Corticosteroid Insensitivity in Smokers with Asthma

Corticosteroids are the most effective treatment for asthma, but the therapeutic response varies considerably between individuals. Several clinical studies have found that smokers with asthma are insensitive to the beneficial effects of short- to medium-term inhaled corticosteroid treatment compared with non-smokers with asthma. It is estimated that 25% of adults in most industrialized countries smoke cigarettes, and similar surveys amongst asthmatic individuals suggest that the prevalence of smoking in this grouping mirrors that found in the general population. Therefore, cigarette smoking is probably the most common cause of corticosteroid insensitivity in asthma. Cigarette smoking and asthma are also associated with poor symptom control and an accelerated rate of decline in lung function. The mechanism of corticosteroid insensitivity in smokers with asthma is currently unexplained but could be due to alterations in airway inflammatory cell phenotypes, changes in glucocorticoid receptor alpha/beta ratio, and/or reduced histone deacetylase activity. Smoking cessation should be encouraged in all smokers with asthma. Short-term benefits include improvements in lung function and asthma control. However, the numbers of sustained quitters is disappointingly small. Additional or alternative drugs need to be identified to treat those individuals who are unable to stop smoking or who have persistent symptoms following smoking cessation.     

Systemic sensitivity to corticosteroids in smokers with asthma.

Cigarette smokers with asthma are insensitive to the therapeutic effects of corticosteroids. It is not known whether this insensitivity to corticosteroids in smokers affects tissue sites beyond the airways. A total of 75 asthmatic subjects (39 smokers) and 78 healthy controls (30 smokers) were recruited to an observational study. The cutaneous and peripheral blood lymphocyte responses to corticosteroids were measured. The cutaneous vasoconstrictor response to topical beclometasone was measured by applying different concentrations of beclometasone solutions to the skin in a random double-blind manner. The degree of blanching at each concentration was graded after 18 h. The sensitivity of peripheral blood lymphocytes to corticosteroids was assessed by measuring the suppressive effect of dexamethasone on lymphocyte proliferation stimulated by phytohaemagglutinin (PHA). Total mean+/-sd cutaneous vasoconstrictor response score to beclometasone was reduced in smokers with asthma to 5.39+/-3.58 versus 7.26+/-3.05 in never-smokers with asthma; and in all smokers to 6.47+/-3.33 versus 7.86+/-2.81 in all never-smokers. The sensitivity to corticosteroids of lymphocytes stimulated by PHA was similar between groups. In conclusion, smokers with asthma have an impaired cutaneous vasoconstrictor response to topical corticosteroids compared with never-smokers with asthma. This finding suggests that the insensitivity to corticosteroids in smokers with asthma affects tissue sites other than the airways.     

Small airway function improvement after smoking cessation in smokers without airway obstruction

OBJECTIVE: Studying smokers with normal spirometry requires monitoring tools of the peripheral lung. A validated multiple breath washout technique was used to assess possible recovery of smoking-induced small airway malfunction in acinar and conductive lung zones. METHODS: Eighty-seven smokers with a smoking history of at least 10 pack-years but absence of spirometric airflow obstruction were invited for assessment of lung function and small airway function at baseline and after 1 wk, 3 mo, 6 mo, and 12 mo of smoking cessation. A control group of 16 persistent smokers was studied at the same time intervals. MEASUREMENTS AND MAIN RESULTS: Of the 87 smokers, 66, 32, 28, and 21% successfully ceased smoking for 1 wk, 3 mo, 6 mo, and 12 mo, respectively. Lung function parameters remained essentially unaffected by smoking cessation. Ventilation heterogeneity showed transient improvements after 1 wk in the acinar lung compartment with a return to baseline afterwards. By contrast, there were persistent improvements in the conductive airway compartment; for example, smokers who successfully quit smoking for 12 mo (n=18) showed a 30 and 42% reduction of conductive airways abnormality after 1 wk and 1 yr, respectively. CONCLUSIONS: Smokers with early signs of small airway malfunction who successfully quit smoking show sustained improvements of conductive airway malfunction. In contrast, acinar airway malfunction quickly returns to baseline after a transient improvement.     

Changes in airway hyperresponsiveness following smoking cessation: comparisons between Mch and AMP

BACKGROUND: Given the observed association between smoking, inflammation and airway hyperresponsiveness (AHR) one may predict that smoking cessation may improve AHR. However, only a few studies have investigated the effect of smoking on AHR and their results appear to be conflicting depending on the stimulus used in their bronchoprovocation protocol. The aim of the current study was to compare changes in AHR between direct (methacholine (Mch)) and indirect (adenosine 5'monophosphate (AMP)) stimuli before and at different time points after smoking cessation in smokers with allergic rhinitis (+/-asthma). METHODS: We have prospectively studied changes in AHR to inhaled Mch and AMP in smokers with allergic rhinitis (+/-asthma), before and at 6 and 12 months after smoking cessation. RESULTS: It was found that 28% (16/57) of the participants had quit smoking by the end of the study. No significant change in AHR was observed in smoking cessation failures. A significant improvement in AHR to AMP but not Mch was observed 6 months after smoking cessation in quitters; a 1.2 doubling concentrations change in PC20 AMP was measured whereas only a 0.4 doubling concentrations change was observed for PC20 Mch. However, after 12 months smoking cessation the improvement in AHR became significant for both AMP and Mch, their dose-response curves being displaced to the right to a similar extent (1.4 and 1.1 doubling concentrations for AMP and Mch, respectively). CONCLUSION: Smoking cessation can improve AHR in smokers who quit with a 6 months improvement being reported for the airways response to AMP but not Mch. AMP challenge may detect earlier changes in AHR in smokers during smoking cessation.     

Smoking cessation improves both direct and indirect airway hyperresponsiveness in COPD.

Smoking induces chronic obstructive pulmonary disease (COPD) and is associated with airway inflammation and airway hyperresponsiveness (AHR). It has not been studied in COPD whether direct (methacholine) and indirect (adenosine-5'-monophosphate (AMP)) stimuli are associated with airway inflammation and neither whether smoking cessation improves these features. The current authors cross-sectionally investigated the relationship of AHR to methacholine and AMP with lung function and inflammatory cells in the sputum of 33 smokers with COPD. In addition, changes in these parameters were prospectively assessed in 14 smokers who successfully quit smoking for 1 yr. The presence of AHR to both methacholine and AMP was associated with lower lung function, but not with sputum inflammation. AHR to methacholine and AMP improved significantly after a 1-yr smoking cessation, yet this was unrelated to changes in sputum cell counts. The numbers of neutrophils and epithelial cells significantly increased with smoking cessation. Both direct and indirect airway hyperresponsiveness are associated with lower lung function, but not with sputum inflammation in chronic obstructive pulmonary disease. Interestingly, 1-yr smoking cessation improved both direct and indirect airway hyperresponsiveness, yet without a significant association with changes in lung function or sputum inflammation. Thus, other factors are likely to induce these improvements, e.g. a reduction in stimulation of irritant receptors, airway wall changes or mucus hypersecretion.     

Smoking and airway inflammation in patients with mild asthma.

STUDY OBJECTIVES: Cigarette smoking is common in asthmatic patients, and we investigated the impact of cigarette smoking on airway inflammation in asthma. DESIGN: Single-center observational study of airway inflammation in asthmatic and healthy smokers and nonsmokers. SETTING: Asthma research unit in a university hospital. PATIENTS OR PARTICIPANTS: Sixty-seven asthmatic and 30 nonasthmatic subjects classified as smokers or nonsmokers. Asthmatics had chronic, stable asthma and were not receiving inhaled or oral steroids at the time of the study. INTERVENTIONS: We examined induced-sputum cell counts and levels of interleukin (IL)-8 and eosinophilic cationic protein (ECP). Bronchial hyperreactivity was assessed using methacholine challenge. MEASUREMENTS AND RESULTS: Asthmatic smokers had higher total sputum cell counts than nonsmoking asthmatics and both smoking and nonsmoking healthy subjects. Smoking was associated with sputum neutrophilia in both asthmatics and nonasthmatics (median, 47% and 41%, respectively) compared with nonsmokers (median, 23% and 22%, respectively), and sputum IL-8 was increased in smokers compared with nonsmokers, both in subjects with asthma (median, 945 pg/mL vs 660 pg/mL, respectively) and in healthy subjects (median, 1,310 pg/mL vs 561 pg/mL, respectively). Sputum eosinophils and ECP levels were higher in both nonsmoking and smoking asthmatics than in healthy nonsmokers. In smoking asthmatics, lung function (FEV(1) percent predicted) was negatively related to both sputum IL-8 (r = - 0.52) and sputum neutrophil proportion (r = - 0.38), and sputum IL-8 correlated positively with smoking pack-years (r = 0.57) and percent neutrophil count (r = 0.51). CONCLUSIONS: In addition to the eosinophilic airway inflammation observed in patients with asthma, smoking induces neutrophilic airway inflammation; a relationship is apparent between smoking history, airway inflammation, and lung function in smoking asthmatics.     

Smoking cessation--but not smoking reduction--improves the annual decline in FEV1 in occupationally exposed workers

INTRODUCTION: Individuals exposed both to cigarette smoke and respiratory pollutants at work incur a greater risk of development of airway hyperresponsiveness (AHR) and accelerated decline in forced expiratory volume in 1 s (FEV1) than that incurred by subjects undergoing each exposure separately. We examined whether smoking cessation or smoking reduction improves AHR and thereby slows down the decline in FEV1 in occupationally exposed workers. METHODS: We examined 165 workers (137 males and 28 females) participating in a smoking cessation programme. Nicotine tablets were used for smoking cessation or smoking reduction. Respiratory symptoms were assessed by questionnaire, FEV1 by spirometry and AHR by methacholine challenge test. At 1 year, subjects were classified into quitters, reducers, or continuing smokers. RESULTS: Sixty-seven subjects completed the study (32 quitters; 17 reducers; 18 continuing smokers). Respiratory symptoms improved markedly in quitters (P<0.001 for all comparisons) and less so in reducers (P values between 0.163 and 0.027). At 1 year, FEV1 had slightly but significantly improved in quitters (P=0.006 vs. smokers; P=0.038 vs. reducers) and markedly deteriorated in reducers and continuing smokers. Concurrent, 1-year change in AHR did not differ significantly among the groups. CONCLUSION: In occupationally exposed workers, stopping smoking markedly improved respiratory symptoms and, in males, slowed the annual decline in FEV1. Smoking reduction resulted in smaller improvements in symptoms but deterioration in FEV1. These findings were independent of AHR. While smoking cessation should remain the ultimate goal in workplace cessation programmes more studies are necessary to better ascertain the benefits of smoking reduction.     

Smoking Prevalence and Cessation Characteristics among U.S. Adults With and Without COPD: Findings from the 2011 Behavioral Risk Factor Surveillance System

Introduction: Cigarette smoking is a major cause of chronic obstructive pulmonary disease, (COPD) but many persons with COPD continue to smoke. Quitting can help prevent the development of and complications from COPD. This study examined whether smoking and cessation behaviors differed among adults with a) COPD, b) asthma, c) other chronic conditions only, or d) no chronic conditions. Methods: Smoking and chronic disease status was obtained from 488,909 adults aged > 18 years using the Behavioral Risk Factor Surveillance System; 9,476 current smokers and recent quitters in 5 states responded to additional questions about cessation. We computed age-adjusted prevalence of smoking and past-year quit attempts, and used bivariate and multivariable logistic regression to identify correlates of past-year quit attempts. Results: Similar to the overall sample, in the 5-state sample, 47.3% of adults with COPD were current smokers versus 23.1% of those with asthma, 28.8% of adults with other chronic conditions, and 20.0% of those with no chronic conditions. Those with COPD did not differ significantly from those with asthma, other chronic diseases, or no chronic disease in having made a past-year quit attempt (59.7% versus 64.0%, 61.5%, and 53.9%, respectively). Smokers with COPD were significantly more likely than those with no chronic disease to have used cessation treatment resources, including a quitline, counseling, or medication (p < 0.001). Conclusions: Adults with COPD were just as likely as those without COPD to make a past-year quit attempt; however, approximately 40% of smokers with COPD did not try to quit.     

Helping smokers to decide on the use of efficacious smoking cessation methods: a randomized controlled trial of a decision aid

AIMS: Most smokers attempt to stop smoking without using help. We evaluated the efficacy of a decision aid to motivate quitters to use efficacious treatment. SETTING AND PARTICIPANTS, A total of 1,014 were recruited from a convenience sample of 3,391 smokers who intended to quit smoking within 6 months. DESIGN AND Smokers were assigned randomly to either receive the decision aid or no intervention. The decision aid was expected to motivate quitters to use efficacious cessation methods and contained neutral information on treatment methods, distinguishing between efficacious and non-efficacious treatments. MEASUREMENTS Baseline questionnaire and follow-ups were used 2 weeks and 6 months after the start of the intervention. FINDINGS: The decision aid increased knowledge of cessation methods and induced a more positive attitude towards these methods. Furthermore, 45% reported increased confidence about being able to quit and 43% said it helped them to choose between treatments. However, no clear effect on usage of treatment aids was found, but the intervention group had more quit attempts (OR=1.52, 95% CI 1.14-2.02) and higher point prevalence abstinence at 6-month follow-up (20.2% versus 13.6%; OR=1.51, 95% CI=1.07-2.11). CONCLUSIONS An aid to help smokers decide to use efficacious treatment when attempting to quit smoking had a positive effect on smoking cessation, while failing to increase the usage of efficacious treatment. This finding lends support to the notion that the mere promotion of efficacious treatments for tobacco addiction might increase the number of quit attempts, irrespective of the actual usage of treatment.     

Effect of 1-year smoking cessation on airway inflammation in COPD and asymptomatic smokers.

Smoking cessation is the only treatment in patients with chronic obstructive pulmonary disease (COPD) effective in slowing down disease progression. Its effect on airway inflammation in COPD is unknown, although cross-sectional studies suggest ongoing inflammation in ex-smokers. In order to elucidate the effect of smoking cessation on airway inflammation, 28 smokers with COPD (mean age: 55 yrs; forced expiratory volume in one second: 71% predicted) and 25 asymptomatic smokers with normal lung function (aged 50 yrs) were included in a 1-yr smoking cessation programme. Effects of smoking cessation on airway inflammation were investigated in bronchial biopsies (baseline, 12 months) and sputum samples (baseline, 2, 6 and 12 months). In the 12 candidates with COPD who successfully ceased smoking, airway inflammation persisted in bronchial biopsies, while the number of sputum neutrophils, lymphocytes, interleukin (IL)-8 and eosinophilic-cationic-protein levels significantly increased at 12 months. In the 16 asymptomatic smokers who successfully quitted, inflammation significantly reduced (i.e. number of sputum macrophages, percentage of eosinophils and IL-8 levels) or did not change. The current authors suggest that the observed persistent airway inflammation in patients with chronic obstructive pulmonary disease is related to repair of tissue damage in the airways. It remains to be elucidated whether this reflects a beneficial or detrimental effect.     

Patterns and predictors of smoking cessation in an elderly cohort

OBJECTIVES: To identify subject characteristics that predict smoking cessation and describe patterns of cessation and recidivism in a cohort of elderly smokers. DESIGN: Prospective cohort study. SETTING: Piedmont region, North Carolina. PARTICIPANTS: Five hundred seventy‐three subjects enrolled in the North Carolina Established Populations for Epidemiologic Studies of the Elderly who responded “yes” to question 179 on the baseline survey (Do you smoke cigarettes regularly now?) and survived at least 3 years, until the next in‐person follow‐up (1989/90). Subjects were classified as quitters (n=100) or nonquitters (n=473) based on subsequent smoking behavior. MEASUREMENTS: Reported smoking behavior, demographic characteristics of the smokers at baseline or subsequent interviews, 7‐year mortality. RESULTS: After controlling for all characteristics studied, subjects who quit smoking were more likely to be female (P=.03) and showed a trend toward greater likelihood of a recent cancer diagnosis (P=.11). Recidivism was observed in only 16% (19/119) of subjects who reported no smoking in 1989/90. The percentage of subjects who died during 7 years of follow‐up was 44.0% of quitters, compared with 51.6% of nonquitters. Smoking cessation was not associated with a statistically significant decrease in risk of death after controlling for other variables (odds ratio=0.78, 95% confidence interval=0.48–1.26). CONCLUSION: Smoking cessation in this elderly cohort was associated with different subject characteristics from those that predict successful cessation in younger populations, suggesting that older smokers may have unique reasons to stop smoking. Further study is needed to assess potential motives and benefits associated with smoking cessation at an advanced age.     

Biomarkers Predicting Response to Corticosteroid Therapy in Asthma

International guidelines on the management of asthma support the early introduction of corticosteroids to control symptoms and to improve lung function by reducing airway inflammation. However, not all individuals respond to corticosteroids to the same extent and it would be an advantage to be able to predict the response to corticosteroid treatment. Several biomarkers have been assessed following treatment with corticosteroids including measures of lung function, peripheral blood and sputum indices of inflammation, exhaled gases and breath condensates. The most widely examined measures in predicting a response to corticosteroids are airway hyperresponsiveness, exhaled nitric oxide (eNO) and induced sputum. Of these, sputum eosinophilia has been demonstrated to be the best predictor of a short-term response to corticosteroids. More importantly, directing treatment at normalizing the sputum eosinophil count can substantially reduce severe exacerbations. The widespread utilization of sputum induction is hampered because the procedure is relatively labor intensive. The measurement of eNO is simpler, but incorporating the assessment of NO in an asthma management strategy has not led to a reduction in exacerbation rates. The challenge now is to either simplify the measurement of a sputum eosinophilia or to identify another inflammatory marker with a similar efficacy as the sputum eosinophil count in predicting both the short- and long-term responses to corticosteroids.     

Changes in blood pressure and body weight following smoking cessation in women

OBJECTIVE: Few have studied the long-term effects of smoking and smoking cessation on weight gain and blood pressure increase and compared with the age-related increases experienced by most adults. This study compared the development of weight and blood pressure in female never smokers, continuing smokers and smokers who quit smoking. DESIGN: Weight, systolic (SBP) and diastolic (DBP) blood pressure and smoking habits were assessed at baseline and re-assessed after a mean follow-up of 9.0 +/- 5.8 years. SETTING: Population-based cohort. SUBJECTS: A total of 2381 female never smokers and 1550 female smokers. At the re-examination, 388 of the smokers had quit smoking. RESULTS: Mean weight gain was 7.6 +/- 6.1, 3.2 +/- 5.8 and 3.7 +/- 5.2 kg, respectively, in quitters, continuing smokers and never smokers (P < 0.001). In women without blood pressure treatment, mean SBP increase was 20.9 +/- 16.8, 19.1 +/- 15.8 and 16.1 +/- 16.3 mmHg, respectively, in these groups (P < 0.001). Mean DBP increase was 6.2 +/- 8.7, 5.7 +/- 9.3 and 3.1 +/- 8.0 mmHg, respectively (P < 0.001). After adjustments for potential confounders, the increased weight gain in quitters remained highly significant. The differences in SBP and DBP increase were attenuated after adjustments, but remained significant. Incidence of hypertension (> or = 160/95 mmHg or treatment) was significantly higher in quitters [adjusted odds ratio (OR): 1.8; CI: 1.4-2.5] when compared with continuing smokers (OR: 1.3; CI: 1.07-1.6) and never smokers (reference). CONCLUSION: Over a long follow-up, weight gain was approximately 3-4 kg higher in quitters when compared with continuing smokers or never smokers. Although the differences in blood pressure increase were moderate, smoking cessation was associated with an increased incidence of hypertension.     

Effectiveness of a smoking cessation intervention in older adults

AIMS: To: (a) identify characteristics of older smokers considering cessation of smoking; (b) evaluate a cessation intervention plus access to nicotine replacement therapy (NRT); (c) identify predictors of those who successfully quit; and (d) evaluate the effectiveness of the intervention in those AGED >or = 75 years. DESIGN: Self-selection of: (a) a cessation of smoking programme; or (b) ongoing smoking. SETTING: Teaching hospital, Perth, Western Australia. PARTICIPANTS: A larger study recruited smokers and never smokers: from this the 215 community-dwelling smokers (>or= 5 cigarettes/day) aged >or= 68 years (171 males) were enrolled. INTERVENTION: Brief intervention with telephone support and access to NRT versus no intervention. MEASUREMENTS: (a) Profile of older adults planning to quit smoking compared with continuing smokers; (b) cessation at 6 months defined as 30-day point prevalence validated via expired carbon monoxide; and (c) factors predictive of successful cessation. FINDINGS: There were 165 intervention participants. Compared with the 50 continuing smokers, participants in the intervention were younger and had significantly less years of regular smoking, more previous quit attempts and greater nicotine dependence scores. At 6 months, the point prevalence of ex-smokers was 25% (n = 42) with 20% (n = 33) being abstinent throughout the study. No continuing smoker had ceased smoking. Among the intervention group, logistic regression showed that those who used NRT (OR 4.36), were male (OR 3.17), had higher anxiety (OR 1.67) or rejected 'more colds and coughs' as a reason for quitting (OR 2.91) were more likely to be successful quitters. Of those aged >or= 75 years (n = 77), 25% matched cessation criteria. CONCLUSIONS: Older smokers can be engaged successfully in a brief intervention plus NRT as aids to cessation of smoking. The intervention was also effective in the older subgroup of participants. Social factors may provide an additional means of motivating older smokers to quit.     

Smoking and timing of cessation: impact on pulmonary complications after thoracotomy

STUDY OBJECTIVE: The benefit of smoking cessation just prior to surgery in preventing postoperative pulmonary complications has not been proven. Some studies actually show a paradoxical increase in complications in those quitting smoking only a few weeks or days prior to surgery. We studied the effect of smoking and the timing of smoking cessation on postoperative pulmonary complications in patients undergoing thoracotomy. DESIGN AND SETTING: Prospective study conducted in a tertiary care cancer center in 300 consecutive patients with primary lung cancer or metastatic cancer to the lung who were undergoing anatomical lung resection. RESULTS: The groups studied were nonsmokers (21%), past quitters of > 2 months duration (62%), recent quitters of < 2 months duration (13%), and ongoing smokers (4%). Overall pulmonary complications occurred in 8%, 19%, 23%, and 23% of these groups, respectively, with a significant difference between nonsmokers and all smokers (p = 0.03) but no difference among the subgroups of smokers (p = 0.76). The risk of pneumonia was significantly lower in nonsmokers (3%) compared to all smokers (average, 11%; p < 0.05), with no difference detected among subgroups of smokers (p = 0.17). Comparing recent quitters and ongoing smokers, no differences in pulmonary complications or pneumonia were found (p = 0.67). Independent risk factors for pulmonary complications were a lower diffusing capacity of the lung for carbon monoxide (Dlco) [odds ratio [ OR] per 10% decrement, 1.41; 95% confidence interval [ CI], 1.17 to 1.70; p = 0.01) and primary lung cancer rather than metastatic disease (OR, 3.94; 95% CI, 1.34 to 11.59; p = 0.003). Among smokers, a lower Dlco percent predicted (OR per 10% decrement, 1.42; 95% CI, 1.16 to 1.75; p = 0.008) and a smoking history of > 60 pack-years (OR, 2.54; 95% CI, 1.28 to 5.04; p = 0.0008) were independently associated with overall pulmonary complications. CONCLUSIONS: In patients undergoing thoracotomy for primary or secondary lung tumors, there is no evidence of a paradoxical increase in pulmonary complications among those who quit smoking within 2 months of undergoing surgery. Smoking cessation can safely be encouraged prior to surgery.     

Spirometry and smoking cessation advice in general practice: a randomised clinical trial

RATIONALE: To assess the success rate of smoking cessation with the "minimal intervention strategy" in general practice, and to determine the influence of spirometry on this success rate. METHODS: Training in smoking cessation advice was given to 16 general practitioners (GPs). During 12 weeks, these GPs screened their practice population for smoking habits, the degree of dependence on nicotine, and the motivation to quit smoking. Patients willing to stop were randomised to a group that underwent a single office spirometry, or to a control group. The GPs were asked to support the attempts with the minimal intervention strategy. Success rates were compared after 6, 12 and 24 months. RESULTS: On a population of 5590 patients, 1206 smokers were identified (22%). To the vulnerable group, identified following the Prochaska and Di Clemente scheme, the proposal was made to change smoking behaviour. Two hundred and twenty-one patients undertook an attempt of smoking cessation. Nicotine replacement therapy (NRT) or bupropion was prescribed in 51% of the attempts. Sixty-four sustained quitters were counted after 6 months (29%), 43 after 1 year (19%) and 33 after 2 years (15%). We found a small but statistically non-significant difference in success rate in favour of the group that underwent office spirometry. CONCLUSION: GPs can motivate almost 20% of their smoking population to quit smoking. The success rate with the minimal intervention strategy was 19% after 1 year and 15% after 2 years. We found no arguments in favour of confronting smokers with their lung function as a tool for enhancing smoking cessation.     

Smoking cessation in primary care clinics

OBJECTIVES: To document smoking cessation rates achieved by applying the 1996 Agency for Health Care Policy and Research (AHCPR) smoking cessation guidelines for primary care clinics, compare these quit rates with historical results, and determine if quit rates improve with an additional motivational intervention that includes education as well as spirometry and carbon monoxide measurements. DESIGN: Randomized clinical trial. SETTING: Two university-affiliated community primary care clinics. PATIENTS: Two hundred five smokers with routinely scheduled appointments. INTERVENTION: All smokers were given advice and support according to AHCPR guidelines. Half of the subjects received additional education with spirometry and carbon monoxide measurements. MEASUREMENTS AND MAIN RESULTS: Quit rate was evaluated at 9-month follow-up. Eleven percent of smokers were sustained quitters at follow-up. Sustained quit rate was no different for intervention and control groups (9% vs 14%; [OR] 0.6; 95% [CI] 0.2, 1.4). Nicotine replacement therapy was strongly associated with sustained cessation (OR 6.7; 95% CI 2.3, 19.6). Subjects without insurance were the least likely to use nicotine replacement therapy ( p =.05). Historical data from previously published studies showed that 2% of smokers quit following physician advice, and additional support similar to AHCPR guidelines increased the quit rate to 5%. CONCLUSIONS: The sustained smoking cessation rate achieved by following AHCPR guidelines was 11% at 9 months, which compares favorably with historical results. Additional education with spirometry did not improve the quit rate. Nicotine replacement therapy was the strongest predictor of cessation, yet was used infrequently owing to cost. These findings support the use of AHCPR guidelines in primary care clinics, but do not support routine spirometry for motivating patients similar to those studied here.