Angiotensin converting enzyme (ACE) catalyzes the conversion of angiotensin I to angiotensin II (a potent vasopressor) and plays an important role in homeostasis of blood pressure. ACE has been shown to be associated primarily with the luminal surfaces of lung vascular endothelial cells making it a possible target for phosgene and ozone. Sixty-day-old male Sprague Dawley rats were exposed to 0.5 ppm phosgene, 1.0 ppm ozone, or air for 4 hr. Rats were sacrificed immediately and 24 hr. postexposure. ACE activity was measured in lung, lavage fluid, lavage fluid cells, and serum. Both phosgene and ozone exposed rats showed no changes in ACE activity in either lavage fluid or serum compared to air controls. Whole lung ACE activity was significantly higher immediately and marginally higher 24 hours postexposure to phosgene with increases of 34% and 16%, respectively. Phosgene exposed rats also showed a significant increase in ACE activity in the lavage fluid cells. These increases were 50% and 54% above controls at 0 and 24 hr postexposure, respectively. The cell type most likely affected was the alveolar macrophage. No significant effects were seen following ozone exposure.