Carbon monoxide poisoning explained

Carbon monoxide poisoning

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, and CO poisoning is 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, heart and even death. 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 early detection with the use of household carbon monoxide detectors.


Common sources of CO that may lead to poisoning include house fires, furnaces or heaters, wood-burning stoves, motor vehicle exhaust, propane-fueled equipment such as portable camping stoves, ice resurfacers,[3] forklifts,[4] and gasoline-powered tools such as high-pressure washers, concrete cutting saws, power trowels, floor buffers, and welders used in buildings or semi-enclosed spaces.[5] CO poisoning can also occur in scuba diving due to faulty or badly sited diving air compressors. Generators and propulsion engines on boats, especially houseboats, have resulted in fatal carbon monoxide exposures.[6] Another source is exposure to the organic solvent methylene chloride, which is metabolized to CO by the body.[7]

0.1 ppmNatural background atmosphere level (MOPITT)
0.5 to 5 ppmAverage background level in homes[8]
5 to 15 ppmLevels near properly adjusted gas stoves in homes
100 to 200 ppmMexico City central area from automobiles[9]
5,000 ppmChimney of a home wood fire[10]
7,000 ppmUndiluted warm car exhaust
30,000 ppmUndiluted cigarette smoke


Early symptoms of carbon monoxide poisoning such as headaches, nausea, and fatigue, are often mistaken for the flu because the deadly gas goes undetected in a home. Prolonged exposure can lead to brain damage and even death.


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. 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.[11]

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, which can even occur in those accidentally exposed who do not have pre-existing depression.[12] 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.


Long term, repeated exposures present a greater risk to persons with coronary heart disease and in pregnant patients.[13] 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/vomiting. Upon removal from exposure, the symptoms usually resolve themselves.[14]


Carbon monoxide is a significantly toxic gas, although patients may demonstrate varied clinical manifestations with different outcomes, even under similar exposure conditions.[15] [16] 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.

Carbon monoxide is life-threatening to humans and other aerobic forms of 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. One report concluded that carbon monoxide exposure can lead to significant loss of lifespan after exposure due to damage to the heart muscle.[17]

The effects produced by carbon monoxide in relation to ambient concentration 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
1,600 ppm (0.16%)Dizziness, nausea, and convulsions within 45 minutes. Insensible within 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.


The precise mechanisms by which toxic effects are induced by CO are not fully understood. Known mechanisms include carbon monoxide binding to hemoglobin reducing oxygen transportation, binding to myoglobin decreasing its oxygen storage capacity, and binding to mitochondrial cytochrome oxidase inhibiting cellular respiration.


Carbon monoxide has a significant affinity to the iron sites in hemoglobin, the principal oxygen-carrying compound in blood. The affinity between hemoglobin and carbon monoxide is about 230 times stronger than the affinity between hemoglobin and oxygen.[18] CO binds to hemoglobin, producing carboxyhemoglobin (COHb); the traditional belief is that carbon monoxide toxicity arises from the formation of carboxyhemoglobin, which decreases the oxygen-carrying capacity of the blood. This inhibits the transport, delivery, and utilization of oxygen.[19]

Because hemoglobin is a tetramer with four oxygen binding sites, binding of CO at one of these sites also increases the oxygen affinity of the remaining 3 sites, which interferes with normal release of oxygen. This causes hemoglobin to retain oxygen that would otherwise be delivered to the tissue.[20] Levels of oxygen available for tissue use are decreased. This situation is described as CO shifting the oxygen dissociation curve to the left. Blood oxygen content is actually increased in the case of carbon monoxide poisoning; because all the oxygen is in the blood, none is being given to the tissues, and this causes tissue hypoxic injury. However, despite CO affecting oxygen availability, other mechanisms may contribute to the crucial effects of CO poisoning.

A sufficient exposure to carbon monoxide can reduce the amount of oxygen taken up by the brain to the point that the victim becomes unconscious, and can suffer brain damage or even death from hypoxia. The brain regulates breathing based upon carbon dioxide levels in the blood, rather than oxygen levels, so a victim can succumb to hypoxia without ever noticing anything up to the point of collapse. Hallmark pathological change following CO poisoning is bilateral necrosis of the pallidum.

Hemoglobin acquires a bright red color when converted to carboxyhemoglobin, so a casualty of CO poisoning is described in textbooks as looking pink-cheeked and healthy. However, this "classic" cherry-red appearance is not always seen in living patients.[21] Care should be taken not to overlook the diagnosis even if this color is not present.


Carbon monoxide also has a high affinity for myoglobin. CO bound to myoglobin may impair cardiac output and result in cerebral ischemia. A delayed return of symptoms has been reported and appears to result following a recurrence of increased carboxyhemoglobin levels; this effect may be due to late release of CO from myoglobin, which subsequently binds to hemoglobin.[1]

Cytochrome oxidase

A second mechanism involves co-effects on the mitochondrial respiratory enzyme chain that is responsible for effective tissue utilization of oxygen. CO does not bind to cytochrome oxidase with the same affinity as oxygen, so it likely requires significant intracellular hypoxia before binding. This binding interferes with aerobic metabolism and efficient adenosine triphosphate (ATP) synthesis. Cells respond by switching to anaerobic metabolism, causing anoxia, lactic acidosis, and eventual cell death.[22]

Other mechanisms

Another mechanism that is thought to have a significant influence on delayed effects involves formed blood cells and chemical mediators, which cause brain lipid peroxidation. CO causes endothelial cell and platelet release of nitric oxide, and the formation of oxygen free radicals including peroxynitrite. In the brain, this causes further mitochondrial dysfunction, capillary leakage, leukocyte sequestration, and apoptosis.[23] The end result is lipid peroxidation (degradation of unsaturated fatty acids), which causes delayed reversible demyelinization of white matter in the central nervous system, and can lead to edema and focal areas of necrosis within the brain.[20]

This brain damage occurs mainly during the recovery period and results in cognitive defects (especially affecting memory and learning) and movement disorders. The movement disorders are related to a predilection of CO to damage the basal ganglia.[23] These delayed neurological effects may develop over days following the initial acute poisoning.


Carbon monoxide poisoning can have significant fetal effects. CO causes fetal tissue hypoxia by decreasing the release of maternal oxygen to the fetus, and by carbon monoxide crossing the placenta and combining with fetal hemoglobin, which has a 10 to 15% higher affinity for CO than adult hemoglobin.[1] Elimination of carbon monoxide is also slower in the fetus, leading to an accumulation of CO. The level of fetal morbidity and mortality in acute carbon monoxide poisoning is significant, so despite maternal wellbeing, severe fetal poisoning can still occur. Due to these effects, pregnant patients are treated with normal or hyperbaric oxygen for longer periods of time than non-pregnant patients.


Diagnosis is usually performed by measuring levels of carbon monoxide found in the blood. This 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%.[24]

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.[25] 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.[26]

The use of a pulse oximeter is not effective in the diagnosis of carbon monoxide poisoning. A patient who is suffering from carbon monoxide poison will most likely have a normal SpO2 reading.

Differential diagnosis

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, chest pain, and migraine or other headaches.[27] This often makes the diagnosis of carbon monoxide poisoning difficult.


Prevention remains a vital public health issue, requiring public education on the safe operation of appliances, heaters, fireplaces, and internal-combustion engines, as well as increased emphasis on the installation of carbon monoxide detectors. Carbon monoxide alarms are usually installed in homes around heaters and other equipment. If a high level of CO is detected, the device sounds an alarm, giving people in the area a chance to ventilate the area or safely leave the building. Unlike smoke detectors, they do not need to be placed near ceiling level. The Consumer Product Safety Commission says that "carbon monoxide detectors are as important to home safety as smoke detectors are," and recommends that each home should have at least one carbon monoxide detector.

The 2009 edition of NFPA 720, the carbon monoxide detector guidelines published by the National Fire Protection Association (NFPA),[28] mandates the placement of carbon monoxide detectors/alarms on every level of the residence, including the basement, in addition to outside sleeping areas. In new homes, electrically powered CO detectors must have battery backup and be interconnected to assure early warning of occupants at all levels.

NFPA 720-2009 is also the first national carbon monoxide standard to address CO devices in non-residential buildings.[29] These guidelines, which now pertain to schools, healthcare centers, nursing homes and more, include three main points: 1) A secondary power supply must operate all carbon monoxide notification appliances for at least 12 hours, 2) CO detectors must be on the ceiling in the same room as permanently installed fuel-burning appliances, 3) CO detectors must be located on every habitable level and in every HVAC zone of the building.

CO devices, which retail for USD$20-$60 and are widely available, can either be battery-operated or AC powered (with or without a battery backup). Since CO is colorless and odorless (unlike smoke from a fire), detection in a home environment is impossible without such a warning device. Some state and municipal governments, including those of Ontario, Canada, and New York City, require installation of CO detectors in new units. Massachusetts and Illinois began to require a detector in all residences on January 1, 2007.[30] [31]

As of October 2008, more than a dozen U.S. states had passed state legislation regarding CO, and bills were pending in other states [32] . CO legislation on the county and municipal level does exist in some states that do not yet have state-wide legislation. State and local laws regarding detector installation and the types of occupancies (such as private homes, schools, medical centers, etc.) that must install these devices vary greatly.[33]


First aid for carbon monoxide poisoning is to immediately remove the victim from the exposure without endangering oneself and obtaining medical treatment. Patients who are unconscious may require CPR on site.

The main medical treatment for carbon monoxide poisoning is administering 100% oxygen by a tight fitting oxygen mask. Oxygen hastens the dissociation of carbon monoxide from hemoglobin, improving tissue oxygenation by reducing its biological half-life. Hyperbaric oxygen is also used in the treatment of CO poisoning; hyperbaric oxygen also increases carboxyhemoglobin dissociation and does so to a greater extent than normal oxygen. Hyperbaric oxygen may also facilitate the dissociation of CO from cytochrome oxidase.

A significant controversy in the medical literature is whether or not hyperbaric oxygen actually offers any extra benefits over normal high flow oxygen in terms of increased survival or improved long term outcomes. There have been clinical trials[26] [34] [35] [36] [37] [38] in which the two treatment options have been compared; of the six performed, four found hyperbaric oxygen improved outcome and two found no benefit for hyperbaric oxygen. Some of these trials have been criticized for apparent flaws in their implementation.[39] [40] [41] A recent robust review of all the literature on carbon monoxide treatment concluded that the role of hyperbaric oxygen is unclear and the available evidence neither confirms nor denies a clinically meaningful benefit. The authors suggested a large, well designed, externally audited, multicentre trial to compare normal oxygen with hyperbaric oxygen.[2]

Further specific treatment for other complications such as seizure, cardiac abnormalities, pulmonary edema, and acidosis may be required. The delayed development of neuropsychiatric impairment is one of the most serious complications of poisoning, with extensive follow up and treatment often being required.


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.[42] 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.[43] 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."[44]


As other poisons such as cyanide and arsenic were placed under increasingly stringent legal restrictions, town gas, with its high levels of carbon monoxide, became a common method of suicide by poisoning. Suicide has often been committed by inhaling the exhaust fumes of a running car engine, particularly in an enclosed space such as a garage. In the past, motor car exhaust may have contained up to 25% carbon monoxide; but newer cars have catalytic converters, which can eliminate over 99% of carbon monoxide produced.[45] However, even cars with catalytic converters can produce substantial carbon monoxide if an idling car is left in an enclosed space.

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.[46] 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.[47]

Carbon monoxide poisoning and "haunted houses"

Symptoms of carbon monoxide poisoning include listlessness, depression, dementia, emotional disturbances, and hallucinations. Many of the phenomena generally associated with haunted houses, including strange visions and sounds, feelings of dread, illness, and the sudden, apparently inexplicable death of all the occupants, can be readily attributed to carbon monoxide poisoning.

In one famous case, carbon monoxide poisoning was clearly identified as the cause of an alleged haunting. Dr. William Wilmer, an ophthalmologist, described the experiences of one of his patients in a 1921 article published in the American Journal of Ophthalmology. "Mr. and Mrs. H." moved into a new home, but soon began to complain of headaches and fatigue. They began to hear bells and footsteps during the night, accompanied by strange physical sensations and sightings of mysterious figures. When they began to investigate the symptoms, they discovered the previous residents of the house had similar experiences. An examination of their furnace found it to be severely damaged, resulting in incomplete combustion and forcing most of the fumes, including carbon monoxide, into the house rather than up the chimney.[48]

A report published in 2005 described a 23-year old female victim of carbon monoxide poisoning, found delirious and hyperventilating, who saw a "ghost" while in the shower. A new gas water heater had just been installed in her home, apparently improperly, which flooded the house with carbon monoxide when the victim closed all the exterior windows and doors and took a shower.[49]

See also

External links

Notes and References

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  29. NFPA 720: Standard for the Installation of Carbon Monoxide (CO) Detection and Warning Equipment, 2009 Edition,
  30. Massachusetts General Laws, Chapter 148, Section 26F 1/2. Also known as "Nicole's Bill". Enacted November 4, 2005.
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