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Cardiovascular disease is the leading cause of death globally The past few decades have shown that especially low- and middle-income countries have undergone rapid industrialization, urbanization, economic development and market globalization. Although these developments led to many positive changes in health outcomes and increased life expectancies, they all also caused inappropriate dietary patterns, physical inactivity and obesity. Evidence shows that a large proportion of the cardiovascular disease burden can be explained by behavioural factors such as low physical activity, unhealthy diet and smoking. Controlling these risk factors from early ages is important for maintaining cardiovascular health. Even in patients with genetic susceptibility to cardiovascular disease, risk factor modification is beneficial.Despite the tremendous advances in the medical treatment of cardiovascular risk factors to reduce overall cardiovascular risk, the modern lifestyle which has led to greater sedentary time, lower participation in active transport and time spent in leisure or purposeful physical activity, unhealthy diets and increased exposure to stress, noise and pollution have diminished the beneficial effects of contemporary medical cardiovascular prevention strategies. Therefore attenuating or eliminating these health risk behaviours and risk factors is imperative in the prevention of cardiovascular diseases., (© 2020. The Author(s).)

Background and Aims: The economic evaluation of tobacco control policies requires the adoption of assumptions about the impact of changes in smoking status on health-related quality of life (HRQoL). Estimates for such impacts are necessary for different populations. This paper aims to test whether smoking status has an independent effect on HRQoL over and above the effect derived from the increased likelihood of suffering a tobacco related disease, and to calculate utility values for the Spanish population., Methods: Using data from the Spanish Encuesta Nacional de Salud of 2011-12, we estimate statistical models for HRQoL as measured by the EQ-5D-5L instrument as a function of smoking status. We include a comprehensive set of controls for biological, clinical, lifestyle and socioeconomic characteristics., Results: Smoking status has an independent, statistically significant effect on HRQoL. However, the size of the effect is small. The typical smoking related diseases, such as lung cancer, are associated with a reduction in HRQoL about 5 times larger than the difference between current smokers and never smokers., Conclusion: Attributing substantive HRQoL gains to quitting smoking as well as accounting for the concomitant HRQoL gain derived from a smaller likelihood of contracting tobacco related diseases might lead to an overestimation of the benefits of tobacco control policies. Nonetheless, the relatively large drops in HRQoL associated with being diagnosed with diseases that might be causally linked to tobacco suggest that such diseases should not be omitted from the economic evaluations of tobacco control policies.

The social cost of drugs is the monetary cost of both the consequences of their trade and their consumption. In this paper, drugs considered are tobacco and alcohol, which are legal, plus those that are illegal. The social cost is the sum of the external cost: value of loss in quality of life, value of years of life lost and value of loss in productivity, plus public expenditure. Public expenditure consists of public spending on medical care, prevention, and law enforcement, minus savings from unpaid pensions and taxes levied on tobacco and alcohol. The parameters for the calculations have used the recommendations of a French governmental working group (2013) Quinet, L'évaluation socioéconomique des investissements publics [Internet], Centre d'Analyse Stratégique, 2013, http://www.strategie.gouv.fr/sites/strategie.gouv.fr/files/archives/CGSP_Evaluation_socioeconomique_17092013.pdf , and the health data were derived from the scientific literature. The social costs are €122 billion for tobacco, €118 billion for alcohol, and €8.7 billion for illegal drugs. The largest fraction of the costs (53, 56, and 31 %, respectively) derives from the number of deaths, 79,000 for tobacco, 49,000 for alcohol, and 1600 for illegal drugs, given the high cost of a year of life lost (€115,000). The external cost corresponds to 86, 97, and 68 % of the social cost, respectively, for tobacco, alcohol, and illegal drugs. The annual drug-related net expenditure represents €13.9, €3.0, and €2.3 billion, respectively, for tobacco, alcohol, and illegal drugs. The tax revenues on tobacco and alcohol, €10.4 and €3.2 billion, represent less than half of the corresponding healthcare costs, which are €25.9 and €7.7 billion.

Background: In January 2011 Spain modified clean air legislation in force since 2006, removing all existing exceptions applicable to hospitality venues. Although this legal reform was backed by all political parties with parliamentary representation, the government's initiative was contested by the tobacco industry and its allies in the hospitality industry. One of the most voiced arguments against the reform was its potentially disruptive effect on the revenue of hospitality venues. This paper evaluates the impact of this reform on household expenditure at restaurants and bars and cafeterias., Methods and Empirical Strategy: We used household expenditure micro-data for years 2006-2012 to estimate models for the probability of observing expenditures and the expected level of expenditure. We applied a before-after analysis with a wide range of controls for confounding factors and a flexible modeling of time effects in order to identify the effects of the reform., Results: Our results suggest that the reform caused a 2% reduction in the proportion of households containing smokers but did not cause reductions in households' expenditures on restaurant services or on bars and cafeteria services.

The nicotine metabolites, cotinine and trans-3'-hydroxycotinine (3HC) are considered as superior biomarkers for identifying tobacco exposure. More importantly, the ratio of 3HC to cotinine is a good indicator to phenotype individuals for cytochrome P450 2A6 activity and to individualize pharmacotherapy for tobacco addiction. In this paper, a simple, robust and novel method based on surface-enhanced Raman spectroscopy coupled with thin-layer chromatography (TLC) was developed to directly quantify the biomarkers in human urine samples. This is the first time surface-enhanced Raman spectroscopy (SERS) was used to detect cotinine and 3HC in urine samples. The linear dynamic range for the detection of cotinine is from 40 nM to 8 μM while that of 3HC is from 1 μM to 15 μM. The detection limits are 10 nM and 0.2 μM for cotinine and 3HC, respectively. The proposed method was further validated by quantifying the concentration of both cotinine and 3HC in smokers' urine samples. This TLC-SERS method allows the direct detection of cotinine in the urine samples of both active and passive smokers and the detection of 3HC in smokers.

In this paper, we sustain that non-smokers who might be at risk of starting to smoke or relapsing can benefit from anti-smoking policies such as tax hikes and smoking bans because these are mechanisms that enhance their self-control with regard to tobacco consumption. We formalize this conjecture by proposing a model where starting/relapsing might result from time inconsistent preferences in a way that mirrors the inability of some smokers to carry out the decision to quit. Subsequently, we specify econometric models that allow us to test the implications of such conjecture using information on smoking behavior at the individual level from the Catalan Health Survey of 2006. The empirical results support our conjecture and suggest that the welfare gains derived from the reinforcement of self-control caused by tax hikes and smoking bans will accrue not only to smokers but also to the rest of the population.

Cigarette smoking is the predominant risk factor for bladder cancer in males and females. The tobacco carcinogens are metabolized by various xenobiotic metabolizing enzymes such as N-acetyltransferases (NAT) and glutathione S-transferases (GST). Polymorphisms in NAT and GST genes alter the ability of these enzymes to metabolize carcinogens. In this paper, we conduct a statistical analysis based on logistic regressions to assess the impact of smoking and metabolizing enzyme genotypes on the risk to develop bladder cancer using a case-control study from Tunisia. We also use the generalized ordered logistic model to investigate whether these factors do have an impact on the progression of bladder tumors.

The objective of this paper is to analyze interdependencies between cigarette and alcohol consumption in rural China, using panel data for 10 years (1994-2003) for rural areas of 26 Chinese provinces. There have been many studies in which cigarette and alcohol consumption have been considered separately but few to date for China on interactions between the consumption of these two products. Taxes are often recommended as a tool to reduce alcohol and cigarette consumption. If cigarettes and alcohol are complements, taxing one will reduce the consumption of both and thus achieve a double public health dividend. However, if they are substitutes, taxing one will induce consumers to increase consumption of the other, offsetting the public health benefits of the tax. Our results indicate that the demands for both cigarettes and alcohol are very sensitive to the price of alcohol, but not to the price of cigarettes or to income. This suggests that taxes on alcohol can have a double dividend. On the other hand, an increase in cigarette taxes may not be effective in curbing cigarette or alcohol consumption in rural China.

Rationale: Growing proportions of smokers in the USA do not smoke everyday and can be referred to as light and intermittent smokers (LITS). Despite a current prevalence of LITS in the USA estimated at 25-33% of all smokers, a systematic review of the literature on this group of smokers has yet to be written., Objectives: The aim of this paper is to review and evaluate research on LITS and to identify, describe and discuss commonalities and differences between LITS and daily smokers., Methods: The primary databases used to search for publications were Pub Med (National Library of Medicine) and SCOPUS (Elsevier)., Results: LITS inhale smoke and have post-smoking blood nicotine concentrations that are broadly equivalent to those found in daily smokers. However, LITS differ from daily smokers with regard to cigarette consumption and frequency of cigarette use, sociodemographic and socioeconomic characteristics, motives, personality traits, dependence, withdrawal and craving, response to smoking-related cues, quitting perception, past-smoking status, and initiation., Conclusions: In contrast to daily smokers, LITS show few or no signs of dependence as currently defined by DSM-IV criteria, appear to exercise more self-control, seem to be less impulsive, and their smoking experience is primarily associated with positive rather than negative reinforcement. Conclusions drawn from the reviewed literature highlight the multivariate factors that must be taken into account when defining LITS and emphasize the importance of further research on this increasing fraction of smokers. The potential implications of increased LITS prevalence on smoking-related disease risks remain to be thoroughly investigated.

Rationale: Although considerable progress has been made, we do not yet fully understand the behavioral and neurobiological basis of nicotine reinforcement, and without this knowledge, treatment strategies aimed at reducing smoking remain deficient., Objectives: This review describes an original perspective on nicotine reinforcement, which arises from substantial evidence of complex interactions between nicotine and nonpharmacological stimuli. We hypothesize that nicotine reinforcement derives from at least two sources: (1) primary reinforcement, an action that requires response-dependent drug administration and is capable of conveying secondary reinforcing effects on associated stimuli, and (2) the reinforcement-enhancing effect of nicotine, which directly enhances behavior maintained by salient nonnicotine stimuli and does not require a contingent relationship between drug administration and reinforced operant responding. Although novel for nicotine, this hypothesis has origins in an extensive literature on the reinforcing effects of psychostimulants. Empirical support for this hypothesis, based largely on animal models of reinforcement, will be presented., Conclusions: Animal models of drug reinforcement have evolved to reflect our growing awareness of the multidimensional nature of drug dependence in humans. Investigating the interaction between nicotine and nonpharmacological stimuli within the context of the drug self-administration paradigm in rats has generated new insights into the paradox of how nicotine, an apparently weak primary reinforcer, can sustain the robust behavior observed in self-administration and in smoking. The hypothesis presented in this paper--that nicotine acts as both a primary reinforcer and an enhancer of other nonnicotine reinforcers--provides important direction for future investigations into the neurobiology of nicotine reinforcement and treatments for smoking cessation.

Rationale: Two seemingly contrary theories describe the learning mechanisms that mediate human addictive behaviour. According to the classical incentive theories of addiction, addictive behaviour is motivated by a Pavlovian conditioned appetitive emotional response elicited by drug-paired stimuli. Expectancy theory, on the other hand, argues that addictive behaviour is mediated by an expectancy of the drug imparted by cognitive knowledge of the Pavlovian (predictive) contingency between stimuli (S+) and the drug and of the instrumental (causal) contingency between instrumental behaviour and the drug., Aims and Method: The present paper reviewed human-nicotine-conditioning studies to assess the role of appetitive emotional conditioning and explicit contingency knowledge in mediating addictive behaviour., Results: The studies reviewed here provided evidence for both the emotional conditioning and the expectancy accounts. The first source of evidence is that nicotine-paired S+ elicit an appetitive emotional conditioned response (CR), albeit only in participants who expect nicotine. Furthermore, the magnitude of this emotional state is modulated by nicotine deprivation/satiation. However, the causal status of the emotional response in driving other forms of conditioned behaviour remains undemonstrated. The second source of evidence is that other nicotine CRs, including physiological responses, self-administration, attentional bias and subjective craving, are also dependent on participants possessing explicit knowledge of the Pavlovian contingencies arranged in the experiment. In addition, several of the nicotine CRs can be brought about or modified by instructed contingency knowledge, demonstrating the causal status of this knowledge., Conclusions: Collectively, these data suggest that human nicotine conditioned effects are mediated by an explicit expectancy of the drug coupled with an appetitive emotional response that reflects the positive biological value of the drug. The implication of this conclusion is that treatments designed to modify the expected value of the drug may prove effective.

Objectives: The paper presents results of collaborative research on cadmium as an endocrine disruptor. To detect steroidogenic alterations in cycling and pregnant rats following cadmium exposures in vivo (at 3 or 5 mg/kg as a single s.c. dose) and in vitro (from 0 through 2000 microM Cd(2+)) whole-ovary culture was used. To evaluate steroid productions in rats fed low iron (10 ppm) and concomitantly exposed to cadmium (5 mg/kg total dose by s.c.-implanted osmotic pumps) during 19 days of pregnancy whole-placenta culture was also used. In human placental tissue cadmium and progesterone concentrations were assessed in relation to cigarette smoking., Methods: Cultures of minced ovaries were evaluated for 1-h basal steroid production and following 1-h production stimulated with either human chorionic gonadotropin (hCG) or hCG and pregnenolone. Placental cultures were evaluated for average 1-h progesterone production following 3 h of unstimulated production. Steroid hormones were evaluated by specific radioimmunoassay. Placental cadmium concentrations were analyzed by atomic absorption spectrometry., Results: In-vivo cadmium exposure interfered with normal steroidogenesis in cycling rats and in early pregnancy, with ovarian estradiol production the most affected. Under in-vitro cadmium exposure the most affected was ovarian production of progesterone and testosterone in cycling (proestrous) rats with medial inhibitory concentrations under 500 micro M Cd(2+). Cadmium interfered with the steroidogenic pathway at more than one site. Linear and additive effects of low-iron feeding and concomitant cadmium exposure during pregnancy on placental progesterone production were found. In humans, we found that the placentas of smoking mothers contained twice as much cadmium and approximately half the amount of progesterone than did the placentas of non-smoking mothers., Conclusions: Results of the research on cadmium-induced steroidogenic effects using cultures of whole rat ovary and/or placenta as well as human placental tissues point to cadmium as an endocrine disruptor that may compromise pregnancy outcome and fetal viability.

Platelet monoamine oxidase (MAO) activity has been shown to be inversely associated with personality traits such as sensation seeking, impulsiveness and extraversion. Those personality traits have also been linked to vulnerability for substance abuse, e.g. tobacco smoking and early onset or "type 2" alcoholism. Compounds in cigarette smoke have been shown to be inhibitors of MAO, which has led several authors to claim that there is no association between alcoholism, which is the most studied psychiatric condition, and platelet MAO if the effect of smoking is removed. With regard to the association between personality and platelet MAO, authors have in general been cautious. In the present paper we describe a number of results which show that there is such an association, both in clinical series if the effect of smoking is removed and in series where smoking have never taken place. A cornerstone in this regard is the significant association between platelet MAO activity and both behaviour/personality, voluntary alcohol intake and biochemical measures of CNS serotonergic activity in non-human primates. Strong evidence that the regulation of platelet MAO activity takes place on a transcriptional level with an involvement of transcription factors, likely to also regulate central monoaminergic activity, are presented.

Activation of arterial blood pressure has been shown to influence higher central nervous activity. In animals, induction of sleep-like states and increases of seizure and pain thresholds in response to baroreceptor stimulation have been reported. In certain human groups, mechanical stimulation of the carotid baroreceptors also increases pain thresholds. The present paper examines the hypothesis that smokers show baroreceptor dependent antinociception as compared to non-smokers. It is speculated that one effect which rewards smoking is the nicotine induced phasic blood pressure increase which leads to baroreceptor stimulation and dampens pain perception. One hundred and twenty subjects were investigated using a recently developed mechanical baroreceptor stimulation technique and an electrical pain stimulus. The group of heavy smokers showed the predicted effect: their pain thresholds were enhanced during conditions of increased baroreceptor activity as compared to the control condition. The group of medium, light and non-smokers, however, did not show this effect. Neither blood lipid levels nor diastolic or systolic blood pressure paralleled the group differences on baroreceptor dependent antinociception. In heavy smokers, the nicotine induced phasic blood pressure increases might have baroreceptor dependent pain dampening effects, which might be among the reinforcing qualities of smoking.

This paper reports on a double blind trial of the effect of buspirone, 15 mg per day, on cigarette withdrawal symptoms and ability of smokers to maintain abstinence during treatment. A total of 61 smokers were randomly assigned to active or placebo conditions. They were maintained on their drug for 2 weeks prior to attempting abstinence and then for a further 4 weeks of abstinence. Subjects attended weekly group sessions of a psychological treatment programme. There was no evidence that the side effects in the active drug group were worse than those in the placebo group. Although there was no significant difference between active and placebo conditions on withdrawal symptoms, smokers in the active drug condition were more than twice as likely to maintain abstinence for the duration of the study than those in the placebo condition (47% versus 16%, chi square = 5.3, P less than 0.025). The results provide preliminary evidence for short-term efficacy of buspirone as an aid to smoking cessation at a low dose. They also provide evidence of a dissociation between withdrawal symptoms and successful abstinence.

This paper describes the results of a postmortem study of the effects of tobacco smoking on the concentrations of 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) as well as the binding of [3H]-8-hydroxy-(di-n-propylamino)-tetralin ([3H]-8-OH-DPAT) and [3H]-ketanserin in six discrete regions of human brain. Smoking was associated with significant decreases in the concentrations of 5-HIAA in the hippocampal neocortex (P less than 0.001), hippocampal formation (P less than 0.05) and the median raphe nuclei (P less than 0.05). The 5-HT level of the hippocampal formation was also significantly reduced in smokers (P less than 0.05). These changes were accompanied by significant increases in the binding of [3H]-8-OH-DPAT in the hippocampal neocortex (P less than 0.01) and hippocampal formation (P less than 0.05). [3H]-Ketanserin binding in the brain regions studied was unaffected by smoking. It is concluded that smoking is associated with a regionally selective decrease in the activity of the serotonergic system of the human hippocampus.

In the present pilot study, an attempt was made to shape and maintain cigarette smoking behavior in rhesus monkeys both with and without the simultaneous use of other reinforcers. Initially, 14 monkeys were trained to suck air and puff on cigarettes using sweetened liquid reinforcer. After smoking had been established, the sweetened liquid reinforcement was removed. Smoking without this reinforcement, referred to as 'voluntary smoking,' was then observed during 20-h daily sessions. Of 14 monkeys studied, 2 have engaged in voluntary smoking for 2 years or longer. The maximum figures recorded for any single 20-h session were 3,271 puffs (20 cigarettes) in one monkey and 16,384 puffs (47 cigarettes) in the other. Although the baseline variability of smoking by these monkeys was quite high, low-nicotine and nicotine-free cigarettes seemed to lead to clear decreases in smoking. In 2 other monkeys that did not perform voluntary smoking, smoking was reestablished under a random-time or a tandem schedule for sweetened liquid reinforcement. Within this situation ('schedule-controlled smoking') schedule manipulations also led to changes in intake of cigarette smoke. The voluntary smoking model described in the present paper should be useful for studying the factors involved in initiating and maintaining smoking behavior and for studying the psychopharmacological effects of smoking, while the schedule-controlled smoking model should be useful for studying the physiological effects of smoking and for studying th relationship of smoking with various disease entities.