Skip to main content

Main menu

  • Home
  • Current issue
  • Past issues
  • Authors/reviewers
    • Instructions for authors
    • Submit a manuscript
    • Institutional open access agreements
    • Peer reviewer login
  • Alerts
  • Subscriptions
  • ERS Publications
    • European Respiratory Journal
    • ERJ Open Research
    • European Respiratory Review
    • Breathe
    • ERS Books
    • ERS publications home

User menu

  • Log in
  • Subscribe
  • Contact Us
  • My Cart
  • Log out

Search

  • Advanced search
  • ERS Publications
    • European Respiratory Journal
    • ERJ Open Research
    • European Respiratory Review
    • Breathe
    • ERS Books
    • ERS publications home

Login

European Respiratory Society

Advanced Search

  • Home
  • Current issue
  • Past issues
  • Authors/reviewers
    • Instructions for authors
    • Submit a manuscript
    • Institutional open access agreements
    • Peer reviewer login
  • Alerts
  • Subscriptions

Smoking cessation and vaccination

Maria Montes de Oca, Maria Eugenia Laucho-Contreras
European Respiratory Review 2023 32: 220187; DOI: 10.1183/16000617.0187-2022
Maria Montes de Oca
1School of Medicine, Universidad Central de Venezuela and Hospital Centro Médico de Caracas, Caracas, Venezuela
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • For correspondence: montesdeoca.maria@gmail.com
Maria Eugenia Laucho-Contreras
2Research Department, Fundación Neumológica Colombiana, Bogotá, Colombia
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • Article
  • Figures & Data
  • Info & Metrics
  • PDF
Loading

Abstract

A significant proportion of COPD patients (∼40%) continue smoking despite knowing that they have the disease. Smokers with COPD exhibit higher levels of nicotine dependence, and have lower self-efficacy and self-esteem, which affects their ability to quit smoking. Treatment should be adapted to the needs of individual patients with different levels of tobacco dependence. The combination of counselling plus pharmacotherapy is the most effective cessation treatment for COPD. In patients with severe COPD, varenicline and bupropion have been shown to have the highest abstinence rates compared with nicotine replacement therapy. There is a lack of evidence to support that smoking cessation reduction or harm reduction strategies have benefits in COPD patients. The long-term efficacy and safety of electronic cigarettes for smoking cessation need to be evaluated in high-risk populations; therefore, it is not possible to recommend their use for smoking cessation in COPD. Future studies with the new generation of nicotine vaccines are necessary to determine their effectiveness in smokers in general and in COPD patients.

Abstract

∼40% of COPD patients continue smoking. They have high nicotine dependence, and low self-efficacy and self-esteem. Combined counselling and pharmacotherapy is the best treatment. There is no evidence on e-cigarette or harm reduction benefits in COPD. https://bit.ly/3BATHeK

Introduction

Cigarette consumption is the leading risk factor for COPD, especially in developed countries. However, COPD can result from other environmental exposures, such as passive smoking exposure or indoor pollution from biomass, repeated infections, poverty and genetic factors that can alter lung growth during early life.

A systematic review and meta-analysis that aimed at identifying risk factors for COPD in nonsmoking adults showed that second-hand smoking was the main risk factor in this population [1]. Among patients included in the analysis, 56% had active smoking as the risk factor and 44% were nonsmokers; in the latter population, 46.9% of patients had passive smoke exposure. Therefore, smoking (active or passive) was associated with 76% of COPD cases. Patients who were exposed to smoke as passive smokers and who were healthy had a probability of developing COPD of 94.6% (pooled OR 52.97, 95% CI 44.65–62.83) [1].

There is evidence that about half of COPD cases are due to accelerated loss of lung function related to adult smoking. The rest are due to failure to achieve normal lung function in early adulthood, followed by age-appropriate decline rates [2–5]. Therefore, the pathogenesis of COPD may begin before birth since passive fetal exposure to smoke in utero is associated with an increased risk of COPD in adults, independently of subsequent active smoking, as well as passive smoke exposure in childhood or active smoking in adolescence [2, 5]. For all these reasons, smoking cessation has been considered as the single most cost-effective strategy to prevent and reduce disease progression. Nevertheless, despite the existence of different effective smoking cessation interventions, the evidence shows that the chances of COPD patients sustaining quitting smoking are still relatively low [6].

Importance of smoking cessation in COPD

In integrated care programmes for patients with COPD, part of the standard care is to help the patient in their attempts to stop smoking. For decades, the benefits of quitting smoking have been proven beyond any doubt. Anthonisen et al. [7] in the Lung Health Study (smokers with mild COPD) showed that all-cause mortality was significantly lower in people who received smoking cessation intervention compared with those who received no intervention (8.83 versus 10.38 per 1000 person-years; p=0.03) after 14.5 years of follow-up. Anthonisen et al. [8] also report that smoking cessation significantly reduces the age-related decline in forced expiratory volume in 1 s (FEV1) (−72 mL per 5 years for sustained quitters versus −301 mL per 5 years for continued smokers). It has also been reported that quitting smoking improves daily symptoms [9] and decreases exacerbations [10], which are the main markers of disease activity and progression [11].

Tobacco dependence

Tobacco is the second most used psychoactive substance worldwide, with more than 1 billion smokers globally [12]. Tobacco dependence is a chronic relapsing disease driven by nicotine addiction, often requiring multiple therapeutic interventions and long-term support. Nicotine is the leading psychoactive agent in tobacco and electronic cigarettes (e-cigarettes). This agent acts as an agonist at nicotinic acetylcholine receptors (nAChRs), localised throughout the brain and peripheral nervous system [13]. Both brain localisation and the type of nAChR are critical elements in mediating the various effects of nicotine. However, other factors, such as the rate of nicotine delivery, may also modulate the addictive effects of nicotine [14, 15].

The reward obtained from nicotine is related to the mesolimbic pathway, which has dopaminergic neurons in the ventral tegmental area (VTA). These neurons project to the nucleus accumbens and the prefrontal cortex. These regions express several nAChR subtypes in dopaminergic, GABAergic and glutamatergic neurons. This distribution causes nicotine administration to increase dopamine levels by firing dopaminergic neurons into striatal and extra-striatal areas (such as the ventral pallidum). The subject experiences a feeling of reward, mediated primarily by the action of nicotine on the α4- and β2-containing nAChRs in the VTA [16].

The genetic basis of nicotine dependence has been widely studied. In the Older Finnish Twin Cohort (n=2923 monozygous and n=6018 dizygous), the authors reported that genetic factors are important in the amount smoked and smoking cessation, and are largely independent of genetic influences on age at initiation [17]. Other findings have linked increased vulnerability to nicotine addiction and increased cigarette smoking per day to allelic variation in the CHRNA5–CHRNA3–CHRNB54 gene cluster, which encodes α5, α3 and β4 nAChR subunits [18, 19]. Allelic variation in CYP2A6 (encoding the enzyme cytochrome P450 2A6, which metabolises nicotine) has been associated with less predisposition to nicotine dependence. These allelic variations result in slow metabolism of nicotine, so individuals consume less nicotine per day, experience less severe withdrawal symptoms and are more successful at quitting smoking than people with normal or fast metabolism. The slow nicotine metabolism is due to an increase in the duration of action at the receptor, letting its levels build up over time. Thus, lower levels of intake are needed to maintain nAChR activation [20–22].

Other studies in large samples showed different genes associated with alcohol and nicotine addiction or dependence [23]. However, in patients with COPD specifically, two single nucleotide polymorphisms in CHRNA3/5 (rs8034191 and rs1051730) were associated with the Fagerström test in active smokers and in those with nicotine dependence [24].

Epidemiological aspects of smoking in COPD

Despite the clear evidence of the benefits of smoking cessation in COPD, a significant proportion (over a third) of patients continue to smoke even knowing that they have moderate-to-severe disease and are experiencing significant symptoms.

Several studies in different populations worldwide have evaluated the smoking status in patients with COPD. The proportion of COPD patients who are current smokers varies considerably between populations and world regions (figure 1). In population-based studies the proportion of current-smoker COPD patients ranged from 34% in Spain to almost 48% in China, with an average of 35.6% [25–28], whereas in observational studies the proportion ranged from 30% (Daxas in COPD Therapy (DINO) study) to 43.4% (COPDGene cohort) [29–33]. On the other hand, an analysis of individuals with COPD enrolled in some COPD pharmacological clinical trials showed that the proportion of current smokers ranged between 20% and 48%, with an average of 38% [34–43].

FIGURE 1
  • Download figure
  • Open in new tab
  • Download powerpoint
FIGURE 1

Prevalence of current-smoker COPD patients in different settings.

Assessment and approach to the smoking patient with COPD (motivation and tobacco dependence)

There are differences in clinical characteristics between smokers with and without COPD. Smokers with COPD exhibit higher dependence on nicotine, smoke more cigarettes per day, have higher cotinine concentrations, and have lower self-efficacy and self-esteem than those without the disease, all of which affect their ability to quit smoking [44–46]. These characteristics are neither linked to a lack of motivation to quit (because this was similar between smokers with and without COPD) nor to differences in the stage of the self-change process or the number of quit attempts [45, 46]. Nevertheless, depression has been reported to be more frequent in smokers with COPD, a fact that can influence the behaviour of these patients [47]. Regarding treatment, smokers with COPD seem to have similar susceptibility to smoking cessation interventions compared with those without COPD. Results from real-world studies and clinical trials have shown that the combination of brief or intensive counselling in smokers with COPD had comparable abstinence rates over 1 year to smokers in general [48–51]. However, a study showed that 1-year quit rates in smokers with COPD were higher than in those without COPD [52].

Other studies have investigated the clinical characteristics of patients with COPD who continue smoking versus sustainers quitting smoking [6, 48, 53, 54]. The main characteristics associated with current smoking in COPD patients are younger age, longer duration of smoking, fewer daily cigarettes, lower socioeconomic status, earlier stages of the disease, milder symptoms, poor quality of life and worse self-perceived general health [6, 53, 54]. Self-efficacy in smokers with COPD is usually low [46]. Perception of better health might be associated with higher self-efficacy to abstain from smoking, leading to more successful quit attempts. At the same time, psychological distress, including depressive symptoms, might contribute to unsuccessful attempts to quit smoking in COPD patients [6].

The approach to smokers with COPD, and smokers in general, should consider the mental situation in which the subject is in at the time of consultation, paying particular attention to aspects linked to tobacco consumption (motivation and dependence).

An accurate evaluation of motivation to classify the patient according to the Prochaska–DiClemente phase model [55] (table 1), as well as the strengthening of motivation and the construction of self-efficacy, is essential to increase the chances of quitting smoking in patients with COPD. The stages of change for smoking cessation represent a cycle. Therefore, patients may return to a previous state several times before absolute abstinence. Due to this cycle, it is crucial to establish the patient's current stage frequently and continue providing a positive support system, as it may take multiple quit attempts before cessation. It is not recommended to initiate pharmacotherapy for smoking cessation until the patient is in the preparation stage.

View this table:
  • View inline
  • View popup
TABLE 1

Stages of change for smoking cessation (Prochaska–DiClemente model [55])

Stopping smoking is complex and smokers often fail due to nicotine addiction; therefore, an accurate evaluation of nicotine dependence is crucial in the cessation process. As in any smoker subject, assessment of smokers with COPD involves evaluation of the number of pack-years, degree of physical dependence on nicotine using the Fagerström test [56] or its short version (Heaviness of Smoking Index) [57], analysis of previous attempts to quit and determination of carbon monoxide levels in exhaled air (figure 2). Some indicators of high nicotine dependence (figure 2) are smoking within 30 min after waking up, nocturnal smoking, consuming ≥20 cigarettes per day and a score of 7−10 points on the Fagerström scale or 5–6 points on the Heaviness of Smoking Index.

FIGURE 2
  • Download figure
  • Open in new tab
  • Download powerpoint
FIGURE 2

Assessment of smokers with COPD.

Smoking cessation interventions in patients with COPD

Advice, counselling interventions and spirometry as a motivational tool

A Cochrane review in general smokers showed that individual counselling was more effective than minimal contact when pharmacotherapy was not offered to participants (risk ratio 1.57, 95% CI 1.40–1.77) and was estimated to increase cessation by 40–80% after at least 6 months [58]. On the other hand, a pooled analysis of smokers with and without pharmacotherapy indicated that more intensive counselling has a small benefit over less intensive counselling (risk ratio 1.29, 95% CI 1.09–1.53) [58].

In patients with COPD, offering straightforward advice to quit or smoking cessation counselling (SCC) by healthcare professionals is an effective smoking cessation intervention, especially when combined with pharmacological treatment. A network meta-analysis in COPD patients showed a trend of SCC alone to be superior to usual care (OR 1.82, 95% CI 0.96–3.44; p=0.07) [59]. The odds of prolonged abstinence for SCC in combination with nicotine replacement therapy (NRT) were 5 times higher compared with no intervention or usual care (OR 5.08, 95% CI 4.32–5.97; p<0.0001), 3 times higher compared with SCC alone (OR 2.80, 95% CI 1.49–5.26; p=0.001) and 1.5 times higher compared with SCC in combination with an antidepressant (OR 1.53, 95% CI 0.71–3.30; p=0.28) [59]. Other systematic reviews reported average 12-month continuous abstinence rates of 1.4% for usual care, 2.6% for minimal counselling (<90 min), 6% for intensive counselling (≥90 min) and 12.3% for intensive counselling with pharmacotherapy [60].

Regarding the effectiveness of high-intensity compared with low-intensity counselling interventions in patients with COPD, a meta-analysis showed that the odds ratios were not significant for the comparisons of high-intensity SCC alone versus low-intensity SCC alone (OR 1.46, 95% CI 0.44–4.90; p=0.54) and high-intensity SCC in combination with an antidepressant versus low-intensity SCC in combination with an antidepressant (OR 1.55, 95% CI 0.35–6.91; p=0.56) [59]. Only high-intensity SCC plus NRT was significantly more effective than low-intensity SCC plus NRT (OR 1.81, 95% CI 1.04–3.15; p=0.04) [59]. Therefore, it is unclear whether more intensive individual counselling is more effective when combined with pharmacotherapy. On the other hand, high-intensity behavioural treatment increased abstinence rates when compared with usual care (risk ratio 25.38, 95% CI 8.03–80.22) or low-intensity behavioural treatment (risk ratio 2.18, 95% CI 1.05–4.49) [6].

Obtaining lung function testing and providing those results to individuals who smoke has been proposed as a motivational tool to improve smoking cessation. A systematic review showed insufficient evidence to determine whether providing lung function values to patients improves smoking cessation compared with other methods [61]. A subsequent systematic review of seven randomised controlled trial (RCT) studies showed mixed results [62]. Two of the studies found an improved rate of smoking cessation when smokers were provided with lung function results in addition to SCC, whereas the other five studies showed no significant differences [62]. Therefore, there is not enough evidence to support that providing lung function results (FEV1 and/or lung age) to smokers contributes to a higher rate of smoking cessation.

Pharmacotherapy: controllers (NRT patch, bupropion and varenicline) and relievers (rapidly acting NRT)

Given that nicotine dependence in patients with COPD is usually high, these patients should be treated with various interventions (counselling, psychological-behavioural support and pharmacological treatment). The results of a meta-analysis indicated that smokers with COPD who receive a combination of high-intensity behavioural support and medication were more than twice as likely to quit as those who receive behavioural support alone [6].

In general, pharmacological treatments for smoking cessation include controller medications that aim at long-term abstinence (nicotine patch, bupropion and varenicline) and those that rapidly relieve acute cravings and withdrawal symptoms (fast-acting nicotine). The pharmacological approach to smoking cessation in COPD depends on the severity of dependence and the presence and intensity of withdrawal symptoms during treatment. Treatment should be adapted to the needs of individual patients with different levels of tobacco dependence. Once treatment starts, the pharmacotherapy intensity should be adjusted up or down, guided by the level of control of tobacco dependence. Table 2 shows the doses and duration of pharmacological treatments to quit smoking.

View this table:
  • View inline
  • View popup
TABLE 2

Doses and duration of pharmacological treatments to quit smoking

Pharmacological treatment compared with placebo in smokers with COPD

Some studies have compared simple controller pharmacotherapy (NRT, bupropion, nortriptyline and varenicline) with placebo in smokers with COPD [6, 63]. A meta-analysis showed that all pharmacotherapy groups (except for nortriptyline) increased the chance of quitting smoking compared with placebo [6]. Prolonged abstinence rates in the pharmacotherapy groups ranged from 14% to 27%, while in the placebo group rates ranged from 5% to 9% [6]. The pooled (6–12 months follow-up) risk ratio for prolonged abstinence at the most extended follow-up was 2.53 (95% CI 1.83–3.50) compared with placebo and for each one of the pharmacotherapy groups was: NRT (12 months follow-up) 2.60 (95% CI 1.29–5.24), bupropion (6 months follow-up) 2.03 (95% CI 1.26–3.28), varenicline (12 months follow-up) 3.34 (95% CI 1.88–5.92) and nortriptyline (6 months follow-up) 2.54 (95% CI 0.87–7.44) [6].

Comparison between different pharmacological interventions and combined controller therapies in smokers with COPD

A study that compared bupropion with NRT patch showed a prolonged abstinence rate at 12 months of 16% in the bupropion group and 21% in the NRT patch group (risk ratio 0.74, 95% CI 0.27–2.05) [64]. In another study which enrolled patients with severe and very severe COPD, varenicline and bupropion yielded higher abstinence rates compared with NRT patch [65]. Continuous abstinence rates through weeks 9 to 24 were 38.2% for NRT, 55.6% for bupropion and 58.3% for varenicline [65]. Varenicline was more effective than nicotine patch in inducing sustained abstinence (OR 1.98, 95% CI 1.25–3.12) and as effective as bupropion at 6 months follow-up (OR 1.43, 95% CI 0.49–2.2) [65]. Nevertheless, the group who had received varenicline compared with bupropion smoked a higher number of cigarettes daily [65].

Combination of controller therapies to induce smoking cessation has also been considered a valid approach to increase the overall efficacy of the intervention. In COPD patients, a study assigned an intervention programme with counselling and advice about NRT (and additional bupropion-SR in one of the programmes) or usual care [66]. The results indicate that the two intervention groups were equally effective in terms of abstinence rates (risk ratio 2.25, 95% CI 0.87–5.85; p=0.10) [66]. However, there might have been some issues interfering with combination effectiveness such as the inclusion of some unmotivated COPD smokers, less intensive counselling, and poor compliance with the use of bupropion and NRT [66]. Combinations of varenicline with other controller therapies have also been proposed for smoking cessation; however, there are no studies that have assessed the effectiveness of these combinations in patients with COPD.

Smoking reduction-to-quit interventions for reducing harm and increasing long-term quitting

Quitting smoking is the best thing that a COPD patient can do to reduce the harm caused by smoking. However, some patients may not want to do this or feel that they cannot stop smoking completely. On the other hand, relapse is common during smoking cessation; therefore, harm reduction has been considered as an alternative approach for smokers with COPD unable or unwilling to quit. The possible approaches to reduce the exposure to toxins from smoking include reducing the amount of tobacco used and using less toxic products, e.g. pharmaceutical nicotine and potential reduced-exposure tobacco products.

It has been postulated that in smokers who cannot quit abruptly, reducing smoking increases the probability of quitting in the future. In general smokers, a meta-analysis did not show clear evidence that reduction-to-quit interventions resulted in better quit rates than no smoking cessation intervention (risk ratio 1.74, 95% CI 0.90–3.38) [67]. In addition, the comparison between reduction and abrupt smoking cessation interventions showed no difference in long-term quitting rates (risk ratio 1.01, 95% CI 0.87–1.17) [67]. A subgroup analysis found some evidence that reduction-to-quit interventions may be more effective than abrupt quitting interventions if varenicline is used as an aid to reduction; this result was based on a single study and should be viewed with caution [67].

On the other hand, another meta-analysis that evaluated the effects of interventions aimed at reducing the health harm of continued tobacco use in smokers who are unable or unwilling to quit found that none of the studies directly tested whether harm reduction strategies reduced the harms to health caused by smoking (long-term change in health status) [68]. Most of the studies tested NRT as an intervention to assist reduction and the pooled analysis showed that people unwilling to quit can be helped to cut down the number of cigarettes they smoke (reduction of ≥50% in cigarettes per day: risk ratio 1.75, 95% CI 1.44–2.13) and to quit smoking in the long-term (risk ratio 1.87, 95% CI 1.43–2.44) using NRT [68]. There is a lack of evidence to support the use of other aids (bupropion, varenicline, e-cigarettes or snus (oral tobacco product)) to reduce the harm caused by continuous tobacco smoking [68] and to support that reducing the number of cigarettes smoked daily can improve health or help patients with COPD to quit smoking completely in the long-term.

E-cigarettes for smoking cessation

The use of e-cigarettes has increased probably due to the presumption that it is associated with less damage, as well as reducing the symptoms of anxiety and withdrawal from tobacco by sharing the same visual and sensory characteristics.

A meta-analysis showed a significant association of e-cigarette use with COPD (adjusted for cigarette smoking and other covariates), with a pooled adjusted OR of 1.49 (95% CI 1.36–1.65) for e-cigarette users compared with non-e-cigarette users [69]. The authors concluded that e-cigarette use has consequences for asthma and COPD, which is of concern for respirology and public health [69].

There is a perception that e-cigarette use is safer or an effective NRT during the smoking cessation process. A recent study assessed the effectiveness, tolerability and safety of using e-cigarettes for smoking cessation [70]. There was moderate-certainty evidence (limited by imprecision) that quit rates were higher in people randomised to nicotine e-cigarettes than in those to NRT (risk ratio 1.53, 95% CI 1.21–1.93) and low-certainty evidence (limited by very serious imprecision) that the rate of occurrence of adverse events was similar (risk ratio 0.98, 95% CI 0.80–1.19) between groups [70].

On the other hand, the results of a trial aimed at evaluating the 1-year efficacy of e-cigarettes compared with NRT as a smoking cessation treatment in general smokers showed that the abstinence rate was 18% for the e-cigarette group and 9.9% for the NRT group (risk ratio 1.83, 95% CI 1.30–2.58) [71]. However, an important finding to highlight in this study was that among participants with 1-year abstinence, 80% were using e-cigarettes at 52 weeks in the e-cigarette group in comparison with 9% of those in the NRT [71].

There is very limited information on the health consequences (COPD outcomes) of e-cigarette use among smokers with COPD, as well as on their effectiveness to help these patients attenuate the consumption of cigarettes or achieve long-term smoking abstinence.

A small retrospective study in 48 patients with COPD who had reported regular daily use of e-cigarettes found that patients were able to quit or substantially reduced their tobacco consumption by switching to regular e-cigarette use, with improvement in COPD exacerbations, FEV1 decline, COPD Assessment Test (CAT) scores and 6-min walk distance (6MWD) [72]. Subsequently, the same group of authors prospectively assessed respiratory parameters in 44 COPD patients who ceased or substantially reduced conventional cigarette use with e-cigarettes [73]. They reported a decline in the use of conventional cigarettes in the e-cigarette user group and improvements in exacerbation rates, CAT scores and 6MWD, but no change in lung function over the 3-year period [73].

The possible evidence of respiratory health benefits of e-cigarette use from these studies in COPD patients contrasts with the results of two large observational studies [74, 75] and with the concerns raised in experimental models (i.e. cell cultures and animal models) that suggest that chronic exposure to e-cigarettes may elicit features of COPD/emphysema and damage the airway epithelium, among other harmful effects in the respiratory system [76–83]. A study in two prospective large cohorts (COPDGene (n=3536) and SPIROMICS (n=1060)) that aimed to determine the usage of e-cigarettes in older adults at risk for or with COPD showed that e-cigarette users had a heavier conventional cigarette smoking history (higher nicotine dependence), worse pulmonary-related health outcomes (more chronic bronchitis and exacerbations) and were less likely to reduce or quit smoking conventional cigarettes [74]. Another large prospective study showed an increased risk of respiratory disease among former (incidence risk ratio 1.28, 95% CI 1.09–1.50) and current e-cigarette users (incidence risk ratio 1.31, 95% CI 1.08–1.59) even when adjusted for cigarette and other combustible tobacco product use, demographic characteristics, and chronic health conditions [75]. Therefore, these findings do not support a reduction in harm using e-cigarettes, and may even suggest higher nicotine exposure and higher risk of respiratory diseases [74, 75].

Taking into account the incomplete information on the safety and efficacy of e-cigarettes as an aid for smoking cessation, it is necessary to carry out a frequent and balanced review of the probable benefits and damages with which they are associated before recommending their use. The long-term efficacy and safety of e-cigarettes for smoking cessation also need to be evaluated in larger high-risk populations. Therefore, based on the available evidence and on the largely unknown long-term health effects of e-cigarettes, it is not possible to recommend this intervention for smoking cessation or for reducing conventional cigarette use in patients with COPD.

Nicotine vaccine

The idea of an immunotherapy approach for treating addictions can be found in the literature since the 1960s [84]. The development of vaccines related to drug abuse is a public health approach that has been explored for over a decade. The nicotine vaccine is intended to treat drug abuse through active immunisation by inducing nicotine-specific monoclonal antibodies (nic-mAbs) to sequester and reduce nicotine distribution inside the brain.

The nicotine-blocking effect of nic-mAbs has been successfully studied in pre-clinical models, with up to ∼80% reduction in brain nicotine levels within minutes of an intravenous dose of nicotine [85, 86]. nic-mAbs are particularly effective in reducing the early distribution of nicotine to the brain, which is important because the greatest reinforcing and subjective effects occur within the first few minutes of smoking [87]. However, a Cochrane systematic review including four studies with a total of 2642 smokers found no evidence that nicotine vaccines improve long-term smoking cessation [88]. None of the included studies detected a significant difference in long-term cessation between participants who received the vaccine and those who received placebo. The risk ratio for 12-month cessation in active and placebo groups was 1.35 (95% CI 0.82–2.22) in the NIC002 trial and 1.74 (95% CI 0.73–4.18) in one NicVAX trial [88]. However, one RCT in 301 smokers evaluating 200 and 400 µg doses of NicVAX (a nic-mAb) showed that subjects with the highest serum antinicotine antibody response (top 30% by area under the curve) were more likely to attain 6 weeks of continuous abstinence from weeks 19 through 26 than the placebo recipients (24.6% versus 12%; OR 2.69, 95% CI 1.14–6.37; p=0.0024) [89].

A recent systematic review that included 15 clinical trials (11 RCTs, three non-RCTs and one cohort study) demonstrated conflicting information around the vaccine [90]. Factors that contributed to these findings were the inclusion of low or unsustained antibody response between individuals and continued nicotine use despite the antibody response. The explanation is not straightforward because there are many challenges and complexities associated with nicotine dependence (genetic factors, drug design and clinical trial designs). Many of the trials for nic-mAbs are not published in peer-reviewed journals after completion, which suggests that this is related to insignificant findings. However, there are several conclusions from those first clinical studies: the nicotine vaccines need to generate high levels of antibodies and improve the design, maybe using nanoparticles instead of a protein conjugate [84, 90]. Future studies with the new generation of nicotine vaccines will be necessary to clarify whether they are more effective in human trials.

Smoking cessation during the coronavirus disease 2019 pandemic in smokers with COPD

The recent coronavirus disease 2019 (COVID-19) pandemic resulted in more than 600 million cases and 6 million deaths worldwide [91]. COPD patients and smokers are at increased risk of poor outcomes and severe disease from COVID-19 [92]. The biological explanation could be the upregulation of the angiotensin-converting enzyme 2 receptors and the epithelial damage present in COPD patients and smokers. Another explanation is more mechanistic and involves hand-to-face movement, which would accelerate viral transmission [93], making the care of COPD patients with COVID-19 particularly challenging.

In a recent consensus built from surveys of COPD patients and doctors during the pandemic, there was a consensus (84% of participants) that remote care, although it limits face-to-face interaction, should reinforce smoking cessation [94].

The impact of the COVID-19 pandemic on smoking behaviour is complex and unclear. A recent systematic review that included 11 publications (58 052 participants) found that smoking consumption decreased during the pandemic in most cases [95]. Fear and social restrictions could be leading to an excellent opportunity to reduce or quit smoking.

Regarding patients with COPD, it is important to highlight the need to: 1) warn the population of the increased risk that smokers have of contracting COVID-19 and of the worse prognosis of the disease, 2) highlight the importance of quitting smoking through new methods such as applications or remote evaluations of outpatients, 3) discourage the use of new electronic nicotine devices and water pipes, which can favour the development of this disease, and 4) emphasise the importance of smoke-free environments, as well as continue generating evidence on the impact of smoking on the development of COVID-19 [96]. To the best of our knowledge, there is no evidence of the development of unique measurements to increase smoking cessation in COPD patients during the pandemic.

The efficacy of vaccination is related to the capacity to produce high levels of antibodies against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Several studies evaluated the relationship between antibody levels after vaccination and smoking status [97–99]. One study found that smoking is a risk factor for low antibody titres even 3 months after the second dose of mRNA vaccination against SARS-CoV-2 independent from the Brinkman index or cigarettes per day [97]. The age-adjusted antibody titres were lower in ever-smokers in comparison with never-smokers (median (interquartile range) −174 (−378 to 145) and 90 (−174 to 512) U·mL−1, respectively; p<0.0001).

In summary, rather than an obstacle, the COVID-19 pandemic represents an opportunity to discuss smoking cessation with COPD patients, highlighting the benefits of improving their response to the virus, their prognosis and their response to the vaccination.

Footnotes

  • Provenance: Commissioned article, peer reviewed.

  • Number 1 in the Series “Non-pharmacological interventions in COPD: state of the art and future directions” Edited by Geert M. Verleden and Wim Janssens

  • This article has an editorial commentary: https://doi.org/10.1183/16000617.0028-2023

  • Conflict of interest: M. Montes de Oca has received honoraria for lectures on COPD from AstraZeneca and GSK, outside the submitted work. M.E. Laucho-Contreras has received an honorarium for Medical Affairs Staff from GSK Colombia and owns GSK stock, all outside the submitted work.

  • Received September 30, 2022.
  • Accepted December 8, 2022.
  • Copyright ©The authors 2023
http://creativecommons.org/licenses/by-nc/4.0/

This version is distributed under the terms of the Creative Commons Attribution Non-Commercial Licence 4.0. For commercial reproduction rights and permissions contact permissions{at}ersnet.org

References

  1. ↵
    1. Cunalata-Paredes AV,
    2. Gea-Izquierdo E
    . COPD in the major nonsmoking adult: a systematic review and meta-analysis. Arch Environ Occup Health 2021; 76: 319–329. doi:10.1080/19338244.2020.1828243
    OpenUrl
  2. ↵
    1. Martinez FJ,
    2. Han MK,
    3. Allinson JP, et al.
    At the root: defining and halting progression of early chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2018; 197: 1540–1551. doi:10.1164/rccm.201710-2028PP
    OpenUrlPubMed
    1. Bui DS,
    2. Lodge CJ,
    3. Burgess JA, et al.
    Childhood predictors of lung function trajectories and future COPD risk: a prospective cohort study from the first to the sixth decade of life. Lancet Respir Med 2018; 6: 535–544. doi:10.1016/S2213-2600(18)30100-0
    OpenUrlCrossRefPubMed
    1. Lange P,
    2. Celli B,
    3. Agusti A, et al.
    Lung-function trajectories leading to chronic obstructive pulmonary disease. N Engl J Med 2015; 373: 111–122. doi:10.1056/NEJMoa1411532
    OpenUrlCrossRefPubMed
  3. ↵
    1. Martinez FD
    . Early-life origins of chronic obstructive pulmonary disease. N Engl J Med 2016; 375: 871–878. doi:10.1056/NEJMra1603287
    OpenUrlCrossRefPubMed
  4. ↵
    1. van Eerd EA,
    2. van der Meer RM,
    3. van Schayck OC, et al.
    Smoking cessation for people with chronic obstructive pulmonary disease. Cochrane Database Syst Rev 2016; 8: CD010744. doi:10.1002/14651858.CD010744.pub2
    OpenUrl
  5. ↵
    1. Anthonisen NR,
    2. Skeans MA,
    3. Wise RA, et al.
    The effects of a smoking cessation intervention on 14.5-year mortality: a randomized clinical trial. Ann Intern Med 2005; 142: 233–239. doi:10.7326/0003-4819-142-4-200502150-00005
    OpenUrlCrossRefPubMed
  6. ↵
    1. Anthonisen NR,
    2. Connett JE,
    3. Murray RP
    . Smoking and lung function of Lung Health Study participants after 11 years. Am J Respir Crit Care Med 2002; 166: 675–679. doi:10.1164/rccm.2112096
    OpenUrlCrossRefPubMed
  7. ↵
    1. Willemse BW,
    2. Postma DS,
    3. Timens W, et al.
    The impact of smoking cessation on respiratory symptoms, lung function, airway hyperresponsiveness and inflammation. Eur Respir J 2004; 23: 464–476. doi:10.1183/09031936.04.00012704
    OpenUrlAbstract/FREE Full Text
  8. ↵
    1. Bauer CMT,
    2. Morissette MC,
    3. Stampfli MR
    . The influence of cigarette smoking on viral infections: translating bench science to impact COPD pathogenesis and acute exacerbations of COPD clinically. Chest 2013; 143: 196–206. doi:10.1378/chest.12-0930
    OpenUrlCrossRefPubMed
  9. ↵
    1. Singh D,
    2. Roche N,
    3. Halpin D, et al.
    Current controversies in the pharmacological treatment of chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2016; 194: 541–549. doi:10.1164/rccm.201606-1179PP
    OpenUrlCrossRefPubMed
  10. ↵
    1. GBD 2019 Tobacco Collaborators
    . Spatial, temporal, and demographic patterns in prevalence of smoking tobacco use and attributable disease burden in 204 countries and territories, 1990–2019: a systematic analysis from the Global Burden of Disease Study 2019. Lancet 2021; 397: 2337–2360. doi:10.1016/S0140-6736(21)01169-7
    OpenUrlCrossRefPubMed
  11. ↵
    1. Wittenberg RE,
    2. Wolfman SL,
    3. De Biasi M, et al.
    Nicotinic acetylcholine receptors and nicotine addiction: a brief introduction. Neuropharmacology 2020; 177: 108256. doi:10.1016/j.neuropharm.2020.108256
    OpenUrl
  12. ↵
    1. Picciotto MR,
    2. Addy NA,
    3. Mineur YS, et al.
    It is not “either/or”: activation and desensitization of nicotinic acetylcholine receptors both contribute to behaviors related to nicotine addiction and mood. Prog Neurobiol 2008; 84: 329–342. doi:10.1016/j.pneurobio.2007.12.005
    OpenUrlCrossRefPubMed
  13. ↵
    1. Jensen KP,
    2. Valentine G,
    3. Gueorguieva R, et al.
    Differential effects of nicotine delivery rate on subjective drug effects, urges to smoke, heart rate and blood pressure in tobacco smokers. Psychopharmacology 2020; 237: 1359–1369. doi:10.1007/s00213-020-05463-6
    OpenUrl
  14. ↵
    1. Le Foll B,
    2. Piper ME,
    3. Fowler CD, et al.
    Tobacco and nicotine use. Nat Rev Dis Primers 2022; 8: 19. doi:10.1038/s41572-022-00346-w
    OpenUrl
  15. ↵
    1. Broms U,
    2. Silventoinen K,
    3. Madden PA, et al.
    Genetic architecture of smoking behavior: a study of Finnish adult twins. Twin Res Hum Genet 2006; 9: 64–72. doi:10.1375/twin.9.1.64
    OpenUrlCrossRefPubMed
  16. ↵
    1. Saccone NL,
    2. Wang JC,
    3. Breslau N, et al.
    The CHRNA5-CHRNA3-CHRNB4 nicotinic receptor subunit gene cluster affects risk for nicotine dependence in African-Americans and in European-Americans. Cancer Res 2009; 69: 6848–6856. doi:10.1158/0008-5472.CAN-09-0786
    OpenUrlAbstract/FREE Full Text
  17. ↵
    1. Bierut LJ,
    2. Stitzel JA,
    3. Wang JC, et al.
    Variants in nicotinic receptors and risk for nicotine dependence. Am J Psychiatry 2008; 165: 1163–1171. doi:10.1176/appi.ajp.2008.07111711
    OpenUrlCrossRefPubMed
  18. ↵
    1. Liakoni E,
    2. Edwards KC,
    3. St Helen G, et al.
    Effects of nicotine metabolic rate on withdrawal symptoms and response to cigarette smoking after abstinence. Clin Pharmacol Ther 2019; 105: 641–651. doi:10.1002/cpt.1238
    OpenUrl
    1. Ray R,
    2. Tyndale RF,
    3. Lerman C
    . Nicotine dependence pharmacogenetics: role of genetic variation in nicotine-metabolizing enzymes. J Neurogenet 2009; 23: 252–261. doi:10.1080/01677060802572887
    OpenUrlCrossRefPubMed
  19. ↵
    1. Strasser AA,
    2. Malaiyandi V,
    3. Hoffmann E, et al.
    An association of CYP2A6 genotype and smoking topography. Nicotine Tob Res 2007; 9: 511–518. doi:10.1080/14622200701239605
    OpenUrlCrossRefPubMed
  20. ↵
    1. Liu M,
    2. Jiang Y,
    3. Wedow R, et al.
    Association studies of up to 1.2 million individuals yield new insights into the genetic etiology of tobacco and alcohol use. Nat Genet 2019; 51: 237–244. doi:10.1038/s41588-018-0307-5
    OpenUrlCrossRefPubMed
  21. ↵
    1. Kim DK,
    2. Hersh CP,
    3. Washko GR, et al.
    Epidemiology, radiology, and genetics of nicotine dependence in COPD. Respir Res 2011; 12: 9. doi:10.1186/1465-9921-12-9
    OpenUrlCrossRefPubMed
  22. ↵
    1. Menezes AM,
    2. Perez-Padilla R,
    3. Jardim JR, et al.
    Chronic obstructive pulmonary disease in five Latin American cities (the PLATINO study): a prevalence study. Lancet 2005; 366: 1875–1881. doi:10.1016/S0140-6736(05)67632-5
    OpenUrlCrossRefPubMed
    1. Fang L,
    2. Gao P,
    3. Bao H, et al.
    Chronic obstructive pulmonary disease in China: a nationwide prevalence study. Lancet Respir Med 2018; 6: 421–430. doi:10.1016/S2213-2600(18)30103-6
    OpenUrl
    1. Schauer GL,
    2. Wheaton AG,
    3. Malarcher AM, et al.
    Smoking prevalence and cessation characteristics among U.S. adults with and without COPD: findings from the 2011 Behavioral Risk Factor Surveillance System. COPD 2014; 11: 697–704. doi:10.3109/15412555.2014.898049
    OpenUrl
  23. ↵
    1. Soriano JB,
    2. Alfageme I,
    3. Miravitlles M, et al.
    Prevalence and determinants of COPD in Spain: EPISCAN II. Arch Bronconeumol 2021; 57: 61–69. doi:10.1016/j.arbr.2020.07.017
    OpenUrl
  24. ↵
    1. Meeraus WH,
    2. Mullerova H,
    3. El Baou C, et al.
    Predicting re-exacerbation timing and understanding prolonged exacerbations: an analysis of patients with COPD in the ECLIPSE cohort. Int J Chron Obstruct Pulmon Dis 2021; 16: 225–244. doi:10.2147/COPD.S279315
    OpenUrl
    1. Criner RN,
    2. Labaki WW,
    3. Regan EA, et al.
    Mortality and exacerbations by global initiative for chronic obstructive lung disease groups ABCD: 2011 versus 2017 in the COPDGene cohort. Chronic Obstr Pulm Dis 2019; 6: 64–73. doi:10.15326/jcopdf.6.1.2018.0130
    OpenUrl
    1. Lassan S,
    2. Keszegh J,
    3. Lassanova M
    . Characteristics of COPD patients treated with single-inhaler triple therapy in real-life clinical practice. Bratisl Lek Listy 2022; 123: 27–36. doi:10.4149/BLL_2022_005
    OpenUrl
    1. Kardos P,
    2. Mokros I,
    3. Sauer R, et al.
    Health status in patients with COPD treated with roflumilast: two large noninterventional real-life studies: DINO and DACOTA. Int J Chron Obstruct Pulmon Dis 2018; 13: 1455–1468. doi:10.2147/COPD.S159827
    OpenUrl
  25. ↵
    1. Worth H,
    2. Buhl R,
    3. Criee CP, et al.
    The ‘real-life’ COPD patient in Germany: the DACCORD study. Respir Med 2016; 111: 64–71. doi:10.1016/j.rmed.2015.12.010
    OpenUrl
  26. ↵
    1. Vestbo J,
    2. Anderson JA,
    3. Brook RD, et al.
    Fluticasone furoate and vilanterol and survival in chronic obstructive pulmonary disease with heightened cardiovascular risk (SUMMIT): a double-blind randomised controlled trial. Lancet 2016; 387: 1817–1826. doi:10.1016/S0140-6736(16)30069-1
    OpenUrlPubMed
    1. Singh D,
    2. Papi A,
    3. Corradi M, et al.
    Single inhaler triple therapy versus inhaled corticosteroid plus long-acting beta2-agonist therapy for chronic obstructive pulmonary disease (TRILOGY): a double-blind, parallel group, randomised controlled trial. Lancet 2016; 388: 963–973. doi:10.1016/S0140-6736(16)31354-X
    OpenUrlCrossRefPubMed
    1. Vestbo J,
    2. Papi A,
    3. Corradi M, et al.
    Single inhaler extrafine triple therapy versus long-acting muscarinic antagonist therapy for chronic obstructive pulmonary disease (TRINITY): a double-blind, parallel group, randomised controlled trial. Lancet 2017; 389: 1919–1929. doi:10.1016/S0140-6736(17)30188-5
    OpenUrlCrossRefPubMed
    1. Calverley PMA,
    2. Anzueto AR,
    3. Carter K, et al.
    Tiotropium and olodaterol in the prevention of chronic obstructive pulmonary disease exacerbations (DYNAGITO): a double-blind, randomised, parallel-group, active-controlled trial. Lancet Respir Med 2018; 6: 337–344. doi:10.1016/S2213-2600(18)30102-4
    OpenUrl
    1. Papi A,
    2. Vestbo J,
    3. Fabbri L, et al.
    Extrafine inhaled triple therapy versus dual bronchodilator therapy in chronic obstructive pulmonary disease (TRIBUTE): a double-blind, parallel group, randomised controlled trial. Lancet 2018; 391: 1076–1084. doi:10.1016/S0140-6736(18)30206-X
    OpenUrlCrossRefPubMed
    1. Lipson DA,
    2. Barnhart F,
    3. Brealey N, et al.
    Once-daily single-inhaler triple versus dual therapy in patients with COPD. N Engl J Med 2018; 378: 1671–1680. doi:10.1056/NEJMoa1713901
    OpenUrlCrossRefPubMed
    1. Ferguson GT,
    2. Rabe KF,
    3. Martinez FJ, et al.
    Triple therapy with budesonide/glycopyrrolate/formoterol fumarate with co-suspension delivery technology versus dual therapies in chronic obstructive pulmonary disease (KRONOS): a double-blind, parallel-group, multicentre, phase 3 randomised controlled trial. Lancet Respir Med 2018; 6: 747–758. doi:10.1016/S2213-2600(18)30327-8
    OpenUrlCrossRefPubMed
    1. Rabe KF,
    2. Martinez FJ,
    3. Ferguson GT, et al.
    Triple inhaled therapy at two glucocorticoid doses in moderate-to-very-severe COPD. N Engl J Med 2020; 383: 35–48. doi:10.1056/NEJMoa1916046
    OpenUrlCrossRefPubMed
    1. Jenkins CR,
    2. Wen FQ,
    3. Martin A, et al.
    The effect of low-dose corticosteroids and theophylline on the risk of acute exacerbations of COPD: the TASCS randomised controlled trial. Eur Respir J 2021; 57: 2003338. doi:10.1183/13993003.03338-2020
    OpenUrlAbstract/FREE Full Text
  27. ↵
    1. Zheng J,
    2. Baldi S,
    3. Zhao L, et al.
    Efficacy and safety of single-inhaler extrafine triple therapy versus inhaled corticosteroid plus long-acting beta2 agonist in eastern Asian patients with COPD: the TRIVERSYTI randomised controlled trial. Respir Res 2021; 22: 90. doi:10.1186/s12931-021-01683-2
    OpenUrl
  28. ↵
    1. Shahab L,
    2. Jarvis MJ,
    3. Britton J, et al.
    Prevalence, diagnosis and relation to tobacco dependence of chronic obstructive pulmonary disease in a nationally representative population sample. Thorax 2006; 61: 1043–1047. doi:10.1136/thx.2006.064410
    OpenUrlAbstract/FREE Full Text
  29. ↵
    1. Jimenez-Ruiz CA,
    2. Masa F,
    3. Miravitlles M, et al.
    Smoking characteristics: differences in attitudes and dependence between healthy smokers and smokers with COPD. Chest 2001; 119: 1365–1370. doi:10.1378/chest.119.5.1365
    OpenUrlCrossRefPubMed
  30. ↵
    1. Crowley TJ,
    2. Macdonald MJ,
    3. Walter MI
    . Behavioral anti-smoking trial in chronic obstructive pulmonary disease patients. Psychopharmacology 1995; 119: 193–204. doi:10.1007/BF02246161
    OpenUrlCrossRefPubMed
  31. ↵
    1. Wagena EJ,
    2. Arrindell WA,
    3. Wouters EF, et al.
    Are patients with COPD psychologically distressed? Eur Respir J 2005; 26: 242–248. doi:10.1183/09031936.05.00010604
    OpenUrlAbstract/FREE Full Text
  32. ↵
    1. Tonnesen P,
    2. Mikkelsen K,
    3. Bremann L
    . Nurse-conducted smoking cessation in patients with COPD using nicotine sublingual tablets and behavioral support. Chest 2006; 130: 334–342. doi:10.1378/chest.130.2.334
    OpenUrlCrossRefPubMed
    1. Tashkin DP,
    2. Rennard S,
    3. Taylor Hays J, et al.
    Lung function and respiratory symptoms in a 1-year randomized smoking cessation trial of varenicline in COPD patients. Respir Med 2011; 105: 1682–1690. doi:10.1016/j.rmed.2011.04.016
    OpenUrlCrossRefPubMed
    1. Tashkin D,
    2. Kanner R,
    3. Bailey W, et al.
    Smoking cessation in patients with chronic obstructive pulmonary disease: a double-blind, placebo-controlled, randomised trial. Lancet 2001; 357: 1571–1575. doi:10.1016/S0140-6736(00)04724-3
    OpenUrlCrossRefPubMed
  33. ↵
    1. Gratziou C,
    2. Florou A,
    3. Ischaki E, et al.
    Smoking cessation effectiveness in smokers with COPD and asthma under real life conditions. Respir Med 2014; 108: 577–583. doi:10.1016/j.rmed.2014.01.007
    OpenUrlPubMed
  34. ↵
    1. Stratelis G,
    2. Molstad S,
    3. Jakobsson P, et al.
    The impact of repeated spirometry and smoking cessation advice on smokers with mild COPD. Scand J Prim Health Care 2006; 24: 133–139. doi:10.1080/02813430600819751
    OpenUrlCrossRefPubMed
  35. ↵
    1. Karadogan D,
    2. Onal O,
    3. Sahin DS, et al.
    Factors associated with current smoking in COPD patients: a cross-sectional study from the Eastern Black Sea region of Turkey. Tob Induc Dis 2018; 16: 22. doi:10.18332/tid/90665
    OpenUrl
  36. ↵
    1. Hirai K,
    2. Tanaka A,
    3. Homma T, et al.
    Characteristics of and reasons for patients with chronic obstructive pulmonary disease to continue smoking, quit smoking, and switch to heated tobacco products. Tob Induc Dis 2021; 19: 85. doi:10.18332/tid/142848
    OpenUrl
  37. ↵
    1. Prochaska JO,
    2. DiClemente CC
    . Stages and processes of self-change of smoking: toward an integrative model of change. J Consult Clin Psychol 1983; 51: 390–395. doi:10.1037/0022-006X.51.3.390
    OpenUrlCrossRefPubMed
  38. ↵
    1. Heatherton TF,
    2. Kozlowski LT,
    3. Frecker RC, et al.
    The Fagerström Test For Nicotine Dependence: a revision of the Fagerström Tolerance Questionnaire. Br J Addict 1991; 86: 1119–1127. doi:10.1111/j.1360-0443.1991.tb01879.x
    OpenUrlCrossRefPubMed
  39. ↵
    1. John U,
    2. Meyer C,
    3. Schumann A, et al.
    A short form of the Fagerström Test for Nicotine Dependence and the Heaviness of Smoking Index in two adult population samples. Addict Behav 2004; 29: 1207–1212. doi:10.1016/j.addbeh.2004.03.019
    OpenUrlCrossRefPubMed
  40. ↵
    1. Lancaster T,
    2. Stead LF
    . Individual behavioural counselling for smoking cessation. Cochrane Database Syst Rev 2017; 3: CD001292. doi:10.1002/14651858.CD001292.pub3
    OpenUrlCrossRefPubMed
  41. ↵
    1. Strassmann R,
    2. Bausch B,
    3. Spaar A, et al.
    Smoking cessation interventions in COPD: a network meta-analysis of randomised trials. Eur Respir J 2009; 34: 634–640. doi:10.1183/09031936.00167708
    OpenUrlAbstract/FREE Full Text
  42. ↵
    1. Hoogendoorn M,
    2. Feenstra TL,
    3. Hoogenveen RT, et al.
    Long-term effectiveness and cost-effectiveness of smoking cessation interventions in patients with COPD. Thorax 2010; 65: 711–718. doi:10.1136/thx.2009.131631
    OpenUrlAbstract/FREE Full Text
  43. ↵
    1. Wilt TJ,
    2. Niewoehner D,
    3. Kane RL, et al.
    Spirometry as a motivational tool to improve smoking cessation rates: a systematic review of the literature. Nicotine Tob Res 2007; 9: 21–32. doi:10.1080/14622200601078509
    OpenUrlCrossRefPubMed
  44. ↵
    1. Westerdahl E,
    2. Engman KO,
    3. Arne M, et al.
    Spirometry to increase smoking cessation rate: a systematic review. Tob Induc Dis 2019; 17: 31. doi:10.18332/tid/106090
    OpenUrlPubMed
  45. ↵
    1. Antoniu SA,
    2. Buculei I,
    3. Mihaltan F, et al.
    Pharmacological strategies for smoking cessation in patients with chronic obstructive pulmonary disease: a pragmatic review. Expert Opin Pharmacother 2021; 22: 835–847. doi:10.1080/14656566.2020.1858796
    OpenUrl
  46. ↵
    1. Gorecka D,
    2. Bednarek M,
    3. Nowinski A, et al.
    Wyniki leczenia uzaleznienia od nikotyny chorych na przewlekła obturacyjna chorobé płuc. [Effect of treatment for nicotine dependence in patients with COPD.] Pneumonol Alergol Pol 2003; 71: 411–417. doi:10.5603/ARM.28222
    OpenUrlPubMed
  47. ↵
    1. Jimenez Ruiz CA,
    2. Ramos Pinedo A,
    3. Cicero Guerrero A, et al.
    Characteristics of COPD smokers and effectiveness and safety of smoking cessation medications. Nicotine Tob Res 2012; 14: 1035–1039. doi:10.1093/ntr/nts001
    OpenUrlCrossRefPubMed
  48. ↵
    1. Hilberink SR,
    2. Jacobs JE,
    3. Breteler MH, et al.
    General practice counseling for patients with chronic obstructive pulmonary disease to quit smoking: impact after 1 year of two complex interventions. Patient Educ Couns 2011; 83: 120–124. doi:10.1016/j.pec.2010.04.009
    OpenUrlCrossRefPubMed
  49. ↵
    1. Lindson N,
    2. Klemperer E,
    3. Hong B, et al.
    Smoking reduction interventions for smoking cessation. Cochrane Database Syst Rev 2019; 9: CD013183. doi:10.1002/14651858.CD013183.pub2
    OpenUrlPubMed
  50. ↵
    1. Lindson-Hawley N,
    2. Hartmann-Boyce J,
    3. Fanshawe TR, et al.
    Interventions to reduce harm from continued tobacco use. Cochrane Database Syst Rev 2016; 10: CD005231. doi:10.1002/14651858.CD005231.pub3
    OpenUrlPubMed
  51. ↵
    1. Wills TA,
    2. Soneji SS,
    3. Choi K, et al.
    E-cigarette use and respiratory disorders: an integrative review of converging evidence from epidemiological and laboratory studies. Eur Respir J 2021; 57: 1901815. doi:10.1183/13993003.01815-2019
    OpenUrlAbstract/FREE Full Text
  52. ↵
    1. Hartmann-Boyce J,
    2. McRobbie H,
    3. Butler AR, et al.
    Electronic cigarettes for smoking cessation. Cochrane Database Syst Rev 2021; 9: CD010216. doi:10.1002/14651858.CD010216.pub5
    OpenUrlPubMed
  53. ↵
    1. Montes de Oca M
    . Smoking cessation/vaccinations. Clin Chest Med 2020; 41: 495–512. doi:10.1016/j.ccm.2020.06.013
    OpenUrl
  54. ↵
    1. Polosa R,
    2. Morjaria JB,
    3. Caponnetto P, et al.
    Evidence for harm reduction in COPD smokers who switch to electronic cigarettes. Respir Res 2016; 17: 166. doi:10.1186/s12931-016-0481-x
    OpenUrlCrossRefPubMed
  55. ↵
    1. Polosa R,
    2. Morjaria JB,
    3. Prosperini U, et al.
    Health effects in COPD smokers who switch to electronic cigarettes: a retrospective-prospective 3-year follow-up. Int J Chron Obstruct Pulmon Dis 2018; 13: 2533–2542. doi:10.2147/COPD.S161138
    OpenUrlCrossRefPubMed
  56. ↵
    1. Bowler RP,
    2. Hansel NN,
    3. Jacobson S, et al.
    Electronic cigarette use in US adults at risk for or with COPD: analysis from two observational cohorts. J Gen Intern Med 2017; 32: 1315–1322. doi:10.1007/s11606-017-4150-7
    OpenUrlPubMed
  57. ↵
    1. Xie W,
    2. Kathuria H,
    3. Galiatsatos P, et al.
    Association of electronic cigarette use with incident respiratory conditions among US adults from 2013 to 2018. JAMA Netw Open 2020; 3: e2020816. doi:10.1001/jamanetworkopen.2020.20816
    OpenUrl
  58. ↵
    1. Garcia-Arcos I,
    2. Geraghty P,
    3. Baumlin N, et al.
    Chronic electronic cigarette exposure in mice induces features of COPD in a nicotine-dependent manner. Thorax 2016; 71: 1119–1129. doi:10.1136/thoraxjnl-2015-208039
    OpenUrlAbstract/FREE Full Text
    1. Higham A,
    2. Bostock D,
    3. Booth G, et al.
    The effect of electronic cigarette and tobacco smoke exposure on COPD bronchial epithelial cell inflammatory responses. Int J Chron Obstruct Pulmon Dis 2018; 13: 989–1000. doi:10.2147/COPD.S157728
    OpenUrlCrossRefPubMed
    1. Higham A,
    2. Rattray NJ,
    3. Dewhurst JA, et al.
    Electronic cigarette exposure triggers neutrophil inflammatory responses. Respir Res 2016; 17: 56. doi:10.1186/s12931-016-0368-x
    OpenUrlCrossRefPubMed
    1. Lerner CA,
    2. Sundar IK,
    3. Yao H, et al.
    Vapors produced by electronic cigarettes and e-juices with flavorings induce toxicity, oxidative stress, and inflammatory response in lung epithelial cells and in mouse lung. PLoS One 2015; 10: e0116732. doi:10.1371/journal.pone.0116732
    OpenUrlCrossRefPubMed
    1. Hwang JH,
    2. Lyes M,
    3. Sladewski K, et al.
    Electronic cigarette inhalation alters innate immunity and airway cytokines while increasing the virulence of colonizing bacteria. J Mol Med 2016; 94: 667–679. doi:10.1007/s00109-016-1378-3
    OpenUrlCrossRefPubMed
    1. Reidel B,
    2. Radicioni G,
    3. Clapp PW, et al.
    E-cigarette use causes a unique innate immune response in the lung, involving increased neutrophilic activation and altered mucin secretion. Am J Respir Crit Care Med 2018; 197: 492–501. doi:10.1164/rccm.201708-1590OC
    OpenUrlCrossRefPubMed
    1. Farber HJ,
    2. Conrado Pacheco Gallego M,
    3. Galiatsatos P, et al.
    Harms of electronic cigarettes: what the healthcare provider needs to know. Ann Am Thorac Soc 2021; 18: 567–572. doi:10.1513/AnnalsATS.202009-1113CME
    OpenUrl
  59. ↵
    1. Bravo-Gutierrez OA,
    2. Falfan-Valencia R,
    3. Ramirez-Venegas A, et al.
    Lung damage caused by heated tobacco products and electronic nicotine delivery systems: a systematic review. Int J Environ Res Public Health 2021; 18: 4079. doi:10.3390/ijerph18084079
    OpenUrlPubMed
  60. ↵
    1. Truong TT,
    2. Kosten TR
    . Current status of vaccines for substance use disorders: a brief review of human studies. J Neurol Sci 2022; 434: 120098. doi:10.1016/j.jns.2021.120098
    OpenUrl
  61. ↵
    1. Keyler DE,
    2. Roiko SA,
    3. Benlhabib E, et al.
    Monoclonal nicotine-specific antibodies reduce nicotine distribution to brain in rats: dose- and affinity-response relationships. Drug Metab Dispos 2005; 33: 1056–1061. doi:10.1124/dmd.105.004234
    OpenUrlAbstract/FREE Full Text
  62. ↵
    1. Beerli RR,
    2. Bauer M,
    3. Buser RB, et al.
    Isolation of human monoclonal antibodies by mammalian cell display. Proc Natl Acad Sci USA 2008; 105: 14336–14341. doi:10.1073/pnas.0805942105
    OpenUrlAbstract/FREE Full Text
  63. ↵
    1. Henningfield JE,
    2. Miyasato K,
    3. Jasinski DR
    . Abuse liability and pharmacodynamic characteristics of intravenous and inhaled nicotine. J Pharmacol Exp Ther 1985; 234: 1–12.
    OpenUrlAbstract/FREE Full Text
  64. ↵
    1. Hartmann-Boyce J,
    2. Cahill K,
    3. Hatsukami D, et al.
    Nicotine vaccines for smoking cessation. Cochrane Database Syst Rev 2012; 8: CD007072. doi:10.1002/14651858.CD007072.pub2
    OpenUrlPubMed
  65. ↵
    1. Hatsukami DK,
    2. Jorenby DE,
    3. Gonzales D, et al.
    Immunogenicity and smoking-cessation outcomes for a novel nicotine immunotherapeutic. Clin Pharmacol Ther 2011; 89: 392–399. doi:10.1038/clpt.2010.317
    OpenUrlCrossRefPubMed
  66. ↵
    1. Hu Y,
    2. Smith D,
    3. Frazier E, et al.
    The next-generation nicotine vaccine: a novel and potent hybrid nanoparticle-based nicotine vaccine. Biomaterials 2016; 106: 228–239. doi:10.1016/j.biomaterials.2016.08.028
    OpenUrl
  67. ↵
    1. World Health Organization
    . WHO Coronavirus (COVID-19) Dashboard. 2022. https://covid19.who.int Date last accessed: 16 December 2022.
  68. ↵
    1. Alqahtani JS,
    2. Oyelade T,
    3. Aldhahir AM, et al.
    Prevalence, severity and mortality associated with COPD and smoking in patients with COVID-19: a rapid systematic review and meta-analysis. PLoS One 2020; 15: e0233147. doi:10.1371/journal.pone.0233147
    OpenUrlCrossRefPubMed
  69. ↵
    1. Alqahtani JS,
    2. Alghamdi SM,
    3. Aldhahir AM, et al.
    Key toolkits of non-pharmacological management in COPD: during and beyond COVID-19. Front Biosci 2021; 26: 246–252. doi:10.52586/4938
    OpenUrl
  70. ↵
    1. Wu F,
    2. Burt J,
    3. Chowdhury T, et al.
    Specialty COPD care during COVID-19: patient and clinician perspectives on remote delivery. BMJ Open Respir Res 2021; 8: e000817. doi:10.1136/bmjresp-2020-000817
    OpenUrlAbstract/FREE Full Text
  71. ↵
    1. Almeda N,
    2. Gomez-Gomez I
    . The impact of the COVID-19 pandemic on smoking consumption: a systematic review of longitudinal studies. Front Psychiatry 2022; 13: 941575. doi:10.3389/fpsyt.2022.941575
    OpenUrl
  72. ↵
    1. World Health Organization
    . Coronavirus Disease (COVID-19): Tobacco. 2022. www.who.int/emergencies/diseases/novel-coronavirus-2019/question-and-answers-hub/q-a-detail/coronavirus-disease-covid-19-tobacco Date last accessed: 16 December 2022.
  73. ↵
    1. Nomura Y,
    2. Sawahata M,
    3. Nakamura Y, et al.
    Age and smoking predict antibody titres at 3 months after the second dose of the BNT162b2 COVID-19 vaccine. Vaccines 2021; 9: 1042. doi:10.3390/vaccines9091042
    OpenUrl
    1. Watanabe M,
    2. Balena A,
    3. Tuccinardi D, et al.
    Central obesity, smoking habit, and hypertension are associated with lower antibody titres in response to COVID-19 mRNA vaccine. Diabetes Metab Res Rev 2022; 38: e3465. doi:10.1002/dmrr.3465
    OpenUrlPubMed
  74. ↵
    1. MacKenzie JS,
    2. MacKenzie IH,
    3. Holt PG
    . The effect of cigarette smoking on susceptibility to epidemic influenza and on serological responses to live attenuated and killed subunit influenza vaccines. J Hyg 1976; 77: 409–417. doi:10.1017/S0022172400055790
    OpenUrlCrossRefPubMed
PreviousNext
Back to top
View this article with LENS
Vol 32 Issue 167 Table of Contents
European Respiratory Review: 32 (167)
  • Table of Contents
  • Index by author
Email

Thank you for your interest in spreading the word on European Respiratory Society .

NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address.

Enter multiple addresses on separate lines or separate them with commas.
Smoking cessation and vaccination
(Your Name) has sent you a message from European Respiratory Society
(Your Name) thought you would like to see the European Respiratory Society web site.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
Print
Citation Tools
Smoking cessation and vaccination
Maria Montes de Oca, Maria Eugenia Laucho-Contreras
European Respiratory Review Mar 2023, 32 (167) 220187; DOI: 10.1183/16000617.0187-2022

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero

Share
Smoking cessation and vaccination
Maria Montes de Oca, Maria Eugenia Laucho-Contreras
European Respiratory Review Mar 2023, 32 (167) 220187; DOI: 10.1183/16000617.0187-2022
del.icio.us logo Digg logo Reddit logo Technorati logo Twitter logo CiteULike logo Connotea logo Facebook logo Google logo Mendeley logo
Full Text (PDF)

Jump To

  • Article
    • Abstract
    • Abstract
    • Introduction
    • Importance of smoking cessation in COPD
    • Tobacco dependence
    • Epidemiological aspects of smoking in COPD
    • Assessment and approach to the smoking patient with COPD (motivation and tobacco dependence)
    • Smoking cessation interventions in patients with COPD
    • Smoking reduction-to-quit interventions for reducing harm and increasing long-term quitting
    • E-cigarettes for smoking cessation
    • Nicotine vaccine
    • Smoking cessation during the coronavirus disease 2019 pandemic in smokers with COPD
    • Footnotes
    • References
  • Figures & Data
  • Info & Metrics
  • PDF

Subjects

  • COPD and smoking
  • Tweet Widget
  • Facebook Like
  • Google Plus One

More in this TOC Section

Series

  • The role of vaccination in COPD
  • Pulmonary rehabilitation and physical interventions
  • The role of diet and nutrition in the management of COPD
Show more Series

Nonpharmacological interventions in COPD: state of the art and future directions

  • The role of vaccination in COPD
  • Pulmonary rehabilitation and physical interventions
  • The role of diet and nutrition in the management of COPD
Show more Nonpharmacological interventions in COPD: state of the art and future directions

Related Articles

Navigate

  • Home
  • Current issue
  • Archive

About the ERR

  • Journal information
  • Editorial board
  • Press
  • Permissions and reprints
  • Advertising
  • Sponsorship

The European Respiratory Society

  • Society home
  • myERS
  • Privacy policy
  • Accessibility

ERS publications

  • European Respiratory Journal
  • ERJ Open Research
  • European Respiratory Review
  • Breathe
  • ERS books online
  • ERS Bookshop

Help

  • Feedback

For authors

  • Instructions for authors
  • Publication ethics and malpractice
  • Submit a manuscript

For readers

  • Alerts
  • Subjects
  • RSS

Subscriptions

  • Accessing the ERS publications

Contact us

European Respiratory Society
442 Glossop Road
Sheffield S10 2PX
United Kingdom
Tel: +44 114 2672860
Email: journals@ersnet.org

ISSN

Print ISSN: 0905-9180
Online ISSN: 1600-0617

Copyright © 2023 by the European Respiratory Society