The authors have previously found that ascorbic acid (AA) deficiency in guinea pigs enhances the pulmonary toxicity of nitrogen dioxide (NO2). The present study showed that exposure to NO2 (4.8 ppm, 3 hr) significantly increased lung lavage fluid protein (a sensitive indicator of pulmonary edema) only in guinea pigs fed rabbit chow (a diet not supplemented with vitamin C) for at least 7 days, at which time lung AA was about 50% of normal. The rabbit chow diet did not cause reduced body weight as did commercial synthetic scorbutic diets, even when they were supplemented with AA. After 14 days of feeding rabbit chow, lung AA was reduced to 15% of control. At this time, alpha-tocopherol (AT) in the same lungs was reduced to 85% of control, and lung nonprotein sulfhydryls (NPSH) were increased to 114% of control. Exposure of the guinea pigs to NO2 (4.5 ppm, 16 hr) increased wet lung weight and further altered the antioxidants in deficient (but not normally fed) animals in the following manner: NPSH content was increased to 130% of control, AT was decreased to 74% of control, and AA was increased from 15 to 50% of control.