Carbon monoxide poisoning happens when people breathe in too much carbon monoxide (CO). Symptoms are often similar to the flu and may include headache, dizziness, weakness, vomiting, chest pain, and confusion. Very high levels of CO can cause loss of consciousness, irregular heartbeats, seizures, or death. The "cherry red skin" appearance is rare. Long-term effects may include tiredness, memory problems, and difficulty moving. According to the Threshold Limit Value – Time Weighted Average, humans can safely be exposed to 25 mL of CO per cubic meter for 8 hours each day over a 40-hour work week.

Carbon monoxide is a colorless and odorless gas that does not cause irritation at first. It forms when organic matter burns incompletely, such as in cooking equipment, motor vehicles, or heaters that use carbon-based fuels. Carbon monoxide mainly causes harm by joining with hemoglobin to form carboxyhemoglobin (COHb or HbCO), which stops blood from carrying oxygen and removing carbon dioxide as carbaminohemoglobin. Other proteins, such as myoglobin, Cytochrome P450, and mitochondrial cytochrome oxidase, are also affected, along with other cellular targets.

Diagnosis is usually based on HbCO levels over 3% in non-smokers and over 10% in smokers. The usual limit for carboxyhemoglobin tolerance is 15% COHb, meaning harm is seen when levels exceed this. The FDA previously set a threshold of 14% COHb in some clinical trials. In general, 30% COHb is considered severe poisoning. The highest non-fatal carboxyhemoglobin level reported was 73% COHb.

Prevention efforts include using carbon monoxide detectors, ensuring gas appliances are properly vented, keeping chimneys clean, and maintaining vehicle exhaust systems. Treatment typically involves giving 100% oxygen and supportive care until symptoms disappear and HbCO levels drop below 3% for non-smokers or 10% for smokers.

Carbon monoxide poisoning is common, causing over 20,000 emergency room visits yearly in the United States. It is the most common cause of fatal poisoning in many countries. In the U.S., non-fire-related cases cause over 400 deaths annually. Poisonings are more frequent in winter, often due to portable generators during power outages. People have known about CO's harmful effects for a long time. The discovery that hemoglobin is affected by CO began with an investigation by James Watt and Thomas Beddoes in 1793 and was later confirmed by Claude Bernard between 1846 and 1857.

Background

Carbon monoxide is not harmful to all living things, and its effects depend on the amount present, a concept known as hormesis. Small amounts of carbon monoxide are naturally created in many organisms through enzyme-driven and non-enzyme-driven reactions. It acts as a signaling molecule called a gasotransmitter and may help treat certain medical conditions. In prokaryotes, some bacteria can produce, use, and respond to carbon monoxide, while others are harmed by it. No harmful effects on plants that use photosynthesis have been found.

The dangers of carbon monoxide come from its strong binding to the heme group in hemoproteins, which disrupts cell functions. For example, it binds to hemoglobin to form carboxyhemoglobin, blocking oxygen transport and cellular respiration. Breathing large amounts of carbon monoxide can cause oxygen deprivation, brain damage, and death.

Research by Esther Killick shows that different species and people may tolerate carbon monoxide differently. A person’s tolerance depends on factors such as genetics (like hemoglobin changes), activity levels, breathing rate, pre-existing heart or brain conditions, blood flow, anemia, sickle cell disease, geography, air pressure, and metabolism.

Carbon monoxide is naturally produced through many biological reactions, such as when the enzyme heme oxygenase breaks down heme into biliverdin and bilirubin. Most carbon monoxide in the body is stored as carboxyhemoglobin at safe levels below 3% HbCO.

Small amounts of carbon monoxide can be helpful, and enzymes create it during times of stress. Scientists are developing drugs called carbon monoxide-releasing molecules to use its benefits. In the past, researchers like Thomas Beddoes, James Watt, Tiberius Cavallo, James Lind, and Humphry Davy studied the medical uses of carbon monoxide in institutions such as the Pneumatic Institution.

Signs and symptoms

Carbon monoxide exposure at 100 parts per million (ppm) or higher is harmful to human health. The World Health Organization (WHO) states that the highest safe level of carbon monoxide in indoor air over 24 hours is 4 milligrams per cubic meter (mg/m³), which equals 3.5 ppm at 20°C. For short-term exposure, levels should not exceed 10 mg/m³ (8.7 ppm at 20°C) in 8 hours, 35 mg/m³ (31 ppm at 20°C) in 1 hour, or 100 mg/m³ (87 ppm at 20°C) in 15 minutes.

Carbon monoxide poisoning affects organs that rely heavily on oxygen, such as the brain and heart. Early signs of acute poisoning include headache, nausea, tiredness, and a general feeling of illness. These symptoms may be mistaken for illnesses like the flu or food poisoning. Headache is the most common symptom and is often described as dull, continuous, and located in the forehead. Prolonged exposure can cause heart problems, such as a fast heartbeat, low blood pressure, and irregular heartbeats. Brain-related symptoms include confusion, dizziness, difficulty walking, seizures, unconsciousness, and even death. Other possible effects are heart muscle damage, irregular heart rhythms, lung issues, high blood sugar, muscle damage, kidney failure, skin sores, and vision or hearing problems. Long-term heart damage from carbon monoxide exposure may reduce lifespan.

After acute poisoning, some people may experience delayed neurological issues, such as trouble with thinking, memory loss, confusion, and mood changes. These problems can appear up to 40 days after poisoning and may affect up to half of those poisoned. Factors like older age, loss of consciousness during poisoning, and initial brain or nerve issues may increase the risk of delayed problems.

Long-term exposure to low levels of carbon monoxide can cause ongoing headaches, dizziness, depression, confusion, memory loss, nausea, hearing issues, and vomiting. It is unclear if low-level exposure causes permanent brain damage. Symptoms often improve after leaving the exposure, unless severe poisoning occurred. One case showed lasting memory and learning problems after three years of exposure to low carbon monoxide levels from a faulty furnace.

Long-term exposure may worsen heart conditions and increase the risk of hardening of the arteries (atherosclerosis). People with heart disease or pregnant women are at higher risk from long-term exposure.

In animal studies, carbon monoxide may worsen hearing loss caused by loud noises. In humans, hearing loss has been reported after carbon monoxide poisoning, even without loud noise exposure.

A classic sign of carbon monoxide poisoning is a red, healthy-looking appearance, often seen in people who have died. However, this "cherry-red" look is not useful for diagnosing living patients. During autopsies, dead people poisoned by carbon monoxide may appear unusually lifelike in color, unlike the usual pale or blue appearance of non-poisoned dead individuals. This red color is similar to how carbon monoxide is used to preserve meat in the food industry.

Epidemiology

The exact number of carbon monoxide poisoning cases is unknown because many mild cases are not noticed. Based on available information, carbon monoxide poisoning is the leading cause of injury and death from poisoning worldwide. Poisoning is more common during winter months because people use more gas furnaces, gas or kerosene heaters, and kitchen stoves indoors. If these devices are broken or not used properly, they can produce dangerous levels of carbon monoxide. Poisoning and detection also increase during power outages when people may use fuel-burning heaters, stoves, or grills indoors, even if these are meant for outdoor use only.

In the United States, more than 40,000 people visit doctors each year for carbon monoxide poisoning. In Australia, 95% of carbon monoxide poisoning deaths are linked to gas space heaters. In many developed countries, carbon monoxide causes more than half of all fatal poisonings. In the United States, about 200 people die yearly from carbon monoxide poisoning related to home heating equipment. Carbon monoxide poisoning contributes to about 5,613 smoke inhalation deaths each year in the United States. The CDC reports that over 500 Americans die yearly from accidental carbon monoxide poisoning, and more than 2,000 die from intentional poisoning. Between 1979 and 1988, 56,133 carbon monoxide poisoning deaths occurred in the United States, with 25,889 being suicides and 30,244 accidental. In New Zealand, 206 people died from carbon monoxide poisoning in 2001 and 2002, which was 43.9% of all poisoning deaths in the country. In South Korea, 1,950 people were poisoned by carbon monoxide between 2001 and 2003, with 254 deaths. In Jerusalem, 3.53 people per 100,000 were poisoned yearly from 2001 to 2006. In Hubei, China, 218 poisoning deaths were reported over 10 years, with 16.5% caused by carbon monoxide.

Carbon monoxide is produced when organic materials burn with limited oxygen, preventing complete conversion to carbon dioxide (CO₂). Sources include cigarette smoke, house fires, faulty furnaces, heaters, wood stoves, vehicle exhaust, generators, propane equipment, and gasoline-powered tools. Exposure often occurs when these devices are used indoors or in small spaces.

Children have been poisoned by riding in the back of pickup trucks. People have been poisoned when car exhaust pipes are blocked by snow. Exhaust gases can enter a vehicle’s cabin if there is a leak between the exhaust manifold and shroud. Generators and boat engines, especially on houseboats, have caused fatal carbon monoxide exposure.

Poisoning can also occur from using a self-contained underwater breathing apparatus (SCUBA) if the diving air compressor is faulty. In caves, carbon monoxide can build up in enclosed spaces due to decomposing organic matter. In coal mines, incomplete combustion during explosions can produce afterdamp, a gas with up to 3% carbon monoxide that can be deadly after one breath. After an explosion, connected mines may become dangerous due to afterdamp spreading between them, as seen in the Trimdon Grange explosion, which killed miners in the Kelloe mine.

Another source is exposure to dichloromethane, a chemical in some paint strippers. The body converts this chemical into carbon monoxide. In November 2019, the U.S. Environmental Protection Agency banned dichloromethane in consumer paint strippers.

Preventing carbon monoxide poisoning is a key public health goal. This includes educating people about safely using appliances, heaters, fireplaces, and engines, as well as installing carbon monoxide detectors. Carbon monoxide is tasteless, odorless, and colorless, so it cannot be detected by sight or smell.

The U.S. Consumer Product Safety Commission says carbon monoxide detectors are as important as smoke detectors. It recommends at least one detector per home, ideally on each floor. These devices are affordable and available in battery- or AC-powered models, with or without backup batteries. They are usually placed near heaters or other equipment. When carbon monoxide levels rise, the detector sounds an alarm, allowing people to leave and ventilate the area. Unlike smoke detectors, carbon monoxide detectors do not need to be placed near the ceiling.

Carbon monoxide detectors are now standard in many areas. In the U.S., NFPA 720–2009, a guideline by the National Fire Protection Association, requires detectors on every floor of a home, including basements, and outside sleeping areas. New homes must have AC-powered detectors with battery backup and interconnected systems for early warnings. These guidelines also apply to schools, hospitals, and other buildings.

Gas companies often advise having gas appliances checked yearly. While NFPA standards are not always laws, some areas, like Massachusetts, require detectors in all homes with potential carbon monoxide sources. This rule was created after a child died from a blocked heating vent. Other places may not have laws or only require detectors for new homes or during sales.

The following exposure limits (rounded values) ensure carboxyhemoglobin (COHb) levels do not exceed 2.5%, even during light or moderate activity:

• 100 mg/m³ (87 ppm) for 15 minutes
• 60 mg/m³ (52 ppm) for 30 minutes
• 30 mg/m³ (26 ppm) for 1 hour
• 10 mg/m³ (9 ppm) for 8 hours
• 7 mg/m³ (6 ppm) for 24 hours (for indoor air quality, to avoid exceeding 2% COHb from long-term exposure).

Diagnosis

Carbon monoxide poisoning can be hard to diagnose because its symptoms often resemble those of other illnesses or infections, such as the flu. A history of possible carbon monoxide exposure, like being near a fire, may suggest poisoning, but the diagnosis is confirmed by measuring carbon monoxide levels in the blood. This is done by comparing the amount of carboxyhemoglobin (a substance formed when carbon monoxide binds to hemoglobin) to the total hemoglobin in the blood.

In healthy people, carboxyhemoglobin levels may be up to 5%, while heavy smokers may reach up to 9%. People who are sick from carbon monoxide poisoning often have levels between 10% and 30%. Those who die from poisoning may have levels as high as 30% to 90% after death.

Even after carboxyhemoglobin levels return to normal, some people may still feel symptoms of poisoning. A normal carboxyhemoglobin level found during a late-stage examination does not always rule out poisoning.

Carbon monoxide levels in blood can be measured using laboratory methods like spectrophotometry or chromatography to confirm poisoning or help with forensic investigations. A CO-oximeter is a device that measures carboxyhemoglobin levels. Pulse CO-oximeters use a non-invasive finger clip, similar to a pulse oximeter, to estimate carboxyhemoglobin by passing light through the fingertip and measuring how different types of hemoglobin absorb the light. Regular pulse oximeters are not effective for diagnosing carbon monoxide poisoning because they cannot distinguish carboxyhemoglobin from oxyhemoglobin. Breath CO monitoring is another method, but it requires the person to inhale deeply and hold their breath to release carbon monoxide from the blood into the lungs. This is not possible for unresponsive individuals, making these devices less useful in emergency situations.

Many conditions must be considered when diagnosing carbon monoxide poisoning. Early symptoms, especially from low-level exposure, are often unclear and may be mistaken for other illnesses, such as flu-like viral infections, depression, chronic fatigue syndrome, chest pain, or headaches. Carbon monoxide is sometimes called a "great mimicker" because its symptoms vary and are not specific. Other conditions that may be considered include acute respiratory distress syndrome, altitude sickness, lactic acidosis, diabetic ketoacidosis, meningitis, methemoglobinemia, or poisoning from opioids or toxic alcohols.

Treatment

The first step in treating carbon monoxide poisoning is to move the affected person away from the source of exposure as quickly as possible, ensuring no one else is harmed. If the person is unconscious, cardiopulmonary resuscitation (CPR) may be needed at the scene. Giving oxygen through a non-rebreather mask reduces the time it takes for carbon monoxide to leave the body. When breathing normal air, carbon monoxide has a half-life of 320 minutes, but with oxygen, this time shortens to 80 minutes. Oxygen helps carbon monoxide separate from carboxyhemoglobin, allowing hemoglobin to return to its normal state. Because carbon monoxide poisoning can harm a baby, pregnant women are given oxygen for longer periods than non-pregnant individuals.

Hyperbaric oxygen therapy is sometimes used to treat carbon monoxide poisoning. This treatment increases the speed at which carbon monoxide separates from carboxyhemoglobin and cytochrome oxidase more than regular oxygen. At three times normal atmospheric pressure, hyperbaric oxygen reduces the half-life of carbon monoxide to 23 minutes, compared to 80 minutes with regular oxygen. Hyperbaric oxygen may also help deliver oxygen to tissues through plasma, bypassing the usual process involving hemoglobin. However, it is unclear whether hyperbaric oxygen provides additional benefits beyond regular high-flow oxygen in terms of survival or long-term recovery. Some studies suggest hyperbaric oxygen improves outcomes, while others find no difference. These studies have been criticized for methodological issues. A review of all available research concluded that the effectiveness of hyperbaric oxygen remains uncertain. Experts recommend a large, well-designed study to compare hyperbaric oxygen with regular oxygen. While hyperbaric oxygen is used for severe cases, its advantages over standard oxygen are not fully proven.

Other complications, such as seizures, low blood pressure, heart problems, fluid buildup in the lungs, and acidosis, may require additional treatment. Low blood pressure is treated with intravenous fluids, and vasopressors may be used for heart muscle weakness. Heart rhythm issues are managed with standard advanced cardiac life support protocols. Severe acidosis may be treated with sodium bicarbonate, though this is debated because acidosis might increase oxygen availability to tissues. In some cases, oxygen therapy alone may be sufficient for acidosis. Delayed brain damage, confirmed through MRI or CAT scans, is a serious complication of carbon monoxide poisoning. Long-term follow-up and supportive care are often needed for neurological damage. Outcomes are hard to predict, especially for individuals who experience cardiac arrest, coma, acidosis, or have high carboxyhemoglobin levels. One study found that about 30% of people with severe carbon monoxide poisoning die. Electroconvulsive therapy (ECT) may increase the risk of delayed neurological problems after poisoning. A device that releases carbon dioxide to encourage faster breathing (called ClearMate) may also be used.

Pathophysiology

The exact ways carbon monoxide harms the body are not fully understood. However, some known effects include carbon monoxide attaching to hemoglobin, myoglobin, and a mitochondrial enzyme called cytochrome c oxidase. This attachment reduces the amount of oxygen that can reach the body’s tissues. It also causes damage to brain lipids through a process called lipid peroxidation.

Carbon monoxide spreads more easily in the body than oxygen. The main source of carbon monoxide in the human body is an enzyme called heme oxygenase, which is found in most cells and platelets. Most carbon monoxide produced naturally in the body binds to hemoglobin, forming a compound called carboxyhemoglobin. A simple explanation for carbon monoxide’s harmful effects is that high levels of carboxyhemoglobin reduce the blood’s ability to carry oxygen to tissues. Hemoglobin has a much stronger bond with carbon monoxide than with oxygen—about 240 times stronger. Some genetic changes, like the Hb-Kirklareli mutation, make hemoglobin bind carbon monoxide even more strongly, up to 80,000 times stronger than oxygen. This can lead to carboxyhemoglobin levels as high as 16% in the blood.

Hemoglobin is a protein made of four parts, each containing a heme group that binds oxygen. Each red blood cell has about 250 million hemoglobin molecules, meaning each cell has around 1 billion sites where oxygen can attach. When carbon monoxide binds to one of these sites, it increases the bond between hemoglobin and oxygen at the other sites. This causes hemoglobin to hold onto oxygen instead of releasing it to tissues, which can be as harmful as if carbon monoxide had bound to all sites. Oxygen delivery is influenced by two processes called the Bohr effect and Haldane effect. When oxygen is inhaled, it binds to hemoglobin, causing a shape change that allows more oxygen to attach to other sites. When blood reaches tissues, oxygen is released because the local environment becomes more acidic, a result of carbon dioxide being converted to carbonic acid. Oxygen-rich blood (arterial blood) has a slightly higher pH (about 7.407) than oxygen-poor blood (venous blood, about 7.371). This pH difference helps hemoglobin release oxygen. When blood returns to the lungs, carbon dioxide is exhaled, reducing acidity and allowing hemoglobin to rebind oxygen. Carbon monoxide does not release from hemoglobin in acidic environments, so it remains attached. This causes venous blood in poisoned individuals to appear bright red, like arterial blood, instead of the usual dark red of deoxygenated blood.

At high levels, carboxyhemoglobin interferes with oxygen use by blocking oxygen delivery to cells and reducing the formation of carbaminohemoglobin, which helps carry carbon dioxide. This can lead to severe oxygen shortages (hypoxia) and acid buildup (acidosis) in the body. Carbon monoxide also binds to myoglobin, a protein in muscles that stores oxygen. It binds to myoglobin about 60 times more strongly than oxygen, which can reduce muscle oxygen use, lower heart output, and cause low blood pressure. This may lead to brain oxygen shortages (ischemia). Symptoms can sometimes return later due to delayed release of carbon monoxide from myoglobin, which then binds to hemoglobin again.

Carbon monoxide also affects the mitochondria, the energy-producing parts of cells. It binds to cytochrome c oxidase, an enzyme needed for energy production, but not as strongly as oxygen. This binding disrupts energy production, forcing cells to switch to less efficient processes that produce lactic acid and lower oxygen levels. This can lead to cell death. Carbon monoxide stays attached to cytochrome c oxidase for a long time, prolonging these effects.

Another effect involves blood cells and chemicals that cause damage to brain lipids. Carbon monoxide triggers the release of nitric oxide and oxygen-free radicals like peroxynitrite. These chemicals harm brain mitochondria, cause blood vessel leaks, and lead to cell death in the brain. This damage results in lipid peroxidation, which can cause delayed brain issues like Grinker myelinopathy, a condition where brain white matter is damaged. This may lead to memory and learning problems, movement disorders, and damage to brain areas like the white matter, globus pallidus, cerebellum, hippocampus, and cerebral cortex.

In pregnant women, carbon monoxide poisoning can harm the fetus. It reduces oxygen delivery from the mother to the fetus and crosses the placenta to bind with fetal hemoglobin, causing more severe oxygen shortages in the fetus. Fetal hemoglobin has a slightly higher affinity for carbon monoxide than adult hemoglobin, making the fetus more vulnerable. Carbon monoxide is also removed more slowly from the fetus, increasing its buildup. This can lead to serious harm or death in the fetus.

History

Humans have had a complicated relationship with carbon monoxide since they first learned to control fire around 800,000 BC. Early humans may have discovered the dangers of carbon monoxide when they used fire in their homes. The development of metalworking and smelting technologies during the Bronze Age (around 6,000 BC) also exposed people to carbon monoxide. In addition to its toxic effects, some Native American groups may have experienced the effects of carbon monoxide on the nervous system during spiritual fire rituals.

Early civilizations created myths to explain the origin of fire, such as the Greek gods Vulcan, Pkharmat, and Prometheus, who brought fire to humans. Aristotle (384–322 BC) was the first to record that burning coals produce toxic fumes. A Greek doctor named Galen (129–199 AD) suggested that changes in air composition caused harm when inhaled. Symptoms of carbon monoxide poisoning were described in writings from around 130 AD by Cassius Iatrosophista. Other ancient writers, such as Julian the Apostate and Caelius Aurelianus, also noted signs of carbon monoxide poisoning caused by coal fumes.

Historical records mention that carbon monoxide was used for suicide in ancient Rome. Emperor Lucius Verus used smoke to kill prisoners. Many deaths have been linked to carbon monoxide poisoning, including Emperor Jovian, Empress Fausta, and Seneca. The most famous death possibly caused by carbon monoxide poisoning may have been Cleopatra or Edgar Allan Poe.

In the 1500s, coal miners believed sudden deaths were caused by evil spirits. Carbon monoxide poisoning was often linked to supernatural beliefs, witchcraft, and other paranormal ideas for centuries, including in modern times, as seen in investigations by Carrie Poppy.

In 1697, Georg Ernst Stahl referred to toxic vapors as "carbonarii halitus," which may have been carbon monoxide. Friedrich Hoffmann conducted the first scientific study of carbon monoxide poisoning from coal in 1716, rejecting the idea that deaths were caused by demons. Herman Boerhaave tested the effects of carbon monoxide on animals in the 1730s. Joseph Priestley first created carbon monoxide in 1772, calling it "heavy inflammable air," and Carl Wilhelm Scheele isolated it from coal in 1773, identifying it as the toxic substance.

In the late 1790s, scientists like Thomas Beddoes and James Watt studied the risks of carbon monoxide poisoning, focusing on how it affects the body when inhaled. These studies often took place at the Pneumatic Institution.

In 1800, William Cruickshank discovered that carbon monoxide is made of one carbon atom and one oxygen atom, marking the start of modern research on the gas. James Watt first suggested how carbon monoxide causes harm in 1793. Later, Adrien Chenot and Claude Bernard confirmed this mechanism in the mid-1800s.

The first controlled study on carbon monoxide poisoning was conducted in 1973.

Carbon monoxide has harmed coal miners for centuries. In mining, it is known as "whitedamp." John Scott Haldane identified carbon monoxide as the deadly part of "afterdamp," a gas from fires, after examining miners who died in explosions. By 1911, Haldane introduced using small animals like canaries to detect dangerous carbon monoxide levels underground. Canaries were replaced by electronic gas detectors in 1986.

In 1858, Felix Hoppe-Seyler developed the first method to detect carboxyhemoglobin using color changes. In 1880, Josef von Fodor created the first method to measure its levels.

Oxygen was first used to treat carbon monoxide poisoning in the late 1700s. In 1799, Humphry Davy was treated with oxygen after inhaling toxic fumes. In 1814, Samuel Witter created an oxygen treatment plan for carbon monoxide poisoning. Oxygen was also used for malaria in 1830 because its symptoms matched those of carbon monoxide poisoning. Hyperbaric oxygen therapy was tested on rats in 1895 and later used on humans in the 1960s.

The worst carbon monoxide disaster was the Balvano train disaster in 1944, Italy, when a train carrying illegal passengers stalled in a tunnel, killing over 500 people.

Over 50 people died from smoke inhalation during the Branch Davidian Massacre in 1993.

On December 14, 2024, 12 people died from carbon monoxide poisoning in Gudauri, Georgia, after fuel oil generators were placed in a closed area near their rooms.

In ancient times, Hannibal used coal fumes to kill Roman prisoners during the Second Punic War.

In 1874, stray dogs were killed using a carbon monoxide gas chamber. In 1884, an article in Scientific American described using carbon monoxide gas chambers for slaughtering animals and euthanasia.

During World War II, the Nazis used carbon monoxide gas in gas vans at Chelmno and other extermination camps to kill over 700,000 people. This method was also used in gas chambers at Treblinka, Sobibor, and Belzec. Carbon monoxide was first used in the Holocaust during "Action T4," where IG Farben supplied the gas in pressurized tanks to mental hospitals like Hartheim Euthanasia Centre. Exhaust fumes from military vehicles were also used to supply gas to the chambers.