Ozone is a major environmental oxidant pollutant. Following ozone inhalation, there are a number of marked pulmonary responses depending on the extent and duration of exposure. Recently it has been established that ozone exposure may also result in cardiac injury. In this study we show that exposure of mice to 800 ppb ozone for as little as 6 h results in a 16% decrease in cardiac protein synthesis rates (p < .02). The fall in protein synthesis is due primarily to a reduced rate of ribosomal efficiency (40%) in the hearts of ozone-exposed mice. This change in cardiac protein metabolism is accompanied by increased levels of two markers of tissue injury: edema and protein carbonyl content. It is unlikely, however, that these observations represent a direct action of ozone on the heart, but rather an indirect effect, possibly mediated by lipid peroxidation products generated in the lung.