The initial stage of inflammation of COPD is induced by releasing of leukocyte endothelial adhesion molecules. The aim of this study is to investigate the levels of LFA-1, Mac-1, and sICAM-1 in stable patients with COPD, healthy smokers and non-smokers, and to determine the role of adhesion molecules in the development of COPD.We investigated Mac-1, LFA-1 and sICAM-1, which are adhesion molecules in the peripheral blood samples of stable patients with COPD (n= 50), healthy smokers (n= 25), and healthy non-smokers (n= 15). Furthermore, patients with COPD were divided into two groups as smoking COPD patients (n= 35), and biomass COPD patients (n= 15).The level of sICAM-1 was measured quantitatively with ELISA method. Flow cytometry was used for Mac-1 and LFA-1 levels. No statistically significant difference was found in LFA-1 and sICAM-1 levels among the groups (p>0.05). But Mac-1 levels were higher in the healthy smokers when compared to stable patients with COPD (97.8±2.5 vs 92.3±5.9, p<0.05) and no statistically significant difference was found between non-smokers and smokers (p>0.05). In addition, while there was statistically significant difference between smoking COPD patients and healthy smokers in terms of Mac-1 levels (93.7±6.6 vs 97.8±2.5, p<0.05), no difference was found between biomass COPD patients and other groups (p>0.05). There was a negative correlation between FEV j and both Mac-1 level (r=-0.302, p=O.O37), and sICAM-1 (r=-0.346, p<0.001). In addition, there was a negative correlation between LFA-1 level and Pa- CO2 (r=-0.387, p=0.007). As a result, we found that there was an increase in adhesion molecules through inducing of inflammation and other stimulants because of smoking. However, we also determined that there were no important changes in releasing of adhesion molecules in stable patients with COPD.