Effects of Smoking Cessation

Based on solid evidence, cigarette smoking causes cancers of the lung, oral cavity and pharynx, larynx, esophagus, bladder, kidney, pancreas, stomach, uterine cervix, colon and rectum, liver, and acute myeloid leukemia.[2] Smoking avoidance and smoking cessation result in decreased incidence and mortality from cancer.[3]

Description of the Evidence

• Study Design: Evidence obtained from a randomized controlled trial (RCT).
• Internal Validity: Good.
• Consistency: Good.
• Magnitude of Effects on Health Outcomes: The relative risk (RR) of several cancers is much greater in cigarette smokers compared with nonsmokers (depending on the anatomical site of the cancer and the intensity and duration of smoking, the RR can range from twofold to tenfold or greater in smoking populations). A reduction of 15% is seen in the RR of all-cause mortality in heavy smokers subjected to intensive clinical cessation interventions.
• External Validity: Good.

Counseling and Smoking Cessation

Based on solid evidence, counseling by a health professional improves smoking cessation rates.

Description of the Evidence

• Study Design: Evidence obtained from RCTs.
• Internal Validity: Good.
• Consistency: Good.
• Magnitude of Effects on Health Outcomes: Counseling improves cessation rates (odds ratio [OR], 1.44; 95% credibility interval, 1.22–1.70).[4]
• External Validity: Good.

Physician or Nurse Advice and Smoking Cessation

Based on solid evidence, brief advice from a physician or nurse to stop smoking improves smoking cessation rates.

Description of the Evidence

• Study Design: Evidence obtained from RCTs.
• Internal Validity: Good.
• Consistency: Good.
• Magnitude of Effects on Health Outcomes: Physician advice improves cessation rates (RR, 1.76; 95% confidence interval [CI], 1.58–1.96).[5] Nurse advice improves cessation rates (RR, 1.29; 95% CI, 1.21–1.38).[6]
• External Validity: Good.

Pharmacological Treatment and Smoking Cessation

Based on solid evidence, drug treatments, including nicotine replacement therapies (NRTs) (gum, patch, spray, lozenge, and inhaler), selected antidepressant therapies (e.g., bupropion), and nicotinic receptor agonist therapy (varenicline), result in better smoking cessation rates than placebo.

Description of the Evidence

• Study Design: Evidence obtained from RCTs.
• Internal Validity: Good.
• Consistency: Good.
• Magnitude of Effects on Health Outcomes: NRT treatments, alone or in combination, improve cessation rates over placebo after 6 months (RR, 1.55; 95% CI, 1.49–1.61).[7] Treatment with bupropion improves cessation rates over placebo after 6 months (OR, 1.94; 95% CI, 1.72–2.19; RR, 1.60; 95% CI, 1.49–1.72).[8] Varenicline therapy treatment improves cessation rates over placebo after 6 months (RR, 2.32; 95% CI, 2.15–2.51).[9]
• External Validity: Good.

Pharmacological Treatment Combined With Counseling and Smoking Cessation

Based on solid evidence, drug treatments combined with counseling by a health professional result in better smoking cessation rates than drug treatments with minimal or no counseling support.

Description of the Evidence

• Study Design: Evidence obtained from RCTs.
• Internal Validity: Good.
• Consistency: Good.
• Magnitude of Effects on Health Outcomes: Drug treatments combined with counseling (behavioral support) improve cessation rates after 6 months over drug treatments combined with minimal or no counseling support (RR, 1.83; 95% CI, 1.68–1.98).[6,10]
• External Validity: Good.

References

1. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans: Tobacco smoke and involuntary smoking. IARC Monogr Eval Carcinog Risks Hum 83: 1-1438, 2004. [PMC free article: PMC4781536] [PubMed: 15285078]
2. U.S. Department of Health and Human Services: The Health Consequences of Smoking—50 Years of Progress: A Report of the Surgeon General. U.S. Department of Health and Human Services, CDC, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014. Also available online. Last accessed August 12, 2024.
3. U.S. Department of Health and Human Services: Smoking Cessation: A Report of the Surgeon General. 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, 2020. Also available online. Last accessed June 14, 2024.
4. Hartmann-Boyce J, Livingstone-Banks J, Ordóñez-Mena JM, et al.: Behavioural interventions for smoking cessation: an overview and network meta-analysis. Cochrane Database Syst Rev 1: CD013229, 2021. [PMC free article: PMC11354481] [PubMed: 33411338]
5. Stead LF, Buitrago D, Preciado N, et al.: Physician advice for smoking cessation. Cochrane Database Syst Rev 2013 (5): CD000165, 2013. [PMC free article: PMC7064045] [PubMed: 23728631]
6. Rice VH, Heath L, Livingstone-Banks J, et al.: Nursing interventions for smoking cessation. Cochrane Database Syst Rev 12 (12): CD001188, 2017. [PMC free article: PMC6486227] [PubMed: 29243221]
7. Hartmann-Boyce J, Chepkin SC, Ye W, et al.: Nicotine replacement therapy versus control for smoking cessation. Cochrane Database Syst Rev 5 (5): CD000146, 2018. [PMC free article: PMC6353172] [PubMed: 29852054]
8. Hajizadeh A, Howes S, Theodoulou A, et al.: Antidepressants for smoking cessation. Cochrane Database Syst Rev 5 (5): CD000031, 2023. [PMC free article: PMC10207863] [PubMed: 37230961]
9. Livingstone-Banks J, Fanshawe TR, Thomas KH, et al.: Nicotine receptor partial agonists for smoking cessation. Cochrane Database Syst Rev 5 (5): CD006103, 2023. [PMC free article: PMC10169257] [PubMed: 37142273]
10. Stead LF, Koilpillai P, Fanshawe TR, et al.: Combined pharmacotherapy and behavioural interventions for smoking cessation. Cochrane Database Syst Rev 3 (3): CD008286, 2016. [PMC free article: PMC10042551] [PubMed: 27009521]

Background

In the United States, smoking-related illnesses accounted for an estimated 480,000 deaths each year.[1,2] On average, these deaths occur 12 years earlier than would be expected, so the aggregate annual loss exceeds 5 million life-years.[3] These deaths are primarily due to smoking’s role as a major cause of cancer, cardiovascular disease, and chronic lung disease. The known adverse health effects also include other respiratory diseases and symptoms, nuclear cataract, hip fractures, reduced female fertility, diabetes, erectile dysfunction, rheumatoid arthritis, and diminished health status. Maternal smoking during pregnancy is associated with fetal growth restriction, low birth weight, and complications of pregnancy.[2] About 30% of cancer deaths in the United States are attributable to smoking.[4]

Tobacco products are the single, major avoidable cause of cancer, causing more than 155,000 deaths among smokers in the United States annually due to various cancers.[5] Most cancers of the lung, trachea, bronchus, larynx, pharynx, oral cavity, nasal cavity, and esophagus are attributable to tobacco products, particularly cigarettes. Smoking is also causally associated with cancers of the pancreas, kidney, bladder, stomach, colon, rectum, liver, and cervix, and with myeloid leukemia.[2,6]

Smoking also has substantial effects on the health of nonsmokers. Environmental or secondhand tobacco smoke is implicated in causing lung cancer, coronary heart disease, stroke, nasal irritation, and reproductive effects in women (low birth weight in newborns of these women).[2] Among children, secondhand smoke exposure is causally associated with sudden infant death syndrome, lower respiratory tract illnesses, otitis media, middle ear effusion, exacerbated asthma, and respiratory effects such as cough, wheeze, and dyspnea.[2]

Environmental tobacco smoke has the same components as inhaled mainstream smoke, although in lower absolute concentrations, between 1% and 10%, depending on the constituent. Carcinogenic compounds in tobacco smoke include the polycyclic aromatic hydrocarbons (PAHs), including the carcinogen benzo[a]pyrene (BaP) and the nicotine-derived tobacco-specific nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK).[7] Elevated biomarkers of tobacco exposure, including urinary cotinine, tobacco-related carcinogen metabolites, and carcinogen-protein adducts, are seen in passive or secondhand smokers.[8-11]

In 2021, 13.1% of adult men and 10.1% of adult women in the United States were current smokers, and 24.1% of adult men and 13.6% of adult women reported the use of any tobacco product.[12] Cigarette smoking is particularly common among American Indian and Alaska Native individuals. The prevalence of smoking also varies inversely with education, and was highest among adults who had earned a General Educational Development diploma (30.1%) and generally decreased with increasing years of education.[12] From 2011 to 2014, significant declines occurred in the use of cigarettes among middle school (4.3% to 2.5%) and high school (15.8% to 9.2%) students.[13] Cigarette smoking prevalence among male and female high school students increased substantially during the 1990s in all ethnic groups, with rates between 20% and 30%. However, by 2022, the cigarette smoking rate in high school students declined to 2%.[4,14,15] (Also available online.)

The effect of tobacco use on population-level health outcomes is illustrated by the example of lung cancer mortality trends. Smoking by women increased between 1940 and the early 1960s, resulting in a greater than 600% increase in female lung cancer mortality since 1950. Lung cancer is now the leading cause of cancer death in women.[14,16] In the last 30 years, prevalence of current cigarette use has generally decreased, though far more rapidly in men. Lung cancer mortality in men peaked in the 1980s, and has been declining since then; this decrease has occurred predominantly in squamous cell and small cell carcinomas, the histological types most strongly associated with smoking.[14] Variations in lung cancer mortality rates by state also more or less parallel long-standing state-specific differences in tobacco use. Among men, the average annual age-adjusted lung cancer death rates from 2017 to 2021 were highest in Mississippi (64.3 per 100,000),[4] where 22% of men in Mississippi were current smokers in 2021, and lowest in Utah (18.8 per 100,000), where only 8% of men smoked. Among women, lung cancer death rates were highest in Kentucky (43.8 per 100,000), where 21% of women were current smokers, and lowest in Utah (13.9 per 100,000), where only 6% of women smoked.[4,14,17,18]

Tobacco Use Interventions

Many health risks related to tobacco smoking can be reduced by smoking cessation. Smokers who quit smoking before age 50 years have up to half the risk of dying within 15 years compared with people who continue to smoke, and the risk of dying is reduced substantially even among individuals who stop smoking after age 70 years.[19] The risk of lung cancer is 30% to 50% lower than that of continuing smokers after 10 years of abstinence, and the risk of oral and esophageal cancer is halved within 5 years of cessation.[19] Smokers who quit also lower their risk of cervical, gastric, and bladder cancer.[16,19,20]

Several approaches at the policy, legislative, and regulatory levels have been attempted to effect widespread reduction in or prevention of commencement of tobacco use. Various efforts at the community, state, and national level have been credited with reducing the prevalence of smoking over time. These efforts include, reducing minors’ access to tobacco products, disseminating effective school-based prevention curricula together with media strategies, raising the cost of tobacco products, using tobacco excise taxes to fund community-level interventions including mass media, providing proven quitting strategies through health care organizations, and adopting smoke-free laws and policies.[21,22]

Pharmacological Interventions to Assist in Tobacco Cessation

Pharmacological agents have been used successfully to aid in the cessation of smoking in the general population.[35] Since the original AHCPR guidelines [36] were published in 1996, various nicotine replacement products have been approved for over-the-counter sale, and additional evidence of the effectiveness of therapies for smoking cessation has been published.[37-40] Pharmacotherapy of smoking cessation, including NRTs (gum, patch, spray, lozenge, and inhaler) and non-nicotine medications (e.g., bupropion and varenicline), results in statistically significant increases in smoking cessation rates over those of a placebo.[41]

A growing number of smoking cessation pharmacotherapies have demonstrated efficacy in significantly increasing rates of smoking cessation. The choice of therapy should be individualized based on several factors, including past experience, patient and/or physician preference, and potential agent side effects. As more is learned about specific genetic variants that influence a smoker's response to smoking cessation pharmacotherapies—such as polymorphisms in genes encoding enzymes involved in nicotine metabolism—this information could eventually be integrated into smoking cessation treatment planning.[42] Presently, the evidence is not yet sufficient to be integrated into clinical practice.

The following sections summarize available pharmacological interventions to assist in tobacco cessation. More comprehensive information is available from product package inserts.

Pharmacotherapy Combinations and Adaptations

Strategies to enhance the effectiveness of pharmacotherapy for smoking cessation have been explored, including combining medications and adjusting dosages and/or treatment duration.[69] As noted previously, a recent meta-analysis concluded that combining a fast-acting NRT with the nicotine patch (i.e., combined NRT) resulted in higher 6-month cessation rates compared with the nicotine patch alone (RR, 1.27; 95% CI, 1.17–1.37). The analysis included moderate-certainty evidence (limited by imprecision) indicating that 21 mg patches are more effective than 14 mg patches (RR, 1.48; 95% CI, 1.06–2.08) but that 42 mg patches are just as effective as 21 mg (24-hour) patches (RR, 1.09; 95% CI, 0.93–1.29). A subset of studies tested the effect of preloading NRT prior to quit day versus starting NRT on the quit day. In that subset, there was moderate-certainty evidence, limited by risk of bias, of a positive effect of preloading NRT on abstinence (RR, 1.25; 95% CI, 1.08–1.44). There was no reliable evidence of an effect of duration of single or combined NRT use on abstinence.[45] In another meta-analysis, results (based on three trials) indicated that the combination of bupropion and varenicline may result in higher 6-month cessation rates compared with varenicline alone (RR, 1.21; 95% CI, 0.95–1.55), but there was insufficient evidence to suggest that combining bupropion plus NRT increases smoking cessation rates over those of NRT alone (RR, 1.17; 95% CI, 0.95–1.44).[49]

A 2015 meta-analysis including randomized trials that compared the combination of varenicline and NRT therapy with varenicline alone showed a statistically significant association with benefit for the combination, especially if precessation treatment with a nicotine patch was given.[70] In a subsequent double-blind, 2 × 2 factorial randomized clinical trial, 1,251 individuals who smoked were randomly assigned to receive smoking cessation counseling and varenicline monotherapy for 12 weeks, varenicline plus NRT (patch) for 12 weeks, varenicline monotherapy for 24 weeks, or varenicline plus NRT for 24 weeks.[71] For the primary outcome of abstinence at 52 weeks, there was no significant interaction between medication type and medication duration (OR, 1.03; 95% CI, 0.91–1.17; P = .66). The abstinence rate was 24.8% for individuals randomly assigned to 24-week treatment duration versus 24.3% for those randomly assigned to 12-week treatment duration (risk difference, -0.4%; 95% CI, -5.2% to 4.3%; OR, 1.01; 95% CI, 0.89–1.15). The abstinence rate was 24.3% for individuals randomly assigned to varenicline-combination therapy versus 24.8% for those randomly assigned to varenicline monotherapy (risk difference, 0.4%; 95% CI, -4.3% to 5.2%; OR, 0.99; 95% CI, 0.87–1.12). Adverse effects across the four treatment groups included nausea (24.0%–30.9%) and insomnia ( 24.4%–30.5%). These findings do not support the addition of NRT to varenicline or the extension of varenicline or combination therapy beyond the standard 12 weeks.[71]

In a double-blind, placebo-controlled, sequential, multiple-assignment randomized trial (SMART), 490 individuals who smoke were randomly assigned to receive 6 weeks of varenicline (2 mg/d) or combined NRT (21 mg/d patch and 2 mg lozenges as needed) and smoking cessation counseling. After 6 weeks, abstainers continued their assigned medication and nonabstainers were randomly assigned again to continue the initially assigned medication at the initial dose, switch between varenicline and combined NRT at the initial dose, or increase the varenicline (3 mg/d) or combined NRT (42 mg/d patch) dose for an additional 6 weeks.[72]

At 12 weeks, the probability of abstinence for those initially randomly assigned to varenicline who were abstinent at 6 weeks and continued on treatment (not randomized again) was 72% (95% credible interval [Crl], 65%–78%) compared with 78% (95% Crl, 69%–85%) for those initially randomly assigned to combined NRT who were abstinent at 6 weeks and continued on treatment. The posterior probability of a nonzero difference between these two conditions was 88% (absolute risk difference [ARD], 6%; 95% CrI, -5% to 16%). The probability of abstinence at 12 weeks (end of treatment) for the individuals initially assigned to varenicline who were not abstinent at 6 weeks was 20% (95% CrI, 16%–26%) for those who increased their varenicline dosage, 0% for those who switched to combined NRT, and 3% (95% CrI, 1%–4%) for those who were assigned to the continued-varenicline treatment group (ARD, -3%; 95% CrI, -4% to -1%). There was a more than 99% posterior probability that continuing varenicline at the initial dosage was worse than switching to a higher dosage. Increasing the varenicline dosage had an ARD of 18% (95% CrI, 13%–24%) and a more than 99% posterior probability of conferring benefit. The probability of abstinence at 12 weeks for the individuals initially assigned to combined NRT who were not abstinent at 6 weeks was 8% (95% CrI, 6%–10%) for those who continued at the initial dosage, 14% (95% CrI, 10%–18%) for those who increased their dosage, and 14% (95% CrI, 10%–18%) for those who switched to varenicline (ARD, 6%; 95% CrI, 6%–11%). There was a more than 99% posterior probability that either strategy conferred benefit over continuing at the initial dosage. The secondary outcome of continuous abstinence at 6-months post-quit indicated that only increased dosages of varenicline and combined NRT provided benefit over continuation of the initial treatment dosages. Relative to continuing the same medication, there was no evidence indicating an increased risk of adverse events associated with the dosage increases for either medication. Additionally, no major differences in treatment adherence were reported between treatment groups.

In summary, these results suggest that individuals who are not able to abstain from smoking after initial treatment with varenicline benefit most from increasing the varenicline dose. For the individuals who continue to smoke after initial treatment with combined NRT, switching to varenicline or increasing the dose of combined NRT resulted in similar end-of-treatment abstinence probabilities. The secondary outcome of continuous abstinence at 6 months favored the dose-increase conditions for both varenicline and combined NRT, relative to continuation.[72]

Smoking Reduction

Among smokers who are interested in quitting but not ready to make an immediate quit attempt, gradually decreasing the number of cigarettes smoked per day leading up to a quit attempt may prove to be a viable intervention strategy. This reduce to quit approach was tested in the context of an RCT. In this study, both the intervention group and control group received counseling with the goals of reducing the number of cigarettes smoked per day by 75% or greater by week 8 and to quit smoking entirely by week 12.[73] The intervention group (n = 760) also received smoking cessation pharmacotherapy (varenicline at a maintenance dose of 1 mg bid for 24 weeks), whereas the control group (n = 750) received placebo tablets. For the primary end point of self-reported smoking abstinence during weeks 15 through 24, a statistically significant RD of 25.2% (varenicline group, 32.1% vs. placebo group, 6.9%; 95% CI, 21.4%–29.0%) was observed. The clinical significance of this finding is that it provides evidence of benefit for a pharmacotherapy-enhanced intervention aimed to motivate smokers who are interested in quitting, but not yet ready to quit, to start by cutting down on the number of cigarettes per day as a lead-in to a subsequent quit attempt.

For a smoker who wants to quit, an important practical question is whether a quit attempt is more likely to successfully result in smoking cessation if it involves abruptly stopping smoking or gradually decreasing the number of cigarettes smoked per day leading up to a quit attempt. U.S. evidence-based guidelines recommend abrupt quitting as the preferred approach,[74] but guidelines from other countries vary on this matter. To directly test this question, 697 smokers who wanted to quit were recruited from 31 primary care clinics in England, and randomly assigned to either a gradual or abrupt smoking cessation intervention.[75] In this noninferiority trial, both groups were provided with access to NRT during the two weeks before the planned quit date. In the gradual cessation group, plans were made to cut down the number of cigarettes per day by 75% by the planned quit date. However, the abrupt cessation group was advised to follow usual smoking patterns until stopping smoking entirely on the planned quit date. Both groups were provided with NRT after the quit date and throughout the trial. For the primary end point of prolonged validated smoking abstinence at 4 weeks, the gradual cessation arm was less likely to quit smoking than the abrupt cessation arm (39.2% vs. 49.0%); a difference that was statistically significant (RD, -9.8%; 95% CI, 2.5%–17.1%). The statistically significantly lower likelihood of smoking cessation in the gradual versus abrupt intervention arms persisted during follow-up at 8 weeks (29.2% vs. 36.6%; RD, -7.4%; 95% CI, 0.4%–14.3%) and 6 months (15.5% vs. 22.0%; RD, -6.5%; 95% CI, 0.7%–12.2%). Baseline patient preferences for a gradual or abrupt quit attempt indicated that smokers who preferred the gradual quitting approach had a lower likelihood of smoking abstinence at 4 weeks (38% vs. 52%), suggesting that patient preferences for these methods may be a marker for other factors associated with successful quitting, such as motivation to quit. However, even when stratified by baseline patient preferences, the gradual cessation method resulted in lower likelihood of cessation both among those who preferred the gradual approach (34.6% vs. 42.0%) and those who preferred the abrupt approach (45.8% vs. 58.1%). The overall clinical significance of this study is that it provides evidence that in the setting of a pharmacotherapy-aided quit attempt among smokers interested in quitting, quitting abruptly is a more effective smoking cessation strategy than gradually cutting down on the number of cigarettes smoked before making a quit attempt. This result holds true regardless of smoker preferences in methods. A quit attempt regardless of method should never be discouraged, but abrupt cessation appears to be the most effective strategy. In this context, abrupt cessation is distinct from making an unaided quit attempt (i.e., quitting “cold turkey”).[76]

A systematic review of this topic revealed substantial heterogeneity in the results across studies, but the results showed that gradual cessation was associated with a 6% lower likelihood of smoking cessation than abrupt cessation, although this finding was not statistically significant (RR, 0.94; 95% CI, 0.79–1.13).[76] In an updated review of 51 trials that included more than 22,000 participants, the authors concluded, with moderate-certainty evidence, that long-term (≥ 6 months) abstinence rates did not differ in participants who were randomly assigned to either a gradual cessation intervention or an abrupt quitting intervention (RR, 1.01; 95% CI, 0.87–1.17; I² = 29%; 22 studies, 9,219 participants).[77] When comparing the effects of a gradual cessation intervention with no smoking cessation intervention on abstinence rates, the authors reported low-certainty evidence (limited by inconsistency, imprecision, and risk of bias) that was inconclusive (RR, 1.74; 95% CI, 0.90–3.38; I² = 45%; 6 studies, 1,599 participants). The authors also reported low-certainty evidence that suggested gradual reduction methods may be more effective when combined with pharmacotherapy (RR, 1.68; 95% CI, 1.09–2.58; I² = 78%; 11 studies, 8,636 participants). A subgroup analysis of these 11 studies reported the same conclusions, with moderate-certainty evidence, specifically when fast-acting NRT or varenicline was used as pharmacotherapy (P < .001, I² = 80% for subgroup differences).[77]

Among dependent smokers, complete abstinence from smoking is the ultimate goal. Even in instances when complete abstinence from smoking is not achieved, smoking cessation pharmacotherapies may benefit individual health—and ultimately the public’s health—if the smoker reduces the number of cigarettes smoked. The relationship between cigarette smoking and lung cancer, and other smoking-associated malignancies, is strongly dose-dependent. Thus, an individual smoker who is unable to achieve abstinence or who is not motivated to quit smoking may benefit by using pharmacotherapies (or other means) to reduce the number of cigarettes smoked per day. NRT has thus generated attention as a viable means of “harm reduction.” In studies that randomly assigned smokers who were not trying to quit to NRT or placebo, a greater proportion of those randomly assigned to NRT compared with placebo reduced the number of cigarettes per day.[78,79] However, the impact of NRT on smoking reduction appears not to be sustained in the long run.[80] Less evidence is available for bupropion, varenicline, and psychosocial interventions as a means of harm reduction. A potential problem with such a harm reduction strategy would be if it prevented cessation among smokers who would have otherwise quit smoking. Evidence shows that smoking reduction is actually associated with increased likelihood of future cessation.[79,81] Another potential negative aspect of harm reduction would be if smokers reduced the number of cigarettes smoked per day but modified the way the cigarettes were smoked in such a way that exposure to tobacco toxins was not actually reduced (e.g., by inhaling more deeply). Compensatory behaviors such as inhaling more deeply or smoking more of a cigarette are attempts by the smoker to try to maintain nicotine levels, so the use of supplemental NRT presumably safeguards against this. Evidence from studies of smoking reduction with NRT that measured smoking biomarkers indicates that compensation occurs, but not to such an extent that it would be expected to outweigh the reduction in exposure from the reduced number of cigarettes per day.[78]

Financial Incentive Programs for Smoking Cessation

Financial incentive programs can offer additional support for smoking cessation efforts. Results from a recent randomized trial suggest that the efficacy of such programs may be influenced greatly by the way rewards are disbursed.[82,83]

The trial randomly assigned 2,538 participants to either one of four incentive programs or usual care. The four programs were combinations of scope (two programs targeted individuals, and two targeted groups of six participants) and incentive structure (one of the individual-focused programs and one of the group-focused programs provided rewards of approximately $800 to participants who achieved cessation at 6 months; the others required an initial refundable deposit of $150, supplemented with $650 in reward payments for successful cessation). The rationale for the four intervention arms was based on behavioral observations that 1) people are more loss averse than gain seeking and 2) collaboration/competition with others can bolster intervention efficacy.[82]

Two main dimensions of the intervention effects were explored:

1. Acceptance of the intervention.
2. Efficacy of the intervention.

Both intent-to-treat and per-protocol analyses were performed, with an in-depth sensitivity analysis for potential biases accompanying the latter. In the intent-to-treat analyses (which evaluated the overall efficacy of the interventions), all of the financial incentive arms demonstrated significantly higher 6-month abstinence rates than did usual care (9.4%–16%, compared with 6% for usual care). The 6-month abstinence rates were similar between the group-focused and individual-focused arms (13.7% and 12.1%, respectively; P = .29), but the reward-based programs were associated with higher abstinence rates than were the deposit-based ones (15.7% vs. 10.2%; P < .001).[82]

However, per-protocol analyses that accounted for the dramatically lower acceptance rate for the deposit-based interventions than for the reward-based interventions (14% vs. 90%) estimated that 6-month abstinence rates could be 13.2 percentage points (95% CI, 3.1–22.8) higher in the deposit-based programs than in the reward-based programs among the estimated 13.7% of participants who would participate in either type of program. That is, deposit-based interventions may be more efficacious than reward-based interventions but harder to get people to commit to.[82]

A Changing Marketplace for Tobacco Products and Nicotine-Delivery Devices

The expansion in the marketplace of tobacco products and devices that deliver nicotine poses new challenges to tobacco control.[84-88] Examples of nontraditional tobacco products in the U.S. market include small cigars, water pipe tobacco smoking (“hookah”), and new types of flavored, smokeless tobacco products modeled after Swedish snus. Prominent among non–tobacco-containing nicotine delivery devices are electronic cigarettes (or “e-cigarettes”) that have experienced a rapid upsurge in use and are now marketed by the major U.S. tobacco companies.[84,85] Monitoring this expansion in products, how the products are used (e.g., product switching, multiple use, and use for tobacco cigarette smoking cessation), and the harms and benefits associated with their use compared with the use of tobacco cigarettes is critical to the development of more effective tobacco control strategies.

Research to determine the potential risks and benefits of these new products is just emerging, and initial findings are mixed.[89,90] The potential benefits of e-cigarettes as a smoking cessation aid for adult smokers is further complicated by two additional factors. First, there has been a marked increase in the use of e-cigarettes by adolescents, with current (past 30-day) e-cigarette use by high school seniors rising dramatically over the last 3 years to 27.5% in 2019.[91] Second, the product has evolved rapidly, with newer electronic nicotine delivery systems, such as JUUL, more quickly and effectively delivering nicotine to the lungs and more closely mimicking cigarettes in terms of their pharmacokinetics.

In one study, 886 adults who attended the U.K. National Health Service stop-smoking services were randomly assigned to either starter packs of nicotine replacement medication or e-cigarettes. At 1 year, biochemically confirmed abstinence was 18.0% in the e-cigarette group compared with 9.9% in the nicotine-replacement group (P < .001). However, at 1 year, 80% of abstinent e-cigarette users were still using e-cigarettes, compared with 9% of abstinent nicotine-replacement medication users still using their products.[92] In contrast, a recent pragmatic trial randomly assigned smokers who were employed at 54 companies to access one of four interventions, which included usual care (information and motivational text messages), FDA-approved cessation medications, e-cigarettes, and financial incentives. The authors found that financial incentives added to free FDA-approved cessation medications resulted in higher quit rates than did cessation medications alone, and among smokers who received usual care, the addition of free cessation medications or e-cigarettes did not provide an added benefit.[93]

Evidence suggests that cessation interventions delivered during children's pediatric visits to parents who smoked boost cessation rates.[74] A recent cluster randomized clinical trial [94] demonstrated higher quit rates 2 years after cessation interventions were delivered during pediatric visits, although there were a limited number of clusters (n = 10) included in the trial.

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Purpose of This Summary

This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about the prevention and cessation of cigarette smoking and the control of tobacco use. It is intended as a resource to inform and assist clinicians in the care of their patients. It does not provide formal guidelines or recommendations for making health care decisions.

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PDQ® Screening and Prevention Editorial Board. PDQ Cigarette Smoking. Bethesda, MD: National Cancer Institute. Updated <MM/DD/YYYY>. Available at: https://www.cancer.gov/about-cancer/causes-prevention/risk/tobacco/quit-smoking-hp-pdq. Accessed <MM/DD/YYYY>. [PMID: 26389444]

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