Chronic obstructive pulmonary disease (COPD) is a complex disease in which multiple genes, as well as cigarette smoking, are involved. The proteinase-antiproteinase imbalance is thought to have a crucial role in the pathogenesis of smoking related COPD. It is proposed that overexpression of matrix metalloproteinases (MMPs) leads to excessive extracellular matrix protein degradation, which influences lung parenchyma destruction and inflammation in COPD. The aim of this study was to investigate association of MMPs selected functional polymorphisms, which alter transcriptional activity, with COPD. The genotypes of 86 COPD patients and 100 control subjects (50 smokers and 50 nonsmokers) were determined by polymerase chain reaction followed by restriction fragment length polymorphisms of the MMP9 (C-1562T) and MMP12 (A-82G) and conformation sensitive gel electrophoresis of the MMP1 (G-1607GG) genes variants. We observed statistically significant increase in frequency of the MMP9 (-1562T) allele (20% versus 11%, p=0.047) and heterozygotes for MMP9 gene variant (36% versus 18%, p=0.026) in COPD group in comparison with smoker control subjects. No differences were observed in alleles or genotypes frequencies of the MMP1 and MMP12 genes polymorphisms between groups. In summary, we demonstrated that presence of MMP9 (-1562T) polymorphism, which is associated with higher level of gene expression and consequently increased extracellular matrix protein degradation, might be involved in COPD development in smokers. These data suggest possible role of MMP9 gene polymorphism, but not MMP1 and MMP12, in etiology of smoking related COPD.