risks of smoking in China was low compared to developed countries. Current smokers in China were less likely than non-smokers and former smokers to acknowledge the consequences of smoking. Current smokers who were more aware of the health consequences of smoking were more likely to intend to quit smoking. Conclusion These findings highlight the need to increase awareness about the health effects of smoking in China, particularly among current smokers to increase quitting.

Yang Y; Wang JJ; Wang CX; Li QA; Yang GH. Awareness of tobacco-related health hazards among adults in China. Biomedical and Environmental Sciences 23(6): 437-444, 2010. (14 refs.)

Objective To determine the level of awareness of the hazards of tobacco smoking and secondhand smoke inhalation among adults in China. Methods Household surveys were conducted with a total of 13 354 respondents aged 15 years or over from 100 counties of 28 Chinese provinces using a stratified multi-stage geographically clustered sample design. Results The findings revealed that 81.8% of the population was aware that smoking causes serious diseases, and 27.2% and 38.7% were aware that smoking causes stroke and heart attack, respectively. Only 64.3% of respondents were aware that secondhand smoke can cause serious diseases, and 27.5%, 51.0%, and 52.6% were aware that secondhand smoke causes heart disease in adults, lung disease in children and lung cancer in adults, respectively. Awareness regarding smoking-related hazards across all participants was significantly associated with several factors, including gender, smoking status, urban/rural residency, education level and exposure to tobacco control publicity in the last 30 days. Awareness regarding tobacco-related hazards in smokers was significantly associated with urban/rural residency, education level, exposure to tobacco control publicity in the last 30 days, and physician's advice. Awareness relating to the hazards of inhaling secondhand smoke was associated with smoking status, urban/rural residency, age, education level, and exposure to tobacco control publicity in the last 30 days. Medical professionals were found to know more about the health hazards of tobacco compared with people in other types of employment. Conclusions Overall awareness of the health hazards of tobacco has improved in the last 15 years in China, but is still relatively poor. Improved means of communicating information and more effective warning labels on cigarette packaging are necessary for increasing public awareness of tobacco hazards, particularly among rural residents and people with less education.

Yu RJ; Zhao LY; Lu L. Regional grey and white matter changes in heavy male smokers. PLoS ONE 6(11): e-article 27440, 2011. (34 refs.)

Cigarette smoking is highly prevalent in the general population but the effects of chronic smoking on brain structures are still unclear. Previous studies have found mixed results regarding regional grey matter abnormalities in smokers. To characterize both grey and white matter changes in heavy male smokers, we investigated 16 heavy smokers and 16 matched healthy controls, using both univariate voxel-based morphometry (VBM) and multivariate pattern classification analysis. Compared with controls, heavy smokers exhibited smaller grey matter volume in cerebellum, as well as larger white matter volume in putamen, anterior and middle cingulate cortex. Further, the spatial patterns of grey matter or white matter both discriminated smokers from controls in these regions as well as in other brain regions. Our findings demonstrated volume abnormalities not only in the grey matter but also in the white matter in heavy male smokers. The multivariate analysis suggests that chronic smoking may be associated with volume alternations in broader brain regions than those identified in VBM analysis. These results may better our understanding of the neurobiological consequence of smoking and inform smoking treatment.

Agnihotri R; Pandurang P; Kamath SU; Goyal R; Ballal S; Shanbhogue AY et al. Association of cigarette smoking with superoxide dismutase enzyme levels in subjects with chronic periodontitis. Journal of Periodontology 80(4): 657-662, 2009. (29 refs.)

Background: Smoking, which is an important risk factor for periodontitis, induces oxidative stress in the body and causes an imbalance between reactive oxygen species (ROS) and antioxidants, such as superoxide dismutase (SOD). In the present study, the influence of smoking on the periodontium was determined by estimating the levels of SOD in light and heavy smokers with periodontitis. Methods: Seventy subjects in the age range of 20 to 55 years, including 60 smokers and 10 non-smokers (controls), were selected. Clinical parameters recorded were plaque index (PI), probing depth (PD), and attachment loss (AL). Smokers were divided into light smokers (<10 cigarettes/day) and heavy smokers ( >= 10 cigarettes/day) and into three subgroups: healthy, mild periodontitis, and moderate periodontitis. Gingival crevicular fluid (GCF) and saliva samples were collected. SOD levels were analyzed using spectrophotometric assay. Results: The mean levels of SOD in the GCF and saliva of smokers were decreased compared to controls. Intra- and intergroup analyses showed a significant reduction in the levels of SOD in the GCF and saliva of heavy smokers compared to light smokers and the control group. Conclusions: There was a progressive reduction in SOD levels from healthy non-smokers to light smokers to heavy smokers. These findings. high light the need to augment the efforts of smoking-cessation programs. The benefits of reduced smoking and improved antioxidant levels may motivate smoking cessation.

Zvolensky MJ; McMillan KA; Gonzalez A; Asmundson GJG. Chronic musculoskeletal pain and cigarette smoking among a representative sample of Canadian adolescents and adults. Addictive Behaviors 35(11): 1008-1012, 2010. (35 refs.)

The present investigation sought to examine the relation between specific types of chronic musculoskeletal pain and cigarette smoking among a large representative sample of adolescents and adults residing in Canada. Specifically, we examined the relations between chronic back pain, arthritis, and daily smoking status. As predicted, individuals with chronic back pain were more likely to smoke than those without chronic back pain or arthritis; this association remained significant after controlling for sociodemographics and any lifetime anxiety or mood disorder. An opposite, albeit less robust, association was evident for the prescence of lifetime arthritis and smoking. Future work is needed to better understand the mechanisms underlying the association between chronic pain and smoking.