Human exposure to carbon monoxide can occur from automobile emissions, industrial processes, sidestream or mainstream cigarette smoke, and poorly ventilated appliances such as space heaters and gas stoves. Most researchers consider the major mechanism for the toxicity of carbon monoxide to be its ability to compete with oxygen for binding to hemoglobin, the protein that transports oxygen through the bloodstream and releases it to cells and tissues. Some researchers speculate that an additional mechanism for carbon monoxide toxicity may involve carbon monoxide binding to myoglobin in the heart muscle cells called myocytes. Drs. Beatrice and Jonathan Wittenberg at the Albert Einstein College of Medicine sought evidence for this additional mechanism of the cardiotoxicity of carbon monoxide. The investigators isolated myocytes from rat hearts and exposed them in a chamber for one hour to gas mixtures containing a wide range of both oxygen and carbon monoxide concentrations. In this way they produced carboxymyoglobin levels ranging from 0% to 100% of the total myoglobin. One strength of the experimental design was the absence of hemoglobin, which also binds avidly to carbon monoxide. The investigators made simultaneous measurements of oxygen uptake and carboxymyoglobin content, and also determined the effect of increasing carboxymyoglobin levels on ATP synthesis. Thus, they correlated carboxymyoglobin levels in the exposure chamber with oxygen uptake and energy production by the myocytes.