The Effects of Smoking Cessation on the Risk of Chronic Obstructive Pulmonary Disease Exacerbations

Health Services Research and Development, VA Puget Sound Health Care System, 1660 S. Columbian Way (152), Seattle, WA 98108, USA.
Journal of General Internal Medicine (Impact Factor: 3.42). 02/2009; 24(4):457-63. DOI: 10.1007/s11606-009-0907-y
Source: PubMed


Smoking cessation has been demonstrated to reduce the rate of loss of lung function and mortality among patients with mild to moderate chronic obstructive pulmonary disease (COPD). There is a paucity of evidence about the effects of smoking cessation on the risk of COPD exacerbations.
We sought to examine whether smoking status and the duration of abstinence from tobacco smoke is associated with a decreased risk of COPD exacerbations.
We assessed current smoking status and duration of smoking abstinence by self-report. Our primary outcome was either an inpatient or outpatient COPD exacerbation. We used Cox regression to estimate the risk of COPD exacerbation associated with smoking status and duration of smoking cessation.
We performed a cohort study of 23,971 veterans who were current and past smokers and had been seen in one of seven Department of Veterans Affairs (VA) primary care clinics throughout the US.
In comparison to current smokers, ex-smokers had a significantly reduced risk of COPD exacerbation after adjusting for age, comorbidity, markers of COPD severity and socio-economic status (adjusted HR 0.78, 95% CI 0.75-0.87). The magnitude of the reduced risk was dependent on the duration of smoking abstinence (adjusted HR: quit < 1 year, 1.04; 95% CI 0.87-1.26; 1-5 years 0.93, 95% CI 0.79-1.08; 5-10 years 0.84, 95% CI 0.70-1.00; > or = 10 years 0.65, 95% CI 0.58-0.74; linear trend <0.001).
Smoking cessation is associated with a reduced risk of COPD exacerbations, and the described reduction is dependent upon the duration of abstinence.

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    • "Smoking cessation has been shown to decelerate the progression of the disease and reduce mortality [1] [2]. In addition, smoking cessation is associated with a significant reduction of COPD exacerbations [3] and hospital admissions [4]. Data on predictors of smoking cessation relies almost entirely on population studies [5] [6]. "
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    ABSTRACT: Smoking cessation is the cornerstone of COPD management, but difficult to achieve in clinical practice. The effect of comorbidities on smoking cessation and risk factors for mortality were studied in a cohort of 739 COPD patients recruited in two Finnish University Hospitals. The diagnosis of COPD was done for the first time on average 5.5 years prior to the enrollment. Data from the medical records and followup questionnaires (years 0, 1, 2, and 4) have been analyzed. The patients’ lung function varied greatly; mean FEV 1 58% of predicted. A total of 60.2% of men and 55.6% of women had been able to quit smoking. Alcohol abuse (OR 2.1, 95% CI 1.4–3.3) and psychiatric conditions (OR 1.8, 95% CI 1.2–2.7) were strongly related to low success rates of quitting. Among current smokers high nicotine dependency was again explained by alcohol abuse and psychiatric conditions. Non-quitters were younger than quitters, but their mortality rates remained significantly higher even when the model was adjusted for impairment of lung functions and comorbidities. In conclusion, co-existing addiction and psychiatric diseases significantly decreased the success rates in smoking cessation and increased mortality among the patients.
    Pulmonary Medicine 11/2012; 2012(5):725024. DOI:10.1155/2012/725024
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    • "Vestbo et al.14 reported that smoking additionally caused annual reduction of pulmonary function of 21±4 mL in a study conducted on patients with moderate to severe COPD. Au et al.15 reported that smoking cessation reduced the frequency of acute exacerbation in COPD patients, and that risk reduction was correlated with period of smoking cessation in a study conducted on current and ex-smokers. However, no significant difference in the current and previous smoking history and smoking amount was found between the two groups in this study. "
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    ABSTRACT: Chronic obstructive pulmonary disease (COPD) is now regarded as a heterogenous disease, with variable phenotypes. Acute exacerbation of COPD is a major event that alters the natural course of disease. The frequency of COPD exacerbation is variable among patients. We analyzed clinical features, according to the frequency of acute exacerbation in COPD. Sixty patients, who visited Gyeongsang National University Hospital from March 2010 to October 2010, were enrolled. Patients were divided into two groups, according to their frequency of acute exacerbation. Frequent exacerbator is defined as the patient who has two or more exacerbation per one year. We reviewed patients' medical records and investigated modified Medical Research Council (MMRC) dyspnea scale, smoking history and frequency of acute exacerbation. We also conducted pulmonary function test and 6-minute walking test, calculated body mass index, degree of airway obstruction and dyspnea and exercise capacity (BODE) index and measured CD146 cells in the peripheral blood. The number of frequent exacerbators and infrequent exacerbators was 20 and 40, respectively. The frequent exacerbator group had more severe airway obstruction (forced expiratory volume in one second [FEV(1)], 45% vs. 65.3%, p=0.001; FEV(1)/forced vital capacity, 44.3% vs. 50.5%, p=0.046). MMRC dyspnea scale and BODE index were significantly higher in the frequent exacerbator group (1.8 vs. 1.1, p=0.016; 3.9 vs. 2.1, p=0.014, respectively). The fraction of CD146 cells significantly increased in the frequent exacerbator group (2.0 vs. 1.0, p<0.001). Frequent exacerbator had more severe airway obstruction and higher symptom score and BODE index. However, circulating endothelial cells measured by CD146 needed to be confirmed in the future.
    Tuberculosis and Respiratory Diseases 04/2012; 72(4):367-73. DOI:10.4046/trd.2012.72.4.367
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    • "Cigarette smoking is the most important environmental risk factor for the development of COPD [1-3]. Cigarette smoking intensity is known to be associated with clinical features of COPD such as the rate of lung function decline [2,4] and COPD exacerbation frequency [5,6]. In addition, it is correlated with symptoms of chronic bronchitis even in healthy smokers [7]. "
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    ABSTRACT: Cigarette smoking is the principal environmental risk factor for developing COPD, and nicotine dependence strongly influences smoking behavior. This study was performed to elucidate the relationship between nicotine dependence, genetic susceptibility to nicotine dependence, and volumetric CT findings in smokers. Current smokers with COPD (GOLD stage ≥ 2) or normal spirometry were analyzed from the COPDGene Study, a prospective observational study. Nicotine dependence was determined by the Fagerstrom test for nicotine dependence (FTND). Volumetric CT acquisitions measuring the percent of emphysema on inspiratory CT (% of lung <-950 HU) and gas trapping on expiratory CT (% of lung <-856 HU) were obtained. Genotypes for two SNPs in the CHRNA3/5 region (rs8034191, rs1051730) previously associated with nicotine dependence and COPD were analyzed for association to COPD and nicotine dependence phenotypes. Among 842 currently smoking subjects (335 COPD cases and 507 controls), 329 subjects (39.1%) showed high nicotine dependence. Subjects with high nicotine dependence had greater cumulative and current amounts of smoking. However, emphysema severity was negatively correlated with the FTND score in controls (ρ = -0.19, p < .0001) as well as in COPD cases (ρ = -0.18, p = 0.0008). Lower FTND score, male gender, lower body mass index, and lower FEV1 were independent risk factors for emphysema severity in COPD cases. Both CHRNA3/5 SNPs were associated with FTND in current smokers. An association of genetic variants in CHRNA3/5 with severity of emphysema was only found in former smokers, but not in current smokers. Nicotine dependence was a negative predictor for emphysema on CT in COPD and control smokers. Increased inflammation in more highly addicted current smokers could influence the CT lung density distribution, which may influence genetic association studies of emphysema phenotypes.
    Respiratory research 01/2011; 12(1):9. DOI:10.1186/1465-9921-12-9 · 3.09 Impact Factor
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