This paper reviews the available evidence concerning the atherogenic potential of carbon monoxide. The evidence comes from two different types of studies--epidemiology studies on populations of humans chronically exposed to carbon monoxide, and animal studies conducted under conditions of controlled exposure to carbon monoxide. Data from both epidemiology and animal studies suggest that carbon monoxide is not atherogenic. Therefore, the increased levels of atherosclerosis associated with smoking as reported in epidemiology studies of human smokers probably cannot be attributed to CO exposure.