ASSESSMENT OF PULMONARY FUNCTION, OXIDATIVE STRESS, AND HEMATOLOGICAL CHANGES IN CHRONIC SMOKERS

Abstract

Background: Cigarette smoking is a major risk factor for pulmonary dysfunction, exerting harmful effects through interconnected physiological, biochemical, and hematological mechanisms. In addition to impairing lung function, smoking induces oxidative stress, systemic inflammation, and alterations in hematological parameters, contributing to tissue injury and disease progression.

Objective: To evaluate smoking-induced changes in pulmonary physiology, antioxidant defense systems, and associated hematological alterations.

Methods: A comparative cross-sectional study was conducted including smokers (n = 60) and age-matched non-smokers (n = 60) from Lahore. Pulmonary function was assessed using spirometry, measuring forced vital capacity (FVC), forced expiratory volume in one second (FEV₁), and FEV₁/FVC ratio. Oxidative stress was evaluated by serum malondialdehyde (MDA), while antioxidant status was assessed via superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx). Hematological parameters including hemoglobin (Hb), hematocrit (Hct), total leukocyte count (TLC), and platelet count were also measured. Statistical analysis was performed using independent t-test and Pearson correlation, with p < 0.05 considered significant.

Results: Smokers demonstrated a significant reduction in pulmonary function parameters compared to non-smokers: FEV₁ (2.10 ± 0.45 vs 3.05 ± 0.50 L), FVC (3.00 ± 0.60 vs 3.80 ± 0.55 L), and FEV₁/FVC ratio (70.2 ± 6.5% vs 80.5 ± 5.8%), all p < 0.001. Biochemically, smokers showed significantly elevated MDA levels (5.8 ± 1.2 vs 3.1 ± 0.9 µmol/L, p < 0.001) and reduced antioxidant enzyme activity (SOD, catalase, GPx; p < 0.001). Hematological analysis revealed higher hemoglobin (15.8 ± 1.2 vs 14.2 ± 1.0 g/dL, p < 0.001) and hematocrit levels (48 ± 4% vs 42 ± 3%, p < 0.001), along with elevated total leukocyte count (9.8 ± 2.1 vs 6.5 ± 1.8 ×10⁹/L, p < 0.001) and mild thrombocytosis (p < 0.05). A significant negative correlation was observed between MDA and FEV₁ (r = –0.62, p < 0.001).

Conclusion: Smoking significantly impairs pulmonary function and disrupts antioxidant defense systems, accompanied by hematological alterations such as polycythemia and leukocytosis. These findings highlight the combined role of oxidative stress, systemic inflammation, and physiological dysfunction in the pathogenesis of smoking-related pulmonary disease.