['The respiratory tract is the primary route of exposure to inhaled toxicants such as environmental pollutants and tobacco smoke. Metabolic activation of xenobiotics is a contributor to the onset of lung diseases. Enzymes such as CYP1A1/1B1 and CYP2A6/2A13 activate polycyclic aromatic hydrocarbons and nitrosamines, respectively. Yet, few in vitro models retaining both adequate morphology and metabolic activities are currently available to investigate smoke toxicity.', 'We characterised the expression and activity of the toxicologically relevant metabolic enzymes CYP1A1/1B1 and CYP2A6/2A13 in polarised primary tracheobronchial epithelial cells cultured at the air-liquid interface. Metabolic activity was compared with NCI-H292 and A549, two commonly used lung epithelial cell models.', 'We report that CYP activity and inducibility is conserved in polarised primary tracheobronchial epithelial cells for 7- and 28-days cultured at the air-liquid interface. In comparison, NCI-H292 cells did not show CYP2A6/2A13 activity whilst A549 cells did not display significant metabolic activity for CYP1A1/1B1 or CYP2A6/2A13.'] Is cYP1A1/1B1 and CYP2A6/2A13 activity conserved in cultures of differentiated primary human tracheobronchial epithelial cells?