Acute exposure to ozone (O 3 ) has been reported to possess beneficial effects in the injured myocardium. We have demonstrated that chronic O 3 exposure elicits cardiac dysfunction in rats. These results suggest that acute and chronic exposures to O 3 have different effects on myocardial function. On the contrary exposure to acute ozone levels has shown to cause lung injury. Although effects of chronic exposure to ozone on the lung has not been determined, it is reasonable to suggest that ozone mediated toxicity may be tissue specific. It appears that in chronic cardiac injury subsequent to an ischemic insult, lipid raft proteins such as caveolin-1 and caveolin-3 play vital roles in the generation of death and survival signaling in the heart. In lung injury subsequent to acute O 3 exposure, dramatic reductions in caveolin-1 levels were associated with increases in lung TNF-α. Our previous studies showed increased expressions of myocardial TNF-α after chronic O 3 exposure. In the present study we wanted to determine the regulatory role of caveolin-1 and caveolin-3 in hearts and lungs from rats exposed to chronic O 3 levels. Sprague Dawley rats were exposed 8 hrs/day for 28 and 56 days to filtered air or 0.8 ppm O 3 . In order to assess the chronic effects to O 3 , levels of caveolin-1 and caveolin-3 in the lung and heart tissue were measured 24 hrs after termination of the O 3 exposure. Caveolin-1 levels in hearts from the ozone exposed groups were significantly decreased compared to air exposed rats; while caveolin-1 levels in lungs from the same animals were not different from the air exposed group. On the other hand caveolin-3 levels in hearts from the ozone exposed groups increased and decreased after 4 and 8 week of ozone exposure compared to air exposed rats; while caveolin-3 levels in lungs from the same animals were not different from the air exposed group. These novel findings suggest the interesting possibility that caveolin expressions subsequent to chronic ozone exposure may be tissue specific.