 The objective of this study is to investigate molecular, cytological and genetic features of occupational chronic obstructive pulmonary disease COPD in conditions of different occupational exposures. In order to achieve this goal serum pro-inflammatory cytokines and standard inflammation markers level, hemostasis, cytological analysis of bronchoalveolar lavage fluid and association of single nucleotide polymorphisms SNPs rs1800470 transforming growing factor β1 TGF β1 gene, rs1828591 hedgehog interacting protein HHIP gene, rs4129267 interleukin 6 receptor IL-6R gene, rs1051730 nicotinic acetylcholine receptor 3 CHRNA3 gene with COPD in subjects exposed to silica dust and in those exposed to polycyclic aromatic hydrocarbons exhaust will be investigated. The relationship between genotype and phenotype characteristics, such as an inflammation activity, assessed by C-reactive protein hsCRP and tumor necrosis factor alpha TNF α serum concentration, in different occupational COPD groups will be studied. The hypothesis is that the mechanisms underlying disease development and progression are different due to environmental risk factor that reflex in differs in disease attributes - molecular biomarkers, cytology results and genetic susceptibility between COPD due to dust, COPD due to chemicals and COPD in smokers therefore COPD can be subdivided into ecological phenotypes according to environmental risk factor. 