Smoking cessation is the single most effective, and cost-effective, intervention in most people to reduce the risk of developing COPD and stop its progression.360 While there is evidence from epidemiological studies that non-smokers can develop chronic airflow obstruction,457,458 tobacco smoke remains the most important cause of COPD worldwide, with up to 50% of smokers being noted to develop the condition.390 FEV1 declines at about 60 mL per year in susceptible smokers, compared to the decline with normal aging of about 30 mL per year in non-smokers.459 The accelerated decline in lung function is related to current and past exposure to cigarette smoke. For example, evidence has shown that current smokers have a steeper decline in lung function than
function, but the subsequent rate of decline in lung function is likely to revert to normal (Figure 31).461
Figure 31. Time-course of COPD461
*The figure shows the rate of loss of FEV1 for a hypothetical, susceptible smoker, and the potential effect
of stopping smoking early or late in the course of COPD. Other susceptible smokers will have different rates of loss, thus reaching ‘disability’ at different ages. The normal FEV1 ranges from below 80% to
above 120%, so this will affect the starting point for the patient’s data.
Smoking cessation is the only evidence-based treatment that has been proven to slow down the development of COPD by preventing further deterioration of lung function. The most rigorous evaluation of smoking cessation and the rate of decline in lung function was the US Lung Health Study. In a prospective RCT, 5,887 smokers with mild-to-moderate airway obstruction were randomised to one of two smoking cessation groups (smoking cessation ± ipratropium therapy) or to a control group. Participants in the two smoking intervention groups showed significantly smaller declines in FEV1 than those in the control group.462 Participants who stopped smoking experienced an improvement in FEV1 in the year after quitting (an average of 47 mL or 2%). The subsequent rate of decline in FEV1 among sustained quitters was half the rate among continuing smokers, 31 mL versus 62 mL, comparable to that of never-smokers.463 Interestingly, further follow-ups showed that participants who made several attempts to quit smoking, even with subsequent relapses, had less loss of lung function at comparable cumulative doses of cigarettes than those who continued to smoke.464 However, reductions of up to 50% in smoking amount had no observable effect on the decline in FEV1.465
There is also evidence that the slowed decline in FEV1 is sustained years after quitting. An 11-year follow-up of the Lung Health Study demonstrated that differences in lung function between treatment groups persisted; sustained quitters had an FEV1 rate of decline of 26.7 mL per year, intermittent quitters lost 47.5 ml year, and those who continued to smoke throughout the 11 years declined by 60.0 mL per year.466
A 14.5-year follow-up on mortality among participants from the Lung Health Study showed that death rates were significantly higher in the usual care group than in the intervention groups (10.38 per 1000 person-years versus 8.83 per 1,000 person-years;
P < 0.05). When survival was analysed according to smoking habit, mortality was 6.04 per 1,000 person-years in sustained quitters, 7.77 per 1,000 person-years in intermittent quitters and 11.09 per 1,000 person-years in continuing smokers. Death rates were significantly related to smoking habit from coronary heart disease (P < 0.05), cardiovascular disease (P < 0.001), lung cancer (P < 0.01) and other causes (P < 0.05).467
In addition to preventing accelerated decline in lung function, smoking cessation has been shown to significantly improve respiratory symptoms468 and airway hyper- responsiveness469 in patients with COPD. The role of smoking cessation on underlying inflammatory processes in the lungs is less clear. Data from well-designed studies regarding the effects on inflammation and remodelling are lacking, and the few available studies show contradictory results.470 It has been shown that bronchial epithelial remodelling was reduced by smoking cessation;471 however, acute inflammatory processes are ongoing,471-473 which may simply reflect a repair process but not ongoing damage to the lung tissue.470
The GOLD guidelines recommend that all smokers, including those who may be at risk for COPD as well as those who already have the disease, should be offered the most intensive smoking cessation intervention feasible.360 Currently, accepted best practice is summarised by a five-step plan for intervention, published by the US Public Health Service (Table 54).474 The plan provides a strategic framework helpful to healthcare professionals interested in helping their patients to stop smoking. Cessation of smoking is a process rather than a single event, and smokers move between various stages of
For a patient ready to quit, appropriate treatment should be initiated, with the formulation of a quit plan. For a patient not ready to make a quit attempt, a brief intervention designed to promote the motivation to quit should be provided.475
Table 54. Brief strategies to help a willing patient to quit smoking474 1.ASK - systematically identify smokers at every visit
Implement an office-wide system that ensures that, for every patient at every visit, smoking status is queried and documented.
2.ADVISE - strongly urge all smokers to quit
In a clear, strong and personalised manner, urge every smoker to quit.
3.ASSESS - determine willingness to make a quit attempt
Ask every smoker if he or she is willing to make a quit attempt at this time (e.g. within the next 30 days).
4.ASSIST - aid the patient in quitting
Help the patient with a quit plan; provide practical counselling; provide intra-treatment social support; recommend the use of approved pharmacotherapy unless contraindicated; provide supplementary materials.
5.ARRANGE - schedule follow-up contact
Schedule follow-up contact; whether in person or via telephone.
There is good evidence that health professionals can substantially increase quitting and readiness to quit in the population. Even a brief (three-minute) period of counselling to urge a smoker to quit results in smoking cessation rates of 5-10%.476 Furthermore, collaborative efforts among health professionals are more effective than interventions by only one type of health professional; a survey of 1,723 smokers found that being asked about smoking by two or more types of professionals substantially increased the odds of recent quitting (OR 2.37; 95% CI 1.15-4.88).477
Pharmacotherapy is an important cornerstone in the treatment of nicotine dependence. Various forms of nicotine replacement therapy (NRT) (chewing gum, transdermal patches, inhalers, sublingual tablets and lozenges) are effective and well tolerated. Various forms of NRT increase the rate of quitting by 50-70%.478 Antidepressants, such as bupropion and nortriptylline, and nicotine receptor partial agonists, such as varenicline, are also very effective, but a not as well tolerated than NRT.479,480 It is imperative that smoking cessation interventions involve combinations of psychological and social support mechanisms, in addition to pharmacotherapy. A systematic review of RCTs on smoking cessation interventions conducted on patients with COPD, concluded
that combination treatment (psychosocial plus pharmacological intervention) is superior to no treatment or psychosocial intervention alone.481