Aetiology
Tobacco smoking usually begins in adolescence or early adulthood (typically before the age of 24 years).[9] Smoking behaviour is influenced by biological, genetic, behavioural, social, and environmental factors. Smoking initiation is more likely in households with current smokers where parental approval is more likely and there is greater access to cigarettes.[41] Studies of twins and adoptees suggest that there is a modest genetic influence on regular use of cigarettes that probably interacts with environmental factors.[42] Low socioeconomic status is associated with increased smoking rates, with the prevalence among those living below the poverty line in the US at 24.7%, versus 14.8% in those with a high income.[4] Smoking is more prevalent in people with a history of mental health illness or substance use disorder (SUD).[43] Over 53% of people with SUD die of smoking-related causes.[44] The rate of smoking among those with schizophrenia is over 70%.[43][45] People with HIV/AIDS have high smoking rates (40% to 75%), and the proportion of deaths among people with HIV/AIDS from diseases related to smoking is substantial.[46] Other risk factors for a person deciding to initiate smoking include having peers who smoke, living in a neighbourhood with a high density of tobacco outlets, not participating in team activities, having a high sensation-seeking propensity, and being exposed to smoking in movies.[47]
Adolescents who use nicotine e-cigarettes have been found to be at least 3 times more likely than those who do not to start smoking combustible cigarettes.[48][49][50] Cultural and psychological pressures appear to play a role in nicotine use among high school and middle school students, especially for e-cigarettes. In a national youth survey of middle and high school students in the US, the most common reason for first trying them was "a friend used them" (57.8%), and the most cited reason for current use was "I am feeling anxious, stressed, or depressed" (43.4%).[51] Moreover, 75.7% reported exposure to tobacco product advertisements, reflecting the broad reach of marketing and its intended impact in recruiting younger people.[51]
Pathophysiology
Daily cigarette smokers typically keep smoking because they are addicted to nicotine. The binding of nicotine with neuronal nicotinic acetylcholine receptors stimulates the central nervous mesolimbic dopamine system, which is thought to mediate reinforcement and reward.[52] Nicotine is a very addictive substance with both positive reinforcing effects and nicotine withdrawal symptoms during periods of abstinence. Nicotine withdrawal symptoms may include:
Dysphoric or depressed mood
Irritability, frustration, anger, and anxiety
Increased appetite and weight gain.
The dopaminergic pathway is targeted by existing pharmacotherapies for smoking cessation (nicotine replacement therapy [NRT], varenicline, and bupropion).[1] Nicotine medicines act on nicotinic acetylcholine receptors (nAChRs) to mimic or replace the effects of nicotine from tobacco.[52]
The principal action of NRT is the relief of withdrawal symptoms when a person stops tobacco use, which reduces motivation to smoke, but other benefits include positive reinforcement, particularly for the arousal and stress-relieving effects.[52] Different modes of delivery of NRT affect the speed of nicotine delivery and the degree of positive reinforcement.[52] Combining different modes of delivery of NRT, such as an NRT patch and rapid-delivery formulations (e.g., nasal spray, gum, lozenge), can increase the chances of successfully stopping smoking.[53]
Varenicline activates nAChRs and blocks the binding of nicotine from tobacco to the nAChR (although to a lesser extent than nicotine), resulting in reduced withdrawal symptoms and less reward from a lapse to smoking.[1]
Bupropion (an atypical antidepressant) is a noradrenaline/dopamine reuptake inhibitor that alters nicotine-mediated dopamine responses and can alleviate withdrawal symptoms and reduce the severity of nicotine cravings.[1]
There is emerging evidence to suggest that genetic variation among smokers may affect smoking cessation success; for example, the minor alleles of four single nucleotide polymorphisms (SNPs) within CHRNA3 or CHRNA5 appear to be risk alleles for cessation failure, and may also indicate a preference for treatment with bupropion over NRT.[54]
Behavioural aspects also contribute to the persistence of smoking and the high relapse rates after cessation.[55] The repetitive nature of smoking reinforces this activity, and there can be learned associations with other pleasurable activities (for example, meals and socialising) and with attempts to regulate mood to cope with stresses.[52] Relapses often occur in social situations or during periods of situational stress.
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