Late August 2000, two deaths were reported at Lake Powell, Arizona. A family vacationing on a rented house boat turned on an electrically generator to power an air conditioner and a television. About fifteen minutes later, the two brothers jumped of to swim at the deck at the stern.Situated immediately below was the exhaust port of the generator. Within two minutes both boys were overcome by the carbon monoxide in the exhaust, which had become concentrated in the space under the deck. Both drowned.
Carbon monoxide (CO), a colorless, odorless gas, is responsible for more than half of yearly deaths due to poisoning worldwide. CO has an approximately 250-fold greater affinity for hemoglobin than does oxygen. Consequently, relatively low levels of CO can have substantial and tragic effects. Hemoglobin combines with CO to form a compound called carboxyhemoglobin , or COHb.
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Co is logically produced as a result of human activities. Engines and furnace exhausts are important sources, as CO is a by product of fossil fuel incomplete combustion.Some CO is also produced by natural processes. In the atmosphere CO levels are rarely dangerous, ranging from less than 0.05 part per million (ppm) in remote areas to 3 to 4 ppm in some cities of the northern hemisphere.
Many of the accidental deaths reported involve undetected CO buildup in enclosed spaces, such as when a household furnace malfunctions or leaks, venting CO into a home. However CO poisoning can also occur in open spaces, as unsuspecting people at work may inhale the exhausts from generators, outboard motors, tractor engines, recreational vehicles, or lawns mowers.
Due to the tight binding of CO to hemoglobin, COHb accumulates overtime as people are exposed to a constant low level of CO. In an average healthy individual, 1% or less of the total hemoglobin is complexed as COHb. since CO is a product of tobacco smoke, many smokers have COHb levels that range between 3-8% of total hemoglobin, the level rises to 15% for chain smokers.
COHb levels equilibrate at 50% in people who breathe air containing 570ppm of CO for several hours.
At levels of less than 10% of total hemoglobin, symptoms are rarely noticed. At 15% , the individual experiences mild headaches. At 20% to 30%, the headache is severe and is accompanied to nausea, dizziness, confusion, disorientation and some visual disturbances.
At 30% to 50%, neurological symptoms becomes more severe, individuals loose consciousness and sink into coma.
CO binding to hemoglobin is affected by many factors, exercise included and changes in air altitude. Because of their higher base levels of COHb, smokers exposed to a source of CO develop symptoms faster than non smokers most times.
Individuals with lungs, heart or blood diseases that reduce availability of oxygen to tissues may also develop symptoms at lower levels of exposure. Fetuses are also at high risk because fetal hemoglobin has a higher affinity for CO than adult hemoglobin. Cases of CO exposure resulting in fetal death has been reported.
The effects of CO interactions is not limited to hemoglobin. It binds to other heme proteins and a variety of metallo proteins. This responsible for long term effects of acute but nonfatal CO poisoning.
When CO poisoning is suspected, rapid removal of the person from the source is essential.When this done Oxygen begins to replace the CO in hemoglobin and COHb levels drops slowly. If oxygen is administered with a mask, the rate of exchange can be increased about fourfold.
Carbon monoxide detectors in all homes are highly recommended. This is a simple and inexpensive measure to avoid possible tragedy.
