High-nicotine Cigarettes Research Articles

Nicotinic Receptor Alpha-5 Subunit Gene Polymorphism is Associated With Heavy Smoking Under a Range of Nicotine Dosing Conditions.

This study aimed to assess the role of the rs16969968 variant of nicotinic receptor alpha-5 subunit in regulating smoking behavior and nicotine intake in response to nicotine manipulations among dependent smokers in a naturalistic environment. Sixty-nine adults (19 females) smoking 10 or more cigarettes per day (CPD) were asked to complete four 2-week study phases during which they smoked exclusively one of two types of Spectrum nicotine research cigarettes (FTC nicotine yield 0.8 and 1.6 mg, respectively), their usual brand of cigarettes, or their usual brand of cigarettes while wearing a 21-mg nicotine patch. Measurements included rs16969968 genotype, number of CPD, smoking topography, and plasma cotinine. Compared to controls (G/G carriers), A allele carriers reported smoking 4 to 5 more CPD across all conditions (all ps < .05). Mean total smoke volume per day and cotinine were greater in A allele carriers than in controls (ps = .05, .046, respectively). No significant genotype differences were found in smoking compensation indices for the switch from medium to high-nicotine-yield cigarettes. Nicotine patch-induced reductions in cigarettes smoked per day and total smoke volume per day showed significant interactions between genotype and pre-patch levels, with heavier smokers showing greater effects of genotype (p = .052 and p = .006, respectively). Results suggest that the rs16969968 variants regulate the heaviness of smoking primarily by their impact on daily numbers of cigarettes smoked, but no genotype differences were found in smoking compensation after switching from medium to high-nicotine cigarettes. The differences in daily cigarette consumption between rs16969968 risk-allele carriers and controls are shown to be consistent regardless of manipulations of cigarette nicotine content and transdermal nicotine supplementation and markedly greater among dependent smokers than those observed in the general smoker populations. G/G allele carriers, relative to A allele carriers, appeared to be more sensitive to the nicotine patch manipulation, reducing their smoking to a greater extent. These findings support continued efforts in the development of personalized intervention strategies to reduce the rs16969968-conveyed genetic propensity for heavy smoking.

Electronic Cigarette Aerosol Is Cytotoxic and Increases ACE2 Expression on Human Airway Epithelial Cells: Implications for SARS-CoV-2 (COVID-19).

Tobacco smoking has emerged as a risk factor for increasing the susceptibility to infection from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) via increased expression of angiotensin-converting enzyme-2 (ACE2) in the lung, linked to coronavirus disease 2019 (COVID-19) development. Given the modifiable nature of electronic cigarettes and the delivery of high concentrations of nicotine, we investigate whether electronic cigarette vaping has the potential to increase susceptibility to SARS-CoV-2 infection. We exposed BEAS-2B cells (bronchial epithelium transformed with Ad12-SV40 2B) and primary small airway epithelial cells (SAECs) to electronic cigarette aerosol condensates produced from propylene glycol/vegetable glycerin or commercially bought e-liquid (±added nicotine) and cigarette smoke extract to investigate if electronic cigarette exposure, like cigarette smoke, increases the expression of ACE2 in lung epithelial cells. In BEAS-2B cells, cytotoxicity (CCK-8), membrane integrity (LDH), and ACE2 protein expression (immunofluorescence) were measured for both 4- and 24 h treatments in BEAS-2B cells and 4 h in SAECs; ACE2 gene expression was measured using quantitative polymerase chain reaction (qPCR) for 4 h treatment in BEAS-2B cells. Nicotine-free condensates and higher concentrations of nicotine-containing condensates were cytotoxic to BEAS-2B cells. Higher LDH release and reduced membrane integrity were seen in BEAS-2B cells treated for 24 h with higher concentrations of nicotine-containing condensates. ACE2 protein expression was observably increased in all treatments compared to cell controls, particularly for 24 h exposures. ACE2 gene expression was significantly increased in cells exposed to the locally bought e-liquid condensate with high nicotine concentration and cigarette smoke extract compared with cell controls. Our study suggests that vaping alone and smoking alone can result in an increase in lung ACE2 expression. Vaping and smoking are avoidable risk factors for COVID-19, which, if avoided, could help reduce the number of COVID-19 cases and the severity of the disease. This is the first study to utilize electronic cigarette aerosol condensates, novel and developed in our laboratory, for investigating ACE2 expression in human airway epithelial cells.

Adolescent nicotine and tobacco smoke exposure enhances nicotine self-administration in female rats

Most people start experimenting with tobacco products or e-cigarettes in early adolescence and become habitual smokers in late adolescence or adulthood. These studies investigated if exposure to tobacco smoke or nicotine during early and mid-adolescence affects nicotine intake in late adolescence and early adulthood. Male and female rats were exposed to tobacco smoke from low- and high-nicotine SPECTRUM cigarettes or nicotine (0.3 mg/kg, twice a day) from postnatal day (P) 24–42. The self-administration sessions started at P55. The rats self-administered nicotine for 14–15 days under a fixed-ratio 1 schedule, and on the first day, the maximum number of infusions was twenty. Exposure to smoke from high, but not low, nicotine cigarettes during adolescence increased nicotine self-administration in female but not male rats. Adolescent treatment with nicotine facilitated nicotine self-administration. On the first day of nicotine self-administration, nicotine-treated rats reached the maximum number of infusions before the saline-treated control rats. Nicotine intake was also higher in the nicotine-treated female rats than in the saline-treated females. There was no sex difference in nicotine intake in controls when the data from the studies were combined. Smoke exposure led to a dose-dependent increase in plasma nicotine and cotinine levels in adolescent rats. Exposure to smoke from high-nicotine cigarettes and 0.3 mg/kg of nicotine led to plasma nicotine and cotinine levels that are similar to those in tobacco users. These findings indicate that in females, but not males, exposure to nicotine during adolescence may facilitate smoking and e-cigarette use later in life.

Exposure to smoke from high- but not low-nicotine cigarettes leads to signs of dependence in male rats and potentiates the effects of nicotine in female rats

Nicotine is only mildly rewarding, but after becoming dependent, it is difficult to quit smoking. The goal of these studies was to determine if low-nicotine cigarettes are less likely to cause dependence and enhance the reinforcing effects of nicotine than regular high-nicotine cigarettes. Male and female rats were exposed to tobacco smoke with a low or high nicotine level for 35 days. It was investigated if smoke exposure affects the development of dependence, anxiety- and depressive-like behavior, and nicotine-induced behavioral sensitization. Smoke exposure did not affect locomotor activity in a small open field or sucrose preference. Mecamylamine precipitated somatic withdrawal signs in male rats exposed to smoke with a high level of nicotine, but not in male rats exposed to smoke with a low level of nicotine or in females. After cessation of smoke exposure, there was a small decrease in sucrose preference in the male rats, which was not observed in the females. Cessation of smoke exposure did not affect anxiety-like behavior in the large open field or the elevated plus maze test. Female rats displayed less anxiety-like behavior in both these tests. Repeated treatment with nicotine increased locomotor activity, rearing, and stereotypies. Prior exposure to smoke with a high level of nicotine increased nicotine-induced rearing in the females. These findings indicate that exposure to smoke with a low level of nicotine does not lead to dependence and does not potentiate the effects of nicotine. Exposure to smoke with a high level of nicotine differently affects males and females.

Smokers’ behavioral intentions in response to a low-nicotine cigarette policy

IntroductionEvidence suggests that reducing the nicotine concentration in cigarettes to sub-addictive levels would reduce use. Until a low-nicotine cigarette policy is enacted, population-level effects are unknown. This study examines the behavioral intentions of current U.S. cigarette smokers if a low-nicotine policy were implemented. MethodsData were drawn from a nationally representative probability-based panel and opt-in panel. Weighted logistic regressions examined likelihood to (1) smoke lower nicotine cigarettes, (2) quit using tobacco, (3) use e-cigarettes, (4) illegally buy high-nicotine cigarettes, and (5) smoke cigars, cigarillos, or little cigars (CLCCs) among smokers, controlling for demographics, tobacco products used, dependence, and intentions to quit cigarettes. Latent class analyses (LCA) characterized patterns of behavioral intentions. ResultsIf a low-nicotine policy were implemented, most participants indicated a likelihood to smoke low-nicotine cigarettes (78.4%) or quit tobacco (61.9%), followed by use e-cigarettes (46.5%). Individuals with greater dependence had greater odds of intending to smoke low-nicotine cigarettes, use e-cigarettes, and illegally buy high-nicotine cigarettes. Current e-cigarette or CLCCs users had higher odds of intending to use these products. LCA revealed that individuals would 1) use low-nicotine cigarettes with low intentions to use other tobacco products or 2) use multiple tobacco products, including low-nicotine cigarettes. ConclusionsA reduced nicotine standard for all combustible tobacco products is needed given that many tobacco users would likely intend to continue to use tobacco products. Differences in intentions by tobacco use and demographic characteristics indicate a need for additional cessation support and education around the harms of continued use of combustible tobacco.

Examining Risk Perceptions Among Daily Smokers Naïve to Reduced Nicotine Content Cigarettes.

The U.S. Food and Drug Administration (FDA) has stated its interest in reducing the addictiveness of combustible cigarettes by lowering their nicotine content. Delineating risk perceptions of reduced nicotine content (RNC) cigarettes prior to federal regulation may inform the content of future educational campaigns accompanying this policy. Five hundred non-treatment-seeking, daily smokers naïve to RNC cigarettes (63.0% male, 51.6% nonWhite, mean [SD] cigarettes per day = 15.69 [7.58], age = 43.44 [11.46]) completed a 10-item RNC cigarette risk perception questionnaire at baseline in two, unrelated experimental studies. We used multinomial logistic regression models to identify demographic (eg, gender) and smoking-related (eg, nicotine dependence) correlates of RNC cigarette risk perceptions. Although the majority of participants did not misperceive RNC cigarettes as less harmful than regular or high nicotine cigarettes, a large portion of the sample held misperceptions about RNC cigarettes' addictiveness (56.4%) and cessation aid potential (63.4%). More than 20% of the sample reported being unsure about RNC-related risks, especially tar content (51.8%). NonWhite smokers were 2.5 to 3 times more likely to be incorrect about multiple RNC cigarette risks (p = .002-.006). If the FDA mandates a reduced nicotine content standard for cigarettes, educational campaigns will be needed to correct misperceptions about RNC cigarettes' addictiveness and potential to aid cessation as well as inform consumers about their safety risks. Campaigns tailored toward nonWhite smokers may also be needed to correct misperceptions of RNC cigarette risks held by this subgroup. The FDA has stated its interest in reducing cigarettes' addictiveness by lowering their nicotine content, enabling smokers to quit. Our findings suggest that most smokers who have not used RNC cigarettes do not perceive these products as less addictive or as cessation tools, stressing a need for future educational campaigns to correct these misperceptions. Campaigns are also needed to educate uninformed smokers about RNC cigarettes and should consider targeting messages toward subgroups likely to hold misperceptions about the risks and benefits of using these products (eg, nonWhite smokers).

Vapours of US and EU Market Leader Electronic Cigarette Brands and Liquids Are Cytotoxic for Human Vascular Endothelial Cells.

The present study was conducted to provide toxicological data on e-cigarette vapours of different e-cigarette brands and liquids from systems viewed as leaders in the e-cigarette market and to compare e-cigarette vapour toxicity to the toxicity of conventional strong high-nicotine cigarette smoke. Using an adapted version of a previously constructed cigarette smoke constituent sampling device, we collected the hydrophilic fraction of e-cigarette vapour and exposed human umbilical vein endothelial cells (HUVECs) to the mixture of compounds present in the vapour of 4 different single-use e-cigarettes, 6 different liquid vapours produced by the same refillable e-cigarette, and one e-cigarette with an exchangeable liquid cartridge. After incubation of cells with various concentrations and for various periods of time we analysed cell death induction, proliferation rates, the occurrence of intra-cellular reactive oxygen species, cell morphology, and we also measured e-cigarette heating coil temperatures. Overall, conventional cigarette smoke extract showed the most severe impact on endothelial cells. However, some e-cigarette vapour extracts showed high cytotoxicity, inhibition of cell proliferation, and alterations in cell morphology, which were comparable to conventional high-nicotine cigarettes. The vapours generated from different liquids using the same e-cigarette show substantial differences, pointing to the liquids as an important source for toxicity. E-cigarette vapour-mediated induction of oxidative stress was significant in one out of the 11 analysed vapours. There is a high variability in the acute cytotoxicity of e-cigarette vapours depending on the liquid and on the e-cigarettes used. Some products showed toxic effects close to a conventional high-nicotine cigarette. Liquid nicotine, menthol content, and the formation of acute intracellular reactive oxygen species do not seem to be the central elements in e-cigarette vapour toxicity.

Nicotine levels after IV nicotine and cigarette smoking in men.

There has been considerable interest in the pharmacodynamics and pharmacokinetics of nicotine and the influence of different routes of administration. However, these variables are often examined in separate studies, and there is less information about the temporal relation between subjective reports and plasma nicotine levels. This study examined the time course and magnitude of plasma nicotine levels and reports of subjective "high" in nicotine-dependent men after 12 or more hrs of abstinence. The effects of two doses of IV nicotine and two doses of nicotine from cigarette smoking were compared, and samples were collected at 2-min intervals. Plasma nicotine levels after smoking a high-nicotine cigarette were significantly greater than after either dose of IV nicotine (p < .001). However, Visual Analog Scale (VAS) ratings of "high" after both doses of IV nicotine and smoking a high-nicotine cigarette did not differ significantly, and followed a similar time course. After smoking a low-nicotine cigarette, VAS ratings of "high" were significantly lower than after either IV nicotine dose or smoking a high-nicotine cigarette (p < .001). Peak levels of "high" were reported within 2 min after IV nicotine administration and the onset of cigarette smoking. Then "high" ratings abruptly decreased, while plasma nicotine rose to peak levels within 4 to 6 min after IV nicotine and 12 to 14 min during cigarette smoking. Plasma nicotine levels did not appear to determine the magnitude or time course of subjective effects under these conditions.

Empirical analysis of the impact of cigarette excise taxes on cigarette consumption: estimates from recent state-level data

The adverse health effects from cigarette smoking account for an estimated 443,000 deaths annually in the U.S. Given this circumstance, this study has two objectives. First, it uses a state-level panel data set for a recent time frame to investigate the impact of federal plus state cigarette excise taxes (along with a variety of other factors) on the aggregate consumption of cigarettes. The study adopts a state-level panel data series spanning the period 2002 through 2007, which is the most recent panel for which data for all of the variables are available. Consistent with a number of previous studies, the PLS estimates in this study find that the higher the cigarette excise tax, the lower the aggregate volume of cigarettes consumed. Of course, this outcome does not address the practical problem of the substitution of high nicotine cigarettes for low nicotine cigarettes in the presence of a significant cigarette tax hike. This circumstance leads to the second objective of this study, namely, to propose a general template for a different kind of cigarette excise tax, one that is tied directly to each cigarette brand’s nicotine and tar content.

A Preliminary Contemporary Panel Data Analysis of the Consumption Impact of Cigarette Taxation

The adverse health effects from cigarette smoking account for an estimated 400,000 deaths annually in the U.S. Given this circumstance, the present study has two objectives. First, using a panel data set for a very recent time frame, it seeks to investigate the impact of federal plus state cigarette excise taxes (along with the influence of other factors) on the aggregate consumption of cigarettes. The study adopts a five-year state-level panel data series spanning the period 2002 through 2006. Consistent with certain previous studies, the estimates in this study find that the higher the cigarette excise tax, the lower the aggregate volume of cigarettes consumed. However, this outcome does not address the practical problem of the substitution of high nicotine cigarettes for low nicotine cigarettes in light of a significant cigarette tax hike. This circumstance leads to the second objective of this study, namely, to formally propose a general form/template for a cigarette excise tax that is tied directly to each cigarette brand’s nicotine and tar content.

Hormones, nicotine, and cocaine: Clinical studies

Nicotine and cocaine each stimulate hypothalamic–pituitary–adrenal and –gonadal axis hormones, and there is increasing evidence that the hormonal milieu may modulate the abuse-related effects of these drugs. This review summarizes some clinical studies of the acute effects of cigarette smoking or IV cocaine on plasma drug and hormone levels and subjective effects ratings. The temporal covariance between these dependent measures was assessed with a rapid (2 min) sampling procedure in nicotine-dependent volunteers or current cocaine users. Cigarette smoking and IV cocaine each stimulated a rapid increase in LH and ACTH, followed by gradual increases in cortisol and DHEA. Positive subjective effects ratings increased immediately after initiation of cigarette smoking or IV cocaine administration. However, in contrast to cocaine's sustained positive effects (< 20 min), ratings of “high” and “rush” began to decrease within one or two puffs of a high-nicotine cigarette while nicotine levels were increasing. Peak nicotine levels increased progressively after each of three successive cigarettes smoked at 60 min intervals, but the magnitude of the subjective effects ratings and peak ACTH and cortisol levels diminished. Only DHEA increased consistently after successive cigarettes. The possible influence of neuroactive hormones on nicotine dependence and cocaine abuse and the implications for treatment of these addictive disorders are discussed.

Effects of Smoking Successive Low- and High-Nicotine Cigarettes on Hypothalamic–Pituitary–Adrenal Axis Hormones and Mood in Men

Smoking one cigarette produces rapid nicotine dose-related increases in hypothalamic-pituitary-adrenal (HPA) axis hormones, mood, and heart rate, but relatively little is known about the effects of smoking several cigarettes successively. Twenty-four healthy adult men who met Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV) criteria for nicotine dependence provided informed consent. After overnight abstinence from smoking, men smoked three low- or high-nicotine cigarettes for 4 min each at 60 min intervals. Samples for nicotine and hormone analysis, Visual Analog Scale (VAS) ratings of subjective effects and heart rate were collected at 4, 8, 12, 16, 20, 30, 40, and 50 min after each cigarette. After low-nicotine cigarettes, nicotine levels, adrenocorticotropin hormone, and heart rate did not increase significantly, cortisol and dehydroepiandrosterone decreased significantly, and positive VAS ratings were lower but parallel to ratings after high-nicotine cigarette smoking. After high-nicotine cigarettes, peak nicotine levels increased monotonically. HPA axis hormones increased after smoking, but peak levels did not differ significantly after successive high-nicotine cigarettes. Positive VAS ratings and heart rate increased after each high-nicotine cigarette, but peak levels were lower after smoking the second and third cigarette. 'Craving' decreased significantly after smoking both low- and high-nicotine cigarettes, then gradually increased during the 60 min interval between cigarettes. These data are consistent with clinical reports that the first cigarette after overnight nicotine abstinence is most salient. Tolerance to the subjective and cardiovascular effects of nicotine developed rapidly during repeated cigarette smoking, but nicotine-stimulated increases in HPA axis hormones did not change significantly.

Effects of Low- and High-Nicotine Cigarette Smoking on Mood States and the HPA Axis in Men

The acute effects of smoking a low- or high-nicotine cigarette on hypothalamic-pituitary-adrenal (HPA) hormones, subjective responses, and cardiovascular measures were studied in 20 healthy men who met American Psychiatric Association Diagnostic and Statistical Manual IV criteria for nicotine dependence. Within four puffs (or 2 min) after cigarette smoking began, plasma nicotine levels and heart rate increased significantly (P<0.01), and peak ratings of 'high' and 'rush' on a Visual Analogue Scale were reported. Reports of 'high', 'rush', and 'liking' and reduction of 'craving' were significantly greater after smoking a high-nicotine cigarette than a low-nicotine cigarette (P<0.05). Peak plasma nicotine levels after high-nicotine cigarette smoking (23.9+/-2.6 ng/ml) were significantly greater than after low-nicotine cigarette smoking (3.63+/-0.59 ng/ml) (P<0.001). After smoking a low-nicotine cigarette, adrenocorticotropin hormone (ACTH), cortisol, dehydroepiandrosterone (DHEA), and epinephrine did not change significantly from baseline. After high-nicotine cigarette smoking began, plasma ACTH levels increased significantly above baseline within 12 min and reached peak levels of 21.88+/-5.34 pmol/l within 20 min. ACTH increases were significantly correlated with increases in plasma nicotine (r=0.85; P<0.0001), DHEA (r=0.66; P=0.002), and epinephrine (r=0.86; P<0.0001). Cortisol and DHEA increased significantly within 20 min (P<0.05) and reached peak levels of 424+/-48 and 21.13+/-2.55 ng/ml within 60 and 30 min, respectively. Thus cigarette smoking produced nicotine dose-related effects on HPA hormones and subjective and cardiovascular measures. These data suggest that activation of the HPA axis may contribute to the abuse-related effects of cigarette smoking.

“Light” smoking and dependence symptoms in high-school students

In high-school students, prevalence of smoking is high but few studies analyzed smoking in the student population according to nicotine content of smoked cigarettes and gender. We analyzed the responses to a questionnaire, including the modified Fagerström Tolerance Questionnaire (FTQ), administered to 555 students (382 males, 173 females) of a professional high school in Palermo, Italy, to assess the prevalence in both genders of: (1) smoking "light" and high nicotine (HN) cigarettes; (2) signs of nicotine dependence and (3) respiratory symptoms. Nicotine content of habitually smoked cigarettes was considered as "light" if 0.8 mg; as high if >0.8 mg. Forty-four percent of students smoked, without differences between genders. Two-thirds of the total sample reported "light" cigarette smoking (76.7% of females vs. 62.0% of males, P<0.05). On average, "light" cigarette smoking was associated with lower pack/year and FTQ global score compared to HN smoking. However, when FTQ global score was analyzed by taking into account pack/year, no major difference was found between "light" and HN cigarette smokers. Cough with phlegm and breathlessness were more frequently reported by smoking than non-smoking students, without differences between "light" and HN cigarette smokers. About 50% of smoking students reported having tried to quit, while only 3.4% of students were ex-smokers. "Light" smoking was common in high school students, especially among females. Dependence appeared more influenced by the smoking history than by nicotine content. Respiratory symptoms were similar in "light" and HN cigarette smokers.

Activation of platelets exposed to shear stress in the presence of smoke extracts of low-nicotine and zero-nicotine cigarettes: The protective effect of nicotine

Mainstream and sidestream smoke extracts of both high-tar and low-tar cigarettes have been shown to increase platelet activation directly and to sensitize them to further activation by exposure to mechanical stimuli such as shear stress. However, nicotine has an inhibitory effect on platelet activation, opposite to that of whole cigarette smoke extracts. To distinguish between the nicotine-dependent and non-nicotine-dependent effects of smoke, platelets were exposed to mainstream and sidestream smoke extracts of low-nicotine and zero-nicotine cigarettes in vitro under flow conditions comparable with the normal circulation, and their activation state was measured using a modified prothrombinase-based assay. Both low-nicotine and zero-nicotine extracts caused increased platelet activation upon exposure to shear stress, and they caused significantly greater activation than extracts from ordinary high-tar, high-nicotine cigarettes. That nicotine was crucial was confirmed by adding 50 nM nicotine (comparable with the nicotine level in smokers' plasma) to zero-nicotine smoke extracts and demonstrating a reduction in the shear-dependent rate of platelet activation of more than 75%.

Pharmacologic and sensorimotor components of satiation in cigarette smoking

To examine mechanisms underlying satiation in cigarette smoking, 18 smokers received intravenous (iv) nicotine, alone or in combination with denicotinized cigarette smoke. Nicotine was administered using programmed presentations of either pulsed injections or continuous infusions, with iv saline serving as a control. A high-nicotine cigarette smoke condition (usual brand) was also presented. During each of the six test sessions, subjects were allowed to puff on their usual brands of cigarette ad libitum while the programmed satiation conditions were in force. Administration of iv nicotine caused a small suppression of ad libitum smoking behavior; denicotinized smoke produced a significantly larger reduction, showing that short-term satiation is more dependent on the presentation of smoke than delivery of nicotine per se. However, denicotinized smoke alone did not have as much effect as puffs from the usual brands of cigarettes. The combination of iv nicotine and denicotinized smoke puffs produced equivalent satiation to that of the usual brand. Cigarette craving and negative affect were partially relieved by iv nicotine presentations as well as by denicotinized smoke, and again the combination of iv nicotine and denicotinized smoke approximated the effects of the usual brand. The results of this study underscore the importance of both sensorimotor aspects of smoking and the pharmacologic effects of nicotine in tobacco dependence.

Effects of Cigarette Smoking and Nicotine Nasal Spray on Psychiatric Symptoms and Cognition In Schizophrenia

Schizophrenic patients have among the highest rates of smoking of any group of patients. Previous studies have identified psychophysiological and potential nicotinic receptor abnormalities which may be associated with this phenomenon. The effects of acute smoking or acute administration of nicotine nasal spray, after smoking abstinence, on negative symptoms and neurocognitive function have been less extensively studied in experimental designs. This study investigated the effects of smoking of high nicotine or denicotinized cigarettes, and receiving active or placebo nicotine nasal sprays, on positive and negative symptoms and cognitive functions in schizophrenic patients. The study utilized a placebo controlled crossover experimental design with pre- and post-drug evaluations on each experimental day. Smoking high nicotine cigarettes decreased negative symptoms more than denicotinized cigarettes, but smoking neither cigarette changed scores of positive symptoms, anxiety, or depression. Active nicotine nasal spray did not differentially decrease negative symptoms compared with placebo, but did improve performance on a spatial organization task, and tended to improve some measures of verbal memory and two-choice reaction time in schizophrenic patients. Both high and denicotinized cigarettes improved performance on the spatial processing task, but there was no statistically significant differential drug (Cigarette type) effect. These results suggest that acute smoking of cigarettes may transiently decrease negative symptoms in patients with schizophrenia, but it is unclear whether this effect is attributable to nicotine, other components of cigarettes, or the act of smoking. Nicotine nasal spray may modestly improve some selected aspects of cognitive function in schizophrenia.

The DRD4 VNTR polymorphism influences reactivity to smoking cues.

Recent research has indicated that craving for tobacco can be reliably elicited by exposure to smoking cues, suggesting that cue-elicited craving for tobacco may be a useful phenotype for research on genetic factors related to nicotine dependence. Given the potential role of dopamine in cue-elicited craving, the authors examined whether the DRD4 VNTR polymorphism is associated with cue-elicited craving for tobacco. Participants who were homozygous or heterozygous for the 7 repeat (or longer) allele were classified as DRD4 L, and all other participants were classified as DRD4 S. Participants were exposed to smoking cues before smoking either high-nicotine cigarettes or control cigarettes. Analyses suggested that participants in the L group demonstrated significantly greater craving, more arousal, less positive affect, and more attention to the smoking cues than did the participants in the S group.

Effects of cigarette smoking on psychopathology scores in patients with schizophrenia: An experimental study

Cigarette smoking and/or nicotine administration have been shown to transiently ameliorate several psychophysiological deficits in patients with schizophrenia such as indicators of deficient sensory gating and attention, but acute effects of smoking on positive and negative symptoms in schizophrenia have not been evaluated in experimental paradigms. The current study assessed whether smoking of cigarettes, after 6–12 h abstinence, transiently alters the expression of negative and/or positive symptoms in patients with schizophrenia who have a history of regular smoking. In a double‐blind, placebo controlled study patients with schizophrenia participated in two sessions in which they smoked either cigarettes moderately high in nicotine content or denicotinized cigarettes. They were interviewed pre‐and postsmoking to obtain ratings of PANSS and SANS scales, and had blood pressure and pulse serially recorded before and after smoking. Pulse rate and blood pressure were slightly higher after smoking in the high nicotine cigarette session. Negative symptom scores on both scales were significantly lower after cigarette smoking compared to same‐day predrug baseline, but there were no differences in active versus denicotinized cigarette drug effects. These results suggest that acute smoking of cigarettes reduces negative symptoms in patients with schizophrenia in this experimental paradigm. Future work needs to identify the mechanism responsible for this behavioral effect.

Changes in platelet glycoprotein receptors after smoking – a flow cytometric study

Cigarette smoking is accepted to be one of the major factors which increase the risk of coronary artery disease, peripheral vascular disease and stroke. A number of studies have been carried out on the acute and chronic effects of tobacco smoking on platelet activation. An enhancing effect of high nicotine cigarette smoking on platelet aggregation has been reported. Since platelet receptors are involved in the final stage of platelet aggregation, the intention of this study was to investigate platelet receptors in acute and chronic smokers before and after smoking. Nineteen chronic smokers, 18 acute smokers and 18 healthy non-smoking controls were included in the present study. Platelet aggregation was carried out using ristocetin, adenosine diphosphate (ADP) and collagen both before and after smoking in acute and chronic smokers. Flow cytometric studies of platelets were carried out utilizing fluorescein isothiocyanate (FITC)-labelled anti-human fibrinogen antibody in unstimulated and ADP-stimulated platelets, FITC-labelled anti-GP IIb/IIIa antibody, FITC-labelled anti-GP Ib/IX antibody and FITC-labelled P-selectin antibody. The intensity of fluorescence was graded into three groups and expressed in arbitrary units. The interesting data generated in the present work is that in vivo platelet activation occurs immediately after smoking a cigarette which is detected by using FITC-labelled anti-human fibrinogen antibody binding to platelet and by P-selectin expression. It is also quite evident from the present study that a significant number of circulating platelets are in the activated state in chronic smokers. Therefore this study suggests that smoking-induced platelet activation may be an important contributory mechanism for acute coronary events in smokers.