Acute subjective and physiological responses to smoking in adolescents

Aims . To determine the topography of cigarette smoking and the subjective and physiological effects of abstinence and nicotine in adolescents who smoke on a daily versus a non-daily basis.
Design . Repeated measures experiment, non-blinded, involving a single test session.
Setting . Human psychopharmacology laboratory.
Participants . Twenty-one daily and 21 non-daily adolescent cigarette smokers (21 females; 21 males; age 13-18 years) with life-time use greater than 10 cigarettes, responding to radio and print advertisements.
Intervention . Overnight abstinence from cigarettes followed by smoking of a single cigarette furnished by the participant at test.
Measurements . The Fagerstrom Test for Nicotine Dependence, saliva nicotine and cotinine, expired air carbon monoxide (CO), heart rate (HR), self-report scales and smoking topography. Most measurements were performed before and after smoking.
Findings . Saliva nicotine, CO and HR increased, and self-reported intention and desire to smoke decreased, after smoking ( p < 0.001). Fagerstrom scores indicated greater dependence and desire to smoke in daily than in non-daily smokers. HR increased substantially over pre-smoking levels in both groups. Puff topography did not differ between the groups, although collectively these participants appeared to take smaller and more puffs than adult smokers tested under similar conditions.
Conclusion . This study provides initial evidence that adolescent cigarette smokers self-administer physiologically active doses of nicotine very early in their smoking careers. Nicotine dependence in adolescents appears to be a function of the current frequency of cigarette use, and subjective-behavioral consequences of abstinence and smoking are evident even in non-daily smokers.     

Acute effects of smoking and food consumption on breath condensate pH in healthy adults

Acute effects of food and cigarette consumption on exhaled breath condensate (EBC) acidity are insufficiently explored. The study aimed to evaluate potential changes in EBC pH within 2 hours following cigarette or food consumption. In 15 healthy smokers, samples were obtained after 10 hours of abstinence from smoking and then 15, 30, 60, and 120 minutes after smoking 1 cigarette. In 19 healthy nonsmoking adults, EBC samples were obtained in the morning after an overnight fast, and then 30, 60, and 120 minutes following standardized breakfast. Smoking of 1 cigarette after overnight tobacco abstinence induced significant increase in EBC pH during the 2-hour observation period, for approximately 0.60 logarithmic units (repeated-measures analysis of variance [ANOVA], P < .0001). The average presmoking pH value in smokers (7.00 ± 0.50) was significantly lower than average value in nonsmokers (7.62 ± 0.31; P = .0001). No effect of food consumption was found. These results show that cigarette smoking acutely increases EBC pH in healthy smokers. Smoking status and abstinence from smoking before EBC sampling seems to be important in studies evaluating EBC pH and should be standardized or at least stated in the methodology. Acute effects of food were not found under described study conditions in healthy adults.     

Smoking reduction and temporary abstinence: new approaches for smoking cessation

Tobacco use causes enormous morbidity and mortality because of the high risk of smoking-related diseases and the high prevalence of cigarette smoking. Existing smoking cessation methods only help motivated smokers who are ready to quit, but the vast majority of smokers are pre-contemplators who are neither ready nor willing to attempt to quit. This means that a high proportion of smokers are not adequately served by current strategies for treating tobacco dependence. As cigarettes prematurely kill 50% of long-term users, any additional measure that may reduce death or illness should be given serious consideration. Many addicted smokers are now forced to live and work much of their life in environments in which smoking is prohibited. Most smokers are dependent on nicotine and abstinence from smoking results in tobacco withdrawal and craving, which manifest as clinical symptoms within a few hours of smoking the last cigarette. Craving and withdrawal symptoms can be controlled by supplying nicotine from sources other than cigarettes, such as Nicotine Replacement Therapy (NRT). Clinical studies of short-term abstinence show that all NRT formulations relieve tobacco withdrawal symptoms and craving. Most unaided attempts to decrease health risks by reducing smoking fail because smokers revert to their 'usual' nicotine intake. However, using NRT to reduce smoking allows smokers to reduce their cigarette consumption (and intake of toxic substances in smoke) while maintaining their nicotine dose. Data suggest that smokers who use NRT can significantly reduce the withdrawal symptoms and craving caused by abstaining from cigarettes, and thereby reduce the number of cigarettes/day and maintain these reductions for up to 2 years. The data also indicate that, despite some compensatory smoking behaviour, reduced smoking with NRT results in decreased toxin exposure. In smoking reduction studies, this translated into an improvement in variables that impact on health: cardiovascular risk factors and haemorheology parameters moved towards more healthy (i.e. non-smoker) levels, and pulmonary function improved. The improvements in established cardiovascular risk factors provide objective proof that exposure reduction translates into clinically meaningful health benefits. Furthermore, the known reversibility of many smoking-induced diseases, the mainly linear dose-effect curve and the absence of any indication of threshold effects suggest that additional health benefits may result from smoking reduction. Even more importantly, smoking reduction may move smokers along the behavioural model towards the ultimate goal--stopping smoking. In all three large smoking reduction studies, a number of subjects who were unwilling or unable to stop smoking at baseline were abstinent at 4 months and 1 and 2 years, which clearly supports the concept of smoking reduction as a step towards abstinence. Rather than undermining cessation, smoking reduction appears to increase motivation to quit. The importance of allowing smokers to gradually take control of their smoking was reflected by the increasing point prevalence abstinence rates seen in the long-term studies. When encouraging smoking reduction, it should clearly be emphasised that complete cessation remains the ultimate goal, but smokers in the precontemplation stage need to progress along the behavioural model before becoming receptive to messages about quitting. In conclusion, the evidence presented in this review supports reduced smoking as a legitimate treatment approach that could be pursued by those smokers who are currently unable or unwilling to quit. Sustained smoking reduction can be achieved and maintained with NRT. The corresponding reduction in exposure is associated with tangible health benefits, measured using surrogate markers. Smoking reduction also promotes abstinence in smokers who are unable or unwilling to quit smoking abruptly. NRT is well tolerated for smoking reduction, and nicotine intake does not increase during concomitant use of NRT and smoking.     

The effects of acute exercise on attentional bias towards smoking-related stimuli during temporary abstinence from smoking

Rationale   Attentional bias towards smoking-related cues is increased during abstinence and can predict relapse after quitting. Exercise has been found to reduce cigarette cravings and desire to smoke during temporary abstinence and attenuate increased cravings in response to smoking cues.
Objective   To assess the acute effects of exercise on attentional bias to smoking-related cues during temporary abstinence from smoking.
Method   In a randomized cross-over design, on separate days regular smokers ( n  = 20) undertook 15 minutes of exercise (moderate intensity stationary cycling) or passive seating following 15 hours of nicotine abstinence. Attentional bias was measured at baseline and post-treatment. The percentage of dwell time and direction of initial fixation was assessed during the passive viewing of a series of paired smoking and neutral images using an Eyelink II eye-tracking system. Self-reported desire to smoke was recorded at baseline, mid- and post-treatment and post-eye-tracking task.
Results   There was a significant condition × time interaction for desire to smoke, F _(1,18) = 10.67, P  = 0.004, eta² = 0.36, with significantly lower desire to smoke at mid- and post-treatment following the exercise condition. The percentage of dwell time and direction of initial fixations towards smoking images were also reduced significantly following the exercise condition compared with the passive control.
Conclusion   Findings support previous research that acute exercise reduces desire to smoke. This is the first study to show that exercise appears to also influence the salience and attentional biases towards cigarettes.     

Efficacy of N-acetylcysteine in the treatment of nicotine dependence: a double-blind placebo-controlled pilot study

Relapse is the rule rather than the exception in smokers aiming to quit smoking. Recently, evidence has emerged that glutamate transmission plays an important role in relapse. N-acetylcysteine (NAC), a cysteine prodrug, restores glutamate homeostasis and appears to be a potential new treatment for substance dependence. In the current pilot study, the effects of NAC on short-term abstinence of smoking were investigated. Subjects were heavy smokers randomized to receive placebo (n = 12) or NAC 3,600 mg/day (n = 10) in a double-blind fashion during 3.5 days. Subjects were asked to stop smoking and report on nicotine craving, nicotine withdrawal symptoms, and cigarette smoking during treatment. At the end of the treatment, subjects were invited to smoke a cigarette and to rate the rewarding effect of this cigarette. There was no significant effect of NAC on craving (p = 0.23, d = 0.52) and only a statistical trend towards fewer withdrawal symptoms in the NAC condition (p = 0.07, d = 0.80). Interestingly, subjects receiving NAC rated the first cigarette after the abstinence period of 3.5 days as significantly less rewarding than subjects on placebo (p = 0.04, d = 0.85). It is concluded that the results of this pilot study are encouraging and suggest that NAC might be a promising new treatment option for relapse prevention in nicotine dependence.     

Smoking related carcinogen-DNA adducts in biopsy samples of human urinary bladder: identification of N-(deoxyguanosin-8-yl)-4-aminobiphenyl as a major adduct.

The prevalence of covalent modifications to DNA (carcinogen-DNA adducts) in 42 human urinary bladder biopsy samples was investigated by 32P-postlabeling methods, with enhancement by both nuclease P1 treatment and 1-butanol extraction. Total mean carcinogen-DNA adduct levels and the mean levels of several specific adducts were significantly elevated in DNA samples of 13 current smokers, as opposed to 9 never smokers or 20 ex-smokers (5 years abstinence). There was no significant difference between the latter two groups. Several DNA adducts enhanced by nuclease P1 treatment were chromatographically similar to putative hydrocarbon DNA adducts reported earlier for placenta and lung DNA samples obtained from cigarette smokers. Putative aromatic amine adducts were detected by 1-butanol extraction that were not present when the samples were treated with nuclease P1. One of these displayed chromatographic behavior identical to the predominant adduct induced by the human urinary bladder carcinogen, 4-aminobiphenyl, which is present in cigarette smoke. This adduct comigrated in several thin-layer chromatographic systems with a synthetic N-(deoxyguanosin-8-yl)-4-amino[2,2'-3H]biphenyl-3',5'-bisphosphate marker. Moreover, when this adduct was eluted from the thin-layer chromatograms of several individuals and injected onto an HPLC system, the 32P from the human bladder DNA samples coeluted in the same fraction as the tritiated synthetic N-(deoxyguanosin-8-yl)-4-aminobiphenyl marker. These data reinforce an association between cigarette smoking and DNA damage and suggest a molecular basis for the initiation of human urinary bladder cancer by cigarette smoke.     

Lymphocyte subsets in bronchoalveolar lavage fluid and in circulating blood in epidermoid bronchogenic carcinoma

Alveolar macrophages, lymphocyte and granulocyte percentages, together with OKT3+, OKT4+, OKT8+ lymphocyte subsets and OKT4+/OKT8+ ratio, were evaluated in bronchoalveolar lavage (BAL) fluid and in peripheral venous blood (PVB) of neoplastic and nonneoplastic subjects, in order to assess these aspects of immunity in neoplastic disease and to find out if the modifications in the bronchoalveolar environment are correlated to the ones in the circulation blood. BAL was performed in 30 patients undergoing fiberoptic bronchoscopy to ascertain the presence of lung cancer. Twelve of them had positive findings for epidermoid bronchogenic carcinoma, while in the remaining subjects the diagnosis was not confirmed. The 30 examined subjects were then grouped according to their smoking habit. In PVB, no significant difference was seen between neoplastic and nonneoplastic subjects, whereas in BAL the neoplastic patients showed a significant increase of lymphocytes OKT3+ and OKT8+. This tends to confirm that PVB is not a good indicator of organ immunity and may justify the reduced activity of alveolar macrophages in subjects affected by bronchogenic neoplasia. Between smokers and nonsmokers, lymphocyte subsets showed more significant differences than between neoplastic and nonneoplastic subjects (decrease of T4+ lymphocytes, increase of T8+ lymphocytes and, therefore, reduction of T4/T8 ratio); there were also scalar variations in the three groups (smokers with cancer, smokers without cancer and nonsmokers without cancer). Thus, the possible autonomous role of cigarette smoke and the presence of neoplasia in the immunity alterations of the alveolar environment with final joint effects were confirmed. These data may indicate a possible correlation between cigarette smoking, immunological alterations in BAL and the onset of bronchogenic carcinoma.     

An antisense oligodeoxynucleotide to growth hormone messenger ribonucleic acid inhibits lymphocyte proliferation

The role of GH in lymphocyte proliferation was studied by examining the effect of an antisense oligodeoxynucleotide (ODN) complementary to GH mRNA. The results of these studies showed that antisense GH ODN treatment inhibits lymphocyte production of immunoreactive GH (irGH). Lymphocytes treated with the GH antisense ODN produced less irGH than did lymphocytes treated with control sense GH ODN. Antisense GH ODN-mediated inhibition of irGH production resulted in a decrease in lymphocyte proliferation. Cells with the antisense GH ODN had less (87%) incorporation of [3H]thymidine [( 3H]TdR) in both resting and Concanavalin-A-stimulated lymphocytes, whereas the incorporation of [3H]TdR in cells treated with a control ODN was not significantly affected. The effect of the antisense ODN on [3H]TdR incorporation was specific, since it could be reversed by hybridization competition with a complementary GH sense ODN or by the addition of exogenous rat GH. Collectively, the data indicate that lymphocytes synthesize and secrete irGH and that irGH produced by these cells can stimulate proliferation, suggesting that GH may play an autocrine/paracrine role in lymphocyte replication.     

Patterns of change in withdrawal symptoms, desire to smoke, reward motivation and response inhibition across 3 months of smoking abstinence

Aims We have demonstrated previously that acute smoking abstinence is associated with lowered reward motivation and impaired response inhibition. This prospective study explores whether these impairments, along with withdrawal‐related symptoms, recover over 3 months of sustained abstinence. Design Participants completed a 12‐hour abstinent baseline assessment and were then allocated randomly to quit unaided or continue smoking. All were re‐tested after 7 days, 1 month and 3 months. Successful quitters' scores were compared with those of continuing smokers, who were tested after ad libitum smoking. Setting Goldsmiths, University of London. Participants A total of 33 smokers who maintained abstinence to 3 months, and 31 continuing smokers. Measurements Indices demonstrated previously in this cohort of smokers to be sensitive to the effect of nicotine versus acute abstinence: reward motivation [Snaith–Hamilton pleasure scale (SHAPS), Card Arranging Reward Responsivity Objective Test (CARROT), Stroop], tasks of response inhibition [anti‐saccade task; Continuous Performance Task (CPT)], clinical indices of mood [Hospital Anxiety and Depression Scale (HADS)], withdrawal symptoms [Mood and Physical Symptoms Scale (MPSS)] and desire to smoke. Findings SHAPS anhedonia and reward responsivity (CARROT) showed significant improvement and plateaued after a month of abstinence, not differing from the scores of continuing smokers tested in a satiated state. Mood, other withdrawal symptoms and desire to smoke all declined from acute abstinence to 1 month of cessation and were equivalent to, or lower than, the levels reported by continuing, satiated smokers. Neither group showed a change in CPT errors over time while continuing smokers, but not abstainers, showed improved accuracy on the anti‐saccade task at 3 months. Conclusion Appetitive processes and related affective states appear to improve in smokers who remain nicotine‐free for 3 months, whereas response inhibition does not. Although in need of replication, the results suggest tentatively that poor inhibitory control may constitute a long‐term risk factor for relapse and could be a target for intervention.     

Does the reaction of abstaining smokers to the smell of other people's cigarettes predict relapse?

Aims Recent ex‐smokers report a range of reactions to other people's cigarette smoke. We examined the hypothesis that those who find the smell of smoke pleasant and tempting are more likely to relapse than those who have a neutral or even negative reaction to it. Design A total of 1110 consecutive patients who attended for smoking cessation treatment and achieved at least 1 week of validated abstinence provided weekly ratings of their reactions to other people's cigarette smoke together with routine baseline measures and weekly ratings of withdrawal discomfort [measured on the Mood and Physical Symptom Scale (MPPS)]. Findings Twenty‐three per cent of the sample found the smell of other people's cigarette smoke during their first week of abstinence pleasant, and 54% found it tempting. There was only a modest correlation between the two variables. Finding the smoke pleasant was not related to smoking status in the following week, but finding the smoke tempting predicted relapse. Ratings of temptation were related to the severity of withdrawal discomfort and to dependence. Entering MPPS ratings of urges to smoke in the given week into regression analysis resulted in the general urges to smoke, rather than urges elicited by other people's smoke, becoming a significant predictor of smoking status in the following week. In patients who maintained continuous abstinence throughout 4 weeks of treatment the pleasantness ratings remained stable, while the ratings of temptation steadily decreased. Conclusions In abstaining smokers, the like or dislike of other people's smoke is not related to relapse. The temptation to smoke elicited by other people's smoke is related to outcome, but only as an indicator of a general ‘temptation threshold’. Patients who find other people's smoke tempting can be reassured that this reaction will gradually decrease.     

Cigarette smoking increases copy number alterations in nonsmall-cell lung cancer

Cigarette smoking has been a well-established risk factor of lung cancer for decades. How smoking contributes to tumorigenesis in the lung remains not fully understood. Here we report the results of a genome-wide study of DNA copy number and smoking pack-years in a large collection of nonsmall-cell lung cancer (NSCLC) tumors. Genome-wide analyses of DNA copy number and pack-years of cigarette smoking were performed on 264 NSCLC tumors, which were divided into discovery and validation sets. The copy number-smoking associations were investigated in three scales: whole-genome, chromosome/arm, and focal regions. We found that heavy cigarette smokers (>60 pack-years) have significantly more copy number gains than non- or light smokers (≤60 pack-years) (P = 2.46 × 10(-4)), especially in 8q and 12q. Copy number losses tend to occur away from genes in non/light smokers (P = 5.15 × 10(-5)) but not in heavy smokers (P = 0.52). Focal copy number analyses showed that there are strong associations of copy number and cigarette smoking pack-years in 12q23 (P = 9.69 × 10(-10)) where IGF1 (insulin-like growth factor 1) is located. All of the above analyses were tested in the discovery set and confirmed in the validation set. DNA double-strand break assays using human bronchial epithelial cell lines treated with cigarette smoke condensate were also performed, and indicated that cigarette smoke condensate leads to genome instability in human bronchial epithelial cells. We conclude that cigarette smoking leads to more copy number alterations, which may be mediated by the genome instability.     

Cigarette abstinence, nicotine gum, and theophylline disposition

When cigarette smokers with chronic lung disease become acutely ill or require surgery, they are often forced to stop smoking and may use nicotine gum. Smoking is known to accelerate the metabolism of theophylline, but the effects of short-term abstinence or nicotine gum on theophylline metabolism have not been reported. We studied the effects of brief tobacco abstinence and nicotine gum on theophylline elimination in healthy volunteers. Abstinence from smoking for 1 week resulted in a 37.6% decrease in clearance and a 35.8% increase in half-life. Nicotine gum had no effect on theophylline clearance. Our data indicate that at least partial normalization of the enzyme-inducing effects of smoking can be seen after brief cigarette abstinence. For smokers who are taking theophylline chronically, their dose of theophylline will need to be reduced by one fourth to one third after brief tobacco abstinence. Plasma concentration monitoring may be necessary for optimal dosing of theophylline in such patients.     

Do work-place smoking bans cause smokers to smoke “harder”? Results from a naturalistic observational study

The purpose of this study was to investigate whether smokers outside buildings with work-place smoking bans smoke "harder" than those smoking in social settings. An unobtrusive random observational study of smokers followed by structured interview was used, with 143 smokers taking smoking breaks outside their office buildings and 113 smokers in social settings. The main outcome measurements were number of puffs per cigarette and cigarette smoking duration. The mean number of puffs per cigarette for the office building group was 18.7% greater than that for the social settings group (10.7 3.2 vs. 8.7 2.7, t 5.58, df 253, p 0.001); 74.8% of smokers outside offices took more than the mean number of puffs for the group compared to 42.5% of smokers in social settings (c df 1 26.31, p 0.0001). Mean cigarette smoking duration was 30.4% shorter for the work-place group than the social settings group (3.9 1.2 minutes vs. 5.6 2.6 minutes). Of smokers outside offices, 55.2% had a cigarette smoking duration between 3 and 4.59 minutes, while 53.1% of smokers in social settings took 2 31.55, p="0.0001)." Smokers who scored at the 75th percentile on the Fagerstrom Tolerance Scale took a mean 9.5 2.6 puffs per cigarette compared to 9.3 on the scale (t=0.34, df="145," p="0.73)." Regardless of degree of nicotine dependency, smokers leaving work-stations to smoke outside buildings smoked their cigarettes nearly 19% "harder" than cigarettes smoked in social settings. The individual and public health benefits of reduced smoking frequency engendered by work-place smoking bans may be lessened by policies which allow smokers to take smoking breaks. 5 minutes to smoke the observed cigarette (c=df 2.7 puffs by those who scored in the 25th percentile     

Differentiation in the short- and long-term effects of smoking on plasma total ghrelin concentrations between male nonsmokers and habitual smokers

To explore the association between the anorexigenic effects of nicotine and the orexigenic properties of ghrelin, plasma total ghrelin levels were measured in nonsmokers and habitual smokers before and after short-term exposure to cigarette smoke. Thirty-one male smokers and 23 nonsmoking volunteers were matched for age and body mass index. After an overnight fast and abstinence from smoking, they all smoked 2 cigarettes consecutively (same brand, rate of inhalation, and duration of smoking). Total ghrelin concentrations were measured by radioimmunoassay before smoking (baseline), immediately afterward, and 30, 60, and 90 minutes after the second cigarette. Baseline ghrelin levels were not different between smokers and nonsmokers. Smoking did not have an immediate influence on ghrelin concentrations in smokers (analysis of variance for repeated measurements, P=0.74), whereas there was a progressive decline in nonsmokers, reaching statistical significance at 30 minutes (P=.04) and a nadir at 60 minutes (P=.04) after smoking. Moreover, the area under the curve for the changes of ghrelin over time after smoking was lower in nonsmokers than in smokers (-287.2+/-167.1 vs 29.2+/-125.3 ng.min/L, P=.03). In conclusion, fasting plasma total ghrelin concentrations are not different between male smokers and nonsmokers. Smoking does not provoke any short-term change in ghrelin levels in smokers, but induces a decline in nonsmokers. If the anorectic effect of smoking is ghrelin induced, this effect may be present only in people not habituated to smoke exposure. In habitual smokers, ghrelin suppression by short-term smoking could be blunted as a result of desensitization due to prolonged nicotine exposure.     

Cigarette smoke augments the expression and responses of toll-like receptor 3 in human macrophages

Background and objective: Cigarette smoking is the main risk factor for the development of chronic obstructive pulmonary disease (COPD). Recently, toll‐like receptor 3 (TLR3) was shown to recognize pathogen‐associated molecular patterns, especially viral‐derived double‐stranded RNA, and to be involved in immune responses. However, the effects of cigarette smoke on TLR3 remain unclear. In this study, it was examined whether cigarette smoke affects the expression and responses of TLR3 in human macrophages. Methods: The expression of TLR3 in alveolar macrophages from human lung tissues was analysed by immunohistochemistry, and the correlation of TLR3 expression with smoking history and lung function was evaluated. In addition, the effect of cigarette smoke on the expression and responses of TLR3 in macrophage lineage cells was investigated. Results: TLR3‐positive alveolar macrophage numbers were significantly increased in smokers and COPD patients compared with non‐smoking control subjects, but there was no difference between smokers and COPD patients. TLR3‐positive macrophage numbers were positively correlated with smoking history and inversely correlated with corrected carbon monoxide diffusing capacity, but were not correlated with % predicted forced expiratory volume in 1 s. Furthermore, cigarette smoke extract potentiated the expression of TLR3 in monocyte‐derived macrophages and significantly augmented the release of interleukin‐8, as well as total matrix metalloproteinase‐9 activity, in cells treated with TLR3 ligand. Conclusions: These data suggest that cigarette smoke augments the expression and responses of TLR3 in human macrophages, and this may contribute to neutrophilic airway inflammation and parenchymal destruction in the lungs of smokers and patients with COPD.     

Changes in cough reflex sensitivity after cessation and resumption of cigarette smoking

Previous studies have shown that healthy cigarette smokers have diminished cough reflex sensitivity compared to healthy nonsmokers. We have recently demonstrated that cough reflex sensitivity is enhanced soon after smoking cessation, suggesting that diminished cough sensitivity in smokers results from chronic cigarette smoke-induced desensitization of airway cough receptors. In this study, we evaluated cough reflex sensitivity to capsaicin (C(5)) in 11 chronic smokers who had discontinued smoking for at least 2 weeks, and then resumed smoking. Two weeks after smoking cessation there was a significant enhancement of cough reflex sensitivity; mean (+/-SEM) log C(5) decreased from 1.77+/-0.18 to 1.47+/-0.14 (p=0.01). All subjects resumed smoking after 2-12 weeks of abstinence. Repeat capsaicin cough challenge was performed 14-23 days after resumption of smoking. Mean log C(5) increased compared to the last value obtained during the smoking cessation period: 1.42+/-0.15 vs. 1.77+/-0.16 (p=0.0004). Mean log C(5) after resumption of smoking returned to almost exactly the baseline value. Our findings suggest that the sensitivity of airway cough receptors is a dynamic phenomenon, promptly affected and modulated by changes in environmental conditions, such as the presence or absence of cigarette smoke.     

Leaving work to smoke

Work-place smoking bans have not only reduced work-day cigarette consumption but also been associated with going outside to smoke during working hours. We examined the extent of "exiled smoking", estimated how much work-day cigarette consumption can be attributed to it, and examined proximal predictors of both these two variables. Some 794 smokers from 42 medium-sized work-places were surveyed as the baseline for an intervention study. A self-completed questionnaire assessed smoking behaviour on work and non-working days, leaving work to smoke, and beliefs and opinions about smoking and smoking bans. Multiple regressions were used to examine predictors of leaving work to smoke, and of the amount smoked when doing so. Smokers reported consuming an average of 5.4 cigarettes during work breaks, 3.5 of which were associated with deliberately seeking opportunities to smoke; 39% reported leaving work to smoke one or more times per day during non-break periods. Indices of addiction were significant predictors of both leaving work to smoke and of cigarette consumption while doing so. Leaving work to smoke is in part an activity of addicted smokers, presumably to maintain blood nicotine levels. There is the potential to further reduce rates of cigarette consumption associated with work-place smoking bans if this "exiled smoking" can be reduced. This may be easier to achieve in light smokers.     

Does menthol attenuate the effect of bupropion among African American smokers?

Background African Americans have higher tobacco‐related morbidity and mortality and are more likely to smoke menthol cigarettes than their white counterparts. This study examined differences between African American menthol and non‐menthol smokers in smoking characteristics and cessation. Methods The study sample consisted of 600 African American smokers enrolled in a clinical trial that assessed the efficacy of sustained‐release bupropion for smoking cessation. Menthol (n = 471) and non‐menthol (n = 129) smokers were compared on smoking‐related characteristics and abstinence rates at 6 weeks and 6 months. Results Menthol smokers were younger (41.2 versus 52.9 years), more likely to be female (73.7% versus 56.6%) and more likely to smoke their first cigarette within 30 minutes of waking up (81.7% versus 69.8%) compared to non‐menthol smokers (all P < 0.01). Cigarette taste (50% versus 40%, P = 0.054) was rated non‐significantly higher by menthol smokers. Seven‐day point‐prevalence abstinence from smoking at 6 weeks were 28% and 42% (P = 0.006) and at 6 months were 21% and 27% (P = 0.21) for menthol and non‐menthol smokers, respectively. At 6 weeks follow‐up, stepwise logistic regression revealed that among those younger than 50 years, non‐menthol smokers were more likely to quit smoking (odds ratio = 2.0; 95% CI = 1.03–3.95) as were those who received bupropion (odds ratio = 2.12; 95% CI = 1.32–3.39). Conclusion African American menthol smokers had lower smoking cessation rates after 6 weeks of treatment with bupropion‐SR, thereby putting menthol smokers at greater risk from the health effects of smoking. Lower overall cessation rates among African Americans menthol smokers may partially explain ethnic differences in smoking‐related disease risks.     

Changes in cigarette smoking and coffee drinking after alcohol detoxification in alcoholics

Aims. To assess the changes in cigarette smoking and coffee drinking after alcohol detoxification in alcoholics. Design. Evaluation at admission and an average 16 days following discharge. Setting. Alcohol detoxification inpatient programme. Participants. Seventy-three alcohol dependent (DSM-III-R) inpatients . Measurements. Average number of cigarettes and of cups of coffee per day; urine cotinine level. Smokers were classified as moderate on the basis of consuming fewer than 30 cigarettes per day at the time of admission; heavy smokers were those who smoked 30 cigarettes per day or more. Findings. As a group, the smokers (N=58) did not significantly change their cigarette consumption and there was no change in urine cotinine level. Heavy smokers (N=34), however, significantly decreased their cigarette consumption, but urine cotinine was unchanged. Moderate smokers (N=24) significantly increased their cigarette consumption but urine cotinine was not significantly changed. All patients-non-smokers, moderate and heavy smokers-significantly increased their coffee intake. Conclusions. The results suggest that heavy smokers may react to alcohol cues and thus reduce smoking activity when sober. Moderate smokers may increase their smoking rate to cope with alcohol abstinence. These changes appear only to reflect a behavioural adjustment, without modification of patients' nicotine-seeking. Alcoholics may increase their coffee intake to cope with alcohol abstinence.     

The association between cigarette smoking,virologic suppression,and CD4+ lymphocyte count in HIV-Infected Russian women

Cigarette smoking among people living with HIV/AIDS is associated with significant morbidity and mortality, but findings regarding the association between cigarette smoking and HIV viral load and CD4+ lymphocyte counts have been inconsistent. This study characterized the prevalence of cigarette smoking among HIV-infected Russian women and examined the association between smoking frequency and quantity and HIV viral load and CD4+ lymphocyte counts. HIV-infected Russian women (N?=?250; M age?=?30.0) in St. Petersburg, Russia, completed an audio computer-assisted self-interview survey assessing cigarette use, antiretroviral medication adherence, and provided blood samples assayed for HIV viral load and CD4+ lymphocyte counts. The majority (60.4%) reported cigarette smoking in the past month; 49.0% of recent smokers were classified as moderate or heavy smokers, defined as smoking ≥10 cigarettes daily. Viral load status did not differ between infrequent smokers and regular smokers. However, moderate/heavy smokers (relative to light smokers) were more likely to have a detectable viral load (AOR?=?2.3, 95% CI: 1.1, 5.1). There were no significant differences in CD4+ lymphocyte counts by smoking frequency or quantity of cigarettes smoked. Results highlight the need for additional research to examine the association between cigarette smoking and virologic suppression and markers of HIV disease progression. Adverse health consequences of cigarette smoking coupled with a potential link between heavy smoking and poor virologic suppression highlight the need for assessment of cigarette use and provision of evidence-based smoking-cessation interventions within HIV medical care.