We examined the effects of dietary vitamin E level on rat lung response to ozone (O3) inhalation. In one study, we fed 1-month-old Sprague-Dawley (SD) rats a test diet containing 0 or 50 IU vitamin E/kg for 2 months, and then exposed one-half of the animals from each dietary group to 0.8 ppm (1,568 micrograms/m3) O3 intermittently (8 hours daily) and the other half to room air for 7 days. After O3 exposure, we found significant increases in marker enzyme activities in rat lungs from both dietary groups relative to corresponding air-exposed controls, but the magnitude of increases was greater for the 0 IU than the 50 IU group. In another study, we fed 1-month-old SD rats a test diet containing 10, 50, or 500 IU vitamin E/kg for 2 months and then exposed one-half of the animals from each dietary group to 0.8 ppm (1,568 micrograms/m3) O3 continuously and the other half to room air for 4 days. The O3 exposure increased the metabolic activities in rat lungs from all three dietary groups relative to corresponding air-exposed controls, but the magnitude of increases was greater for the 10 IU than the 50 IU or 500 IU group, and the difference between the 50 IU and 500 IU groups was small. Because a greater increase in lung metabolism after O3 exposure is thought to be associated with a greater tissue injury, the results suggest that an absence of dietary vitamin E exacerbates lung injury from O3 inhalation, while its presence protects from injury. However, the magnitude of this protective effect does not increase proportionately with increased dietary vitamin E supplementation beyond a certain level.