Electronic nicotine delivery systems (ENDS), more commonly known as e.cigarettes, are used as a tobacco free nicotine delivery system. ENDS utilise a liquid solution which is drawn over a heating element to produce a vapour which is then inhaled giving rise to the term ‘vaping’. The solution normally contains propylene glycol and vegetable glycerine to generate the vapour together with nicotine and flavourings. Evidence has indicated these ‘carriers’ may affect the function, growth and survival of airway epithelial cells [1][2] H441 or primary bronchial epithelial cells (HBEC) were grown on plastic or cultured on permeable supports at air-liquid interface. PG (0-3%) or PG:VG (55:45, 0-3%) were applied to the medium, directly to the apical (luminal) surface, or the cells were exposed to vapour for 10 minutes. Transepithelial electrical resistance was measured using an electrovoltometer and apical to basolateral permeability was assessed using sodium fluorescein. Glucose uptake across the cell membrane was measured using the Uptake Glo luminescent assay (Promega, UK) or 14C D-glucose. Cytotoxicity was measured using an LDH cytotoxicity assay (Peirce, UK). Mannitol was used as an osmotic control in some experiments. Exposure to 3% PG and 3% PG:VG decreased TEER relative to PBS at 15minutes, 4hrs and 24hrs compared to PBS (3% PG: p<0.001, 3% PG:VG p<0.05, n=5). At 24 hours 3% PG and 3% PG:VG exhibited more fluorescein permeability compared to PBS and mannitol and the permeability coefficient (Papp) was larger for cells exposed to 3% PG than 3%PG/VG. PG elicited a dose dependent inhibition of glucose uptake in proliferating H441 and HBEC. 3% PG inhibited glucose uptake to a similar level as the glucose transport inhibitor cytochalasin B (35 ± 5% and 32 ± 7% of control p < 0.001, n = 9 respectively). PG did not elicit any changes in LDH release. Treatment of air-liquid interface cultures with PG:VG (3%, 15ml apical) inhibited basolateral but not apical glucose uptake (p<0.01, n=4) in H441 cells and the effect was similar in HBEC when compared to a PBS control. Inhibition was less than that induced by the GLUT transport inhibitor phloretin. No effect of PG:VG on uptake was determined when compared to 3% mannitol. These data indicate that exposure to PG:VG reduces TEER, increases permeability and decreases glucose uptake in airway cells. As glucose uptake is a key metabolic requirement for cell growth, survival and is critical for the normal function of the airway epithelium, we hypothesised that propylene glycol (PG) and propylene glycol mixed with vegetable glycerine (PG:VG) inhibited glucose uptake and modified barrier function human airway epithelial cells.