• Users Online: 139
  • Print this page
  • Email this page


 
 
Table of Contents
REVIEW
Year : 2019  |  Volume : 33  |  Issue : 3  |  Page : 125-134

Tobacco and smoking cessation


1 Department of Psychiatry, Changhua Christian Hospital; Department of Psychiatry, Lukang Christian Hospital, Evergreen Campus; Department of Counseling, National Changhua University of Education, Changhua; Department of Occupational Therapy, Asia University, Wufeng; Department of Medicine, Chung Shan Medical University, Taichung, Taiwan
2 Department of Psychiatry, Lukang Christian Hospital, Evergreen Campus, Changhua, Taiwan

Date of Submission29-May-2019
Date of Decision11-Jul-2019
Date of Acceptance11-Jul-2019
Date of Web Publication30-Sep-2019

Correspondence Address:
Nan- Ying Chiu
No. 888, Section 2, Lutung Road, Lukang Town, Changhua County 505
Taiwan
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/TPSY.TPSY_26_19

Rights and Permissions
  Abstract 


Background: Tobacco products have been used by human for a long history. The prevalence of tobacco use varies in different countries. Tobacco use is different from tobacco use disorder. Tobacco use disorder is a problematic pattern of tobacco use leading to significant distress or impairment. Cigarette smoking is a chronic relapsing substance use disorder caused by addiction to nicotine. Tobacco smoke contains over 7,000 different chemical compounds, of which 93 of them are harmful substances. Methods: In this review, the authors intended to address the issues of harmful effects of cigarette smoking and how to cease smoking. Results: Abundant studies showed that tobacco use is the main risk factor of morbidity and mortality in the world. People who use tobacco products should be advised to quit smoking and offered appropriate treatment. It is better for health-care providers to make the smoking cessation treatment as a standard component of medical care. Data from evidence-based literature showed that smoking cessation therapy can significantly raise smoking cessation rates and should be routinely in persons who are willing to quit tobacco smoking. Smoking cessation treatment includes psychosocial interventions and pharmacological treatment, which may be used in combination. Nonpharmacological management may be individual or group sessions, and it may include motivational interviewing, cognitive behavioral therapy, and others. Delivery formats of stop-smoking interventions are varied. Pharmacological therapy includes nicotine replacement treatment and smoking aids such as bupropion and varenicline. Morbidity and mortality rates are decreased with tobacco cessation at any point in time, although cessation before the age of 40 years has the most significant effect. Conclusion: The Tobacco Hazards Prevention Act took effect since 1997 in Taiwan. Rates of Taiwanese tobacco use have been steadily declining. Brilliant achievements in the field of tobacco control in Taiwan draw international attention.

Keywords: comorbidity and mortality of cigarette smoking, nicotine replacement, substance use disorder, varenicline


How to cite this article:
Chiu NY, Chang CJ. Tobacco and smoking cessation. Taiwan J Psychiatry 2019;33:125-34

How to cite this URL:
Chiu NY, Chang CJ. Tobacco and smoking cessation. Taiwan J Psychiatry [serial online] 2019 [cited 2019 Oct 15];33:125-34. Available from: http://www.e-tjp.org/text.asp?2019/33/3/125/268314




  Introduction Top


Tobacco use, especially cigarette smoking, is a major risk of morbidity and mortality and is the leading preventable etiology of death worldwide [1]. Tobacco use is different from tobacco use disorder in that the person is not significantly distressed or impaired due to its use. Tobacco use disorder is a problematic pattern of tobacco use leading to clinically significant impairment or distress. That impairment or distress is manifested over a 12-month period by the presence of at least two criteria as defined by the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). These criteria are designed to measure the physical and/or psychological impact of a person's tobacco use (e.g., tolerance, withdrawal, craving, interference with other activities, performance, or relationships) [2]. By the DSM-5 criteria, tobacco use disorder can be diagnosed in about half of people who use tobacco. The development of tobacco use disorder is multifactorial, including societal, community, and individual factors [3].


  Tobacco Use Prevalence and Patterns Top


Tobacco has been used since the earliest recorded history of the Western hemisphere. Cigarettes began to be mass-produced and marketed in the early 20th century. The resulting annual consumption was increased from < 4 billion cigarettes in 1905 to more than 100 billion 20 years late [4]. The data showed that the number of current smokers is 1.6 billion all over the world. The 2015 Global Burden of Disease Study from 195 countries and territories estimated that 25.0% of men worldwide smoke daily and that 5.4% of women worldwide smoke daily [1]. Tobacco consumption was peaked in the mid-1980s. According to the 2016 fast fact information of the Centers for Disease Control and Prevention of the United States (www.cdc.gov/tobacco/data_statistics/fact_sheets/fast_facts/), and the 2018 report of the World Health Organization [5], the epidemic of tobacco-caused diseases has spread throughout the world, globally about 7.1 million people die annually of tobacco-related diseases, and by 2030, the annual rate is expected to rise to 10 million tobacco-related deaths. Since the 2000s, there has been a steady decline in tobacco smoking in Taiwan [6]. In 2017, 14.5% of the people in the age of 18 and over 18 years smoked cigarettes. In Taiwan, considerable variations exist in smoking prevalence according to gender, age, socioeconomic status, and ethnicity. In 2017, 26.4% of male adults above the age of 18 years and 2.3% of female adults above the age of 18 years used tobacco products in Taiwan [6]. The daily tobacco consumption of smokers above the age of 18 years was 19.2 in Taiwan [6]. The prevalence of smoking among patients with mental illness and substance use disorder was much higher than those in the general population. Exposure to cigarette smoke is common in persons in the general population of nonsmokers, and they are at risk at home, work, or public places when socializing [7].


  The Risks of Tobacco Use Top


Of about 7,000 different chemical compounds which have been identified in cigarette smoke, 93 are carcinogens and harmful substances [6],[8]. Some important components of tobacco smoke include:

  • Nicotine is the substance in cigarettes which is addictive, but it does not cause carcinoma and has, at most, a small effect on risk of cardiovascular (CV) disease.
  • Tar is the name given to all the other chemicals in the smoke particles that are linked to cancer, heart disease, pulmonary disease, and the other diseases caused by smoking.
  • Carbon monoxide (CO) is a gas inhaled by tobacco product users from cigarettes. It is linked to CV disease and has adverse effects in pregnancy.


Unfortunately, it is not just the direct effect of tobacco smoke that causes the damage.

There are some different chemicals in tobacco smoke that are absorbed into bloodstream and find their way to all parts of the body where they cause damage. The effects of smoking can be seen in the heart, blood vessels, and even stomach. In women, components of tobacco smoke can also be found in the cervix.

The causal link between smoking and increased morbidity and mortality is now firmly established [8] (World Health Organization. WHO Global Report: Mortality at www.who.int/iris/handle/10665/44815). In Taiwan, cigarette smoking is responsible for about 27,000 deaths per year recently, i.e., more than 75 deaths per day [6]. On average, one dies from smoking-related diseases every 20 min in Taiwan [6]. On an individual level, this means that long-term regular smokers can expect to lose, on average, 10 years of life. The study in the United Kingdom showed that about half to two-thirds of all long-term smokers die prematurely because of their smoking and do so on average 20 years earlier than if they did not smoke [9].

The main causes of death attributable to cigarette smoking are carcinomas, CV disease, and pulmonary disease [10]. Lung cancer was almost unheard of before the smoking of manufactured cigarettes because smoking was popular at the beginning or the 20th century. The risk of contracting lung cancer for a cigarette smoker is 15 times greater than that of a nonsmoker [11]. The risk accumulates over time and is related to both daily cigarette consumption and duration of smoking. Both 90% of morbidity and mortality of lung cancer are related to using tobacco products [11],[12].

The average smoker has about double the risk of developing CV diseases compared to someone who has never smoked [13]. Those CV diseases include ischemic heart disease, cerebrovascular disease (stroke), aortic aneurysm, myocardial degeneration, and atherosclerosis [14].

Chronic obstructive pulmonary disease (COPD) is smoking-related for the most part, includes chronic bronchitis and emphysema, and is a result of changes in the central and peripheral airways, alveoli, capillaries, and immune system [8]. COPD, as a consequence of smoking, accounts for over one-fifth of all smoking-related deaths [15]. Smokers often talk of having a “smoker's cough;” this is usually a sign of COPD, and they should have their lung function testing to assess how much damage has already been done. If they wait until they are breathless, they will already be well on the way to permanent disability.

There are many other life-threatening diseases caused by smoking. Carcinogens in cigarette smoke are ingested, dispersed, and eliminated throughout the body, and therefore, smoking is linked with a large number of cancers other than lung cancer. They include cancers of the upper respiratory system, esophagus, urinary bladder, kidney, stomach, pancreas and myeloid leukemia [14]. Smoking is also a cause of noncancerous but still life-threatening illnesses, such as ulcers of the stomach and duodenum. About one-third of lifelong smokers avoids premature death despite their cigarette smoking, but none escapes the ill-health effects of smoking [15]. Smoking causes long-term disability, both in those smokers who are killed by smoking cigarettes and those who ultimately die from some other causes. Lifelong chronic smokers expect to experience diseases of old age earlier than nonsmokers. Smoking is strongly linked with nonfatal debilitating diseases including age-related hearing loss and cataract, blindness, chronic back and neck pain, inflammatory bowel disease, diabetes mellitus (Type II), gum disease, osteoarthritis, osteoporosis, as well as rheumatoid arthritis; smoking also causes wrinkles [16]. In addition, smokers are at an increased risk of anesthetic management problems during surgery [17]. Postoperatively, smoking patients' wounds heal more slowly and they are more vulnerable to postsurgical complications than those of nonsmokers [18],[19]. Cigarette smoking decreases the chances of conception in both men and women. In male smokers, it is associated with reduced sperm count [20], and in women, it is linked to hormonal effects that make pregnancy less likely [21]. It is widely recognized that cigarette smoking during pregnancy harms the fetus and the mother. The health risks posed by smoking during pregnancy are threefold: to the mother, the unborn fetus, and eventually, the newly born child [22].

Many people with psychiatric illnesses use tobacco product [5]. A strong link exists between smoking and a range of mental disorders [5], notably schizophrenia, mood disorders, and substance use disorders, but the nature of the relationship remains unclear. Whether smoking causes or exacerbates these conditions, whether they make it more likely that a sufferer will smoke, or whether there is a common underlying cause has yet to be established [23]. Depressed mood is also a withdrawal symptom, and cases of major depressive disorder have been reported following smoking cessation. It is a widely held thought among smokers and nonsmokers that smoking helps relieve stress and anxiety. But evidence suggests that smoking does not help to reduce stress and that when smokers do stop smoking, their stress and anxiety levels actually decrease [23].

Exposure to cigarette smoke is common among nonsmokers, which is passive smoking. Parental smoking is linked to increased risk of childhood respiratory diseases and ear infections [24]. Partner and occupational exposure to tobacco smoke increases risk of lung cancer, respiratory disease, and coronary heart disease [25].


  The Health Benefits of Stopping Smoking Top


Smoking cessation is the single most important thing a person can do to improve their current and future health [8]. The greatest benefit is smokers without smoking-related disease who stop tobacco use before age of 35 years: They can have a normal life expectancy [14]. But smokers who stop later on in life than this age, even into their old ages, can expect to significantly improve their life expectancy [8],[9] [Table 1].
Table 1: Beneficial health changes when smokers stop smoking

Click here to view



  Assessment of Tobacco Use Top


The level of nicotine dependence should be assessed to enable the provision of appropriate treatment and to set success rates in the context of the type of smokers being treated. The number of cigarettes smoked per day is not a stronger indicator of how dependent a smoker is. A simple and reliable way to measure nicotine dependence is to ask: “How soon after waking do you smoke the first cigarette of the day?” If a smoker smokes within 30 min of waking, they are a more dependent smoker and would benefit from more intensive smoking cessation treatment and higher dose medication. This question is taken from the Fagerström Test for Nicotine Dependence (FTND) [26]. In research, the full set of questions is usually used when assessing nicotine dependence [26,27]. In Taiwan, we use this test tool too [6]. The higher the score, the more dependent a smoker being (the maximum score is 10) [26] [Table 2].
Table 2: Fagerström Test for Nicotine Dependence

Click here to view


To assess the interest in quitting smoking and willingness to attend for smoking cessation treatment is crucial. The simplest way of determining whether a person is interested in stopping smoking is to ask them. The stages of change model (or the transtheoretical model) are used by some services to assess motivation to quit smoking [28] but have not been found in research to improve on a simple common-sense approach. The limitation of this model is explored [29],[30]. The stages of change model should not be used because it makes the assessment of readiness to quit smoking more complex and involved than is necessary, may provoke the wrong intervention strategy, and is likely to lead to effective interventions not being offered to people who would have responded.

To assess smoking characteristics is another issue. The cessation rates are lower for more dependent smokers, in more deprived socioeconomic groups, and among those with lower educational levels [31]. Young smokers are less likely to be successful in attempts to stop smoking [31]. The chances of success of quit attempts are also lower in those who live with smokers and those who live alone. Spending more time in the company of smokers appears to be related to lower success rates [32]. Persons with these negative prognostic signs may need more intensive help, for example, telephone contact, higher dose of pharmacotherapy, or combinations of medications.

A CO monitor is an important piece of equipment to have for treating smokers [33]. CO is one of the constituents of cigarette smoke, and when inhaled, it takes the place of oxygen on hemoglobin contained in the red blood cells. CO is linked to coronary heart disease and is associated with adverse effects in pregnancy. CO is an approximate indicator of how much a smoker has smoked. CO is eliminated from the body fairly rapidly (in about 24 hours) and so if a person has not smoked since their quit date, then their CO reading should be below 10 ppm (parts per million) or < 7 ppm above the ambient CO reading [33]. CO monitor not only verifies that persons are not smoking but also is a useful motivational tool. Smokers like to see the change in CO when they stop smoking. A CO monitor is also useful for confirming abstinence before supplying more pharmacotherapies [33].


  Tobacco Withdrawal Syndrome Top


Tobacco withdrawal symptoms are physical and psychological changes that occur following interruption, reduction, or termination of tobacco use [34]. They are temporary and are a product of physical or psychological adaptation to long-term tobacco use, which needs a period of readjustment when tobacco is no longer used.

The withdrawal syndrome comprises a range of symptoms, including irritability/aggression, depression, restlessness, poor concentration, increased appetite, lightheadedness, nighttime awakening, constipation, mouth ulcers, and urges to smoke. Those symptoms, especially urges to smoke, lead to relapse early in a quit attempt. Most withdrawal symptoms last no longer than four weeks, and therefore, assisting smokers through the first four weeks is important [34]. More severe urges to smoke and depressive mood are associated with a greater risk of relapse. There is no evidence that greater weight gain is associated with greater risk of relapse. Smokers expect to feel physically better when they stop smoking, but many report feeling physically worse. Many smokers report increased coughing, chest problems, as well as soreness of the throat and mouth ulcers. The short-term decrease in salivary immunoglobulin A, probably as a result of the stress involved with quit smoking, may explain an increase in respiratory tract infections and oral ulcers.

Some smokers report an increased anxiety at the time of stopping smoking. In the past, this was thought that increased anxiety is not a tobacco withdrawal symptom but just a response to the act of trying to smoking cessation. Nicotine withdrawal symptoms are experienced by many, but not all, smokers when they stop smoking. Most of those symptoms disappear with four weeks. Increased appetite can persist past four weeks. Urges to smoke may go on for a much longer time. But as long as people do not use tobacco, those symptoms will become less frequent. Furthermore, the frequency of each symptom is different – increased appetite and urges to smoke are the highest and lightheadedness is the lowest [35]. The management of tobacco withdrawal syndrome is the key issue while doing smoking cessation.


  Treatment Options of Smoking Cessation Top


Treatment goals of tobacco use disorder are to reduce or stop (a) tobacco use behaviors, (b) harm due to nicotine and other toxins in tobacco, as well as (c) harm due to second-hand smoke exposure in children and other contacts of smokers [36]. The US Preventive Services Task Force (www.uspreventiveservicestaskforce.org/Page/Document/Recommendation) in 2019 recommends that physicians ask all adults about tobacco use, advise those who use tobacco to stop, and provide behavioral interventions and Food and Drug Administration (FDA)-approved pharmacotherapy for smoking cessation. The American College of Cardiology Expert Consensus Decision Pathway on Tobacco Cessation Treatment supplements the US Preventive Services Task Force recommendations for nonpregnant adults, using the 5A's model (a, ask about tobacco use; b, advise quitting smoking; c, assess tobacco effects; d, assist in a plan for smoking cessation; and e, arrange follow-up) [37].

It states that effective treatment is best achieved by a team approach. Intervention should occur at all points of care with all health professionals, including physicians, nursing staff, pharmacists, and other professionals. Counseling should focus on the improvement of health as it pertains to the particular patient, rather than only general information about the harms of persistent smoking. The follow-up should be through in-person visit, phone, or Internet patient portal within 2–4 weeks of initial cessation plan. For the patient who declines cessation treatment, should offer it again at every follow-up. The workers should carefully monitor former smokers for relapse.

Evidence-based treatment is preferable to nonevidence-based methods [38]. Evidence-based strategies include nicotine replacement treatment (NRT), other pharmacotherapies (e.g., sustained-release bupropion and varenicline), as well as counseling, which means that pharmacological interventions and behavioral interventions are the choice for tobacco use disorder. Behavioral interventions include individual counseling, group counseling, telephone counseling, and self-help materials. High-quality evidence indicates that a combination of drug therapy and high-intensity behavioral treatment is more effective than pharmacotherapy and behavioral treatment alone [39].


  Nonpharmacological Behavioral Interventions for Tobacco Use Disorder Top


Nondrug treatments for nicotine dependence include behavioral skills training using cognitive behavioral therapy (CBT) techniques, motivational interviewing (MI), as well as incentives to motivate and to reinforce behavior change [38, 40-43]. Those strategies are often used in combination. Behavioral therapies, based on principles of behavioral and cognitive psychology, are intended to bolster smokers' self-control over their smoking behavior by helping them change unhelpful cognitions and structuring efforts to change smoking behavior through a range of techniques such as goal setting (e.g., setting a quit day), self-monitoring, rewards, and skills training to help smokers learn, practice, and implement techniques to help them resist urges to smoke after quitting. MI is a goal-oriented, client-centered counseling style that attempts to help smokers change behavior through exploring and resolving ambivalence about making changes in their behaviors [42] [Table 3].
Table 3: Behavioral therapies for nicotine dependence

Click here to view


A randomized clinical trial reported recently that addition of financial incentives to free smoking cessation aids (NRT, bupropion, and varenicline) and free e-cigarettes resulted in a significantly higher rate of sustained smoking abstinence (six months or more) than did free smoking cessation aids or free e-cigarettes alone. Smokers who have received only information and motivational text messages with free smoking cessation aids or e-cigarettes have a significantly lower sustained smoking abstinence rate [44]. A physician's advice to quit smoking and brief guidance provided in clinic practice can be made more effective by connecting smokers with other resources available to the treatment team [39]. Behavioral treatments work best when combined with pharmacological smoking treatment and delivered by well-trained tobacco treatment specialists over multiple face-to-face and/or phone sessions with smokers [38],[45].

There are some delivery formats of quit-smoking interventions with evidence of effectiveness [46]. Brief interventions consisting of advice to stop smoking delivered by a physician or nursing staff combined with pharmacotherapy is typically the most common way smokers obtain assistance to quit smoking. Nevertheless, even just advice to quit from a physician has a positive effect on increasing smoking quit rates [47] [Table 4].
Table 4: Delivery formats of quit-smoking interventions with evidence of effectiveness

Click here to view



  Pharmacological Interventions for Smoking Cessation Top


Drug treatment acts synergistically with behavioral counseling to increase quit rates and should be encouraged for virtually all daily smokers and considered on a case-by-case basis for nondaily smokers [48]. The US FDA has approved five nicotine replacement therapy (NRT) products as well as bupropion and varenicline for quit smoking [49].

In the United States, NRT is available as patches, gum, nasal spray, lozenges, and oral inhaler. In Taiwan, we do not have lozenges and nasal spray [6]. NRT provides nicotine to reduce withdrawal symptoms which occur when a smoker stops smoking. But NRT does not replicate the pleasurable effects of smoking. NRT may also reduce the satisfaction from smoking a cigarette if there is a lapse. Each NRT product has about the same efficacy in clinical trials, increasing quit rates with risk ratios of about 1.6 compared with placebo in a meta-analysis [45]. The selection of NRT product can reflect a smoker's preference. NRT products are sold in different strengths. More dependent smokers do better with high doses of nicotine. The patch is generally used as the primary product because compliance is greatest for nicotine patch, lower for nicotine gum, and very low for inhaler. No harm from long-term NRT use has been reported [50]. Oral NRT products produce relatively low blood nicotine levels and require frequent use (once every 1–2 hours) to relieve nicotine withdrawal symptoms. Nicotine from oral products is absorbed through the buccal mucosa in the free-base form [45]. Drinking acidic liquids such as coffee within 10 min of using oral NRT products acidifies the mouth and impairs nicotine absorption. Smokers should be advised to avoid those kinds of beverages before and during product use. The efficacy of NRT for smoking cessation is well-established. Combining nicotine patch with a more quickly absorbed form of NRT is more effective than using a single product, with a risk ratio of 1.34 compared with the use of a single product in a meta-analysis [45]. Although NRT is probably not harmless, it is much less harmful than tobacco use.

Bupropion is an antidepressant. It simulates some of nicotine's effects on the brain by blocking neuronal uptake of dopamine and norepinephrine [51]. It relieves nicotine withdrawal symptoms and reduces the reward from tobacco smoking. Sustained-release bupropion is similar in efficacy to NRT and is effective in smokers with or without depression [52]. It reduces seizure threshold and should not be used in patients who have increased risk of seizures. Bupropion is approved by the FDA for 12 weeks' use, but extended treatment for one year reduces the relapse rate after initial cessation [53]. Combination treatment with bupropion and nicotine patch is more effective than patch alone or bupropion alone [54]. It has also been studied in combination with varenicline, showing enhanced quit rates at 12 and 26 weeks but not at 52 weeks [55].

Varenicline is a partial agonist at the α4 β2 nicotinic cholinergic receptor that mediates brain dopamine release and that is believed to be the primary mediator of nicotine [56]. As a partial agonist, it activates the nicotine receptor, producing about 50% of the maximal effects as nicotine and thereby reducing the intensity of tobacco withdrawal syndrome. It binds tightly to the nicotine receptor, preventing receptor binding by nicotine from cigarette smoke, and reducing the rewarding effects of smoking. Nicotinic receptor antagonism from varenicline results in reduced pleasure from smoking and is believed to explain why some smokers reduce their cigarette consumption even before their designated quit day and why varenicline may reduce the likelihood of transition that an individual who slips and smokes a cigarette will return to regular smoking. Varenicline is proven to be more effective in promoting smoking cessation than single NRT or bupropion in many clinical trials [57]. The recent largest was the Evaluating Adverse Events in a Global Smoking Cessation Study (EAGLES), which included over 8,000 smokers [52]. It compared varenicline, bupropion, nicotine patch, and placebo given for 12 weeks along with brief counseling. Continuous quit rates from 9 to 24 weeks were as follows: varenicline 21.8%, bupropion 16.2%, nicotine patch 15.7%, and placebo 9.2%. Quit rates are higher in smokers without psychiatric illness than those with psychiatric disease, but the relative efficacy across drugs is similar [52]. Extending varenicline for six months to prevent relapse is effective and has been approved by US FDA [58]. Many concerns over adverse events of varenicline were not confirmed by the results of the EAGLES trial, and the FDA removed varenicline's black box warning in 2016.

Some other smoking cessation medications are available. In controlled clinical trials, nortriptyline and clonidine have been shown to enhance smoking cessation, but they are not approved by US FDA for this indication and are rarely used (the 2019 US Preventive Services Task Force at www.uspreventiveservicestaskforce.org/Page/Document/Recommendation and Agency for Healthcare Research and Quality: Treating Tobacco Use and Dependence: 2018 update at www.ahrq.gov/professionals/clinicians-providers/guidelinesrecommendations/tobacco/index.html).

Cytisine (a partial agonist of nicotinic acetylcholine receptors with an affinity for the α4 β2 receptor subtype) has a mechanism similar to varenicline. It has been used as a smoking cessation agent in Europe for decades but is not approved for use in the US despite calls for licensing it worldwide after clinical trials found it to be more effective than placebo for short-term and long-term abstinence [59],[60].

E-cigarettes, also known as electronic nicotine delivery systems (ENDS), differ from cigarettes and other combustible tobacco products in that they do not produce smoke by burning tobacco. E-cigarette device varies considerably in design, such as e-pipe, e-cigar, large-size tank devices, medium-size tank devices, rechargeable e-cigarette, and disposable e-cigarette [61]. They consist of battery-powered atomizers producing nicotine vapor which then cools either in the mouthpiece of the device or in the mouth of a person with a tobacco use to form an aerosol. A Cochrane systematic review concluded that weak evidence exists that ENDS containing nicotine help persons achieve tobacco abstinence in the long-term compared with placebo ENDS and that ENDS have similar efficacy to nicotine patches [62]. From a public health perspective, concerns have been raised that ENDS may serve as a gateway to the use of conventional cigarettes among nonsmoking adolescents [63]. The long-term health consequences of ENDS remain unknown. But the vapor/aerosol created by ENDS contains formaldehyde [64], and e-juice contains carcinogens [65]. Approaches to the use of ENDS in the treatment of nicotine dependence vary by nations. The US Preventive Services Task Force has concluded that not enough evidence exists to recommend ENDS for the treatment of tobacco use disorder. The risk–benefit ratio of using ENDS for smoking cessation remains uncertain [66] [Table 5].
Table 5: FDA-Approved Smoking Cessation Medications

Click here to view



  Prognosis, Relapse Prevention, and Prevention of Smoking Initiation Top


The success rates for long-term tobacco cessation are currently low. More than half of smokers attempt to quit annually, but only about a quarter to a third of those attempting to quit use evidence-based therapies [67]. There are numerous disparities in access to and use of those treatments, including age, gender, race and ethnicity, geographic location, and comorbidities [67]. Despite the blow annual quit rate, in 2015, 59% of adults who had ever smoked had quit, and the rate of tobacco use in the US has been steadily declining [67].

Relapse back to tobacco smoking is part and parcel of nicotine dependence. Every smoker who quits remains prone to relapse [68]. The risk for relapse is greatest early on in the quit attempt, which a sharp drop-off in the first week. By 2–3 months, the risk is considerably reduced, and most of the smokers who have remained abstinent for that period are likely to become lifelong ex-smokers [27]. Smokers report acute stress as a reason for returning to smoking, such as arguments with partner of family member, the pressure is on at work, on holidays, being under the influence of alcohol, being in the company of smokers in a smoking permissive environment, or being too happy or in low mood. There is a lack of evidence to support the use of any specific relapse prevention intervention, although limited methodologically sound research exists on this issue [27].

The prevention of smoking initiation is targeted primarily at youth and young adults [69]. Data showed that few people start to smoke after the age of 26 years and more than 80% of adults who report ever trying cigarette do so by the age of 18 years [69]. There are likely some school-based programs that are effective in reducing smoking initiation; it appears that providing educational session in school may increase efficacy [70]. More research are needed on the best way to give information that may deter the initiation of tobacco use. Public policy measures include increase in cost of tobacco products, limitation of marketing, setting up smoke-free laws and policies, and reduction of tobacco products supply may prevent smoking initiation [71],[72],[73],[74].


  Smoking Cessation Services in Taiwan Top


“Smoking kills” is the number one killer in Taiwan [6]. The Tobacco Hazards Prevention Act took effect since 1997 in Taiwan [75]. The goal is to promote joint efforts by all to prevent tobacco hazards and then to create smoke-free Taiwan for all [75]. Taiwan has been providing smoking cessation therapy paid by health and welfare surcharges since 2002. Nicotine addicts above 18 years of age (those scoring at least 4 points on the FTND or smoking 10 or more cigarettes a day) were provided with two treatment sessions every year, with each treatment providing up to eight weeks of medication and short-term counseling services. The Health Promotion Administration (HPA) of the Ministry of Health and Welfare, Taiwan, announced the Smoking Cessation Action in 2010 and raised funds for Comprehensive Smoking Cessation Network.

To help more smokers quit smoking, the Second-generation Cessation Services Payment Scheme was launched on March 1, 2012. Payment subsides and cessation treatments were expanded from outpatients to inpatients and emergency room patients. The HPA integrated the resources which actively promote smoking cessation within workplaces, school campuses, and other institutes to provide smoking cessation health-care education, counseling, and training [6]. Statistical data released by the HPA reveal that the Taiwan Smokers' Helpline provided services for many smokers, and the smoking cessation success rate reached 42.4% over a period of six months. The six-month success rate of second-generation comprehensive smoking cessation service is 28.8% [6].


  Conclusion Top


The usage of tobacco products by people has a long history. The prevalence of tobacco use is high in most of the countries. A strong link exists between tobacco smoking and psychiatric illnesses. Tobacco use is different from tobacco use disorder. Tobacco use disorder is a problematic pattern of tobacco use, leading to significant distress or impairment. Cigarette smoking is a chronic relapsing substance use disorder caused by addiction to nicotine.

Tobacco smoke contains over 7,000 different chemical compounds, of which 93 of them are harmful substances. Many severe complications of tobacco use are well-known. Tobacco use is the main risk factor of morbidity and mortality in Taiwan and in the world. Because tobacco use is associated with a high burden of morbidity, mortality, and economic loss, all people who use tobacco should be advised to quit smoking and offered treatment for them. The reversible relationship between cigarette smoking and many diseases provides a strong rationale for health-care providers to make the smoking cessation treatment a standard component of medical care. Every patient should be asked about tobacco use at every visit.

Evidence-based therapy can raise smoking cessation rates and should be routinely in persons who are willing to quit tobacco products. Smoking cessation treatment includes psychosocial behavioral and pharmacological approaches, which may be used in combination. Nonpharmacological management may be used in individual or group sessions, and it may include meditational interviewing (MI), cognitive behavioral therapy (CBT), and others. Delivery formats of stop-smoking interventions vary. Pharmacological therapy includes nicotine replacement and smoking aids such as bupropion and varenicline. Morbidity and mortality rates are decreased with tobacco cessation at any point in time, although cessation before the age of 40 years has the most significant effect.


  Acknowledgements Top


The contents of this review contain information on off-label use of released licensed medications. The readers should read package inserts on dosages and adverse effects of the drugs mentioned in this review before prescribing them to their patients.


  Financial Support and Sponsorship Top


Nil.


  Conflicts of Interest Top


There are no conflicts of interest.



 
  References Top

1.
GBD 2015 Tobacco Collaborators: Smoking prevalence and attributable disease burden in 195 countries and territories, 1990-2015: a systematic analysis from the global burden of disease study 2015. Lancet 2017; 389: 1885-906.  Back to cited text no. 1
    
2.
Higa-McMillan CK, Smith RL, Chorpita BF, et al.: Common and unique factors associated with DSM-IV-TR internalizing disorders in children. J Abnorm Child Psychol 2008; 36: 1279-88.  Back to cited text no. 2
    
3.
Kalkhoran S, Benowitz NL, Rigotti NA: Prevention and treatment of tobacco use: JACC health promotion series. J Am Coll Cardiol 2018; 72: 1030-45.  Back to cited text no. 3
    
4.
McNally WD: The tar in cigarette smoke and its possible effects. Am J Cancer 1932; 16: 1502-14.  Back to cited text no. 4
    
5.
World Health Organization, Research for International Tobacco Control: WHO Report on the Global Tobacco Epidemic. Geneva, Switzerland: World Health Organization, 2018.  Back to cited text no. 5
    
6.
Health Promotion Administration: 2018 Taiwan Tobacco Control Annual Report. Taipei: Health Promotion Administration, Taiwan, 2018.  Back to cited text no. 6
    
7.
Glantz SA, Parmley WW: Passive smoking and heart disease. Mechanisms and risk. JAMA 1995; 273: 1047-53.  Back to cited text no. 7
    
8.
U.S. Department of Health and Human Servicesp: The Health Consequences of Smoking: a Report of the Surgeon General. Atlanta, Georgia, USA: Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004.  Back to cited text no. 8
    
9.
Doll R, Peto R, Boreham J, et al.: Mortality in relation to smoking: 50 years' observations on male British doctors. BMJ 2004; 328: 1519.  Back to cited text no. 9
    
10.
Twigg L, Moon G, Walker S: The Smoking Epidemic in England. London: Health Development Agency, 2004.  Back to cited text no. 10
    
11.
Boffetta P, Pershagen G, Jöckel KH, et al.: Cigar and pipe smoking and lung cancer risk: a multicenter study from Europe. J Natl Cancer Inst 1999; 91: 697-701.  Back to cited text no. 11
    
12.
Sastre MT, Mullet E, Sorum PC: Relationship between cigarette dose and perceived risk of lung cancer. Prev Med 1999; 28: 566-71.  Back to cited text no. 12
    
13.
Wald NJ, Hackshaw AK: Cigarette smoking: an epidemiological overview. Br Med Bull 1996; 52: 3-11.  Back to cited text no. 13
    
14.
Royal College of Physicians: Nicotine Addiction in Brain. London: Royal College of Physicians, 2000.  Back to cited text no. 14
    
15.
Peto R, Lopez A, Boreham J, et al.: Mortality from Smoking in Developed Countries 1950-2000. 2nd ed. Oxford, UK: Oxford University Press, 2004.  Back to cited text no. 15
    
16.
Jorgensen LN, Kallehave F, Christensen E, et al.: Less collagen production in smokers. Surgery 1998; 123: 450-5.  Back to cited text no. 16
    
17.
Rhodes JM: Colonic mucus and ulcerative colitis. Gut 1997; 40: 807-8.  Back to cited text no. 17
    
18.
Silverstein P: Smoking and wound healing. Am J Med 1992; 93: 22S-4S.  Back to cited text no. 18
    
19.
Møller AM, Villebro N, Pedersen T, et al.: Effect of preoperative smoking intervention on postoperative complications: a randomised clinical trial. Lancet 2002; 359: 114-7.  Back to cited text no. 19
    
20.
Chia SE, Lim ST, Tay SK, et al.: Factors associated with male infertility: a case-control study of 218 infertile and 240 fertile men. Br J Obstet Gynaecol 2000; 107: 55-61.  Back to cited text no. 20
    
21.
Barbieri RL: The initial fertility consultation: recommendations concerning cigarette smoking, body mass index, and alcohol and caffeine consumption. Am J Obstet Gynecol 2001; 185: 1168-73.  Back to cited text no. 21
    
22.
Benowitz N, Dempsey D: Pharmacotherapy for smoking cessation during pregnancy. Nicotine Tob Res 2004; 6 (Suppl 2): S189-202.  Back to cited text no. 22
    
23.
Taylor G, McNeill A, Girling A, et al. Change in mental health after smoking cessation: systematic review and meta-analysis. BMJ 2014; 348: g1151.  Back to cited text no. 23
    
24.
Cook DG, Strachan DP: Health effects of passive smoking 3. Parental smoking and prevalence of respiratory symptoms and asthma in school age children. Thorax 1997; 52: 1081-94.  Back to cited text no. 24
    
25.
Department of Health: Smoking Kills: a White Paper on Tobacco. London: The Stationary Office, 1998.  Back to cited text no. 25
    
26.
Heatherton TF, Kozlowski LT, Frecker RC, et al.: The Fagerström test for nicotine dependence: a revision of the Fagerström tolerance questionnaire. Br J Addict 1991; 86: 1119-27.  Back to cited text no. 26
    
27.
Hajek P, Stead LF, West R, et al.: Relapse prevention interventions for smoking cessation. Cochrane Database Syst Rev 2005; (1): CD003999.  Back to cited text no. 27
    
28.
DiClemente CC, Prochaska JO, Fairhurst SK, et al.: The process of smoking cessation: an analysis of precontemplation, contemplation, and preparation stages of change. J Consult Clin Psychol 1991; 59: 295-304.  Back to cited text no. 28
    
29.
West R: Time for a change: putting the transtheoretical (stages of change) model to rest. Addiction 2005; 100: 1036-9.  Back to cited text no. 29
    
30.
Sutton S: Back to the drawing board? a review of applications of the transtheoretical model to substance use. Addiction 2001; 96: 175-86.  Back to cited text no. 30
    
31.
Hatziandreu EJ, Pierce JP, Lefkopoulou M, et al.: Quitting smoking in the United States in 1986. J Nat Cancer Inst 1990; 82: 1402-6.  Back to cited text no. 31
    
32.
Richmond RL, Kehoe LA, Webster IW: Multivariate models for predicting abstention following intervention to stop smoking by general practitioners. Addiction 1993; 88: 1127-35.  Back to cited text no. 32
    
33.
McEwen A, Hajek P, McRobbie H, et al.: Manual of Smoking Cessation: a Guide for Counselors and Practitioners. Oxford, United Kingdom: Blackwell Publishing, 2006.  Back to cited text no. 33
    
34.
Hughes JR: Tobacco withdrawal in self-quitters. J Consult Clin Psychol 1992; 60: 689-97.  Back to cited text no. 34
    
35.
West RJ, Hajek P, Belcher M: Severity of withdrawal symptoms as a predictor of outcome of an attempt to quit smoking. Psychol Med 1989; 19: 981-5.  Back to cited text no. 35
    
36.
Jha P, Ramasundarahettige C, Landsman V, et al.:21st-century hazards of smoking and benefits of cessation in the United States. N Engl J Med 2013; 368: 341-50.  Back to cited text no. 36
    
37.
Barua RS, Rigotti NA, Benowitz NL, et al.:2018 ACC expert consensus decision pathway on tobacco cessation treatment: a report of the American College of Cardiology task force on clinical expert consensus documents. J Am Coll Cardiol 2018; 72: 3332-65.  Back to cited text no. 37
    
38.
Stead LF, Koilpillai P, Fanshawe TR, et al.: Combined pharmacotherapy and behavioural interventions for smoking cessation. Cochrane Database Syst Rev 2016; 3: CD008286.  Back to cited text no. 38
    
39.
van Eerd EA, van der Meer RM, van Schayck OC, et al.: Smoking cessation for people with chronic obstructive pulmonary disease. Cochrane Database Syst Rev 2016; (8): CD010744.  Back to cited text no. 39
    
40.
Fiore M, Jaen C, Baker T: Treating Tobacco Use and Dependence: 2008 Update. Washington, DC: US Department of Health and Human Services, Public Health Service, 2008.  Back to cited text no. 40
    
41.
Abrams DB, Niaura R, Brown RA, et al.: The Tobacco Dependence Treatment Handbook: A Guide to Best Practices. New York: The Guilford Press, 2003.  Back to cited text no. 41
    
42.
Lindson-Hawley N, Thompson TP, Begh R: Motivational interviewing for smoking cessation. Cochrane Database Syst Rev 2015; (3): CD006936.  Back to cited text no. 42
    
43.
Cahill K, Hartmann-Boyce J, Perera R: Incentives for smoking cessation. Cochrane Database Syst Rev 2015; (5): CD004307.  Back to cited text no. 43
    
44.
Halpern SD, Harhay MO, Saulsgiver K, et al.: A pragmatic trial of E-cigarettes, incentives, and drugs for smoking cessation. N Engl J Med 2018; 378: 2302-10.  Back to cited text no. 44
    
45.
Stead LF, Perera R, Bullen C, et al.: Nicotine replacement therapy for smoking cessation. Cochrane Database Syst Rev 2012; 11: CD000146.  Back to cited text no. 45
    
46.
Public Health England: Models of Delivery for Stop Smoking Services: Options and Evidence. London, United Kingdom: Public Health England, 2017.  Back to cited text no. 46
    
47.
Stead LF, Buitrago D, Preciado N, et al.: Physician advice for smoking cessation. Cochrane Database Syst Rev 2013; (5): CD000165.  Back to cited text no. 47
    
48.
Halpern SD, French B, Small DS, et al.: Randomized trial of four financial-incentive programs for smoking cessation. N Engl J Med 2015; 372: 2108-17.  Back to cited text no. 48
    
49.
Ferris Wayne G, Connolly GN, Henningfield JE: Brand differences of free-base nicotine delivery in cigarette smoke: the view of the tobacco industry documents. Tob Control 2006; 15: 189-98.  Back to cited text no. 49
    
50.
Schnoll RA, Goelz PM, Veluz-Wilkins A, et al.: Long-term nicotine replacement therapy: a randomized clinical trial. JAMA Intern Med 2015; 175: 504-11.  Back to cited text no. 50
    
51.
Slemmer JE, Martin BR, Damaj MI: Bupropion is a nicotinic antagonist. J Pharmacol Exp Ther 2000; 295: 321-7.  Back to cited text no. 51
    
52.
Anthenelli RM, Benowitz NL, West R, et al.: Neuropsychiatric safety and efficacy of varenicline, bupropion, and nicotine patch in smokers with and without psychiatric disorders (EAGLES): a double-blind, randomised, placebo-controlled clinical trial. Lancet 2016; 387: 2507-20.  Back to cited text no. 52
    
53.
Hays JT, Hurt RD, Rigotti NA, et al.: Sustained-release bupropion for pharmacologic relapse prevention after smoking cessation. A randomized, controlled trial. Ann Intern Med 2001; 135: 423-33.  Back to cited text no. 53
    
54.
Suissa K, Larivière J, Eisenberg MJ, et al.: Efficacy and safety of smoking cessation interventions in patients with cardiovascular disease: a network meta-analysis of randomized controlled trials. Circ Cardiovasc Qual Outcomes 2017; 10. pii: e002458.  Back to cited text no. 54
    
55.
Ebbert JO, Hatsukami DK, Croghan IT, et al.: Combination varenicline and bupropion SR for tobacco-dependence treatment in cigarette smokers: a randomized trial. JAMA 2014; 311: 155-63.  Back to cited text no. 55
    
56.
Rollema H, Chambers LK, Coe JW, et al.: Pharmacological profile of the alpha4beta2 nicotinic acetylcholine receptor partial agonist varenicline, an effective smoking cessation aid. Neuropharmacology 2007; 52: 985-94.  Back to cited text no. 56
    
57.
Cahill K, Lindson-Hawley N, Thomas KH, et al.: Nicotine receptor partial agonists for smoking cessation. Cochrane Database Syst Rev 2016; (5): CD006103.  Back to cited text no. 57
    
58.
Tonstad S, Tønnesen P, Hajek P, et al.: Effect of maintenance therapy with varenicline on smoking cessation: a randomized controlled trial. JAMA 2006; 296: 64-71.  Back to cited text no. 58
    
59.
Walker N, Howe C, Glover M, et al.: Cytisine versus nicotine for smoking cessation. N Engl J Med 2014; 371: 2353-62.  Back to cited text no. 59
    
60.
West R, Zatonski W, Cedzynska M, et al.: Placebo-controlled trial of cytisine for smoking cessation. N Engl J Med 2011; 365: 1193-200.  Back to cited text no. 60
    
61.
U.S. Department of Health and Human Services: E-Cigarette Use among Youth and Young Adults: A Report of the Surgeon General. Atlanta, Georgia, USA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2016.  Back to cited text no. 61
    
62.
Hartmann-Boyce J, McRobbie H, Bullen C, et al.: Electronic cigarettes for smoking cessation. Cochrane Database Syst Rev 2016; 9: CD010216.  Back to cited text no. 62
    
63.
Barrington-Trimis JL, Urman R, Leventhal AM, Gauderman WJ, Cruz TB, Gilreath TD, et al. E-cigarettes, cigarettes, and the prevalence of adolescent tobacco use. Pediatrics 2016;138.  Back to cited text no. 63
    
64.
Bekki K, Uchiyama S, Ohta K, et al.: Carbonyl compounds generated from electronic cigarettes. Int J Environ Res Public Health 2014; 11: 11192-200.  Back to cited text no. 64
    
65.
Kim HJ, Shin HS: Determination of tobacco-specific nitrosamines in replacement liquids of electronic cigarettes by liquid chromatography-tandem mass spectrometry. J Chromatogr A 2013; 1291: 48-55.  Back to cited text no. 65
    
66.
Fiore MC, Jaén CR: A clinical blueprint to accelerate the elimination of tobacco use. JAMA 2008; 299: 2083-5.  Back to cited text no. 66
    
67.
Babb S, Malarcher A, Schauer G, et al.: Quitting smoking among adults – United States, 2000-2015. MMWR Morb Mortal Wkly Rep 2017; 65: 1457-64.  Back to cited text no. 67
    
68.
Office on Smoking and Health National Center for Chronic Disease Prevention and Health Promotion: Preventing Tobacco Use among Youth and Young Adults: A Report of the Surgeon General. Atlanta, Georgia, USA: Department of Health and Human Services, 2012.  Back to cited text no. 68
    
69.
Piasecki TM, Fiore MC, McCarthy DE, et al.: Have we lost our way? the need for dynamic formulations of smoking relapse proneness. Addiction 2002; 97: 1093-108.  Back to cited text no. 69
    
70.
West R, McNeill A, Raw M: Smoking cessation guidelines for health professionals: An update. Health education authority. Thorax 2000; 55: 987-99.  Back to cited text no. 70
    
71.
Flay BR: School-based smoking prevention programs with the promise of long-term effects. Tob Induc Dis 2009; 5: 6.  Back to cited text no. 71
    
72.
Chaloupka FJ: Macro-social influences: the effects of prices and tobacco-control policies on the demand for tobacco products. Nicotine Tob Res 1999; 1 (Suppl 1): S105-9.  Back to cited text no. 72
    
73.
Song AV, Dutra LM, Neilands TB, et al.: Association of smoke-free laws with lower percentages of new and current smokers among adolescents and young adults: an 11-year longitudinal study. JAMA Pediatr 2015; 169: e152285.  Back to cited text no. 73
    
74.
Bonnie RJ, Stratton K, Kwan LY: Public Health Implications of Raising the Minimum Age of Legal Access to Tobacco Products. Washington DC, USA: National Academies Press, 2015.  Back to cited text no. 74
    
75.
Ministry of Health and Welfare: Tobacco Hazards Prevention Act, Amendment Edition. Taipei, Taiwan: Ministry of Health and Welfare, 2009.  Back to cited text no. 75
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]



 

Top
 
  Search
 
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

 
  In this article
   Abstract
  Introduction
   Tobacco Use Prev...
   The Risks of Tob...
   The Health Benef...
   Assessment of To...
   Tobacco Withdraw...
   Treatment Option...
   Nonpharmacologic...
   Pharmacological ...
   Prognosis, Relap...
   Smoking Cessatio...
  Conclusion
  Acknowledgements
   Financial Suppor...
   Conflicts of Int...
   References
   Article Tables

 Article Access Statistics
    Viewed94    
    Printed8    
    Emailed0    
    PDF Downloaded26    
    Comments [Add]    

Recommend this journal