Contents
pdf Download PDF
pdf Download XML
45 Views
15 Downloads
Share this article
Research Article | Volume 11 Issue 7 (July, 2025) | Pages 752 - 757
Clinical Spectrum and Outcomes of Acute Exacerbation of Copd in Smokers versus Non-Smokers
 ,
1
Associate Professor Department of Medicine Government Medical College and Hospital Baramati Dist. Pun
2
2ndAssistant Professor Department of Medicine Government Medical College and hospital Baramati Dist Pune
Under a Creative Commons license
Open Access
Received
June 11, 2025
Revised
June 26, 2025
Accepted
July 12, 2025
Published
July 26, 2025
Abstract

Background: Chronic Obstructive Pulmonary Disease (COPD) is a progressive respiratory condition frequently aggravated by acute exacerbations. Smoking remains a well-established risk factor; however, non-smokers are also significantly affected due to other environmental and occupational exposures. This study aimed to compare the clinical profile and outcomes of acute exacerbation of COPD (AECOPD) in smokers versus non-smokers. Aims: This study compares the clinical features, severity, and outcomes of acute COPD exacerbations in smokers versus non-smokers, aiming to highlight how smoking status influences disease progression and guide more personalized management strategies. Methods: This hospital-based, prospective observational study was conducted in the Department of General Medicine and Pulmonary Medicine at Government Medical College and Hospital, Baramati, Pune, Maharashtra, to evaluate and compare the clinical profile and outcomes of acute exacerbations of chronic obstructive pulmonary disease (AECOPD) among smokers and non-smokers. The study included a total of 100 patients admitted with a confirmed diagnosis of AECOPD. These patients were divided into two groups based on their smoking history: Group A comprised 50 patients with a history of smoking, while Group B included 50 patients with no history of smoking or significant exposure to second-hand smoke. Results: Laboratory and radiological assessments revealed some significant differences between smokers and non-smokers with COPD. The mean WBC count (11.2 ± 3.5 vs. 10.8 ± 3.3 ×10⁹/L; p = 0.48) and CRP levels (32.6 ± 12.8 vs. 29.4 ± 11.6 mg/L; p = 0.21) were comparable between the two groups. However, hyperinflation on chest X-ray was significantly more common among smokers (80%) than non-smokers (60%; p = 0.03). Arterial blood gas analysis showed that smokers had a significantly lower pH (7.34 ± 0.05 vs. 7.37 ± 0.04; p = 0.02) and higher pCO₂ levels (54.1 ± 7.2 vs. 48.9 ± 6.8 mmHg; p = 0.001), indicating greater respiratory acidosis in the smoker group. Conclusion: Laboratory and radiological assessments demonstrated important distinctions between smokers and non-smokers with COPD. While inflammatory markers such as WBC count and CRP levels did not differ significantly, hyperinflation on chest X-ray was notably more frequent in smokers, suggesting more advanced lung involvement. Arterial blood gas analysis further revealed that smokers exhibited greater respiratory acidosis, as evidenced by significantly lower pH levels and higher pCO₂ values. These findings indicate that smoking may contribute to more severe pulmonary dysfunction and impaired gas exchange in COPD patients.

Keywords
INTRODUCTION

Chronic obstructive pulmonary disease (COPD) is a progressive respiratory disorder characterized by airflow limitation that is not fully reversible and is typically associated with an abnormal inflammatory response of the lungs to noxious particles or gases. It represents a major cause of morbidity and mortality worldwide, posing a significant burden on healthcare systems, especially during acute exacerbations (AECOPD), which are defined as episodes of worsening respiratory symptoms beyond normal day-to-day variations that necessitate a change in regular medication [1]. AECOPD is a major contributor to the decline in lung function, quality of life, and survival in COPD patients [2].

 

Tobacco smoking remains the most well-established risk factor for the development and progression of COPD, accounting for approximately 80–90% of all cases globally [3]. However, a considerable number of non-smokers, particularly in developing countries, also develop COPD, often due to chronic exposure to biomass fuels, air pollution, occupational dusts, and secondhand smoke [4]. These exposures are especially common among women in rural areas who cook using biomass stoves and lack proper ventilation. The phenotypic manifestations and outcomes of AECOPD in smokers versus non-smokers may differ significantly due to variation in the underlying pathophysiological mechanisms and inflammatory profiles [5].

 

Smokers with COPD are more likely to exhibit emphysematous changes with predominant small airway involvement, leading to gas exchange abnormalities and frequent exacerbations [6]. In contrast, non-smokers with COPD often demonstrate chronic bronchitis or a restrictive pattern and may present with less severe airflow limitation, yet still experience frequent exacerbations [7]. The severity and frequency of AECOPD are critical prognostic indicators, and their association with smoking status continues to be an area of active investigation. It is unclear whether smokers have worse clinical outcomes during exacerbations than non-smokers or if the underlying etiologies of exacerbation differ between the two groups.

 

The clinical spectrum of AECOPD encompasses a wide range of symptoms including increased dyspnea, cough, sputum production, and purulence, often triggered by bacterial or viral infections, environmental pollutants, or non-compliance with medications [8]. These exacerbations may lead to hospitalization, need for ventilatory support, prolonged hospital stay, and increased healthcare utilization. Recent studies have highlighted that smoking status may influence the immune response during exacerbations, with smokers demonstrating higher neutrophilic inflammation and oxidative stress, which may contribute to more severe presentations and poorer recovery [9].

 

Furthermore, management strategies and outcomes such as duration of hospitalization, need for ICU care, use of systemic corticosteroids or antibiotics, and readmission rates may also vary between smokers and non-smokers. While some studies report increased mortality and morbidity in smokers, others have found that non-smokers with COPD, particularly women, may have an underdiagnosed but equally severe form of the disease [10]. Given these variations, it is essential to evaluate and compare the clinical profile and outcomes of AECOPD between smokers and non-smokers to guide tailored management and resource allocation.

 

This study aims to delineate the clinical characteristics, severity, and outcomes of acute exacerbations of COPD in smokers compared to non-smokers. By identifying potential differences in presentation and prognosis, this research seeks to inform clinicians and public health authorities on how smoking status modulates disease trajectory, thus supporting more personalized approaches to COPD management.

MATERIALS AND METHODS

Study Design: This was a hospital-based, prospective observational study conducted to evaluate and compare the clinical profile and outcomes of acute exacerbations of chronic obstructive pulmonary disease (AECOPD) among smokers and non-smokers.

Department: Department of General Medicine / Pulmonary Medicine

 

Study Duration: Department of Medicine, Government Medical College and Hospital, Baramati, Pune, Maharashtra.

 

Sample Size: A total of 100 patients admitted with a diagnosis of acute exacerbation of COPD were included in the study.

  • Group A (Smokers): 50 patients with a history of smoking
  • Group B (Non-Smokers): 50 patients with no history of smoking or significant second-hand smoke exposure

Inclusion Criteria:

  • Adult patients aged ≥ 40 years admitted with a clinical diagnosis of AECOPD based on GOLD criteria
  • Spirometry-confirmed diagnosis of COPD (available prior to or after clinical stabilization).
  • Patients with clearly documented smoking history (active or former smokers) and non-smokers.

 

Exclusion Criteria:

  • Patients with asthma, bronchiectasis, interstitial lung disease, or other chronic respiratory disorders.
  • Patients with significant cardiac comorbidities causing dyspnea (e.g., congestive heart failure).
  • Patients unwilling or unable to give informed consent.

Statistical Analysis:-

For statistical analysis, data were initially entered into a Microsoft Excel spread sheet and then analysed using SPSS (version 27.0; SPSS Inc., Chicago, IL, USA) and Graph Pad Prism (version 5). Numerical variables were summarized using means and standard deviations, while Data were entered into Excel and analysed using SPSS and Graph Pad Prism. Numerical variables were summarized using means and standard deviations, while categorical variables were described with counts and percentages. Two-sample t-tests were used to compare independent groups, while paired t-tests accounted for correlations in paired data. Chi-square tests (including Fisher’s exact test for small sample sizes) were used for categorical data comparisons. P-values ≤ 0.05 were considered statistically significant.

 

RESULTS

Table 1: Baseline Demographic and Clinical Characteristics

Parameter

Smokers (n=50)

Non-Smokers (n=50)

p-value

Age (years, mean ± SD)

65.2 ± 9.3

61.4 ± 10.1

0.04

Male: Female

46:04:00

28:22:00

<0.001

BMI (kg/m², mean ± SD)

21.1 ± 2.5

23.3 ± 2.7

0.002

Duration of COPD (years)

8.4 ± 3.1

6.2 ± 2.7

0.01

Comorbidities (HTN/DM/IHD)

30 (60%)

34 (68%)

0.38

 

Table 2: Clinical Presentation during Exacerbation

Symptom

Smokers (n=50)

Non-Smokers (n=50)

p-value

Dyspnea (mMRC Grade 3)

42 (84%)

35 (70%)

0.09

Cough with sputum

45 (90%)

36 (72%)

0.02

Wheeze

40 (80%)

32 (64%)

0.08

Fever

18 (36%)

20 (40%)

0.68

SpO at presentation (%)

88.1 ± 4.3

90.6 ± 3.9

0.01

 

Table 3: Laboratory and Radiological Findings

Parameter

Smokers (n=50)

Non-Smokers (n=50)

p-value

WBC count (×10/L)

11.2 ± 3.5

10.8 ± 3.3

0.48

CRP (mg/L)

32.6 ± 12.8

29.4 ± 11.6

0.21

Chest X-ray: Hyperinflation

40 (80%)

30 (60%)

0.03

ABG: pH

7.34 ± 0.05

7.37 ± 0.04

0.02

ABG: pCO (mmHg)

54.1 ± 7.2

48.9 ± 6.8

0.001

 

Table 4: Treatment Modalities and Hospital Course

Parameter

Smokers (n=50)

Non-Smokers (n=50)

p-value

Use of NIV

28 (56%)

18 (36%)

0.04

Need for ICU admission

14 (28%)

6 (12%)

0.04

Length of hospital stay (days)

7.8 ± 2.1

6.2 ± 1.9

0.002

Antibiotics used

45 (90%)

42 (84%)

0.38

Systemic steroids given

48 (96%)

46 (92%)

0.39

 

Table 5: Outcomes and Mortality

Outcome

Smokers (n=50)

Non-Smokers (n=50)

p-value

Clinical improvement

42 (84%)

45 (90%)

0.38

Readmission within 30 days

12 (24%)

6 (12%)

0.12

In-hospital mortality

4 (8%)

1 (2%)

0.17

Post-discharge oxygen dependency

9 (18%)

4 (8%)

0.13

30-day mortality

5 (10%)

2 (4%)

0.24

 

Comparison between smokers (n=50) and non-smokers (n=50) with COPD revealed several significant differences. Smokers were older on average (65.2 ± 9.3 vs. 61.4 ± 10.1 years; p = 0.04) and had a significantly higher male predominance (male: female ratio of 46:4 vs. 28:22; p < 0.001). The mean BMI was significantly lower in smokers compared to non-smokers (21.1 ± 2.5 vs. 23.3 ± 2.7 kg/m²; p = 0.002). Additionally, the duration of COPD was longer among smokers (8.4 ± 3.1 vs. 6.2 ± 2.7 years; p = 0.01). However, the prevalence of comorbidities such as hypertension, diabetes, or ischemic heart disease did not differ significantly between the two groups (60% vs. 68%; p = 0.38).

 

Symptom comparison between smokers and non-smokers with COPD revealed some notable differences. Dyspnea of mMRC Grade 3 was more common in smokers (84%) than in non-smokers (70%), though this difference was not statistically significant (p = 0.09). Cough with sputum was significantly more prevalent among smokers (90% vs. 72%; p = 0.02). Wheeze was also more frequent in smokers (80% vs. 64%), but the difference did not reach statistical significance (p = 0.08). The occurrence of fever was comparable between the two groups (36% vs. 40%; p = 0.68). However, smokers presented with significantly lower oxygen saturation levels (SpO₂) at admission compared to non-smokers (88.1 ± 4.3% vs. 90.6 ± 3.9%; p = 0.01).

 

 Laboratory and radiological assessments revealed some significant differences between smokers and non-smokers with COPD. The mean WBC count (11.2 ± 3.5 vs. 10.8 ± 3.3 ×10⁹/L; p = 0.48) and CRP levels (32.6 ± 12.8 vs. 29.4 ± 11.6 mg/L; p = 0.21) were comparable between the two groups. However, hyperinflation on chest X-ray was significantly more common among smokers (80%) than non-smokers (60%; p = 0.03). Arterial blood gas analysis showed that smokers had a significantly lower pH (7.34 ± 0.05 vs. 7.37 ± 0.04; p = 0.02) and higher pCO₂ levels (54.1 ± 7.2 vs. 48.9 ± 6.8 mmHg; p = 0.001), indicating greater respiratory acidosis in the smoker group.

 The analysis of treatment interventions and outcomes showed that smokers with COPD had significantly greater healthcare needs compared to non-smokers. The use of non-invasive ventilation (NIV) was more frequent among smokers (56%) than non-smokers (36%), with a statistically significant difference (p = 0.04). Similarly, ICU admissions were more common in smokers (28% vs. 12%; p = 0.04). The mean length of hospital stay was also significantly longer in the smoker group (7.8 ± 2.1 days) compared to non-smokers (6.2 ± 1.9 days; p = 0.002). However, no significant differences were observed between the two groups in the use of antibiotics (90% vs. 84%; p = 0.38) or systemic steroids (96% vs. 92%; p = 0.39).

 

Clinical outcomes were generally less favorable in smokers compared to non-smokers, although the differences did not reach statistical significance. Clinical improvement was observed in 84% of smokers and 90% of non-smokers (p = 0.38). Readmission within 30 days occurred more frequently in smokers (24% vs. 12%; p = 0.12), as did in-hospital mortality (8% vs. 2%; p = 0.17) and 30-day mortality (10% vs. 4%; p = 0.24). Additionally, post-discharge oxygen dependency was higher among smokers (18% vs. 8%; p = 0.13), though again, these differences were not statistically significant.

DISCUSSION

The present study highlights several significant differences in the clinical characteristics and outcomes of acute exacerbation of COPD (AECOPD) between smokers and non-smokers. Smokers were older, predominantly male, and had a longer duration of disease, which is consistent with previous literature indicating a higher prevalence of COPD in older male smokers due to cumulative tobacco exposure and delayed diagnosis in men [11,12]. The significantly lower BMI observed in smokers may be attributed to chronic systemic inflammation, higher energy expenditure, and muscle wasting, a pattern noted in earlier studies by Celli et al., who associated low BMI with poor prognosis in COPD [13].

 

Cough with sputum production and wheeze were more prominent among smokers, reflecting the classic phenotype of chronic bronchitis commonly linked to tobacco use. Similar findings were reported by Salvi et al., who observed that sputum production is more prevalent in smokers due to mucous gland hypertrophy and goblet cell hyperplasia [14]. Although dyspnea was more severe in smokers (mMRC Grade 3), the difference was not statistically significant, aligning with findings from Eisner et al., who reported comparable breathlessness in both groups, regardless of smoking history [15].

 

A striking difference was seen in oxygen saturation at presentation, with smokers having significantly lower SpO₂ levels, indicating more severe hypoxemia. Comparable trends were reported by Gan et al., who noted that active smokers tend to have worse gas exchange parameters during exacerbations [16]. Additionally, the greater degree of respiratory acidosis (lower pH and higher pCO₂) in smokers on arterial blood gas analysis is consistent with findings from Papi et al., who reported increased CO₂ retention in smokers due to small airway collapse and ventilation-perfusion mismatch [17].

 

Radiologically, hyperinflation was significantly more common in smokers, reinforcing the emphysematous pattern of COPD associated with smoking. This concurs with CT-based studies by Regan et al., which demonstrated higher emphysema scores in smokers compared to non-smokers with COPD [18].

 

In terms of treatment interventions, smokers had a greater need for non-invasive ventilation and ICU admission, indicating more severe exacerbations. A similar trend was observed in a study by Seemungal et al., where smoking was identified as a risk factor for frequent and severe exacerbations requiring escalated care [19]. The longer hospital stay in smokers also supports earlier findings that tobacco-induced inflammation delays recovery during exacerbation episodes.

 

Although not statistically significant, clinical outcomes such as readmission, mortality, and oxygen dependency were poorer in smokers. These findings are consistent with the work of Hurst et al., who reported a higher risk of exacerbation recurrence and mortality in patients with a smoking history [20]. The lack of statistical significance in these outcomes could be due to the limited sample size or confounding factors such as adherence, socioeconomic status, or environmental exposures in non-smokers.

 

Overall, the findings of this study align with existing literature, underscoring the detrimental impact of smoking on the clinical severity and prognosis of AECOPD. It also reinforces the growing need to recognize non-smoker COPD as a distinct clinical entity with its own challenges, particularly in regions with high exposure to biomass smoke and air pollution. Larger, multicentric studies are warranted to explore this differentiation further and to develop phenotype-specific management strategies.

CONCLUSION

The present study demonstrates that smokers with COPD experience a more severe clinical course during acute exacerbations compared to non-smokers. Smokers were older, had a longer disease duration, and showed greater male predominance and lower BMI, indicating a more advanced disease profile. Symptomatically, they presented more frequently with productive cough and lower oxygen saturation at admission, reflecting a heightened inflammatory and obstructive burden. Laboratory and radiographic findings further supported this, with smokers showing more frequent hyperinflation, lower arterial pH, and higher pCO₂ levels, indicative of greater respiratory acidosis.

 

In terms of management, smokers required more intensive interventions, including a higher need for non-invasive ventilation and ICU care, and had significantly longer hospital stays. Although the differences in mortality, readmissions, and post-discharge oxygen dependency were not statistically significant, trends consistently indicated poorer outcomes among smokers. These findings reinforce the detrimental impact of smoking on disease severity and resource utilization in COPD and highlight the need for aggressive smoking cessation efforts, early intervention, and tailored management strategies in this subgroup to improve long-term outcomes.

REFERENCES
  1. Global Initiative for Chronic Obstructive Lung Disease. Global strategy for the diagnosis, management, and prevention of COPD. 2024 Report.
  2. Hurst JR, Vestbo J, Anzueto A, et al. Susceptibility to exacerbation in chronic obstructive pulmonary disease. N Engl J Med. 2010 Sep 16;363(12):1128-38.
  3. Forey B, Thornton A, Lee PN. Systematic review with meta-analysis of the epidemiological evidence relating FEV1 decline to active smoking. BMC Pulm Med. 2011;11:36.
  4. Salvi SS, Barnes PJ. Chronic obstructive pulmonary disease in non-smokers. Lancet. 2009 Aug 29;374(9691):733-43.
  5. Eisner MD, Balmes J, Katz PP, et al. Lifetime environmental tobacco smoke exposure and the risk of chronic obstructive pulmonary disease. Environ Health. 2005 Mar 21;4(1):7.
  6. Decramer M, Janssens W, Miravitlles M. Chronic obstructive pulmonary disease. Lancet. 2012 Apr 7;379(9823):1341-51.
  7. Jindal SK, Aggarwal AN, Chaudhry K, et al. A multicentric study on epidemiology of chronic obstructive pulmonary disease and its relationship with tobacco smoking and environmental tobacco smoke exposure. Indian J Chest Dis Allied Sci. 2006 Oct-Dec;48(4):23-29.
  8. Sethi S. Infection as a comorbidity of COPD. Eur Respir J. 2010 Jun;35(6):1209-15.
  9. Papi A, Bellettato CM, Braccioni F, et al. Infections and airway inflammation in chronic obstructive pulmonary disease severe exacerbations. Am J Respir Crit Care Med. 2006 May 15;173(10):1114-21.
  10. Gan WQ, Man SF, Postma DS, et al. Female smokers beyond the perimenopausal years are at increased risk of chronic obstructive pulmonary disease: a systematic review and meta-analysis. Respir Res. 2006;7:52.
  11. Vestbo J, Hurd SS, Agustí AG, et al. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2013;187(4):347-65.
  12. Jindal SK, Aggarwal AN, Gupta D. A review of population studies from India to estimate national burden of COPD. Indian J Chest Dis Allied Sci. 2001;43(3):139–47.
  13. Celli BR, Cote CG, Marin JM, et al. The body-mass index, airflow obstruction, dyspnea, and exercise capacity index in COPD. N Engl J Med. 2004;350(10):1005-12.
  14. Salvi SS, Barnes PJ. Chronic obstructive pulmonary disease in non-smokers. Lancet. 2009;374(9691):733-43.
  15. Eisner MD, Anthonisen N, Coultas D, et al. An official American Thoracic Society public policy statement: Novel risk factors and the global burden of chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2010;182(5):693-718.
  16. Gan WQ, Man SF, Senthilselvan A, Sin DD. Association between chronic obstructive pulmonary disease and systemic inflammation: a systematic review and a meta-analysis. Thorax. 2004;59(7):574-80.
  17. Papi A, Bellettato CM, Braccioni F, et al. Infections and airway inflammation in chronic obstructive pulmonary disease exacerbations. Am J Respir Crit Care Med. 2006;173(10):1114-21.
  18. Regan EA, Lynch DA, Curran-Everett D, et al. Clinical and radiologic disease in smokers with normal spirometry. JAMA Intern Med. 2015;175(9):1539-49.
  19. Seemungal TA, Donaldson GC, Paul EA, et al. Effect of exacerbation on quality of life in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 1998;157(5):1418-22.
  20. Hurst JR, Vestbo J, Anzueto A, et al. Susceptibility to exacerbation in chronic obstructive pulmonary disease. N Engl J Med. 2010;363(12):1128-38.
Recommended Articles
Research Article
Surgical versus Medical Management of Concurrent Otitis Media with Effusion in Children Undergoing Adenotonsillectomy
...
Published: 26/07/2025
Research Article
Comparing the Efficacy of Dexamethasone Injection by Submucosal, Intravenous and Intramuscular Routes in Minimizing Post-Operative Discomfort After Mandibular Third Molar Surgery - A Randomized Controlled Trial
...
Published: 26/07/2025
Research Article
Clinical Profile and Short-Term Outcomes of Dengue Patients with Warning Signs versus Without Warning Signs
Published: 26/07/2025
Research Article
Comparison of Macular Changes by Optical Coherencetomography after Phacoemulsification in Diabetic and Non Diabetic
...
Published: 24/07/2025
Chat on WhatsApp
© Copyright Journal of Contemporary Clinical Practice