Carbon monoxide (CO) is a clear, colorless, odorless, and insidious poison that is responsible for hundreds of inadvertent and preventable deaths in the United States each year. The major environmental source of CO is incomplete combustion of carbonaceous fossil fuels. The reason for its toxicity is that it combines with the oxygen-carrying site of hemoglobin, the red protein within red blood cells that is responsible for delivering oxygen from the lung to body tissues. CO has a more than two-hundredfold greater affinity for this oxygen-carrying site than does oxygen. This means that, at sea level, exposure to 1,000 parts per million (ppm) CO in 20 percent oxygen (200,000 ppm) would lead, at equilibrium, to about 50 percent of hemoglobin sites being combined with CO rather than oxygen. Fortunately, it requires eight to twelve hours for maximum blood levels to be achieved when the body encounters a new CO concentration, otherwise mainstream cigarette smoke, which contains even higher levels of CO, might be instantaneously lethal. When CO combines with hemoglobin, the resulting chemical is called carboxy hemoglobin (COHb).
The negative effect of CO on the delivery of oxygen to the tissues extends beyond just the simple blockage of oxygen-combining sites. Each hemoglobin molecule contains four oxygen-carrying sites. Once the first oxygen molecule is released at the tissue level the second, third, and fourth come off even more rapidly. Oxygen release is delayed by CO so that there is even less oxygen delivered than would be expected purely on the basis of the amount of oxygen not being carried by hemoglobin. For this reason, overt symptoms due to lack of oxygen can be observed at COHb levels of approximately 15 to 20 percent, or even less, in healthy people. Levels of COHb over 40 percent can be lethal.
The uptake of CO increases as respiratory rates increase. This puts children at greater risk since they breathe more rapidly, in proportion to their body weight, than adults. This explains the unfortunate situation of a family in an automobile stuck in a snowstorm with the motor running being found with the adults unconscious and the children dead. The fetus is also at higher risk due to the greater affinity of CO for fetal, as compared to adult, hemoglobin.
All cases of fatal CO poisoning are readily preventable. In addition to automobile exhaust, other lethal sources of CO are often related to home heating systems. Blockage of flues, or inappropriate repair work on the home heating source or on ducts, is often responsible for CO toxicity. Symptoms of CO toxicity, such as headache, weakness, and listlessness, tend to be worse in the morning and to go away during the day if people leave the home. Many fatal cases are preceded by visits to physicians or emergency departments with only symptomatic treatment. Home CO alarms are relatively cheap and are an effective means of prevention. CO poisoning occurs more rapidly at high altitude due to the relative lack of oxygen to compete for the oxygen-combining site of hemoglobin. Conversely, symptomatic CO poisoning is treated with oxygen.
CO is also made in the human body through the normal catabolism of heme (oxygen-carrying hemoglobin), which leads to a background concentration in the blood of approximately 0.5 percent COHb. Concentrations of 2 to 3 percent COHb have been associated with an increased risk of angina attacks in susceptible individuals with preexisting arteriosclerotic heart disease. Preventing this adverse consequence is the major basis for
BERNARD D. GOLDSTEIN
(SEE ALSO: Ambient Air Quality [Air Pollution])
Ernst, A., and Zibrak, J. D. (1998). "Carbon Monoxide Poisoning." New England Journal Medicine 339:1603–1608.
Raub, J. A.; Mathieu-Nof, M.; Hampson, M. B.; and Thom, S. R. (2000). "Carbon Monoxide Poisoning— A Public Health Perspective." Toxicology 145(1):1–14.
Tomaszewski, C. (1999). "Carbon Monoxide Poisoning— Early Awareness and Intervention Can Save Lives." Postgrad Medicine 105(1):39–40.