The present study investigated antioxidant status in lavage fluid, lung, liver, heart and kidney in a rat model to simulate an inhalation injury as might be encountered by firefighters and burn victims. Anesthetized rats received either a 20% total body surface area (TBSA) full thickness scald or a sham burn. After a 5 h recovery period, half of the animals in the burn or sham burn groups were exposed to cooled western bark (fir and pine) smoke for 16.25 min. The remaining rats in each group breathed room air. At 1, 12, 24, 48 and 96 h after exposure to the smoke, five rats from each of the four groups were euthanatized and lungs were lavaged by infusing three 5 ml aliquots of normal saline for evaluation of airway cellular content and lung wet to dry weight ratios to estimate lung water content. A second series of five rats/group per time point were euthanatized at the above times and lung, liver, kidney and heart were removed for evaluation of tissue antioxidant enzyme activities and for thiobarbituric acid reactive substances (TBARS) concentrations, as well as for lung histology. Smoke exposure resulted in average plasma carboxyhemoglobin (COHb) of 19+/-2% in the two smoke exposed groups and produced areas of erosion of the tracheal surface, resulting in loss of epithelium and exposed basement membrane. Lung water content was not significantly different among the four groups during the 96-h experimental period. Lung TBARS levels were 2-3-fold higher at 12 h in smoke exposed rats compared with controls. These levels peaked at 24 h and remained significantly elevated at 48 h compared to controls. TBARS were also elevated in liver, but not in heart or kidney in response to burn or combined injury. Minor effects on lung antioxidant enzyme activities were observed after smoke inhalation. These data suggest that smoke inhalation, independent of burn injury, induces an oxidant stress that persists for at least the first 48 h after smoke exposure.