- Carbon monoxide poisoning
Carbon monoxide poisoning Classification and external resources
Spacefilling model of a carbon monoxide molecule
ICD-10 T58 ICD-9 986 DiseasesDB 2020 MedlinePlus 002804 eMedicine emerg/817 MeSH C21.613.455.245
Carbon monoxide poisoning occurs after enough inhalation of carbon monoxide (CO). Carbon monoxide is a toxic gas, but, being colorless, odorless, tasteless, and initially non-irritating, it is very difficult for people to detect. Carbon monoxide is a product of incomplete combustion of organic matter due to insufficient oxygen supply to enable complete oxidation to carbon dioxide (CO2). It is often produced in domestic or industrial settings by older motor vehicles and other gasoline-powered tools, heaters, and cooking equipment. Exposures at 100 ppm or greater can be dangerous to human health.
Symptoms of mild acute poisoning include lightheadedness, confusion, headaches, vertigo, and flu-like effects; larger exposures can lead to significant toxicity of the central nervous system and heart, and even death. Following acute poisoning, long-term sequelae often occur. Carbon monoxide can also have severe effects on the fetus of a pregnant woman. Chronic exposure to low levels of carbon monoxide can lead to depression, confusion, and memory loss. Carbon monoxide mainly causes adverse effects in humans by combining with hemoglobin to form carboxyhemoglobin (HbCO) in the blood. This prevents oxygen binding to hemoglobin, reducing the oxygen-carrying capacity of the blood, leading to hypoxia. Additionally, myoglobin and mitochondrial cytochrome oxidase are thought to be adversely affected. Carboxyhemoglobin can revert to hemoglobin, but the recovery takes time because the HbCO complex is fairly stable.
Treatment of poisoning largely consists of administering 100% oxygen or providing hyperbaric oxygen therapy, although the optimum treatment remains controversial. Oxygen works as an antidote as it increases the removal of carbon monoxide from hemoglobin, in turn providing the body with normal levels of oxygen. The prevention of poisoning is a significant public health issue. Domestic carbon monoxide poisoning can be prevented by early detection with the use of household carbon monoxide detectors. Carbon monoxide poisoning is the most common type of fatal poisoning in many countries. Historically, it was also commonly used as a method to commit suicide, usually by deliberately inhaling the exhaust fumes of a running car engine. Modern cars with electronically controlled combustion and catalytic converters produce so little carbon monoxide that this is much less viable. Carbon monoxide poisoning has also been implicated as the cause of apparent haunted houses. Symptoms such as delirium and hallucinations have led people suffering poisoning to think they have seen ghosts or to believe their house is haunted.
- 1 Signs and symptoms
- 2 Causes
- 3 Pathophysiology
- 4 Diagnosis
- 5 Prevention
- 6 Treatment
- 7 Epidemiology
- 8 Society and culture
- 9 References
- 10 See also
Signs and symptoms
Carbon monoxide is toxic to all aerobic forms of life. It is easily absorbed through the lungs. Carbon monoxide is colorless, odorless, tasteless, and non-irritating, which makes it difficult for humans to detect. Inhaling even relatively small amounts of the gas can lead to hypoxic injury, neurological damage, and even death. Different people and populations may have a different carbon monoxide tolerance level. On average, exposures at 100 ppm or greater is dangerous to human health. In the United States, the OSHA limits long-term workplace exposure levels to less than 50 ppm averaged over an 8-hour period; in addition, employees are to be removed from any confined space if an upper limit ("ceiling") of 100 ppm is reached. Carbon monoxide exposure may lead to a significantly shorter life span due to heart damage. The carbon monoxide tolerance level for any person is altered by several factors, including activity level, rate of ventilation, a pre-existing cerebral or cardiovascular disease, cardiac output, anemia, sickle cell disease and other hematological disorders, barometric pressure, and metabolic rate.
Concentration Symptoms 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; loss of judgment 400 ppm (0.04%) Frontal headache within one to two hours 800 ppm (0.08%) Dizziness, nausea, and convulsions within 45 min; insensible within 2 hours 1,600 ppm (0.16%) Headache, tachycardia, dizziness, and nausea within 20 min; death in less than 2 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. Convulsions, respiratory arrest, and death in less than 20 minutes. 12,800 ppm (1.28%) Unconsciousness after 2-3 breaths. Death in less than three minutes.
The main manifestations of poisoning develop in the organ systems most dependent on oxygen use, the central nervous system and the heart. The initial symptoms of acute carbon monoxide poisoning include headache, nausea, malaise, and fatigue. These symptoms are often mistaken for a virus such as influenza or other illnesses such as food poisoning or gastroenteritis. Headache is the most common symptom of acute carbon monoxide poisoning; it is often described as dull, frontal, and continuous. Increasing exposure produces cardiac abnormalities including fast heart rate, low blood pressure, and cardiac arrhythmia; central nervous system symptoms include delirium, hallucinations, dizziness, unsteady gait, confusion, seizures, central nervous system depression, unconsciousness, respiratory arrest, and even 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 kidney failure, skin lesions, and visual and auditory problems.
One of the major concerns following acute carbon monoxide poisoning is the severe delayed neurological manifestations that may occur. Problems may include difficulty with higher intellectual functions, short-term memory loss, dementia, amnesia, psychosis, irritability, a strange gait, speech disturbances, Parkinson's disease-like syndromes, cortical blindness, and a depressed mood. Depression may even occur in those who did not have pre-existing depression. These delayed neurological sequelae may occur in up to 50% of poisoned patients after 2 to 40 days. It is difficult to predict who will develop delayed sequelae; however, advancing age, loss of consciousness while poisoned, and initial neurological abnormalities may increase the chance of developing delayed symptoms.
Chronic exposure to relatively low levels of carbon monoxide may cause persistent headaches, lightheadedness, depression, confusion, memory loss, nausea and vomiting. It is unknown whether low-level chronic exposure may cause permanent neurological damage. Typically, upon removal from exposure to carbon monoxide, symptoms usually resolve themselves, unless there has been an episode of severe acute poisoning. However, one case noted permanent memory loss and learning problems after a 3-year exposure to relatively low levels of carbon monoxide from a faulty furnace. Chronic exposure may worsen cardiovascular symptoms in some people. Long-term exposures to carbon monoxide present the greatest risk to persons with coronary heart disease and in females who are pregnant.
Concentration Source 0.1 ppm Natural atmosphere level (MOPITT) 0.5 to 5 ppm Average level in homes 5 to 15 ppm Near properly adjusted gas stoves in homes 100 to 200 ppm Exhaust from automobiles in the Mexico City central area 5,000 ppm Exhaust from a home wood fire 7,000 ppm Undiluted warm car exhaust without a catalytic converter
Carbon monoxide is a product of combustion of organic matter under conditions of restricted oxygen supply, which prevents complete oxidation to carbon dioxide (CO2). Sources of carbon monoxide include cigarette smoke, house fires, faulty furnaces, heaters, wood-burning stoves, internal combustion vehicle exhaust, electrical generators, propane-fueled equipment such as portable stoves, and gasoline-powered tools such as leaf blowers, lawn mowers, high-pressure washers, concrete cutting saws, power trowels, and welders. Exposure typically occurs when equipment is used in buildings or semi-enclosed spaces. Poisoning may also occur following the use of a self-contained underwater breathing apparatus (SCUBA) due to faulty diving air compressors. Riding in pickup trucks has led to poisoning in children. Idling automobiles with the exhaust pipe blocked by snow has led to the poisoning of car occupants. Generators and propulsion engines on boats, especially houseboats, has resulted in fatal carbon monoxide exposures. Another source of poisoning is exposure to the organic solvent dichloromethane, found in some paint strippers. Dichloromethane is converted into carbon monoxide by the body. In some caves carbon monoxide can build up in enclosed chambers due to decomposing organic matter.
The precise mechanisms by which the effects of carbon monoxide are induced upon bodily systems, are complex and not yet fully understood. Known mechanisms include carbon monoxide binding to hemoglobin, myoglobin and mitochondrial cytochrome oxidase, and carbon monoxide causing brain lipid peroxidation.
Carbon monoxide has a higher diffusion coefficient compared to oxygen and the only enzyme in the human body that produces carbon monoxide is heme oxygenase which is located in all cells and breaks down heme. Under normal conditions carbon monoxide levels in the plasma are approximately 0 mmHg because it is has a higher diffusion coefficient and the body easily gets rid of any CO made. When CO is not ventilated it binds to hemoglobin, which is the principal oxygen-carrying compound in blood; this produces a compound known as carboxyhemoglobin. The traditional belief is that carbon monoxide toxicity arises from the formation of carboxyhemoglobin, which decreases 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 approximately 230 times stronger than the affinity between hemoglobin and oxygen so 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 oxygen that would otherwise be delivered to the tissue. This situation is described as carbon monoxide shifting the oxygen dissociation curve to the left. Because of the increased affinity between hemoglobin and oxygen during carbon monoxide poisoning, the blood oxygen content is increased. But because all the oxygen stays in the hemoglobin, none is delivered to the tissues. This causes hypoxic tissue injury. Hemoglobin acquires a bright red color when converted into carboxyhemoglobin, so poisoned patients have been described as looking pink-cheeked and healthy. However, this cherry-red appearance is rarely seen in living patients so is not considered a reliable diagnostic sign.
Carbon monoxide also binds to the hemeprotein myoglobin. It has a high affinity for myoglobin, about 60 times greater than that of oxygen. Carbon monoxide bound to myoglobin may impair its ability to utilize oxygen. This causes reduced cardiac output and hypotension, which may result in brain ischemia. A delayed return of symptoms have been reported. This results following a recurrence of increased carboxyhemoglobin levels; this effect may be due to a late release of carbon monoxide from myoglobin, which subsequently binds to hemoglobin.
Another mechanism involves effects on the mitochondrial respiratory enzyme chain that is responsible for effective tissue utilization of oxygen. Carbon monoxide binds to cytochrome oxidase with less affinity than oxygen, so it is possible that it requires significant intracellular hypoxia before binding. This binding interferes with aerobic metabolism and efficient adenosine triphosphate synthesis. Cells respond by switching to anaerobic metabolism, causing anoxia, lactic acidosis, and eventual cell death. The rate of dissociation between carbon monoxide and cytochrome oxidase is slow, causing a relatively prolonged impairment of oxidative metabolism.
Central nervous system effects
The mechanism that is thought to have a significant influence on delayed effects involves formed blood cells and chemical mediators, which cause brain lipid peroxidation (degradation of unsaturated fatty acids). Carbon monoxide 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. The result of these effects is lipid peroxidation, which causes delayed reversible demyelinization of white matter in the central nervous system known as Grinker myelinopathy, which can lead to edema and necrosis within the brain. This brain damage occurs mainly during the recovery period. This may result in cognitive defects, especially affecting memory and learning, and movement disorders. These disorders are typically related to damage to the cerebral white matter and basal ganglia. Hallmark pathological changes following poisoning are bilateral necrosis of the white matter, globus pallidus, cerebellum, hippocampus and the cerebral cortex.
Carbon monoxide poisoning in pregnant women may cause severe adverse fetal effects. Poisoning causes fetal tissue hypoxia by decreasing the release of maternal oxygen to the fetus. Carbon monoxide also crosses the placenta and combines with fetal hemoglobin, causing more direct fetal tissue hypoxia. Additionally, fetal hemoglobin has a 10 to 15% higher affinity for carbon monoxide than adult hemoglobin, causing more severe poisoning in the fetus than in the adult. Elimination of carbon monoxide is slower in the fetus, leading to an accumulation of the toxic chemical. The level of fetal morbidity and mortality in acute carbon monoxide poisoning is significant, so despite mild maternal poisoning or following maternal recovery, severe fetal poisoning or death may still occur.
As many symptoms of carbon monoxide poisoning also occur with many other types of poisonings and infections (such as the flu), the diagnosis is often difficult. A history of potential carbon monoxide exposure, such as being exposed to a residential fire, may suggest poisoning, 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 to the amount of hemoglobin in the blood. Carbon monoxide is produced naturally by the body as a byproduct of converting protoporphyrin into bilirubin. This carbon monoxide also combines with hemoglobin to make carbooxyhemoglobin, but not at toxic levels. The ratio of carboxyhemoglobin to hemoglobin molecules in an average person may be up to 5%, although cigarette smokers who smoke two packs/day may have levels up to 9%.
Serious toxicity occurs with the carboxyhemoglobin to hemoglobin ratio 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. Carboxyhemoglobin levels should be considered as guides to exposure levels rather than guides to effects, as they do not reliably predict clinical course of action or short- and long-term consequences. Patients may continue to experience significant symptoms of CO poisoning long after their blood carboxyhemoglobin concentration has returned to normal. Because of this, for late arriving patients a normal carboxyhemoglobin level does not rule out poisoning.
A CO-oximeter is used to determine carboxyhemoglobin levels. Pulse CO-oximeters estimate carboxyhemoglobin with a non-invasive finger clip similar to a pulse oximeter. These devices function by passing various wavelengths of light through the fingertip and measuring the light absorption of the different types of hemoglobin in the capillaries.
A 2010 study was undertaken to address concerns over the differences in concentration measurements between CO-oximeter results and the results of a standard laboratory blood test. Smaller previous studies had been conducted, however because of specific issues with their study design, the clinical application of CO-oximetry was called into question. In the 2010 study, differences between CO-oximeter results and standard laboratory tests fell outside of the clinically acceptable limits of +/- 5% carboxyhemoglobin in 33.3% of tests. When compared to the laboratory test results, the discrepancies between CO-oximetry tests ranged from -11.6% to +14.4%. Sensitivity in this study was determined to be 48%, while specificity was determined to be 99%. Additionally, because these devices function based on measuring absorbance of light wavelengths, a patient’s skin-tone can affect results, which is specifically of concern when these devices are used on black or Hispanic patients. The researchers concluded, based on their results and a lack of peer-reviewed research on the subject, that CO-oximetry cannot replace standard laboratory analysis in clinical care. CO-oximeters were also not recommended for use as an out-of-hospital triage tool.
The use of a regular pulse oximeter is not effective in the diagnosis of carbon monoxide poisoning as patients suffering from carbon monoxide poisoning may have a normal oxygen saturation level on a pulse oximeter. This is due to the carboxyhemoglobin being misrepresented as oxyhemoglobin.
Breath CO monitoring offers a viable alternative to pulse CO-oximetry. Carboxyhemoglobin levels have been shown to have a strong correlation with breath CO concentration . Because of this, monitoring CO in an exhaled sample allows for a non-invasive means to determine carboxyhemoglobin concentrations and to help diagnose patients experiencing symptoms of CO poisoning. Several models of Breath CO monitors are available commercially, which function based on the use of an electrochemical gas sensor to detect CO. These devices are not susceptible to misrepresenting carboxyhemoglobin as oxyhemoglobin. Monitoring CO via exhaled breath has been demonstrated to be useful in emergency medical services when determining the blood CO levels of individuals who are known or suspected to have received exposure.
There are many conditions to be considered in the differential diagnosis of carbon monoxide poisoning. 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. Carbon monoxide has been called a “great mimicker” due to the presentation of poisoning being diverse and nonspecific. Other conditions included in the differential diagnosis include acute respiratory distress syndrome, altitude sickness, lactic acidosis, diabetic ketoacidosis, meningitis, methemoglobinemia, or opioid or toxic alcohol poisoning.
Detection in biological specimens
Carbon monoxide may be quantitated in blood using spectrophotometric methods or chromatographic techniques in order to confirm a diagnosis of poisoning in hospitalized victims or to assist in the forensic investigation of a case of fatal exposure. Carboxyhemoglobin blood saturations may range up to 8-10% in heavy smokers or persons extensively exposed to automotive exhaust gases. In symptomatic poisoned patients they are often in the 10-30% range, while persons who succumb may have postmortem blood levels of 30-90%.
Carbon monoxide detection
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. In buildings, carbon monoxide detectors are usually installed around heaters and other equipment. If a relatively high level of carbon monoxide is detected, the device sounds an alarm, giving people the chance to evacuate and ventilate the building. Unlike smoke detectors, carbon monoxide detectors do not need to be placed near ceiling level. The United States Consumer Product Safety Commission has stated, "carbon monoxide detectors are as important to home safety as smoke detectors are," and recommends each home have at least one carbon monoxide detector, and preferably one on each level of the building. These devices, which are relatively inexpensive and widely available, are either battery- or AC-powered, with or without battery backup.
The use of carbon monoxide detectors has been standardized in many areas. In the USA, NFPA 720-2009, the carbon monoxide detector guidelines published by the National Fire Protection Association, 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, AC-powered detectors must have battery backup and be interconnected to ensure early warning of occupants at all levels. NFPA 720-2009 is the first national carbon monoxide standard to address devices in non-residential buildings. These guidelines, which now pertain to schools, healthcare centers, nursing homes and other non-residential buildings, includes three main points:
- 1. A secondary power supply (battery backup) must operate all carbon monoxide notification appliances for at least 12 hours,
- 2. Detectors must be on the ceiling in the same room as permanently installed fuel-burning appliances, and
- 3. Detectors must be located on every habitable level and in every HVAC zone of the building.
Initial treatment for carbon monoxide poisoning is to immediately remove the person from the exposure without endangering further people. Those who are unconscious may require CPR on site. Administering oxygen via non-rebreather mask shortens the half life of carbon monoxide to 80 minutes from 320 minutes on normal air. Oxygen hastens the dissociation of carbon monoxide from carboxyhemoglobin, thus turning it back into hemoglobin. Due to the possible severe effects in the fetus, pregnant women are treated with oxygen for longer periods of time than non-pregnant patients.
Hyperbaric oxygen is also used in the treatment of carbon monoxide poisoning, as it may hasten dissociation of CO from carboxyhemoglobin and cytochrome oxidase to a greater extent than normal oxygen. Hyperbaric oxygen at three times atmospheric pressure reduces the half life of carbon monoxide to 23 minutes, compared to 80 minutes for regular oxygen. It may also enhance oxygen transport to the tissues by plasma, partially bypassing the normal transfer through hemoglobin. However it is controversial whether 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 randomized controlled trials 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. A review of all the literature on carbon monoxide poisoning treatment concluded that the role of hyperbaric oxygen is unclear and the available evidence neither confirms nor denies a medically meaningful benefit. The authors suggested a large, well designed, externally audited, multicentre trial to compare normal oxygen with hyperbaric oxygen.
Further treatment for other complications such as seizure, hypotension, cardiac abnormalities, pulmonary edema, and acidosis may be required. Increased muscle activity and seizures should be treated with dantrolene or diazepam; diazepam should only be given with appropriate respiratory support. Hypotension requires treatment with intravenous fluids; vasopressors may be required to treat myocardial depression. Cardiac dysrhythmias are treated with standard advanced cardiac life support protocols. If severe, metabolic acidosis is treated with sodium bicarbonate. Treatment with sodium bicarbonate is controversial as acidosis may increase tissue oxygen availability. Treatment of acidosis may only need to consist of oxygen therapy. The delayed development of neuropsychiatric impairment is one of the most serious complications of carbon monoxide poisoning. Brain damage is confirmed following MRI or CAT scans. Extensive follow up and supportive treatment is often required for delayed neurological damage. Outcomes are often difficult to predict following poisoning, especially patients who have symptoms of cardiac arrest, coma, metabolic acidosis, or have high carboxyhemoglobin levels. One study reported that approximately 30% of people with severe carbon monoxide poisoning will have a fatal outcome.
The true number of incidents of carbon monoxide poisoning is unknown, since many non-lethal exposures go undetected. From the available data, carbon monoxide poisoning is the most common cause of injury and death due to poisoning worldwide. Poisoning is typically more common during the winter months. This thought to be due increased domestic use of gas furnaces, gas or kerosene space heaters, and kitchen stoves during the winter months, which if faulty and/or are used without adequate ventilation, may produce excessive carbon monoxide.
It has been estimated that more than 40,000 people per year seek medical attention for carbon monoxide poisoning in the United States. In many industrialized countries carbon monoxide is the cause of more than 50% of fatal poisonings. In the United States, approximately 200 people die each year from carbon monoxide poisoning associated with home fuel-burning heating equipment. Carbon monoxide poisoning contributes to the approximately 5613 smoke inhalation deaths each year in the United States. The CDC reports, "Each year, more than 500 Americans die from unintentional carbon monoxide poisoning, and more than 2,000 commit suicide by intentionally poisoning themselves." For the 10-year period from 1979 to 1988, 56,133 deaths from carbon monoxide poisoning occurred in the United States, with 25,889 of those being suicides, leaving 30,244 unintentional deaths. A report from New Zealand showed that 206 people died from carbon monoxide poisoning in the years of 2001 and 2002. In total carbon monoxide poisoning was responsible for 43.9% of deaths by poisoning in that country. In South Korea, 1,950 people had been poisoned by carbon monoxide with 254 deaths from 2001 through 2003. A report from Jerusalem showed 3.53 per 100,000 people were poisoned annually from 2001 through 2006. in Hubei, China, 218 deaths from poisoning were reported over a 10 year period with 16.5% being from carbon monoxide exposure.
Before the 1960s most domestic gas supply in the United Kingdom was coal gas (alternatively known as town gas), which in its unburned form contained high levels of carbon monoxide. Carbon monoxide poisoning by intentionally inhaling coal gas was a common suicide method, accounting for nearly half of all suicides in the United Kingdom in the late 1950s. After the British government phased out coal gas in favor of natural gas in the 1960s, the suicide rate in Britain fell by almost a third and has not risen since. The use of coal gas as a suicide method has declined as most domestic gas supply worldwide is now natural gas, which lacks carbon monoxide. Until the invention of catalytic converters, suicide has been committed by inhaling the exhaust fumes of a running car engine, particularly in an enclosed space such as a garage. Before 1975, motor car exhaust contained 4-10% carbon monoxide, but newer cars have catalytic converters that eliminate over 99% of the carbon monoxide produced. However even cars with catalytic converters can produce substantial amounts of carbon monoxide if an idling car is left in an enclosed space such as a closed garage.
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 fossil fuels, or by combining formic acid and sulfuric acid, within a confined space. Such incidents have occurred mostly in connection with group suicide pacts in Asian countries such as Japan, Taiwan, and Hong Kong, but are starting to occur in western countries as well, such as the 2007 suicide of Boston lead singer Brad Delp.
Society and culture
Many of the phenomena generally associated with haunted houses, including strange visions and sounds and feelings of dread, can be attributed to carbon monoxide poisoning, as its symptoms include confusion, delirium, emotional disturbances, and hallucinations. 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 think they were hearing 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.
A report published in 2005 described a 23-year old female victim of carbon monoxide poisoning, found delirious and hyperventilating, who thought she saw a ghost while in the shower. A new gas water heater had just been improperly installed in her home, which flooded the house with carbon monoxide when the victim closed all the exterior windows and doors and took a shower.
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- ^ a b Ong JR, Hou SW, Shu HT, Chen HT, Chong CF, Chong CF (November 2005). "Diagnostic pitfall: carbon monoxide poisoning mimicking hyperventilation syndrome". The American Journal of Emergency Medicine 23 (7): 903–904. doi:10.1016/j.ajem.2005.07.008. PMID 16291452.
- Carbon monoxide breath monitor
- John Scott Haldane
- Undersea and Hyperbaric Medical Society
- Deaths from carbon monoxide poisoning
- Pilot study of risks and long-term effects of carbon monoxide poisoning by Brian Miller, John Ross, Laura MacCalman, Chris Burton and Claudia Pagliari. Institute of Occupational Medicine Research Report TM/11/02
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