Carbon monoxide poisoning explained

Carbon monoxide poisoning
Diseasesdb:2020
Medlineplus:002804
Emedicinesubj:emerg
Emedicinetopic:817
Meshname:Carbon+Monoxide+Poisoning
Meshnumber: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.[1] 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.[2] 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.[3]

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.[4] 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;[5] in addition, employees are to be removed from any confined space if an upper limit ("ceiling") of 100 ppm is reached.[6] Carbon monoxide exposure may lead to a significantly shorter life span due to heart damage.[7] 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.[8] [9] [10]

The acute effects produced by carbon monoxide in relation to ambient concentration in parts per million are listed below:[11] [12]

ConcentrationSymptoms
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.

Acute poisoning

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.[13] These symptoms are often mistaken for a virus such as influenza or other illnesses such as food poisoning or gastroenteritis.[14] Headache is the most common symptom of acute carbon monoxide poisoning; it is often described as dull, frontal, and continuous.[15] Increasing exposure produces cardiac abnormalities including fast heart rate, low blood pressure, and cardiac arrhythmia;[16] central nervous system symptoms include delirium, hallucinations, dizziness, unsteady gait, confusion, seizures, central nervous system depression, unconsciousness, respiratory arrest, and death.[17] 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.[18] [19] [20] [21]

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.[14] [22] Depression may even occur in those who did not have pre-existing depression.[23] These delayed neurological sequelae may occur in up to 50% of poisoned people after 2 to 40 days.[14] 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.[24]

One classic sign of carbon monoxide poisoning is more often seen in the dead rather than the living - people have been described as looking pink-cheeked and healthy. However, since this "cherry-red" appearance is common only in the deceased, and is unusual in living people, it is not considered a useful diagnostic sign in clinical medicine. In pathological (autopsy) examination the ruddy appearance of carbon monoxide poisoning is notable because unembalmed dead persons are normally bluish and pale, whereas dead carbon-monoxide poisoned persons may simply appear unusually life-like in coloration.[25] [26] The colorant effect of carbon monoxide in such postmortem circumstances is thus analogous to its use as a red colorant in the commercial meat-packing industry.

Chronic poisoning

Chronic exposure to relatively low levels of carbon monoxide may cause persistent headaches, lightheadedness, depression, confusion, memory loss, nausea and vomiting.[27] It is unknown whether low-level chronic exposure may cause permanent neurological damage.[14] Typically, upon removal from exposure to carbon monoxide, symptoms usually resolve themselves, unless there has been an episode of severe acute poisoning.[27] 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.[28] Chronic exposure may worsen cardiovascular symptoms in some people.[27] Chronic carbon monoxide exposure might increase the risk of developing atherosclerosis.[29] [30] Long-term exposures to carbon monoxide present the greatest risk to persons with coronary heart disease and in females who are pregnant.[31]

Causes

ConcentrationSource
0.1 ppmNatural atmosphere level (MOPITT)[32]
0.5 to 5 ppmAverage level in homes[33]
5 to 15 ppmNear properly adjusted gas stoves in homes
100 to 200 ppmExhaust from automobiles in the Mexico City central area[34]
5,000 ppmExhaust from a home wood fire[35]
7,000 ppmUndiluted 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.[14] [27] [36] [37] [38] [39] Exposure typically occurs when equipment is used in buildings or semi-enclosed spaces.[14] Poisoning may also occur following the use of a self-contained underwater breathing apparatus (SCUBA) due to faulty diving air compressors.[40] Riding in pickup trucks has led to poisoning in children.[41] Idling automobiles with the exhaust pipe blocked by snow has led to the poisoning of car occupants.[42] Generators and propulsion engines on boats, especially houseboats, has resulted in fatal carbon monoxide exposures.[43] [44] Another source of poisoning is exposure to the organic solvent dichloromethane, found in some paint strippers.[45] Dichloromethane is converted into carbon monoxide by the body.[46] [47] [48] In most light aircraft and some cars the heating system comprises of a shroud around the exhaust. Any perferation in the shroud leaches exhaust gas into the cabin.In some caves carbon monoxide can build up in enclosed chambers due to decomposing organic matter.[49]

Pathophysiology

The precise mechanisms by which the effects of carbon monoxide are induced upon bodily systems, are complex and not yet fully understood.[13] Known mechanisms include carbon monoxide binding to hemoglobin, myoglobin and mitochondrial cytochrome oxidase, and carbon monoxide causing brain lipid peroxidation.[17] [50]

Hemoglobin

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.[51] 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.[50] [52] [53]

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.[54] This situation is described as carbon monoxide shifting the oxygen dissociation curve to the left.[50] 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.[14] Hemoglobin acquires a bright red color when converted into carboxyhemoglobin, so poisoned cadavers and even commercial meats treated with carbon monoxide acquire an unnatural reddish hue.

Myoglobin

Carbon monoxide also binds to the hemeprotein myoglobin. It has a high affinity for myoglobin, about 60 times greater than that of oxygen.[14] Carbon monoxide bound to myoglobin may impair its ability to utilize oxygen.[50] This causes reduced cardiac output and hypotension, which may result in brain ischemia.[14] 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.[2]

Cytochrome oxidase

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.[55] 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.[56] The rate of dissociation between carbon monoxide and cytochrome oxidase is slow, causing a relatively prolonged impairment of oxidative metabolism.[13]

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.[13] In the brain this causes further mitochondrial dysfunction, capillary leakage, leukocyte sequestration, and apoptosis.[57] 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.[54] 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.[57] [58] Hallmark pathological changes following poisoning are bilateral necrosis of the white matter, globus pallidus, cerebellum, hippocampus and the cerebral cortex.[59] [14] [60]

Pregnancy

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.[2] Elimination of carbon monoxide is slower in the fetus, leading to an accumulation of the toxic chemical.[61] 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.[62]

Diagnosis

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.[48] [63] 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.[14] 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.[14] 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%.[64]

As people may continue to experience significant symptoms of CO poisoning long after their blood carboxyhemoglobin concentration has returned to normal people arriving late with a normal carboxyhemoglobin level does not rule out poisoning.[65]

A CO-oximeter is used to determine carboxyhemoglobin levels.[66] [67] Pulse CO-oximeters estimate carboxyhemoglobin with a non-invasive finger clip similar to a pulse oximeter.[68] 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.

The use of a regular pulse oximeter is not effective in the diagnosis of carbon monoxide poisoning as people suffering from carbon monoxide poisoning may have a normal oxygen saturation level on a pulse oximeter.[69] This is due to the carboxyhemoglobin being misrepresented as oxyhemoglobin.[70]

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.[71] [72]

Differential diagnosis

There are many conditions to be considered in the differential diagnosis of carbon monoxide poisoning.[73] [74] 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.[75] Carbon monoxide has been called a “great mimicker” due to the presentation of poisoning being diverse and nonspecific.[73] 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.[74]

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 a person 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 people they are often in the 10-30% range, while persons who succumb may have postmortem blood levels of 30-90%.[76] [77]

Prevention

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.[78] . Gas organizations will often recommend to get gas appliances serviced at least once a year. [79] 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.[80] [81] Unlike smoke detectors, carbon monoxide detectors do not need to be placed near ceiling level.[82] 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[81] and widely available, are either battery- or AC-powered, with or without battery backup.[83] . It is also recommended that scuba divers detect for carbon monoxide contamination in breathing air before diving as the effects of carbon monoxide on the body are increased under pressure. Carbon monoxide is tasteless and odourless so can not be detected by smell [84] . Compressor owners should ensure that their mix is CO Clear by using fixed monotors that work in line with the compressor. Divers should use specialised hand held CO analysers specifically designed for testing scuba cylinders prior to diving.

Standardization

The use of carbon monoxide detectors has been standardized in many areas. In the USA, NFPA 720-2009,[85] 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.[85] 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:[85]

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.

Recommended WHO guidelines

The following guideline values (ppm values rounded) and periods of time-weighted average exposures have been determined in such a way that the carboxyhaemoglobin level of 2.5% is not exceeded, even when a normal subject engages in light or moderate exercise:

Treatment

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.[50] Administering oxygen via non-rebreather mask shortens the half life of carbon monoxide to 80 minutes from 320 minutes on normal air.[17] Oxygen hastens the dissociation of carbon monoxide from carboxyhemoglobin, thus turning it back into hemoglobin.[4] [86] Due to the possible severe effects in the fetus, pregnant women are treated with oxygen for longer periods of time than non-pregnant people.[87]

Hyperbaric oxygen

Hyperbaric oxygen is also used in the treatment of carbon monoxide poisoning, as it may hasten dissociation of CO from carboxyhemoglobin[4] and cytochrome oxidase[88] to a greater extent than normal oxygen. Hyperbaric oxygen at three times atmospheric pressure reduces the half life of carbon monoxide to 23 (~80/3 minutes) minutes, compared to 80 minutes for regular oxygen.[4] It may also enhance oxygen transport to the tissues by plasma, partially bypassing the normal transfer through hemoglobin.[86] 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.[1] [89] [90] [91] [92] [93] There have been randomized controlled trials in which the two treatment options have been compared;[94] [95] [96] [97] [98] [99] of the six performed, four found hyperbaric oxygen improved outcome and two found no benefit for hyperbaric oxygen.[1] Some of these trials have been criticized for apparent flaws in their implementation.[100] [101] [102] 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.[1]

Other

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.[50] Hypotension requires treatment with intravenous fluids; vasopressors may be required to treat myocardial depression.[103] Cardiac dysrhythmias are treated with standard advanced cardiac life support protocols.[14] If severe, metabolic acidosis is treated with sodium bicarbonate. Treatment with sodium bicarbonate is controversial as acidosis may increase tissue oxygen availability.[104] Treatment of acidosis may only need to consist of oxygen therapy.[14] [74] 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.[13] [105] [106] Extensive follow up and supportive treatment is often required for delayed neurological damage.[17] Outcomes are often difficult to predict following poisoning,[107] especially people who have symptoms of cardiac arrest, coma, metabolic acidosis, or have high carboxyhemoglobin levels.[74] One study reported that approximately 30% of people with severe carbon monoxide poisoning will have a fatal outcome.[48] It has been reported that electroconvulsive therapy (ECT) may increase the likelihood of delayed neuropsychiatric sequelae (DNS) after carbon monoxide (CO) poisoning.[108]

Epidemiology

The true number of incidents of carbon monoxide poisoning is unknown, since many non-lethal exposures go undetected.[13] [48] From the available data, carbon monoxide poisoning is the most common cause of injury and death due to poisoning worldwide.[109] Poisoning is typically more common during the winter months.[73] [110] [111] [112] 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.[73] [113] Carbon Monoxide detection and poisoning also increases during power outages.[114] [115] [116]

It has been estimated that more than 40,000 people per year seek medical attention for carbon monoxide poisoning in the United States.[117] In many industrialized countries carbon monoxide is the cause of more than 50% of fatal poisonings.[2] In the United States, approximately 200 people die each year from carbon monoxide poisoning associated with home fuel-burning heating equipment.[118] Carbon monoxide poisoning contributes to the approximately 5613 smoke inhalation deaths each year in the United States.[119] 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."[120] 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.[119] 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.[121] In South Korea, 1,950 people had been poisoned by carbon monoxide with 254 deaths from 2001 through 2003.[122] A report from Jerusalem showed 3.53 per 100,000 people were poisoned annually from 2001 through 2006.[123] in Hubei, China, 218 deaths from poisoning were reported over a 10 year period with 16.5% being from carbon monoxide exposure.[124]

Suicide

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.[125] 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.[126] [127] 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.[128] [129] 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.[130] 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.[131]

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,[132] or fossil fuels, or by combining formic acid and sulfuric acid, within a confined space.[133] [134] [135] Such incidents have occurred mostly in connection with group suicide pacts in Asian countries such as Japan, Taiwan, and Hong Kong,[136] [137] [138] [139] but are starting to occur in western countries as well,[140] [141] [142] such as the 2007 suicide of Boston lead singer Brad Delp.[143]

See also

Notes and References

  1. Buckley NA, Isbister GK, Stokes B, Juurlink DN. Hyperbaric oxygen for carbon monoxide poisoning: a systematic review and critical analysis of the evidence. Toxicological Reviews. 2005. 75–92. 24. 2. 16180928. 10.2165/00139709-200524020-00002.
  2. Omaye ST. Metabolic modulation of carbon monoxide toxicity. Toxicology. 2002. 139–50. 180. 2. 12324190. 10.1016/S0300-483X(02)00387-6. Nov.
  3. Web site: A True Tale Of A Truly Haunted House. Albert Donnay. Ghostvillage.com. October 31, 2004. 2008-12-16.
  4. Raub JA, Mathieu-Nolf M, Hampson NB, Thom SR. Carbon monoxide poisoning-a public health perspective. Toxicology. 2000. 1–14. 145. 1. 10771127. 10.1016/S0300-483X(99)00217-6. April.
  5. Web site: OSHA Fact Sheet: Carbon Monoxide. 2009-09-14. United States National Institute for Occupational Safety and Health.
  6. Web site: Carbon monoxide. - 1917.24. 2010-01-13. United States Department of Labor: Occupational Safety and Health Administration.
  7. Henry CR, Satran D, Lindgren B, Adkinson C, Nicholson CI, Henry TD. Myocardial Injury and Long-term Mortality Following Moderate to Severe Carbon Monoxide Poisoning. JAMA. 2006. 295. 398–402. 10.1001/jama.295.4.398. 16434630. January. 4. Free full text.
  8. Web site: Carbon Monoxide. 2009-09-14. American Lung Association. http://web.archive.org/web/20080528195959/http://www.lungusa.org/site/pp.asp?c=dvLUK9O0E&b=35375. 2008-05-28. yes.
  9. Lipman GS. Carbon monoxide toxicity at high altitude. Wilderness & Environmental Medicine. 2006. 144–145. 17. 2. 16805152. 10.1580/1080-6032(2006)17[144:CMTAHA]2.0.CO;2.
  10. Book: first draft prepared by Mr J. Raub.. Environmental Health Criteria 213 (Carbon Monoxide). International Programme on Chemical Safety, World Health Organization. Geneva. 1999. 9241572132.
  11. Goldstein M. Carbon monoxide poisoning. Journal of Emergency Nursing: JEN: Official Publication of the Emergency Department Nurses Association. 34. 6. 538–542. 2008. December. 19022078. 10.1016/j.jen.2007.11.014.
  12. Struttmann T, Scheerer A, Prince TS, Goldstein LA. Unintentional carbon monoxide poisoning from an unlikely source. The Journal of the American Board of Family Practice. 11. 6. 481–484. 1998. 9876005. Nov.
  13. Hardy KR, Thom SR. Pathophysiology and treatment of carbon monoxide poisoning. Journal of Toxicology. Clinical Toxicology. 1994. 613–629. 32. 6. 7966524. 10.3109/15563659409017973.
  14. Book: Nelson, LH. Goldfrank's toxicologic emergencies. McGraw-Hill. New York. 2002. 7th. 1689–1704. Carbon Monoxide. 0-07-136001-8. Flomenbaum N, Goldfrank LR, Hoffman RL, Howland MD, Neal AL.
  15. Hampson NB, Hampson LA. Characteristics of headache associated with acute carbon monoxide poisoning. Headache. 42. 3. 220–223. 2002. March. 11903546. 10.1046/j.1526-4610.2002.02055.x.
  16. Tritapepe L, Macchiarelli G, Rocco M, Scopinaro F, Schillaci O, Martuscelli E, Motta PM. Functional and ultrastructural evidence of myocardial stunning after acute carbon monoxide poisoning. Critical Care Medicine. 26. 4. 797–801. 1998. April. 9559621. 10.1097/00003246-199804000-00034.
  17. Weaver LK. Clinical practice. Carbon monoxide poisoning. The New England Journal of Medicine. 360. 12. 1217–1225. 2009. March. 19297574. 10.1056/NEJMcp0808891.
  18. Choi IS. Carbon monoxide poisoning: systemic manifestations and complications. Journal of Korean Medical Science. 2001. 253–261. 16. 3. 11410684. June. Free full text. . 3054741.
  19. Marius-Nunez AL. Myocardial infarction with normal coronary arteries after acute exposure to carbon monoxide. Chest. 97. 2. 491–4. 1990. February. 2298080. 10.1378/chest.97.2.491.
  20. Gandini C, Castoldi AF, Candura SM, Locatelli C, Butera R, Priori S, Manzo L. Carbon monoxide cardiotoxicity. Journal of Toxicology. Clinical Toxicology. 39. 1. 35–44. 2001. 11327225. 10.1081/CLT-100102878.
  21. Sokal JA. The effect of exposure duration on the blood level of glucose, pyruvate and lactate in acute carbon monoxide intoxication in man. Journal of Applied Toxicology: JAT. 5. 6. 395–7. 1985. December. 4078220. 10.1002/jat.2550050611.
  22. Choi IS. Delayed neurologic sequelae in carbon monoxide intoxication. Archives of Neurology. 40. 7. 433–435. 1983. July. 6860181.
  23. Roohi F, Kula RW, Mehta N. Twenty-nine years after carbon monoxide intoxication. Clinical Neurology and Neurosurgery. 2001. 92–95. 103. 2. 11516551. 10.1016/S0303-8467(01)00119-6. July.
  24. Myers RA, Snyder SK, Emhoff TA. Subacute sequelae of carbon monoxide poisoning. Annals of Emergency Medicine. 14. 12. 1163–1167. 1985. December. 4061987. 10.1016/S0196-0644(85)81022-2.
  25. Simini B. Cherry-red discolouration in carbon monoxide poisoning. Lancet. 352. 9134. 1154. 1998. October. 9798630. 10.1016/S0140-6736(05)79807-X.
  26. Brooks DE, Lin E, Ahktar J. What is cherry red, and who cares?. The Journal of Emergency Medicine. 2002. 213–214. 22. 2. 11858933. 10.1016/S0736-4679(01)00469-3. February.
  27. Fawcett TA, Moon RE, Fracica PJ, Mebane GY, Theil DR, Piantadosi CA. Warehouse workers' headache. Carbon monoxide poisoning from propane-fueled forklifts. Journal of Occupational Medicine. 1992. 12–15. 34. 1. 1552375. January.
  28. Ryan CM. Memory disturbances following chronic, low-level carbon monoxide exposure. Archives of Clinical Neuropsychology: the Official Journal of the National Academy of Neuropsychologists. 1990. 59–67. 5. 1. 14589544. 10.1016/0887-6177(90)90007-C.
  29. Davutoglu. V. Chronic carbon monoxide exposure is associated with the increases in carotid intima-media thickness and C-reactive protein level. Tohoku J Exp Med. 2009. November. 219. 3. 201–6.
  30. Book: Shephard, Roy. Carbon Monoxide The Silent Killer. 1983. Charles C Thomas. Springfield Illinois. 93–96.
  31. 10.1056/NEJM198911233212102. Allred EN, Bleecker ER, Chaitman BR, Dahms TE, Gottlieb SO, Hackney JD, Pagano M, Selvester RH, Walden SM, Warren J. Short-term effects of carbon monoxide exposure on the exercise performance of subjects with coronary artery disease. The New England Journal of Medicine. 1989. 1426–1432. 321. 21. 2682242. Nov.
  32. Book: Committee on Medical and Biological Effects of Environmental Pollutants. Carbon Monoxide. National Academy of Sciences. Washington, D.C.. 1977. 29. 0-309-02631-8.
  33. Web site: An Introduction to Indoor Air Quality: Carbon Monoxide (CO). Green W. United States Environmental Protection Agency. 2008-12-16.
  34. Book: Singer, Siegfried Fred. The Changing Global Environment. D. Reidel Publishing Company. Dordrecht. 90.
  35. Web site: What Do Carbon Monoxide Levels Mean?. Gosink T. Alaska Science Forum. Geophysical Institute, University of Alaska Fairbanks. 1983-01-28. 2008-12-16.
  36. Marc B, Bouchez-Buvry A, Wepierre JL, Boniol L, Vaquero P, Garnier M. Carbon-monoxide poisoning in young drug addicts due to indoor use of a gasoline-powered generator. Journal of Clinical Forensic Medicine. 8. 2. 54–56. 2001. June. 16083675. 10.1054/jcfm.2001.0474.
  37. Johnson C, Moran J, Paine S, Anderson H, Breysse P. Abatement of toxic levels of carbon monoxide in Seattle ice-skating rinks. American Journal of Public Health. 65. 10. 1087–1090. 1975. 1163706. 10.2105/AJPH.65.10.1087. October. 1776025.
  38. Web site: NIOSH Carbon Monoxide Hazards from Small Gasoline Powered Engines. 2007-10-15. United States National Institute for Occupational Safety and Health.
  39. Fife CE, Smith LA, Maus EA, McCarthy JJ, Koehler MZ, Hawkins T, Hampson NB. Dying to play video games: carbon monoxide poisoning from electrical generators used after hurricane Ike. Pediatrics. 123. 6. e1035–8. 2009. June. 19482736. 10.1542/peds.2008-3273.
  40. Austin CC, Ecobichon DJ, Dussault G, Tirado C. Carbon monoxide and water vapor contamination of compressed breathing air for firefighters and divers. Journal of Toxicology and Environmental Health. 52. 5. 403–423. 1997. December. 9388533. 10.1080/00984109708984073.
  41. Hampson NB, Norkool DM. Carbon monoxide poisoning in children riding in the back of pickup trucks. JAMA. 267. 4. 538–540. 1992. 1370334. 10.1001/jama.267.4.538. January.
  42. Centers for Disease Control and Prevention (CDC). Carbon monoxide poisonings associated with snow-obstructed vehicle exhaust systems—Philadelphia and New York City, January 1996. MMWR: Morbidity and Mortality Weekly Report. 45. 1. 1–3. 1996. January. 8531914.
  43. Centers for Disease Control and Prevention (CDC). Houseboat-associated carbon monoxide poisonings on Lake Powell—Arizona and Utah, 2000. MMWR: Morbidity and Mortality Weekly Report. 49. 49. 1105–1108. 2000. December. 11917924.
  44. Web site: NIOSH Carbon Monoxide Dangers in Boating. 2007-10-15. United States National Institute for Occupational Safety and Health.
  45. van Veen. MP. Fortezza F, Spaans E, Mensinga TT. Non-professional paint stripping, model prediction and experimental validation of indoor dichloromethane levels. Indoor Air. 2002. 12. 2. 92–7.
  46. Kubic VL, Anders MW. Metabolism of dihalomethanes to carbon monoxide. II. In vitro studies. Drug metabolism and disposition. 1975. 104–112. 3. 2. 236156. March.
  47. Dueñas A, Felipe S, Ruiz-Mambrilla M, Martín-Escudero JC, García-Calvo C. CO poisoning caused by inhalation of CH3Cl contained in personal defense spray. The American Journal of Emergency Medicine. 18. 1. 120–121. 2000. January. 10674554. 10.1016/S0735-6757(00)90070-6.
  48. Varon J, Marik PE, Fromm RE Jr, Gueler A. Carbon monoxide poisoning: a review for clinicians. The Journal of Emergency Medicine. 1999. 87–93. 17. 1. 9950394. 10.1016/S0736-4679(98)00128-0.
  49. Book: Dart, RC. Medical toxicology. Williams & Wilkins. Philadelphia. 2004. 1169. 0-7817-2845-2.
  50. Bateman DN. Carbon Monoxide. Medicine. 31. 10. 233. 2003. October. 10.1383/medc.31.10.41.27810.
  51. Book: USMLE Step 1 Lecture Notes: Physiology. 2011. Dunn, Robert B.. Kudrath, W., Passo S.S., Wilson, L.B.. 167–168. 7-3.
  52. Townsend CL, Maynard RL. Effects on health of prolonged exposure to low concentrations of carbon monoxide. Occupational and Environmental Medicine. 59. 10. 708–711. 2002. October. 12356933. 1740215. 10.1136/oem.59.10.708.
  53. Haldane J. The action of carbonic oxide on man. The Journal of Physiology. 1895. 430–462. 18. 16992272. 5-6. 1514663.
  54. Gorman D, Drewry A, Huang YL, Sames C. The clinical toxicology of carbon monoxide. Toxicology. 2003. 25–38. 187. 1. 12679050. 10.1016/S0300-483X(03)00005-2. May.
  55. Gorman DF, Runciman WB. Carbon monoxide poisoning. Anaesthesia and Intensive Care. 19. 4. 506–11. 1991. November. 1750629.
  56. Alonso JR, Cardellach F, Lopez S, Casademont J, Miro O.. Carbon monoxide specifically inhibits cytochrome c oxidase of human mitochondrial respiratory chain. Pharmacology & Toxicology. 2003. 142–146. 93. 3. 12969439. 10.1034/j.1600-0773.2003.930306.x. September.
  57. Blumenthal I. Carbon monoxide poisoning. Journal of the Royal Society of Medicine. 2001. 270–272. 94. 6. 11387414. June. Free full text. 1281520.
  58. Fan HC, Wang AC, Lo CP, Chang KP, Chen SJ. Damage of cerebellar white matter due to carbon monoxide poisoning: a case report. The American Journal of Emergency Medicine. 27. 6. 757.e5–e7. 2009. July. 19751650. 10.1016/j.ajem.2008.10.021.
  59. Prockop LD, Chichkova RI. Carbon monoxide intoxication: an updated review. Journal of the Neurological Sciences. 2007. 122–130. 262. 1-2. 17720201. 10.1016/j.jns.2007.06.037. Nov.
  60. Fukuhara M, Abe I, Matsumura K, Kaseda S, Yamashita Y, Shida K, Kawashima H, Fujishima M. Circadian variations of blood pressure in patients with sequelae of carbon monoxide poisoning. American Journal of Hypertension. 9. 4 Part 1. 300–305. 1996. April. 8722431. 10.1016/0895-7061(95)00342-8.
  61. Greingor JL, Tosi JM, Ruhlmann S, Aussedat M. Acute carbon monoxide intoxication during pregnancy. One case report and review of the literature. Emergency Medicine Journal: EMJ. 18. 5. 399–401. 2001. September. 11559621. 1725677. 10.1136/emj.18.5.399.
  62. Farrow JR, Davis GJ, Roy TM, McCloud LC, Nichols GR. Fetal death due to nonlethal maternal carbon monoxide poisoning. Journal of Forensic Sciences. 35. 6. 1448–1452. 1990. November. 2262778.
  63. Bennetto L, Powter L, Scolding NJ. Accidental carbon monoxide poisoning presenting without a history of exposure: A case report. Journal of Medical Case Reports. 2. 1. 118. 2008. April. 18430228. 10.1186/1752-1947-2-118. 2390579.
  64. Book: Ford MD, Delaney KA, Ling LJ, Erickson T. Clinical toxicology. 2001. 1046. WB Saunders Company. 0-7216-5485-1.
  65. Keleş A, Demircan A, Kurtoğlu G. Carbon monoxide poisoning: how many patients do we miss?. European Journal of Emergency Medicine. 15. 3. 154–157. 2008. June. 18460956. 10.1097/MEJ.0b013e3282efd519.
  66. Rodkey FL, Hill TA, Pitts LL, Robertson RF. Spectrophotometric measurement of carboxyhemoglobin and methemoglobin in blood. Clinical Chemistry. 25. 8. 1388–1393. 1979. August. 455674. 2009-07-17.
  67. Rees PJ, Chilvers C, Clark TJ. Evaluation of methods used to estimate inhaled dose of carbon monoxide. Thorax. 35. 1. 47–51. 1980. January. 7361284. 471219. 10.1136/thx.35.1.47.
  68. Coulange M, Barthelemy A, Hug F, Thierry AL, De Haro L. Reliability of new pulse CO-oximeter in victims of carbon monoxide poisoning. Undersea & Hyperbaric Medicine. 35. 2. 107–111. 2008. 18500075. March.
  69. Vegfors M, Lennmarken C. Carboxyhaemoglobinaemia and pulse oximetry. British Journal of Anaesthesia. 66. 5. 625–626. 1991. May. 2031826. 10.1093/bja/66.5.625.
  70. Barker SJ, Tremper KK. The effect of carbon monoxide inhalation on pulse oximetry and transcutaneous PO2. Anesthesiology. 66. 5. 677–679. 1987. May. 3578881. 10.1097/00000542-198705000-00014.
  71. M.. Jarvis. 1986. Low cost carbon monoxide monitors in smoking assessment. Thorax. 886–887.
  72. Nicholas. Wald. 1981. Carbon monoxide in breath in relation to smoking and carboxyhaemoglobin levels. Thorax. 366–369.
  73. Kao LW, Nañagas KA. Toxicity associated with carbon monoxide. Clinics in Laboratory Medicine. 26. 1. 99–125. 2006. March. 16567227. 10.1016/j.cll.2006.01.005.
  74. Web site: Shochat. Guy N. Toxicity, Carbon Monoxide. emedicine. 17 February 2009. 2009-04-27.
  75. Ilano AL, Raffin TA. Management of carbon monoxide poisoning. Chest. 1990. 165–9. 97. 1. 2403894. 10.1378/chest.97.1.165. Jan. Free full text.
  76. Sato K, Tamaki K, Hattori H, et al. Determination of total hemoglobin in forensic blood samples with special reference to carboxyhemoglobin analysis. For. Sci. Int. 48: 89-96, 1990.
  77. R. Baselt, Disposition of Toxic Drugs and Chemicals in Man, 8th edition, Biomedical Publications, Foster City, CA, 2008, pp. 237-241.
  78. Ernst A, Zibrak JD. Carbon monoxide poisoning. The New England Journal of Medicine. 339. 22. 1603–1608. 1998. November. 9828249. 10.1056/NEJM199811263392206.
  79. Official Website. UK Gas Safe Register: Being Gas Safe.
  80. Yoon SS, Macdonald SC, Parrish RG. Deaths from unintentional carbon monoxide poisoning and potential for prevention with carbon monoxide detectors. JAMA. 1998. 685–687. 279. 9. 9496987. 10.1001/jama.279.9.685. March. Free full text.
  81. Krenzelok EP, Roth R, Full R. Carbon monoxide ... the silent killer with an audible solution. The American Journal of Emergency Medicine. 1996. 484–486. 14. 5. 8765117. 10.1016/S0735-6757(96)90159-X. September.
  82. Web site: CO Alert. Placement of Carbon Monoxide Detectors Important. 2009-01-11.
  83. Web site: Lipinski. Edward R. Keeping Watch on Carbon Monoxide. New York Times. February 14, 1999. 2009-09-09.
  84. http://dspace.rubicon-foundation.org/xmlui/bitstream/handle/123456789/7964/DHM_V38N3_breathing_gas.pdf?sequence=1.
  85. Book: NFPA 720: Standard for the Installation of Carbon Monoxide (CO) Detection and Warning Equipment. National Fire Protection Agency. Quincy, MA. 2009.
  86. Olson KR. Carbon monoxide poisoning: mechanisms, presentation, and controversies in management. The Journal of Emergency Medicine. 1. 3. 233–243. 1984. 6491241. 10.1016/0736-4679(84)90078-7.
  87. Margulies JL. Acute carbon monoxide poisoning during pregnancy. The American Journal of Emergency Medicine. 4. 6. 516–519. 1986. November. 3778597. 10.1016/S0735-6757(86)80008-0.
  88. Brown DB, Mueller GL, Golich FC. Hyperbaric oxygen treatment for carbon monoxide poisoning in pregnancy: a case report. Aviation, Space, and Environmental Medicine. 63. 11. 1011–1014. 1992. November. 1445151.
  89. Juurlink DN, Buckley NA, Stanbrook MB, Isbister GK, Bennett M, McGuigan MA. Juurlink. David N. Hyperbaric oxygen for carbon monoxide poisoning. Cochrane Database of Systematic Reviews. 1. CD002041. 2005. 15674890. 10.1002/14651858.CD002041.pub2. January.
  90. Henry JA. Hyperbaric therapy for carbon monoxide poisoning: to treat or not to treat, that is the question. Toxicological Reviews. 24. 3. 149–150. 2005. 16390211. 10.2165/00139709-200524030-00002.
  91. Olson KR. Hyperbaric oxygen or normobaric oxygen?. Toxicological Reviews. 24. 3. 151. 2005. 16390212. 10.2165/00139709-200524030-00003.
  92. Seger D. The myth. Toxicological Reviews. 24. 3. 155–156. 2005. 16390214. 10.2165/00139709-200524030-00005.
  93. Thom SR. Hyperbaric oxygen therapy for carbon monoxide poisoning: Is it time to end the debates?. Toxicological Reviews. 24. 3. 157–158. 2005. 16390215. 10.2165/00139709-200524030-00006.
  94. Scheinkestel CD, Bailey M, Myles PS, Jones K, Cooper DJ, Millar IL, Tuxen DV. Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: a randomized controlled clinical trial. The Medical Journal of Australia. 1999. 203–210. 170. 5. 10092916. March. Free full text.
  95. Thom SR, Taber RL, Mendiguren II, Clark JM, Hardy KR, Fisher AB. Delayed neuropsychologic sequelae after carbon monoxide poisoning: prevention by treatment with hyperbaric oxygen. Annals of Emergency Medicine. 1995. 474–480. 25. 4. 7710151. 10.1016/S0196-0644(95)70261-X. April.
  96. Raphael JC, Elkharrat D, Jars-Guincestre MC, Chastang C, Chasles V, Vercken JB, Gajdos P.. Trial of normobaric and hyperbaric oxygen for acute carbon monoxide intoxication. Lancet. 1989. 414–419. 2. 8660. 2569600. 10.1016/S0140-6736(89)90592-8. August.
  97. Ducasse JL, Celsis P, Marc-Vergnes JP. Non-comatose patients with acute carbon monoxide poisoning: hyperbaric or normobaric oxygenation?. Undersea & Hyperbaric Medicine. 1995. 9–15. 22. 1. 7742714. March.
  98. Mathieu D, Mathieu-Nolf M, Durak C, Wattel F, Tempe JP, Bouachour G, Sainty JM.. Randomized prospective study comparing the effect of HBO vs 12 hours NBO in non-comatose CO-poisoned patients: results of the preliminary analysis. Undersea & Hyperbaric Medicine. 1996. 7. 23.
  99. Weaver LK, Hopkins RO, Chan KJ, Churchill S, Elliott CG, Clemmer TP, Orme JF Jr, Thomas FO, Morris AH. Hyperbaric oxygen for acute carbon monoxide poisoning. The New England Journal of Medicine. 2002. 1057–1067. 347. 14. 12362006. 10.1056/NEJMoa013121. October.
  100. Gorman DF.. Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: a randomised controlled clinical trial. Unfortunate methodological flaws. The Medical Journal of Australia. 1999. 563. 170. 11. 10397050. June.
  101. Scheinkestel CD, Jones K, Myles PS, Cooper DJ, Millar IL, Tuxen DV. Where to now with carbon monoxide poisoning?. Emergency Medicine Australasia: EMA. 2004. 151–154. 16. 2. 15239731. 10.1111/j.1742-6723.2004.00567.x. April.
  102. Isbister GK, McGettigan P, Harris I.. Hyperbaric oxygen for acute carbon monoxide poisoning. The New England Journal of Medicine. 2003. 557–560. 348. 6. 12572577. 10.1056/NEJM200302063480615. February.
  103. Tomaszewski C. Carbon monoxide poisoning. Early awareness and intervention can save lives. Postgraduate Medicine. 105. 1. 39–40, 43–48, 50. 1999. January. 9924492. 10.3810/pgm.1999.01.496.
  104. Peirce EC. Treating acidemia in carbon monoxide poisoning may be dangerous. Journal of Hyperbaric Medicine. 1. 2. 87–97. 1986.
  105. Devine SA, Kirkley SM, Palumbo CL, White RF. MRI and neuropsychological correlates of carbon monoxide exposure: a case report. Environmental Health Perspectives. 110. 10. 1051–1055. 2002. October. 12361932. 1241033. 10.1289/ehp.021101051.
  106. O'Donnell P, Buxton PJ, Pitkin A, Jarvis LJ. The magnetic resonance imaging appearances of the brain in acute carbon monoxide poisoning. Clinical Radiology. 55. 4. 273–280. 2000. April. 10767186. 10.1053/crad.1999.0369.
  107. Seger D, Welch L. Carbon monoxide controversies: neuropsychologic testing, mechanism of toxicity, and hyperbaric oxygen. Annals of Emergency Medicine. 24. 2. 242–248. 1994. August. 8037390. 10.1016/S0196-0644(94)70136-9.
  108. Chiang. CL. Tseng, MC. Safe use of electroconvulsive therapy in a highly suicidal survivor of carbon monoxide poisoning.. Gen Hosp Psychiatry. 27. 2011. September.
  109. Thom SR. Hyperbaric-oxygen therapy for acute carbon monoxide poisoning. The New England Journal of Medicine. 347. 14. 1105–1106. 2002. October. 12362013. 10.1056/NEJMe020103.
  110. Ernst A, Zibrak JD. Carbon monoxide poisoning. The New England Journal of Medicine. 339. 22. 1603–8. 1998. November. 9828249. 10.1056/NEJM199811263392206.
  111. Centers for Disease Control and Prevention (CDC). Deaths from motor-vehicle-related unintentional carbon monoxide poisoning—Colorado, 1996, New Mexico, 1980-1995, and United States, 1979-1992. MMWR. Morbidity and Mortality Weekly Report. 45. 47. 1029–32. 1996. November. 8965803.
  112. Partrick M, Fiesseler F, Shih R, Riggs R, Hung O. Monthly variations in the diagnosis of carbon monoxide exposures in the emergency department. Undersea & Hyperbaric Medicine: Journal of the Undersea and Hyperbaric Medical Society, Inc. 36. 3. 161–7. 2009. 19860138.
  113. Heckerling PS. Occult carbon monoxide poisoning: a cause of winter headache. The American Journal of Emergency Medicine. 5. 3. 201–4. 1987. May. 3580051. 10.1016/0735-6757(87)90320-2.
  114. Web site: Department of Public Health Warns of Dangers of Carbon Monoxide Poisoning During Power Outages. Tower Generator. 2011-11-23.
  115. Web site: Avoiding Carbon Monoxide poisoning during a power outage. CDC. 2011-11-23.
  116. Klein. Kelly. Herzogg, Perri; Smolinkski, Susan; White, Suzanne. Demand for poison control center services "surged" during the 2003 blackout.. Clinical Toxicology. 2007. 45. 3. 248–254.
  117. Hampson NB. Emergency department visits for carbon monoxide poisoning in the Pacific Northwest. The Journal of Emergency Medicine. 1998. 695–698. 16. 5. 9752939. 10.1016/S0736-4679(98)00080-8. September.
  118. Web site: Carbon Monoxide Detectors Can Save Lives: CPSC Document #5010. US Consumer Product Safety Commission. 2009-04-30. http://web.archive.org/web/20090409030219/http://www.cpsc.gov/CPSCPUB/PUBS/5010.html . 2009-04-09.
  119. Cobb N, Etzel RA. Unintentional carbon monoxide-related deaths in the United States, 1979 through 1988. JAMA. 266. 5. 659–663. 1991. August 7. 1712865. 10.1001/jama.266.5.659.
  120. Web site: Carbon Monoxide poisoning fact sheet. Centers for Disease Control and Prevention. July 2006. pdf. 2008-12-16.
  121. McDowell R, Fowles J, Phillips D. Deaths from poisoning in New Zealand: 2001-2002. The New Zealand Medical Journal. 118. 1225. U1725. 2005. November. 16286939. Free full text.
  122. Song KJ, Shin SD, Cone DC. Socioeconomic status and severity-based incidence of poisoning: a nationwide cohort study. Clinical toxicology (Philadelphia, Pa.). 47. 8. 818–826. 2009. September. 19640232. 10.1080/15563650903158870.
  123. Salameh S, Amitai Y, Antopolsky M, Rott D, Stalnicowicz R. Carbon monoxide poisoning in Jerusalem: epidemiology and risk factors. Clinical Toxicology (Philadelphia, Pa.). 47. 2. 137–41. 2009. February. 18720104. 10.1080/15563650801986711.
  124. Liu Q, Zhou L, Zheng N, Zhuo L, Liu Y, Liu L. Poisoning deaths in China: type and prevalence detected at the Tongji Forensic Medical Center in Hubei. Forensic Science International. 193. 1-3. 88–94. 2009. December. 19854011. 10.1016/j.forsciint.2009.09.013.
  125. Web site: Anderson. Scott. The Urge to End It All. New York Times. July 6, 2008. 2009-05-10.
  126. Wirth I, Strauch H. Suicides in East Berlin from 1980 to 1989. Archiv für Kriminologie. 219. 3-4. 73–88. 2007. March–April. 17539588.
  127. Thomsen AH, Gregersen M. Carbon monoxide deaths caused by town gas in Denmark 1995-99. Ugeskrift for laeger. 169. 21. 2020–2024. 2007. May 21. 17553384.
  128. Skopek MA, Perkins R. Deliberate exposure to motor vehicle exhaust gas: the psychosocial profile of attempted suicide. The Australian and New Zealand Journal of Psychiatry. 32. 6. 830–838. 1998. Dec. 10084348. 10.3109/00048679809073873.
  129. Oström M, Thorson J, Eriksson A. Carbon monoxide suicide from car exhausts. Social Science & Medicine. 42. 3. 447–451. 1996. Feb. 8658238. 10.1016/0277-9536(95)00104-2.
  130. Vossberg B, Skolnick J. The role of catalytic converters in automobile carbon monoxide poisoning: a case report. Chest. 1999. 580–581. 115. 2. 10027464. 10.1378/chest.115.2.580. February. Free full text.
  131. Hampson NB. Intentional carbon monoxide poisoning. Chest. 116. 2. 586–587. 1999. August. 10453903. 10.1378/chest.116.2.586.
  132. Oehme. C. Penning, R. Intentional Carbon monoxide poisoning by burning charcoal. MMW Fortschr Med. 16. 2011. June. 153. 24. 48–9. 21717712.
  133. Yang CC, Ger J, Li CF. Formic acid: a rare but deadly source of carbon monoxide poisoning. Clinical Toxicology. 46. 4. 287–9. 2008. April. 18363119. 10.1080/15563650701378746.
  134. Chung WS, Leung CM. Carbon monoxide poisoning as a new method of suicide in Hong Kong. Psychiatric Services (Washington, D.C.). 2001. 836–837. 52. 6. 11376237. 10.1176/appi.ps.52.6.836. June. Free full text.
  135. Prahlow JA, Doyle BW. A suicide using a homemade carbon monoxide "death machine".. Am J Forensic Med Pathol. 2005. 80–177. 15894855. June. Free full text.
  136. Naito A. Internet suicide in Japan: implications for child and adolescent mental health. Clinical Child Psychology and Psychiatry. 12. 4. 583–597. 2007. October. 18095539. 10.1177/1359104507080990.
  137. Leung CM, Chung WS, So EP. Burning charcoal: an indigenous method of committing suicide in Hong Kong. The Journal of Clinical Psychiatry. 63. 5. 447–450. 2002. May. 12019670. 10.4088/JCP.v63n0512.
  138. Lee DT, Chan KP, Yip PS. Charcoal burning is also popular for suicide pacts made on the internet. BMJ. 330. 7491. 602. 2005. March. 15761009. 554074. 10.1136/bmj.330.7491.602-b.
  139. Pan YJ, Liao SC, Lee MB. Suicide by charcoal burning in Taiwan, 1995-2006. Journal of Affective Disorders. 120. 1-3. 254–7. 2009. April. 19410296. 10.1016/j.jad.2009.04.003.
  140. 10.1258/rsmmsl.49.4.301. Brooks-Lim EW, Sadler DW. Suicide by burning barbecue charcoal: three case reports. Medicine, Science, and the Law. 49. 4. 301–6. 2009. October. 20025107.
  141. Patel F. Carbon copy deaths: carbon monoxide gas chamber. Journal of Forensic and Legal Medicine. 15. 6. 398–401. 2008. August. 18586213. 10.1016/j.jflm.2008.01.004.
  142. Hunt IM, While D, Windfuhr K, Swinson N, Shaw J, Appleby L, Kapur N. Suicide pacts in the mentally ill: a national clinical survey. Psychiatry Research. 167. 1-2. 131–8. 2009. May. 19342106. 10.1016/j.psychres.2008.05.004.
  143. Web site: Police Report On Delp's Death Reveals His Final Message. WMUR. 2007-03-14. 2007-04-30.