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.
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.
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.
Inclusion Criteria:
Exclusion Criteria:
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.
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.
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.
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.