Evaluating blood inflammatory cells in smokers and patients with COPD: implications for COPD management

<bold>Introduction:</bold> Smoking is a major trigger of inflammation and a key contributor to COPD pathogenesis. This study evaluated the blood inflammatory cell populations in smokers with and without COPD, providing insights into COPD management. Methodology: Blood samples from 80 consented patients with and without COPD, sub-grouped into COPD current smokers (COPD-CS, 20) and ex-smokers (COPD-ES, 20), normal lung function smokers (NLFS, 20), and healthy non-smokers (NC, 20), were analysed for inflammatory cells [white cell count (WCC), neutrophils, lymphocytes, monocytes, eosinophils, C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR)] using Sysmex XN2000 full blood count analyser. <bold>Results:</bold> Compared to NC, WCC, neutrophils, lymphocytes, and monocytes counts were markedly higher in COPD groups (p<0.05~<0.001) and in NLFS (p<0.05); eosinophils counts were higher in COPD-ES (p<0.05); ESR levels increased in COPD-CS and NLFS (p<0.05), and CRP levels were higher in COPD groups (p<0.05). Smoking pack-years positively correlated with neutrophils, monocytes, eosinophils, ESR, and CRP in COPD-CS (p<0.03). In addition, lymphocytes and eosinophils positively correlated with pack-years in NLFS (p<0.03). Lung function parameters and blood oxygen saturation in COPD groups were negatively associated with smoking pack-years (p<0.03). <bold>Conclusion:</bold> Increased inflammatory cell levels in COPD groups, particularly in neutrophils, lymphocytes, monocytes, and eosinophils, correlated with smoking history. Elevated ESR and CRP indicate ongoing inflammation, suggesting the need for broad-spectrum anti-inflammatory therapy and smoking cessation to suppress inflammation and prevent further lung damage.