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Allergy Asthma Immunol Res. 2010 October; 2(4): 254–259.
Published online 2010 September 6. doi:  10.4168/aair.2010.2.4.254
PMCID: PMC2946703

Effects of Smoking Cessation on Airflow Obstruction and Quality of Life in Asthmatic Smokers



Smoking elicits airway inflammation and airflow obstruction in patients with asthma, even after smoking cessation. The aim of this study was to examine the effects of smoking cessation on lung function and quality of life (QOL) in asthmatic patients.


Thirty-two patients with asthma who were active smokers were recruited. After education on the effects of smoking on asthma, 22 patients continued to smoke, and 10 quit smoking. All patients were treated with inhaled fluticasone propionate (1 mg/day) for 3 months. We compared forced expiratory volume in 1 s (FEV1), FEV1/forced vital capacity (FVC), forced expiratory flow between 25 and 75% FVC (FEF25-75%), and scores on a QOL questionnaire at baseline, 1, 2, and 3 months.


Quitters showed a greater percent change in FEV1 (19.1±6.3 vs. 7.9±2.4%, P=0.024) and FEV1/FVC (6.5±4.14 vs. 3.5±1.5%, P=0.05) than smokers. Both quitters and smokers showed improved QOL scores after 1, 2, and 3 months of fluticasone treatment.


Patients with asthma who quit smoking showed less airway obstruction, suggesting that smoking cessation is crucial in the management of asthma.

Keywords: Smoking, asthma, lung function, quality of life


Cigarette smoking is an important factor associated with poor symptom control and treatment resistance in patients with asthma.1-3 In our previous study in Korea, 18.8% of patients with asthma were current smokers.4 Asthmatic patients who smoke have more emergency department admissions with exacerbations,5 worse symptom control,6-8 accelerated decline in lung function,9,10 and increased mortality rates11 compared to non-smokers with asthma. Asthmatic smokers have a greater need for rescue medication,12 poorer health-status indices,13 reduced therapeutic response to corticosteroids,2,3 and enhanced airway inflammation.14-16 Thus, a need exists to develop novel therapies to target this subgroup of patients with asthma.

Although previous studies on the effects of smoking on asthma have improved our understanding of airway inflammation and therapeutic response, further research is needed to clarify the role of smoking in asthma. Few studies have examined the effects of smoking cessation on symptoms, lung function, therapeutic responsiveness, and quality of life (QOL). In the present study, we evaluated the effect of smoking cessation on lung function and QOL in patients with asthma during corticosteroid treatment.


Subjects and study protocol

The subjects were recruited from the Asthma Genome Research Center, Soonchunhyang University Bucheon Hospital, Korea. A clinical history was obtained for each patient on the first day of the study using a physician-administered questionnaire. Chest posterior-anterior and Water's view radiography, allergy skin prick tests, and spirometry (including bronchodilator responses after the inhalation of two puffs of 100 µg aerosolized albuterol) were performed. On the second visit, airway hyperresponsiveness (AHR) was measured in cases with predicted values for forced expiratory volume in 1 s (FEV1) ≥70%. All patients showed airway reversibility, as indicated by inhalant bronchodilator-induced improvement of >15% in FEV1 and/or airway hyperreactivity under <10 mg/mL methacholine.17 All asthmatics smoked during the first and second visit. Asthmatics (n=35) with moderate persistent severity had compatible clinical symptoms and physical characteristics according to the Global Initiative for Asthma guidelines.18 All subjects provided informed consent, and the protocols were approved by the local ethics committees. The patients were educated visually in the use of inhaled glucocorticoid (GC) by a trained nurse until their accuracy scores reached 12 (out of a maximum score of 14). GC inhalation was maintained for 3 months. Inhaled GC was 1 mg/day fluticasone propionate, which was self-administered using a multi-dose dry-powder inhaler (two puffs b.i.d.; Diskhaler, GSK, Durham, NC, USA). The patients used short-acting bronchodilators as needed. We educated all patients with asthma regarding the effects of smoking on health. Patients were classified into quitters and continuing smokers. FEV1, FEV1/forced vital capacity (FVC), forced expiratory flow between 25 and 75% FVC (FEF25-75%), and score on the asthma-related QOL questionnaire (AQLQ) at baseline and at 1, 2, and 3 months were compared between groups.

Lung function tests

Baseline FVC and FEV1 measurements were obtained in the absence of recent bronchodilator use (within 8 h) and selected according to the American Thoracic Society criteria.19 Basal and post-bronchodilator FEV1, FVC, and FEF25-75% were measured. AHR was measured via methacholine challenge and was expressed as the provocation concentration that caused a fall in FEV1 of 20% (PC20) in non-cumulative units.20

IgE measurement and skin allergy tests

Total IgE was measured using the UniCAP system (Pharmacia Diagnostics, Uppsala, Sweden). Allergy skin prick tests were performed using commercially available inhalant allergens (Bencard, Devon, UK), which included dust mites (Dermatophagoides farinae and D. pteronyssinus) and histamine (1 mg/mL). No subject had received oral antihistamines in the 3 days preceding the study. All tests included positive (1 mg/mL histamine) and negative (diluent) controls. After 15 min, the mean diameter of the wheals formed by each allergen was compared with that formed by histamine. If the former was the same or larger than the latter (A/H ratio ≥1.0) or the mean diameter was >3 mm, the reaction was deemed positive. Atopy was determined by the presence of an immediate skin reaction to one or more aeroallergens, as described previously.21

QOL measurement

The AQLQ was evaluated at baseline and after 4 weeks of treatment, using a Korean translation of the Juniper AQLQ.22 The answers to each question were scored on a five-point scale, with a score of 1 representing the greatest impairment, and a score of 5 representing no impairment (lower AQLQ scores reflected increased impairment). Items were weighted equally and reported as the mean score for each domain (activity limitation, emotions, symptoms, and exposure to environmental stimuli), along with the overall score.

Statistical analysis

Group differences were compared using two-sample t-tests, Wilcoxon rank-sum tests, and the Pearson χ2 test for normally distributed, skewed, and categorical data, respectively. Data are expressed as the mean and standard error of the mean. A P-value of less than 0.05 was considered statistically significant.


Thirty-five asthmatic patients who were active smokers were recruited for this prospective study (Fig. 1). Three patients withdrew; two patients had restarted smoking, and one patient was not able to complete the QOL. Thus, 32 patients with asthma were enrolled. After education about the effects of smoking on overall health and on asthma in particular, 22 patients continued to smoke, and 10 quit smoking. Descriptive statistics according to smoking status in patients with asthma are shown in Table. Current smokers had a higher number of pack-years compared with patients who quit smoking (23.5±13.6 versus 6.5±2.2, respectively; P=0.001). The level of IgE and atopy prevalence tended to be higher among current smokers than among quitters.

Fig. 1
Study design.
Baseline clinical profiles of the subjects

Both quitters and smokers showed an increase in predicted FEV1 following steroid treatment (baseline versus 1, 2, and 3 months: quitters, 73.6±5.6 versus 91.1±5.2, 92.5±4.3, and 101.1±10.1%; smokers, 68.2±2.4 versus 76.9±3.7, 75.5±4.1, and 78.4±5.9%; Fig. 2A). FEV1/FVC (baseline versus 1, 2, and 3 months: quitters, 68.8±3.3 versus 75.5±2.7, 77.0±4.4, and 87.6±6.3%; smokers, 67.1±1.9 versus 70.5±2.3, 68.5±2.5, and 69.5±3.9%; Fig. 2B) tended to be higher in quitters than in smokers. FEF25-75% was higher in quitters than in smokers (baseline versus 1, 2, and 3 months: quitters, 49.2±6.1 versus 70.8±7.5, 77.0±4.4, and 100.6±18.4%; smokers, 44.5±4.0 versus 60.8±5.9, 56.7±6.1, and 59.5±8.0%; Fig. 2C). Quitters showed a significantly greater increase in percent change in FEV1 and FEV1/FVC than did current smokers at 1 month (FEV1: 19.1±6.3 versus 7.9±2.4%, P=0.024; FEV1/FVC: 6.5±4.14 versus 3.5±1.5%, P=0.05; Fig. 3). Both quitters and smokers showed improved AQLQ scores (baseline versus 1, 2, and 3 months: quitters, 52.1±2.5 versus 62.5±3.1, 68.7±3.5, and 76.8±2.4; smokers, 53.2±1.7 versus 64.3±1.6, 68.9±2.5, and 67.7±3.3; Fig. 4). The percent change in QOL did not differ between quitters and smokers.

Fig. 2
Predicted FEV1 (A), FEV1/FVC (B), and FEF25-75% (C) values during inhaled steroid treatment in quitters and smokers.
Fig. 3
Percent change in predicted forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), FEV1/FVC, and forced expiratory flow between 25 and 75% FVC (FEF25-75%) values in quitters and smokers at 1 month after initiating inhaled steroid treatment. ...
Fig. 4
Changes in quality of life in quitters and smokers at 1, 2, and 3 months after initiating inhaled steroid treatment.


In this study, smoking cessation in patients with asthma improved lung function, indicating that smoking cessation is a very important factor in asthma management.

Both morbidity and mortality due to asthma increase in individuals who smoke compared with those who have never smoked.1-4 Asthmatic smokers show more severe asthmatic symptoms,6 a greater need for rescue medication,12 and poorer health-status indices than never-smokers.12,13 Smoking a ciga rette can cause acute bronchoconstriction, although tobacco smoke does not act as an acute irritant in all patients.23 Baseline FEV1 is directly related to the immediate response to inhaling cigarette smoke,24 suggesting that asthmatic smokers with relatively poor lung function are particularly susceptible to the acute effects of tobacco smoke. Emergency department visits as a result of exacerbated asthma occur more frequently among heavy cigarette smokers after days with high levels of ambient ozone pollution,25 and hospital admission rates for asthma and hospital-based care are higher in smokers.13,18,26 There is conflicting evidence as to whether current smoking is a risk factor for near-fatal or fatal asthma.27,28 In a previous prospective controlled study, subjects who quit smoking achieved considerable improvement in lung function and decreased sputum neutrophil count within 3 months compared with subjects who continued to smoke.29 In our study, patients with asthma who were current smokers tended to have lower baseline FEV1 values than did quitters, suggesting that continued smoking results in a greater decrease in lung function in long-term asthmatic smokers. The differences between our results and those of Chaudhuri et al.29 seem to be due to patient selection and study duration.

Combined cigarette smoking and asthma accelerate the decline in lung function to a greater degree than either factor alone.9,10,30 In a previous study, the synergistic effect of combined asthma and smoking resulted in a 17.8% decline in FEV1 over 10 years.9 In contrast, smoking cessation improved symptoms and bronchial hyper-responsiveness and decreased airway inflammation.3 In our study, asthmatic smokers had a higher number of pack-years (23.5±13.6) than asthmatics who had quit (6.5±2.2, P=0.001), indicating that a long-term addiction is more difficult to break. Therefore, long-term smokers are likely to require more anti-smoking education.

International guidelines for asthma management recommend inhaled corticosteroids as the most effective anti-inflammatory therapy for chronic asthma.18 The evidence for this recommendation is based on clinical studies that have been undertaken largely in patients with asthma who have never smoked or who were former smokers. Asthmatic smokers, however, may be resistant to the beneficial therapeutic effects of corticosteroids due to several clinical factors.2,3 The mechanism underlying corticosteroid resistance in asthmatic smokers is largely unstudied, but may include one or more of the pathways implicated in asthmatic non-smokers and other inflammatory diseases. Alternative or additional treatment to inhaled corticosteroids may be required for asthmatics who are unable to stop smoking or who have persistent symptoms after quitting.14 In our study, patients who quit smoking showed greater improvement in lung function than current smokers, indicating that quitting is an important factor in asthma treatment. Among atopic patients with asthma, smokers are less responsive to inhaled adenosine than non-smokers, which reflects differences in airway inflammation.31 Cigarette smoking may modulate inflammation associated with asthma. In previous studies, cigarette smoking induced airway inflammation in non-asthmatic smokers without airflow obstruction compared to non-smokers.32,33 Normal smokers show increased T-lymphocyte cell counts, particularly CD8 cells,32 and macrophage cell counts within airway walls, higher neutrophil numbers within bronchial secretions, and infiltration of peripheral airways by mononuclear cells and macrophages.16,32,33. In our study, we did not identify the effects of smoking on airway inflammation. Further studies are needed to clarify the effects of smoking on airway inflammation using sputum cells in a larger population of patients with asthma.

Recent studies of outcomes in patients with asthma have focused on clinical and physiological measures.34 Because such clinical measures do not provide a complete, accurate view of the impact of a disease on an individual's physical, social, or emotional well being, health-related QOL measures are increasingly being integrated into clinical research on asthma.22,34,35 AQLQ scores have been used as a tool to measure the outcome of drug treatment. AQLQ scores may reveal benefits of asthma treatment not apparent via objective monitoring and complement clinical and physiological assessments of treatment outcome.36 In the present study, we found that overall AQLQ scores improved in quitters and continuing smokers after treatment with inhaled GCs, indicating that corticosteroids may be valuable in the control of asthma regardless of smoking status. The limitations of this study were that the number of subjects was small and that the smoking group had more pack years; therefore, we could not exclude a long-standing smoking effect on pulmonary function.

In conclusion, patients with asthma who quit smoking showed greater improvement in airway obstruction than patients who continued smoking, suggesting that smoking cessation is of therapeutic benefit in the management of asthma.


This work was supported by a grant from the Korea Health 21 R&D Project, Ministry of Health and Welfare, Republic of Korea (A090548 and A040153).


There are no financial or other issues that might lead to conflict of interest.


1. Thomson NC, Spears M. The influence of smoking on the treatment response in patients with asthma. Curr Opin Allergy Clin Immunol. 2005;5:57–63. [PubMed]
2. Chalmers GW, Macleod KJ, Little SA, Thomson LJ, McSharry CP, Thomson NC. Influence of cigarette smoking on inhaled corticosteroid treatment in mild asthma. Thorax. 2002;57:226–230. [PMC free article] [PubMed]
3. Chaudhuri R, Livingston E, McMahon AD, Thomson L, Borland W, Thomson NC. Cigarette smoking impairs the therapeutic response to oral corticosteroids in chronic asthma. Am J Respir Crit Care Med. 2003;168:1308–1311. [PubMed]
4. Jang AS, Park JS, Lee JH, Park SW, Kim DJ, Uh ST, Kim YH, Park CS. The impact of smoking on clinical and therapeutic effects in asthmatics. J Korean Med Sci. 2009;24:209–214. [PMC free article] [PubMed]
5. Silverman RA, Boudreaux ED, Woodruff PG, Clark S, Camargo CA., Jr Cigarette smoking among asthmatic adults presenting to 64 emergency departments. Chest. 2003;123:1472–1479. [PubMed]
6. Althuis MD, Sexton M, Prybylski D. Cigarette smoking and asthma symptom severity among adult asthmatics. J Asthma. 1999;36:257–264. [PubMed]
7. Siroux V, Pin I, Oryszczyn MP, Le Moual N, Kauffmann F. Relationships of active smoking to asthma and asthma severity in the EGEA study. Epidemiological study on the Genetics and Environment of Asthma. Eur Respir J. 2000;15:470–477. [PubMed]
8. Living in Britain: results from the 2002 General Household Survey [Internet] UK Gov., Office for National Statistics. Available from:
9. Apostol GG, Jacobs DR, Jr, Tsai AW, Crow RS, Williams OD, Townsend MC, Beckett WS. Early life factors contribute to the decrease in lung function between ages 18 and 40: the Coronary Artery Risk Development in Young Adults study. Am J Respir Crit Care Med. 2002;166:166–172. [PubMed]
10. Lange P, Parner J, Vestbo J, Schnohr P, Jensen G. A 15-year follow-up study of ventilatory function in adults with asthma. N Engl J Med. 1998;339:1194–1200. [PubMed]
11. Marquette CH, Saulnier F, Leroy O, Wallaert B, Chopin C, Demarcq JM, Durocher A, Tonnel AB. Long-term prognosis of near-fatal asthma. A 6-year follow-up study of 145 asthmatic patients who underwent mechanical ventilation for a near-fatal attack of asthma. Am Rev Respir Dis. 1992;146:76–81. [PubMed]
12. Gallefoss F, Bakke PS. Does smoking affect the outcome of patient education and self-management in asthmatics? Patient Educ Couns. 2003;49:91–97. [PubMed]
13. Sippel JM, Pedula KL, Vollmer WM, Buist AS, Osborne ML. Associations of smoking with hospital-based care and quality of life in patients with obstructive airway disease. Chest. 1999;115:691–696. [PubMed]
14. Chalmers GW, MacLeod KJ, Thomson L, Little SA, McSharry C, Thomson NC. Smoking and airway inflammation in patients with mild asthma. Chest. 2001;120:1917–1922. [PubMed]
15. McKay A, Komai-Koma M, MacLeod KJ, Campbell CC, Kitson SM, Chaudhuri R, Thomson L, McSharry C, Liew FY, Thomson NC. Interleukin-18 levels in induced sputum are reduced in asthmatic and normal smokers. Clin Exp Allergy. 2004;34:904–910. [PubMed]
16. Van Hove CL, Moerloose K, Maes T, Joos GF, Tournoy KG. Cigarette smoke enhances Th-2 driven airway inflammation and delays inhalational tolerance. Respir Res. 2008;9:42. [PMC free article] [PubMed]
17. Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease (COPD) and asthma. This official statement of the American Thoracic Society was adopted by the ATS Board of Directors, November 1986. Am Rev Respir Dis. 1987;136:225–244. [PubMed]
18. National Asthma Education and Prevention Program. Expert Panel Report: Guidelines for the Diagnosis and Management of Asthma Update on Selected Topics--2002. J Allergy Clin Immunol. 2002;110:S141–S219. [PubMed]
19. American Thoracic Society. Lung function testing: selection of reference values and interpretative strategies. Am Rev Respir Dis. 1991;144:1202–1218. [PubMed]
20. Junifer EF, Cockcroft DW, Hargreave FE. Histamine and methacholine inhalation tests: a laboratory tidal breathing protocol. 2nd ed. Lund: Astra Draco; 1994.
21. Park CS, Kim YY, Kang SY. Collection between RAST and skin test for inhalant offending allergens. Korean J Allergy. 1983;3:1–9.
22. Juniper EF, Guyatt GH, Willan A, Griffith LE. Determining a minimal important change in a disease-specific Quality of Life Questionnaire. J Clin Epidemiol. 1994;47:81–87. [PubMed]
23. Higenbottam TW, Feyeraband C, Clark TJ. Cigarette smoking in asthma. Br J Dis Chest. 1980;74:279–284. [PubMed]
24. Jensen EJ, Dahl R, Steffensen F. Bronchial reactivity to cigarette smoke; relation to lung function, respiratory symptoms, serum-immunoglobulin E and blood eosinophil and leukocyte counts. Respir Med. 2000;94:119–127. [PubMed]
25. Cassino C, Ito K, Bader I, Ciotoli C, Thurston G, Reibman J. Cigarette smoking and ozone-associated emergency department use for asthma by adults in New York City. Am J Respir Crit Care Med. 1999;159:1773–1779. [PubMed]
26. Prescott E, Lange P, Vestbo J. Effect of gender on hospital admissions for asthma and prevalence of self-reported asthma: a prospective study based on a sample of the general population. Thorax. 1997;52:287–289. [PMC free article] [PubMed]
27. Rasmussen F, Taylor DR, Flannery EM, Cowan JO, Greene JM, Herbison GP, Sears MR. Risk factors for hospital admission for asthma from childhood to young adulthood: a longitudinal population study. J Allergy Clin Immunol. 2002;110:220–227. [PubMed]
28. Turner MO, Noertjojo K, Vedal S, Bai T, Crump S, Fitzgerald JM. Risk factors for near-fatal asthma. A case-control study in hospitalized patients with asthma. Am J Respir Crit Care Med. 1998;157:1804–1809. [PubMed]
29. Chaudhuri R, Livingston E, McMahon AD, Lafferty J, Fraser I, Spears M, McSharry CP, Thomson NC. Effects of smoking cessation on lung function and airway inflammation in smokers with asthma. Am J Respir Crit Care Med. 2006;174:127–133. [PubMed]
30. Polosa R, Knoke JD, Russo C, Piccillo G, Caponnetto P, Sarva M, Proietti L, Al-Delaimy WK. Cigarette smoking is associated with a greater risk of incident asthma in allergic rhinitis. J Allergy Clin Immunol. 2008;121:1428–1434. [PubMed]
31. Oosterhoff Y, Jansen MA, Postma DS, Koeter GH. Airway responsiveness to adenosine 5'-monophosphate in smokers and nonsmokers with atopic asthma. J Allergy Clin Immunol. 1993;92:773–776. [PubMed]
32. Saetta M, Turato G, Maestrelli P, Mapp CE, Fabbri LM. Cellular and structural bases of chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2001;163:1304–1309. [PubMed]
33. Roth MD, Arora A, Barsky SH, Kleerup EC, Simmons M, Tashkin DP. Airway inflammation in young marijuana and tobacco smokers. Am J Respir Crit Care Med. 1998;157:928–937. [PubMed]
34. Blaiss MS. Outcomes analysis in asthma. JAMA. 1997;278:1874–1880. [PubMed]
35. Guyatt GH, Feeny DH, Patrick DL. Measuring health-related quality of life. Ann Intern Med. 1993;118:622–629. [PubMed]
36. Juniper EF, Guyatt GH, Epstein RS, Ferrie PJ, Jaeschke R, Hiller TK. Evaluation of impairment of health related quality of life in asthma: development of a questionnaire for use in clinical trials. Thorax. 1992;47:76–83. [PMC free article] [PubMed]

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