Carbon monoxide poisoning occurs after the inhalation of carbon monoxide gas. Carbon monoxide (CO) is a product of combustion of organic matter under conditions of restricted oxygen supply, which prevents complete oxidation to carbon dioxide (CO2). Carbon monoxide is colorless, odorless, tasteless, and non-irritating, making it difficult for people to detect.
Carbon monoxide is a significantly toxic gas with poisoning being the most common type of fatal poisoning in many countries.[1] Symptoms of mild poisoning include headaches, vertigo, and flu-like effects; larger exposures can lead to significant toxicity of the central nervous system and heart. Following poisoning, long-term sequelae often occur. Carbon monoxide can also have severe effects on the fetus of a pregnant woman.
The mechanisms by which carbon monoxide produces toxic effects are not yet fully understood, but hemoglobin, 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.[2] Domestic carbon monoxide poisoning can be prevented by the use of household carbon monoxide detectors.
Sources
0.1 ppm - natural background atmosphere level (MOPITT)
0.5 to 5 ppm - average background level in homes[5]
5 to 15 ppm - levels near properly adjusted gas stoves in homes[6]
100-200 ppm - Mexico City central area from autos etc.[7]
5,000 ppm - chimney of a home wood fire[8]
7,000 ppm - undiluted warm car exhaust[9]
30,000 ppm - undiluted cigarette smoke[10]
Common sources of CO that may lead to poisoning include house fires, furnaces or heaters, wood-burning stoves, motor vehicle exhaust, and propane-fueled equipment such as portable camping stoves, ice resurfacers,[3] forklifts,[4] engine-driven generators,[5] and gasoline-powered tools such as high-pressure washers, concrete cutting saws, power trowels, floor buffers, and welders used in buildings or semienclosed spaces.[6] CO poisoning can also occur in scuba diving due to faulty or badly sited diving air compressors. (See Effects of relying on breathing equipment while underwater for more information.) Generators and propulsion engines on boats --especially houseboats --have resulted in fatal carbon monoxide exposures. [7] Another source is exposure to the organic solvent methylene chloride, which is metabolized to CO by the body.[8]
Polluted air often contains unhealthy levels of carbon monoxide. Many areas of the US have struggled to achieve legislated limits. Significant advances have been made since the implementation by 1990 of a vehicle emissions limit of 3.4 gpm (grams per mile), a large reduction from the previous limit of 87 gpm. [11] [12] [13] [14]
[edit] Epidemiology
Carbon monoxide poisoning is the most common type of fatal poisoning in France and the United States. It has been estimated that more than 40,000 people per year seek medical attention for carbon monoxide poisoning in the United States.[9] In many industrialized countries, carbon monoxide may be the cause of greater than 50% of fatal poisonings.[1] In the U.S., about 200 people die each year from carbon monoxide poisoning associated with home fuel-burning heating equipment.[10] The CDC reports, "Each year, more than 500 Americans die from unintentional CO poisoning, and more than 2,000 commit suicide by intentionally poisoning themselves."[11]
[edit] Suicide
As other poisons such as cyanide and arsenic were placed under increasingly stringent legal restrictions, the carbon monoxide in town gas became the principal method of suicide by poisoning.[citation needed] Suicide was also often committed by inhaling exhaust fumes of running car engines. In the past, motor car exhaust may have contained up to 25% carbon monoxide. Newer cars have catalytic converters, which can eliminate over 99% of carbon monoxide produced.[12] However, even cars with catalytic converters can produce substantial carbon monoxide if an idling car is left in an enclosed space. Furthermore, cars with faulty heaters can produce a sufficient amount of carbon monoxide to cause deaths in some instances. This is due to reduced oxygen availability, and therefore, less efficient combustion.
As carbon monoxide poisoning via car exhaust has become less of a suicide option, there has been an increase in new methods of carbon monoxide poisoning such as burning charcoal or other fossil fuels within a confined space, such as a small room, tent, or car.[13] Such incidents have occurred mostly in connection with group suicide pacts in both Japan and Hong Kong, but are starting to occur in western countries as well, such as the 2007 suicide of Boston lead singer Brad Delp.[14]
[edit] Symptoms
[edit] Acute
The earliest symptoms, especially from low level exposures, are often non-specific and readily confused with other illnesses, typically flu-like viral syndromes, depression, chronic fatigue syndrome, and migraine or other headaches.[15] This often makes the diagnosis of carbon monoxide poisoning difficult. If suspected, the diagnosis can be confirmed by measurement of blood carboxyhemoglobin.
The main manifestations of poisoning develop in the organ systems most dependent on oxygen use: the central nervous system and the heart. The clinical manifestations include tachycardia and hypertension, and central nervous system symptoms such as headache, dizziness, confusion, convulsions, and unconsciousness. CO poisoning may also produce myocardial ischemia, atrial fibrillation, pneumonia, pulmonary edema, hyperglycemia, muscle necrosis, acute renal failure, skin lesions, visual and auditory problems, and respiratory arrest.[16]
One of the major concerns following CO poisoning is the severe neurological manifestations that may occur days or even weeks after an acute poisoning. Common problems encountered are difficulty with higher intellectual functions and short-term memory, dementia, irritability, gait disturbance, speech disturbances, parkinson-like syndromes, cortical blindness, and depression[17] (depression can occur in those accidentally exposed). These delayed sequelae occur in approximately 15 percent of severely poisoned patients after an interval of 2 to 28 days. It is difficult to predict who may develop delayed sequelae; however, advancing age, loss of consciousness while poisoned, and initial neurological abnormalities may indicate a greater chance of developing delayed symptoms. According to the Philadelphia poison control hotline, sequelae are generally not anticipated when exposure is not severe enough to result in loss of consciousness.
[edit] Chronic
Long term, repeat exposures present a greater risk to persons with coronary heart disease and in pregnant patients.[18] Chronic exposure may increase the incidence of cardiovascular symptoms in some workers, such as motor vehicle examiners, firefighters, and welders. Patients often complain of persistent headaches, lightheadedness, depression, confusion, and nausea. Upon removal from exposure, the symptoms usually resolve themselves.[19]
[edit] Toxicity
Carbon monoxide is a significantly toxic gas, although patients may demonstrate varied clinical manifestations with different outcomes, even under similar exposure conditions.[20] Toxicity is also increased by several factors, including: increased activity and rate of ventilation, pre-existing cerebral or cardiovascular disease, reduced cardiac output, anemia or other hematological disorders, decreased barometric pressure, and high metabolic rate.
Under ordinary conditions, it is less dense than air, but during fires, it accumulates on the ground, so that if poisoning causes loss of consciousness, the amount of carbon monoxide inhaled increases and the possibility of fatality is radically increased.
Carbon monoxide is life-threatening to humans and other forms of air-breathing life, as inhaling even relatively small amounts of it can lead to hypoxic injury, neurological damage, and possibly death. A concentration of as little as 0.04% (400 parts per million) carbon monoxide in the air can be fatal. The gas is especially dangerous because it is not easily detected by human senses. Early symptoms of carbon monoxide poisoning include drowsiness and headache, followed by unconsciousness, respiratory failure, and death. First aid for a victim of carbon monoxide poisoning requires access to fresh air; administration of artificial respiration and, if available, oxygen; and, as soon as possible, medical attention.
When carbon monoxide is inhaled, it takes the place of oxygen in hemoglobin, the red blood pigment that normally carries oxygen to all parts of the body. Because carbon monoxide binds to hemoglobin several hundred times more strongly than oxygen, its effects are cumulative and long-lasting, causing oxygen starvation throughout the body. Prolonged exposure to fresh air (or pure oxygen) is required for the CO-tainted hemoglobin (carboxyhemoglobin) to clear.
The effects of carbon monoxide in parts per million are listed below:
35 ppm (0.0035%) Headache and dizziness within six to eight hours of constant exposure
100 ppm (0.01%) Slight headache in two to three hours
200 ppm (0.02%) Slight headache within two to three hours
400 ppm (0.04%) Frontal headache within one to two hours
800 ppm (0.08%) Dizziness, nausea, and convulsions within 45 minutes. Insensible within two hours.
1,600 ppm (0.16%) Headache, dizziness, and nausea within 20 minutes. Death in less than two hours.
3,200 ppm (0.32%) Headache, dizziness and nausea in five to ten minutes. Death within 30 minutes.
6,400 ppm (0.64%) Headache and dizziness in one to two minutes. Death in less than 20 minutes.
12,800 ppm (1.28%)Unconsciousness after 2-3 breaths. Death in less than three minutes.
In addition, a recent report concludes that carbon monoxide exposure can lead to significant loss of lifespan after exposure due to damage to the heart muscle. [21]
[edit] Carboxyhemoglobin
Levels of carbon monoxide bound in the blood can be determined by measuring carboxyhemoglobin, which is a stable complex of carbon monoxide and hemoglobin that forms in red blood cells. Carbon monoxide is produced normally in the body, establishing a low background carboxyhemoglobin saturation. Carbon monoxide also functions as a neurotransmitter. Normal carboxyhemoglobin levels in an average person are less than 5%, whereas cigarette smokers (two packs/day) may have levels up to 9%.[22]
Serious toxicity is often associated with carboxyhemoglobin levels above 25%, and the risk of fatality is high with levels over 70%. Still, no consistent dose response relationship has been found between carboxyhemoglobin levels and clinical effects.[23] Therefore, carboxyhemoglobin levels are more guides to exposure levels than effects as they do not reliably predict clinical course or short- or long-term outcome.[24]
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