Carbon monoxide poisoning usually occurs from breathing too much carbon monoxide (CO). Symptoms are often described as "flu-like" and generally include headaches, dizziness, weakness, vomiting, chest pain, and confusion. A large exposure can lead to loss of consciousness, arrhythmia, seizures, or death. Classically described "cherry red skin" is rare. Long-term complications may include fatigue, memory problems, and movement problems. In those exposed to smoke, cyanide toxicity should also be considered.
Carbon monoxide poisoning can occur by accident or as an attempt to end a person's life. CO is a colorless and odorless gas that initially does not cause irritation. This is generated during incomplete combustion of organic matter. This can happen from motor vehicles, heaters, or cooking utensils that use carbon-based fuels. This can also occur from exposure to methylene chloride. Carbon monoxide mainly causes adverse effects by combining with hemoglobin to form carboxyhemoglobin (HbCO) preventing blood from carrying oxygen. In addition, myoglobin and mitochondria cytochrome oxidase are affected. Diagnosis is based on HbCO levels of more than 3% among non-smokers and more than 10% among smokers.
Efforts to prevent toxicity include carbon monoxide detectors, proper ventilation of gas equipment, keeping the chimney clean, and keeping the vehicle exhaust system in good repair. Treatment of poisoning generally consists of giving 100% oxygen along with supportive care. This should generally be done until symptoms are no longer present and HbCO levels are less than 10%. While hyperbaric oxygen therapy is used for severe poisoning, the benefits of standard oxygen delivery are unclear. The risk of death among those affected was between 1 and 30%.
Carbon monoxide poisoning is relatively common, generating over 20,000 emergency department departments a year in the United States. This is the most common type of fatal poisoning in many countries. In the United States, non-fire-related cases result in more than 400 deaths per year. Poisoning occurs more frequently in winter, especially from the use of portable generators during power outages. The toxic effects of CO have been known since ancient history. The realization that hemoglobin is affected by CO is determined in 1857.
Video Carbon monoxide poisoning
Signs and symptoms
Carbon monoxide is not toxic to all life forms. The harmful effect is due to binding with hemoglobin so that its harm to organisms that do not use this compound is questionable. Thus no effect on photosynthesis plants. It is easily absorbed through the lungs. Inhaling gas can cause hypoxic injury, nervous system damage, and even death. Different people and populations may have different levels of carbon monoxide tolerance. On average, exposure at 100 ppm or greater is harmful to human health. In the United States, OSHA limits long-term workplace exposure levels to less than 50 ppm, on average over an 8-hour period; In addition, employees must be excluded from the confined space if the upper limit ("ceiling") of 100 ppm is reached. Exposure to carbon monoxide can lead to a significantly shorter life span due to heart damage. The level of carbon monoxide tolerance for each person is altered by several factors, including pre-existing levels of activity, ventilation, cerebral or cardiovascular disease, cardiac output, anemia, sickle cell disease and other haematological disorders, barometric pressure, and metabolic rate..
Acute poisoning
The main manifestations of carbon monoxide poisoning develop in organ systems that most depend on the use of oxygen, the central nervous system and the heart. Early symptoms of acute carbon monoxide poisoning include headache, nausea, malaise, and fatigue. These symptoms are often mistaken for viruses such as influenza or other diseases such as food poisoning or gastroenteritis. Headache is the most common symptom of acute carbon monoxide poisoning; often described as boring, frontal, and sustainable. Increased exposure produces cardiac abnormalities including rapid heartbeat, low blood pressure, and cardiac arrhythmias; Central nervous system symptoms include delirium, hallucinations, dizziness, unstable gait, confusion, convulsions, central nervous system depression, unconsciousness, breathing, and death. Less common symptoms of acute carbon monoxide poisoning include myocardial ischemia, atrial fibrillation, pneumonia, pulmonary edema, high blood sugar, lactic acidosis, muscle necrosis, acute renal failure, skin lesions, and visual and auditory problems.
One of the main concerns after acute carbon monoxide poisoning is a potentially delayed neurologic manifestation that may occur. Problems may include difficulties with higher intellectual function, short-term memory loss, dementia, amnesia, psychosis, irritability, strange walking, speech impairment, Parkinson's syndrome, cortical blindness, and depressed mood. Depression can occur in those who do not have pre-existing depression. This delayed neurologic sequelae can occur in up to 50% of people poisoned after 2 to 40 days. It is difficult to predict who will develop a delayed sequel; However, old age, loss of consciousness when poisoned, and early neurological abnormalities may increase the likelihood of delayed symptoms.
One of the classic signs of carbon monoxide poisoning is more often seen in the dead than the living - people have been described as red-looking and healthy (see below). However, since the appearance of "cherry-red" is only common in people who die, and unusual in people who are still alive, it is not considered a useful diagnostic sign in clinical medicine. In pathological examination (autopsy), the apparent appearance of carbon monoxide poisoning is noticeable because dead people not found are usually bluish and pale, whereas dead carbon monoxide poisoners may only look extraordinary in color. The effect of carbon monoxide dye in the postmortem state is thus analogous to its use as a red dye in the commercial meat packing industry.
Chronic poisoning
Chronic exposure to relatively low levels of carbon monoxide can cause persistent headaches, lightheadedness, depression, confusion, memory loss, nausea, hearing loss and vomiting. It is not known whether chronic low-level exposure can cause permanent neurological damage. Usually, once expelled from carbon monoxide exposure, the symptoms usually heal on their own, unless there is a severe episode of acute poisoning. However, one case recorded permanent memory loss and learning problems after 3 years exposure to relatively low levels of carbon monoxide from defective furnaces. Chronic exposure may exacerbate cardiovascular symptoms in some people. Chronic carbon monoxide exposure may increase the risk of developing atherosclerosis. Long-term exposure to carbon monoxide presents the greatest risk to people with coronary heart disease and in pregnant women. In animal experiments, carbon monoxide appears to aggravate hearing impairment caused by noise in conditions of exposure to noise that would have a limited effect on the opposite hearing. In humans, hearing loss has been reported after carbon monoxide poisoning. Unlike the findings in animal studies, noise exposure is not a necessary factor for hearing problems.
Maps Carbon monoxide poisoning
Cause
Carbon monoxide is the product of combustion of organic matter under limited oxygen supply conditions, which prevents complete oxidation of carbon dioxide (CO 2 ). Carbon monoxide sources include cigarette smoke, house fires, broken furnaces, heating, wood burning stoves, exhausts of internal combustion vehicles, electric generators, propane-fueled appliances such as portable stoves, and gasoline-powered tools such as leaf blowers, lawn mowers, pressure washers high, concrete cutter saws, electric shovels, and welders. Exposure usually occurs when equipment is used in a semi-enclosed building or room.
Riding behind a pickup truck has caused poisoning in children. Driving a car with an exhaust pipe blocked by snow has caused car occupants toxicity. Any perforation between the exhaust manifold and the shroud can cause the exhaust gas to reach the cab. Generators and propulsion machines on ships, especially houseboats, have resulted in fatal carbon monoxide exposures.
Toxicity can also occur after the use of a standalone underwater breathing apparatus (SCUBA) due to incorrect air dive compressors.
In the cave carbon monoxide can build in a confined space due to the decomposition of organic matter. In coal mines, incomplete combustion can occur during an explosion resulting in afterdamp production. Gas up to 3% CO and can be fatal with just one breath. Following an explosion in a coal mine, adjacent adjacent sections may become dangerous due to post-mining leakage from mine to mine. Such an event follows the Trimdon Grange blast that killed people at the Kelloe mine.
Another source of poisoning is exposure to organic solvent dichloromethane, which is found in some strippers of paint, because dichloromethane metabolism produces carbon monoxide.
Pathophysiology
The exact mechanism by which the carbon monoxide effect is induced in the body system, is very complex and not yet fully understood. Known mechanisms include carbon monoxide that binds hemoglobin, myoglobin and mitochondrial cytochrome oxidase and limits oxygen supply, and carbon monoxide that causes lipid peroxidation of the brain.
hemoglobin
Carbon monoxide has a higher diffusion coefficient compared to oxygen and the only enzyme in the human body that produces carbon monoxide is the heme oxygenation located in all cells and breaks up the heme. Under normal conditions the carbon monoxide level in plasma is about 0 mmHg because it has a higher diffusion coefficient and the body easily removes any CO that is made. When the CO is unventilated, it binds to hemoglobin, which is the main oxygen-carrying compound in the blood; This produces a compound known as carboxyhemoglobin. The traditional belief is that carbon monoxide toxicity arises from the formation of carboxyhemoglobin, which lowers the oxygen-carrying capacity of the blood and inhibits the transport, delivery, and utilization of oxygen by the body. The affinity between hemoglobin and carbon monoxide is about 230 times stronger than the affinity between hemoglobin and oxygen so that hemoglobin binds to carbon monoxide in preference to oxygen.
Hemoglobin is a tetramer with four oxygen binding sites. The binding of carbon monoxide at one of these sites increases the oxygen affinity of the remaining three sites, which causes the hemoglobin molecule to retain the oxygen to be delivered to the tissues. This situation is described as carbon monoxide which shifts the oxygen dissociation curve to the left. Due to the increased affinity between hemoglobin and oxygen during carbon monoxide poisoning, little oxygen will actually be released in tissues. This causes hypoxia tissue injury. Hemoglobin acquires a bright red color when converted into carboxyhemoglobin, so that the toxic carcasses and even commercial meat treated with carbon monoxide obtain an unnatural reddish color.
Mioglobin
Carbon monoxide also binds to hemeprotein myoglobin. It has a high affinity for myoglobin, about 60 times larger than oxygen. Carbon monoxide bound to myoglobin can impair its ability to utilize oxygen. This results in reduced cardiac output and hypotension, which can lead to brain ischemia. The delayed return of symptoms has been reported. These results follow the recurrence of elevated carboxyhemoglobin levels; this effect may be caused by the late release of carbon monoxide from myoglobin, which then binds to hemoglobin.
Cytochrome oxidase
Another mechanism involves the effect on the chain of mitochondrial respiratory enzymes responsible for effective utilization of oxygen tissue. Carbon monoxide binds to cytochrome oxidase with less affinity than oxygen, so significant intracellular hypoxia may be necessary before binding. This binding interferes with aerobic metabolism and efficient adenosine triphosphate synthesis. The cells respond by switching to anaerobic metabolism, causing anoxia, lactic acidosis, and eventual cell death. The degree of dissociation between carbon monoxide and cytochrome oxidase is slow, causing a relatively prolonged oxidative metabolic disorder.
The effects of the central nervous system
Mechanisms suspected of having a significant effect on delayed effects involve blood cells being formed and chemical mediators, which causes brain lipid peroxidation (degradation of unsaturated fatty acids). Carbon monoxide causes endothelial cells and release of nitric oxide platelets, and the formation of oxygen-free radicals including peroxinitrite. In the brain this causes further mitochondrial dysfunction, capillary leak, leucocyte sequestration, and apoptosis. The result of this effect is lipid peroxidation, which causes reversible demyelination of white matter in the central nervous system known as myelinopathy grinker, which can cause edema and necrosis in the brain. This brain damage occurs mainly during the recovery period. This can lead to cognitive defects, especially affecting memory and learning, and movement disorders. This disorder is usually associated with damage to the white matter of the brain and the basal ganglia. The hallological change of hallmark after poisoning is bilateral necrosis of white matter, globus pallidus, cerebellum, hippocampus and cerebral cortex.
Pregnancy
Carbon monoxide poisoning in pregnant women can cause severe side effects in the fetus. Poisoning causes hypoxia of fetal tissue by reducing the release of mother's oxygen to the fetus. Carbon monoxide also crosses the placenta and joins fetal hemoglobin, leading to more direct fetal tissue hypoxia. In addition, fetal hemoglobin has a 10 to 15% higher affinity for carbon monoxide than adult hemoglobin, leading to more severe poisoning of the fetus than in adults. Carbon monoxide elimination is slower in the fetus, leading to the accumulation of toxic chemicals. The rate of fetal morbidity and mortality in acute carbon monoxide poisoning is significant, so that despite mild maternal toxicity or after maternal recovery, severe fetal toxicity or death can still occur.
Diagnosis
Because many symptoms of carbon monoxide poisoning also occur with many types of poisoning and other infections (such as flu), diagnosis is often difficult. Historical potential carbon monoxide exposures, such as exposure to live fires, may indicate toxicity, but the diagnosis is confirmed by measuring the levels of carbon monoxide in the blood. This can be determined by measuring the amount of carboxyhemoglobin compared with the amount of hemoglobin in the blood.
The ratio of carboxyhemoglobin to the hemoglobin molecule in the average person can reach 5%, although smokers who smoke two packs per day may have a rate of up to 9%. In people who are symptomatically poisoned they are often in the 10-30% range, while people who die may have postmortem blood levels of 30-90%.
Because people can continue to experience significant CO poisoning symptoms long after their carboxyhemoglobin concentration of blood returns to normal, presentation to a normal carboksihemoglobin-level examination (which may occur in end-poisoning countries) does not rule out poisoning.
Measure
Carbon monoxide can be quantified in blood using spectrophotometric or chromatographic methods to confirm the diagnosis of poisoning in a person or to assist in a forensic investigation of a case of fatal exposure.
A CO-oximeter can be used to determine carboxyhemoglobin levels. Pulse CO-oximeters estimate carboxyhemoglobin with non-invasive finger clips similar to pulse oximeter. This device works by passing various wavelengths of light through the fingertips and measuring the absorption of light from different types of hemoglobin in capillaries. The use of regular pulse oximeter is not effective in the diagnosis of carbon monoxide poisoning because people with carbon monoxide poisoning may have normal oxygen saturation levels in the pulse oximeter. This is due to carboxyhemoglobin which is misinterpreted as oxyhemoglobin.
CO Breath monitoring offers an alternative to CO-oximetry pulse. Carboxyhemoglobin levels have been shown to have a strong correlation with respiratory CO concentrations. However, many of these devices require users to take a deep breath and hold their breath to allow CO in the blood to escape into the lungs before measurements can be made. Since this is not possible with an unresponsive person, this device may not be suitable for use in emergency care detection at CO poisoning sites.
Differential diagnosis
There are many conditions to be considered in the differential diagnosis of carbon monoxide poisoning. The earliest symptoms, especially from low-level exposure, are often nonspecific and easily confused with other diseases, usually such as viral syndrome, depression, chronic fatigue syndrome, chest pain, and migraine or other headaches. Carbon monoxide has been called a "great mimicker" because the presentation of toxicity is diverse and non-specific. Other conditions included in the differential diagnosis include acute respiratory distress syndrome, altitude sickness, lactic acidosis, diabetic ketoacidosis, meningitis, methemoglobinemia, or opioid toxic alcohol poisoning.
Prevention
Detector
Prevention remains a critical public health issue, requiring public education about the safe operation of equipment, heating, fireplaces, and internal combustion engines, as well as increased emphasis on mounting carbon monoxide detectors. Carbon monoxide is tasteless and odorless, and therefore can not be detected by visual or odor cues.
The US Consumer Product Safety Commission has stated, "Carbon monoxide detectors are as important as home security as smoke detectors," and recommend every home has at least one carbon monoxide detector, and preferably one at each level of the building. This device, which is relatively inexpensive and widely available, can use batteries or air conditioners, with or without a spare battery. In buildings, carbon monoxide detectors are usually installed around heaters and other equipment. If relatively high levels of carbon monoxide are detected, the device sounds an alarm, giving people a chance to evacuate and build ventilation. Unlike smoke detectors, carbon monoxide detectors need not be placed near the ceiling level.
The use of carbon monoxide detectors has been standardized in many areas. In the US, NFPA 720-2009, a carbon monoxide detector guideline published by the National Fire Protection Association, mandates the placement of carbon monoxide detectors/alarms at every level of residence, including basements, in addition to the sleeping area outside. In new homes, air-powered detectors must have battery backup and interconnect to ensure early warning of occupants at all levels. NFPA 720-2009 is the first national carbon monoxide standard intended for devices in non-residential buildings. This guide, which is now associated with schools, health centers, nursing homes and other non-residential buildings, includes three main points:
- 1. Secondary power supply (battery backup) must operate all means of carbon monoxide notification for at least 12 hours,
- 2. The detector must be on the ceiling in the same room with permanently installed fuel burning equipment, and
- 3. Detectors should be placed at each level that can be occupied and in any HVAC zone of the building.
Gas organizations will often recommend getting gas equipment serviced at least once a year.
Legal requirements
NFPA standards do not need to be enforced by law. In April 2006, the US state of Massachusetts required detectors to be present in all dwellings with a potential source of CO, regardless of age of the building and whether they own or rent. This was imposed by the municipal inspectors, and was inspired by the death of 7-year-old Nicole Garofalo in 2005 because of the snow blocking the home heating vent. Other jurisdictions may not have the requirements or only the detector mandate for new construction or at the time of sale.
Despite similar deaths in vehicles with clogged exhaust pipes (eg in Northeastern United States 1978 and February 2013 snowstorm) and the availability of commercial equipment, there is no legal requirement for automotive CO detectors.
World Health Organization recommendations
The following guideline values ​​(rounded ppm values) and the average time period of weighted exposure have been determined in such a way that a 2.5% carbocysihemoglobin (COHb) rate is not exceeded, even when normal subjects are involved in mild or moderate exercise:
- 100Ã, mg/m3 (87 ppm) for 15 minutes
- 60Ã, mg/m3 (52 ppm) for 30 minutes
- 30Ã, mg/m3 (26 ppm) for 1 hour
- 10 mg/m3 (9 ppm) for 8 hours
For indoor air quality of 7 mg/m3 (6 ppm) for 24 hours (not to exceed 2% COHb for chronic exposure)
Treatment
The initial treatment for carbon monoxide poisoning is to immediately remove people from exposure without harming others. Those who are not aware may need CPR on the site. Giving oxygen through a non-rebreather mask shortens the carbon monoxide half-life from 320 minutes, when breathing normal air, to just 80 minutes. Oxygen accelerates the dissociation of carbon monoxide from carboxyhemoglobin, thus converting it back to hemoglobin. Due to the likelihood of a severe effect on the fetus, pregnant women are treated with oxygen for a longer period of time than non-pregnant people.
Hyperbaric Oxygen
Hyperbaric oxygen is also used in the treatment of carbon monoxide poisoning, because it can accelerate the dissociation of CO from carboxyhemoglobin and cytochrome oxidase to a greater degree than normal oxygen. Hyperbaric oxygen at three times the atmospheric pressure reduces the half-life of carbon monoxide to 23 (~ 80/3 minutes) minutes, compared with 80 minutes for oxygen at normal atmospheric pressure. It can also increase the transport of oxygen to the tissues by the plasma, partially passing through the normal transfer via hemoglobin. However, it is controversial whether hyperbaric oxygen actually offers the added benefit of normal high-flow oxygen, in terms of increased survival or increased long-term outcomes. There are randomized controlled trials where two treatment options have been compared; of the six performed, four found increased oxygen hyperbaric yields and two found no benefit for hyperbaric oxygen. Some of these trials have been criticized for the obvious defects in their implementation. A review of all literatures concludes that the role of hyperbaric oxygen is unclear and the available evidence does not confirm or deny medically meaningful benefits. The authors suggest large multicenter trials, well designed, outside the audit, to compare normal oxygen with hyperbaric oxygen.
More
Further treatment for other complications such as seizures, hypotension, cardiac abnormalities, pulmonary edema, and acidosis may be necessary. Increased muscle activity and seizures should be treated with dantrolene or diazepam; diazepam should only be administered with appropriate respiratory support. Hypotension requires treatment with intravenous fluids; vasopressor may be needed to treat myocardial depression. Cardiac dysrhythmias are treated with advanced standard cardiac life support protocols. If severe, metabolic acidosis is treated with sodium bicarbonate. Treatment with controversial sodium bicarbonate because acidosis can increase tissue oxygen availability. Acidosis treatment may only need to consist of oxygen therapy. The delayed development of neuropsychiatric disorders is one of the most serious complications of carbon monoxide poisoning. Brain damage confirmed after MRI or CAT scan. Extensive and supportive advanced care is often necessary for delayed neurologic damage. The results are often difficult to predict after poisoning, especially people who have symptoms of heart attack, coma, metabolic acidosis, or have high carboxyhemoglobin levels. One study reported that about 30% of people with severe carbon monoxide poisoning would have fatal results. It has been reported that electroconvulsive therapy (ECT) may increase the likelihood of delayed neuropsychiatric sequelae (DNS) after carbon monoxide (CO) poisoning.
Epidemiology
The actual number of cases of carbon monoxide poisoning is unknown, as many non-lethal exposures are undetectable. From the available data, carbon monoxide poisoning is the most common cause of worldwide injury and death from poisoning. Poisoning is usually more common during the winter months. This is due to increased domestic use of gas furnaces, heating of fuel chambers or kerosene, and kitchen stoves during the winter, which, if damaged and/or used without adequate ventilation, can produce excessive carbon monoxide. The detection of carbon monoxide and poisoning also increases during power outages, when electric heaters and cooking utensils become inoperable and residents can temporarily use heating chambers, stoves, and grills (some of which are safe to use outdoors but still burn right in the room).
It is estimated that over 40,000 people per year seek medical attention for carbon monoxide poisoning in the United States. 95% of deaths from carbon monoxide poisoning in the United States are caused by space gas heating. In many countries the carbon monoxide industry is responsible for more than 50% of fatal poisonings. In the United States, about 200 people die each year from carbon monoxide poisoning associated with home fuel burning heating devices. Carbon monoxide poisoning contributes to about 5613 deaths inhaling smoke annually in the United States. The CDC reports, "Every year, over 500 Americans die of accidental carbon monoxide poisoning, and more than 2,000 people commit suicide by deliberately poisoning themselves." For the 10-year period 1979-1988, 56,133 deaths from carbon monoxide poisoning occurred in the United States, with 25,889 people committing suicide, leaving 30,244 unintentional deaths. A report from New Zealand shows that 206 people died from carbon monoxide poisoning in 2001 and 2002. Total carbon monoxide poisoning accounts for 43.9% of deaths from poisoning in the country. In South Korea, 1,950 people have been poisoned by carbon monoxide with 254 deaths from 2001 to 2003. A report from Jerusalem showed 3.53 per 100,000 people were poisoned each year from 2001 to 2006. In Hubei, China, 218 deaths from poisoning were reported above The 10-year period with 16.5% comes from carbon monoxide exposure.
History
The earliest explanation of carbon monoxide poisoning dates from at least 200 BC by Aristotle. The documented cases of carbon monoxide were used as suicide date methods at least 100 BC in ancient Rome. In 350 AD, Roman Emperor Julian suffered carbon monoxide poisoning in Paris, and later described it in his Misopogon: "although the winter weather persisted and continued to increase in severity, yet I do not allow my slaves to heat the house, because I was afraid of removing the moisture on the wall, but I ordered them to bring a burning fire and put in the room a large amount of hot coals, but the embers, though not many of them, came out of the wall of steam and this made me fall asleep. with smoke, I almost choked and then I was taken out. "Misunderstanding about the cause of carbon monoxide poisoning has probably caused the death of Julian's successor, Jovian.
John Scott Haldane identified carbon monoxide as a deadly afterdamp constituent, a gas created by combustion, after examining the bodies of many miners killed in pit explosions. Their skin is colored cherry-pink from carboxyhaemoglobin, a stable compound that forms in the blood by reaction with gas. As a result of his research, he was able to design a respirator for rescue workers. He tested the effects of carbon monoxide on his own body in enclosed spaces, depicting his slow poisoning results. In the late 1890s, he introduced the use of small animals for miners to detect dangerous levels of harmful carbon monoxide underground, both white and walnut rats. With faster metabolism, they exhibit toxic effects before the gas levels become important to the workers, and thus give early warning of the problem. Walnut in the British hole was replaced in 1986 by an electronic gas detector.
As part of the Holocaust during World War II, Nazi Germany used van gas in the Chelmno extermination camp and elsewhere to kill about 700,000 prisoners with carbon monoxide poisoning. This method is also used in gas chambers of several death camps such as Treblinka, Sobibor and Belzec. The gas attack with carbon monoxide begins in the T4 action, the euthanasia program developed by the Nazis in Germany to kill the mentally ill and prewar disabilities begins in earnest. The gas is supplied by IG Farben in pressurized cylinders and fed by tubes to gas chambers built in various mental hospitals, such as Hartheim Euthanasia Center. Many key personnel were recruited from the T4 program to kill more people in gas cars and special gas chambers used in death camps like Treblinka. Exhaust fumes from tank engines for example, are used to supply gas to the chamber.
The use of oxygen as a treatment began in 1868. The use of hyperbaric oxygen in rats after poisoning was studied by Haldane in 1895 while its use in humans began in the 1960s.
Research
Carbon monoxide is produced naturally by the body as a by-product of converting protoporphyrin into bilirubin. This carbon monoxide also combines with hemoglobin to make carboxyhemoglobin, but not at toxic levels.
A small amount of CO is useful and there is an enzyme that produces it at the time of oxidative stress. Drugs are being developed to introduce small amounts of CO during some types of surgery, this drug is called a carbon monoxide release molecule.
References
External links
- Centers for Disease Control and Prevention (CDC) - Carbon Monoxide - NIOSH Workplace Safety and Health Topics
- International Program on Chemical Security (1999). Carbon Monoxide, Environmental Health Criteria 213, Geneva: WHO
Source of the article : Wikipedia
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