BEAR receives several cases of alleged CO poisoning a year. These can be difficult cases, as CO poisoning might occur over a period of time. Often the situation is misunderstood and alleged victims are confused.
In some instances, when CO contamination had been clearly demonstrated the communications channels were not properly coordinated. Here a clear timeline put together by BEAR engineers can help to demonstrate the sequence of events.
Carbon monoxide, with the chemical formula CO, is a colorless, odorless, tasteless yet highly toxic gas. Its molecules consist of one carbon atom covalently bonded to one oxygen atom. There are two covalent bonds and a coordinate covalent bond between the oxygen and carbon atoms.
CO is produced from the partical combustion of carbon-containing compunds, notably in internal-combustion engines. Carbon monoxide froms in preference to the more usual carbon dioxide when there is a reduced availability of oxygen present during the combustion process. Carbon monoxide has significant fuel value, burning in air with a characteristic blue flame, producing carbon dioxide.
Carbon monoxide is a significantly toxic gas and has no odor or color. It is the most common type of fatal poisoning in many countries. Exposures can lead to significant toxicity of the central nervous system and heart. Following poisoning, long-term sequelae often occurs. Carbon monoxide can also have severe effects on the fetus of a pregnant woman. Symptoms of mild poisoning include headaches and dizziness at concentrations less than 100 ppm. Concentrations as low as 667 ppm can cause up to 50% of the body's haemoglobin to be converted to carbosy-haemoglobin (HbCO). Carboxy-haemoglobin is quite stable but this change is reversible. Carboxy-haemoglobin is ineffective for delivering oxygen, resulting in some body parts not receiving oxygen needed. As a result, exposures of this level can be life-threatening. In the United States, OSHA limits long-term workplace exposure levels to 50 ppm.
The mechanisms by which carbon monoxide produces toxic effects are not yet fully understood, but haemoglobin, myoglobin, and mitochondrial cytochrome oxidase are thought to be compromised. Treatment largely consists of administering 100% oxygen or hyperbaric oxygen therapy, although the optimum treatment remains controversial.