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Introduction/Aim: Environmentally persistent free radicals (EPFRs) are newly identified combustion generated environmental stressors. EPFRs are present in substantial numbers attached to atmospheric particulate matter (PM). EPFRs are associated with pulmonary pathology by inducing oxidative stress in the lungs. Oxidative stress in the airway epithelium induces inflammation and cell damage that may initiate or worsen respiratory disease. Redox regulation maintains the equilibrium of pro-oxidant/antioxidant reactions but can be disturbed by environmental exposures. How this impacts on respiratory disease and whether anti-oxidants can provide protection is unknown. The aim of this study was to develop a stress response model in primary human nasal epithelial cells (HNECs) grown at the air-liquid interface (ALI) into a well-differentiated epithelium and to use this model to examine the effect of EPFRs and …