We have investigated the possibility that tumor necrosis factor α (TNF) plays a role in the increased airway permeability and an inflammatory response following an acute ozone (O3) exposure. Male Sprague‐Dawley rats were injected, intraperitoneally, with either rabbit anti‐mouse antibody to TNF (anti‐TNF) or preimmune rabbit serum, 2 h before a 3‐h exposure to O3or purified air. Permeability, as determined by [99mTc] diethylenetriamine pentaacetate (DTPA) transport, total protein and albumin concentrations in the bron‐choalveolar lavage (BAL), and the inflammatory cell response in the BAL were assessed 10 h after the exposure was completed. The O3‐exposed group that was injected with anti‐TNF showed a significant decrease in permeability to DTPA in comparison to the O3‐exposed group injected with preimmune rabbit serum. There was no difference between the anti‐TNF group and the purified air group. In contrast, the total protein and albumin levels in the BAL were significantly greater in both of the O3‐exposed groups than in the purified air group. The concentrations of protein and albumin in the anti‐TNF group did, however, show an attenuating trend when compared to the preimmune O3‐exposed group. The polymorphonuclear leukocytes (PMNs) in BAL of the anti‐TNF group also showed an attenuating trend when compared to the preimmune O3‐exposed group, but both of these O3‐exposed groups were significantly greater than the purified air group. Lung sections stained with naphthol AS‐D chloroacetate esterase showed an increase in the number of stained PMNs in the anti‐TNF group in comparison to the preimmune O3‐ and air‐exposed groups. These data suggest that TNF plays a role in the increase in tracheal permeability as determined by DTPA transport, while the contributing role that TNF plays in bronchoalveolar permeability and the inflammatory response seen following an acute exposure to 0.8 ppm O3is less evident.