CO = Carbon Monoxide

The most common sources of carbon monoxide in deaths are fires, automobile exhaust, defective heaters, and incomplete combustion of burning products, such as charcoal briquets. Carbon monoxide is produced whenever organic materials are burned with an inadequate supply of oxygen necessary to produce complete combustion. Carbon monoxide produces tissue hypoxia by competing with oxygen for binding sites on the oxygen-carrying hemeproteins (hemoglobin, myoglobin, cytochrome c oxidase, cytochrome P-450). The affinity of carbon monoxide for hemeproteins varies from 30 to 500 times as much as oxygen, depending on the hemeproteins. For hemoglobin, it is from 250 to 300 times greater than that for oxygen. It is believed that carbon monoxide has a direct toxic effect at the cellular level by impairing mitochondrial respiration, caused by carbon monoxide’s binding to the cytochrome oxidase complex.  The percent saturation of carbon monoxide is defined as the percentage of hemoglobin combined with carbon monoxide in the form of carboxyhemoglobin. Humidity, high environmental temperature, high altitude and physical activity increase the respiratory rate and, thus, the absorption of carbon monoxide. The recommended maximum allowable exposure limit is 35 ppm over 8 h. For safety purposes, workers exposed to carbon monoxide should never have a blood carboxyhemoglobin level above 5%. In practice, this is not always possible. While non-smokers have blood carboxyhemoglobin levels of 1–3%, smokers often have “normal” levels of carboxyhemoglobin of 5–6%, commonly reach 10% and may even exceed 15%. Blood carboxyhemoglobin levels of 10–14% have been observed in firefighters after a blaze. Elevated levels of carboxyhemoglobin (up to 13%) can also be found in police officers working in tunnels or workers in garages where motor vehicles are running, if the individuals are also smokers. After fires, the second most common source of carbon monoxide in fatalities is inhalation of the exhaust fumes of automobiles. Most such deaths are suicide, but accidental deaths do occur. These are due almost exclusively to a faulty vehicle, though deaths have happened when cars have been trapped in snow. Some deaths have occurred while the vehicle was in motion, and some with partly open windows. The quantity of CO produced by a gasoline engine depends on a number of factors, including idling speed, air–fuel ratio, compression ratio, and the presence of a catalytic converter. Prior to the introduction of catalytic converters, an idling engine could produce 7% CO, while the same engine in a vehicle traveling at 60 mph, with the carburetor adjusted for efficient operation, produced less than 0.5% CO.  Diesel engines have traditionally produced smaller quantities of carbon monoxide than gasoline engines. Catalytic converters have limitations. They do not become fully operational until they and the engine reach a certain temperature. Thus, there is an initial rise in CO exhaust to a high level with a subsequent decline to a constant lower level. The warmer the engine, and, thus, the converter, prior to starting, the lower the maximum CO level. If the catalytic converter becomes overheated, it becomes less efficient. Charcoal briquets are made to smolder, not burn with a flame. The incomplete burning that takes place produces carbon monoxide. Thus, if these grills are used in an unventilated environment such as a residence, garage, trailer, tent, or even a porch, death can be caused by the large amount of carbon monoxide produced. Occasionally, individuals camping out will use charcoal briquets to keep warm. This has resulted in a number of fatal CO poisonings. Carbon monoxide poisoning has also occurred with natural and butane gas heaters following buildup of carbon deposits, with resultant incomplete combustion of gas. Carbon monoxide can get into the air tanks of scuba divers. Here, emitted by gasoline-driven compressors might be accidentally sucked up and mixed with the air being pumped into the scuba air tanks. Carbon monoxide levels in blood and body cavity fluids of decomposed bodies are dependent on the carbon monoxide level of the blood prior to the death. They are not produced by postmortem carbon monoxide formation through the decomposition of hemoglobin, myoglobin, and other substances. The effects of exposure to carbon monoxide are subtle. At levels of 0–10% carboxyhemoglobin saturation, there are generally no symptoms. Levels from 10 to 20% are often symptomless, except for a headache. Between 30–40% CO, there was a throbbing headache, nausea, vomiting, faintness and drowsiness even at rest. As levels approach 40%, the slightest exertion caused faintness. Pulse and respiration are rapid. Blood pressure falls. Between 40–60% CO, there is mental confusion, weakness and loss of coordination. At 56% walk was unaided. At 60% CO and beyond, individuals lose consciousness.

The exhaust might lead into the compartment of the vehicle. Accidental deaths caused by carbon monoxide can be subtle in their presentation. A person might be found dead in a parked car with the ignition on and the motor either running or stalled. Death is caused by carbon monoxide entering a defect in the vehicle. An investigator, however, could mistakenly ascribe the cause of death to heart disease. When more than one individual is found dead in a car whose ignition is on, almost inevitably, death is caused by CO. If more than one person is found dead in a residence, or one individual dead and others comatose, without any evidence of trauma, the first agent one should suspect is carbon monoxide poisoning caused by a defective heating unit. Sometimes, people will try to make a suicide look like an accident. They will be found in a garage, with the door closed, the ignition of the car on, the hood open, and tools on the fender. The expected conclusion is that such individuals were overcome by exhaust fumes while repairing the vehicle.

Carbon monoxide can pass from the maternal to the fetal blood. The carboxyhemoglobin (COHB) concentration of the fetus is dependent on the percent saturation of the mother’s hemoglobin with CO. Saturation of fetal hemoglobin with CO lags behind saturation of the maternal hemoglobin because of the slow dissociation of maternal carboxyhemoglobin. After a time, however, equilibrium will be reached. The final COHB is 10% higher than maternal COHB. Carbon monoxide can produce intrauterine death of the infant even though the mother may survive. The brain is the organ most sensitive to the actions of carbon monoxide. Brain damage is characteristically localized to certain selective areas. If death does not occur immediately, the injury to these areas may increase over hours and days. Carbon monoxide produces selective injury to the cerebral gray matter. Bilateral necrosis of the globus pallidus is the most characteristic lesion, though other affected areas include the cerebral cortex, hippocampus, cerebellum, and substantia nigra. The lesions in the globus pallidus, however, are nonspecific and can be seen in drug overdoses as well. After an asymptomatic interval, the patient can develop severe headache, fever, nuchal rigidity, and neuropsychiatric symptoms. Transitory cortical blindness and memory defects are common. In addition, there can be aphasia, apathy, disorientation, hallucinations, incontinence, slow movements, and muscular rigidity. The permanent sequelae of CO intoxication include dementia, amnestic syndromes, psychosis, paralysis, chorea, cortical blindness, peripheral neuropathy, and incontinence. The delayed neurological syndrome in carbon monoxide intoxication is associated with lesions of the cerebral white matter. These lesions are nonspecific, however, and are found in other conditions associated with hypoxia and hypotension. It appears that a combination of hypotension and hypoxia is necessary to produce these lesions.

Acknowledgements:

The Police Department; 

https://www.politie.nl/mijnbuurt/politiebureaus/05/burgwallen.html and a Chief Inspector – Mr. Erik Akerboom      ©

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