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 motor vehicles that run on gasoline, diesel, propane, methane, or other carbon-based fuels and tools, heaters, and cooking equipment that are powered by carbon-based fuels. Exposures at 100 ppm or greater can be dangerous to human health.
Symptoms of mild acute poisoning will include light-headedness, 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 hemoglobin from releasing oxygen in tissues, effectively 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 automobiles, even with electronically-controlled combustion and catalytic converters, can still produce levels of carbon monoxide which will kill if enclosed within a garage or if the tailpipe is obstructed (for example, by snow) and exhaust gas cannot escape normally. 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.
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 people after 2 to 40 days. It is difficult to predict who will develop delayed sequelae; however, advanced age, loss of consciousness while poisoned, and initial neurological abnormalities may increase the chance of developing delayed symptoms.
One classic sign of carbon monoxide poisoning is more often seen in the dead rather than the living – people have been described as looking red-cheeked and healthy (see below). 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 lifelike in coloration. 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 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. Chronic carbon monoxide exposure might increase the risk of developing atherosclerosis. Long-term exposures to carbon monoxide present the greatest risk to persons with coronary heart disease and in females who are pregnant.
Carbon monoxide as a therapeutic agent
Small amounts of CO are beneficial and enzymes exist that produce it at times of oxidative stress. Drugs are being developed to introduce small amounts of CO during certain kinds of surgery, these drugs are called Carbon monoxide-releasing molecules.
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. As part of the Holocaust during World War II, German Nazis used gas vans to kill an estimated 700,000 prisoners by carbon monoxide poisoning. This method was also used in the gas chambers of several death camps.
Another source of poisoning is exposure to the organic solvent dichloromethane, found in some paint strippers, as the metabolism of dichloromethane produces carbon monoxide. Any perforation between the exhaust manifold and shroud can result in exhaust gases reaching the cabin. In caves carbon monoxide can build up in enclosed chambers due to the presence of decomposing organic matter.
Carbon monoxide shifts the oxygen-dissociation curve to the left.
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 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, little oxygen will actually be released in the tissues. This causes hypoxic tissue injury. 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.
Carbon monoxide also binds to the hemeproteinmyoglobin. 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.
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.
Finger tip carboxyhemoglobin saturation monitor (SpCO%). Note: This is not the same as a pulse oximeter (SpO2%), although some models (such as this one) do measure both the oxygen and carbon monoxide saturation.
Breath CO monitor displaying carbon monoxide concentration of an exhaled breath sample (in ppm) with its corresponding percent concentration of carboxyhemoglobin.
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.
As people may continue to experience significant symptoms of CO poisoning long after their blood carboxyhemoglobin concentration has returned to normal, presenting to examination with a normal carboxyhemoglobin level (which may happen in late states of poisoning) 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.
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. 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. However, many of these devices require the user to inhale deeply and hold their breath to allow the CO in the blood to escape into the lung before the measurement can be made. As this is not possible in a nonresponsive patient, these devices are not appropriate for use in on-scene emergency care detection of CO poisoning.
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%.
Naturally-occurring and beneficial effects of CO
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 carboxyhemoglobin, but not at toxic levels. In fact exploratory therapies include administering carbon monoxide to the patient using carbon monoxide-releasing molecules. 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%.
Carbon monoxide detector connected to a North American power outlet
Carbon monoxide detector recommendations for buildings
Prevention remains a vital public health issue, requiring public education on the safe operation of appliances, heaters, fireplaces, and internal-combustion engines, as well as increased emphasis on the installation of carbon monoxide detectors. Carbon monoxide is tasteless and odourless so can not be detected by smell.
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. 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 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.
The NFPA standard is not necessarily enforced by law. As of April 2006, the U.S. state of Massachusetts require detectors to be present in all residences with potential CO sources, regardless of building age and whether they are owner-occupied or rented. This is enforced by municipal inspectors, and was inspired by the death of 7-year-old Nicole Garofalo in 2005 due to snow blocking a home heating vent. Other jurisdictions may have no requirement or only mandate detectors for new construction or at time of sale.
Gas organizations will often recommend to get gas appliances serviced at least once a year.
Recommended World Health Organisation (WHO) Air Quality guidelines for Europe 2000
The following guideline values (ppm values rounded) and periods of time-weighted average exposures have been determined in such a way that the carboxyhaemoglobin (COHb) level of 2.5% is not exceeded, even when a normal subject engages in light or moderate exercise:
100 mg/m3 (87 ppm) for 15 min
60 mg/m3 (52 ppm) for 30 min
30 mg/m3 (26 ppm) for 1 h
10 mg/m3 (9 ppm) for 8 h
Recommended WHO European Guidelines for Indoor Air Quality 2010
7 mg/m3 (6 ppm) for 24 h (so as not to exceed 2% COHb for chronic exposure)
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 people.
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 (~80/3 minutes) 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 people 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. It has been reported that electroconvulsive therapy (ECT) may increase the likelihood of delayed neuropsychiatric sequelae (DNS) after carbon monoxide (CO) poisoning.
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 is due to increased domestic use of gas furnaces, gas or kerosene space heaters, and kitchen stoves during the winter months, which if faulty and/or used without adequate ventilation, may produce excessive carbon monoxide. Carbon monoxide detection and poisoning also increases during power outages.
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.
^first draft prepared by Mr J. Raub. (1999). Environmental Health Criteria 213 (Carbon Monoxide). Geneva: International Programme on Chemical Safety, World Health Organization. ISBN92-4-157213-2.
^Goldstein M (December 2008). "Carbon monoxide poisoning". Journal of Emergency Nursing: JEN: Official Publication of the Emergency Department Nurses Association34 (6): 538–542. doi:10.1016/j.jen.2007.11.014. PMID19022078.
^Struttmann T, Scheerer A, Prince TS, Goldstein LA (Nov 1998). "Unintentional carbon monoxide poisoning from an unlikely source". The Journal of the American Board of Family Practice11 (6): 481–484. doi:10.3122/jabfm.11.6.481. PMID9876005.
^ abcdefghijklmnLewis Goldfrank; Neal Flomenbaum; Neal Lewin; Mary Ann Howland; Robert Hoffman; Lewis Nelson (2002). "Carbon Monoxide". Goldfrank's toxicologic emergencies (7th ed.). New York: McGraw-Hill. pp. 1689–1704. ISBN0-07-136001-8.
^Tritapepe L, Macchiarelli G, Rocco M, Scopinaro F, Schillaci O, Martuscelli E, Motta PM (April 1998). "Functional and ultrastructural evidence of myocardial stunning after acute carbon monoxide poisoning". Critical Care Medicine26 (4): 797–801. doi:10.1097/00003246-199804000-00034. PMID9559621.
^Marius-Nunez AL (February 1990). "Myocardial infarction with normal coronary arteries after acute exposure to carbon monoxide". Chest97 (2): 491–4. doi:10.1378/chest.97.2.491. PMID2298080.
^Gandini C, Castoldi AF, Candura SM, Locatelli C, Butera R, Priori S, Manzo L (2001). "Carbon monoxide cardiotoxicity". Journal of Toxicology. Clinical Toxicology39 (1): 35–44. doi:10.1081/CLT-100102878. PMID11327225.
^Sokal JA (December 1985). "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: JAT5 (6): 395–7. doi:10.1002/jat.2550050611. PMID4078220.
^ abcdFawcett TA, Moon RE, Fracica PJ, Mebane GY, Theil DR, Piantadosi CA (January 1992). "Warehouse workers' headache. Carbon monoxide poisoning from propane-fueled forklifts". Journal of Occupational Medicine34 (1): 12–15. PMID1552375.
^Ryan CM (1990). "Memory disturbances following chronic, low-level carbon monoxide exposure". Archives of Clinical Neuropsychology: the Official Journal of the National Academy of Neuropsychologists5 (1): 59–67. doi:10.1016/0887-6177(90)90007-C. PMID14589544.
^Davutoglu, V (November 2009). "Chronic carbon monoxide exposure is associated with the increases in carotid intima-media thickness and C-reactive protein level". Tohoku J Exp Med219 (3): 201–6. doi:10.1620/tjem.219.201.
^Shephard, Roy (1983). Carbon Monoxide The Silent Killer. Springfield Illinois: Charles C Thomas. pp. 93–96.
^Allred EN, Bleecker ER, Chaitman BR, Dahms TE, Gottlieb SO, Hackney JD, Pagano M, Selvester RH, Walden SM, Warren J (Nov 1989). "Short-term effects of carbon monoxide exposure on the exercise performance of subjects with coronary artery disease". The New England Journal of Medicine321 (21): 1426–1432. doi:10.1056/NEJM198911233212102. PMID2682242.
^Committee on Medical and Biological Effects of Environmental Pollutants (1977). Carbon Monoxide. Washington, D.C.: National Academy of Sciences. p. 29. ISBN0-309-02631-8.
^Marc B, Bouchez-Buvry A, Wepierre JL, Boniol L, Vaquero P, Garnier M (June 2001). "Carbon-monoxide poisoning in young drug addicts due to indoor use of a gasoline-powered generator". Journal of Clinical Forensic Medicine8 (2): 54–56. doi:10.1054/jcfm.2001.0474. PMID16083675.
^Fife CE, Smith LA, Maus EA, McCarthy JJ, Koehler MZ, Hawkins T, Hampson NB (June 2009). "Dying to play video games: carbon monoxide poisoning from electrical generators used after hurricane Ike". Pediatrics123 (6): e1035–8. doi:10.1542/peds.2008-3273. PMID19482736.
^Austin CC, Ecobichon DJ, Dussault G, Tirado C (December 1997). "Carbon monoxide and water vapor contamination of compressed breathing air for firefighters and divers". Journal of Toxicology and Environmental Health52 (5): 403–423. doi:10.1080/00984109708984073. PMID9388533.
^Centers for Disease Control and Prevention (CDC) (December 2000). "Houseboat-associated carbon monoxide poisonings on Lake Powell—Arizona and Utah, 2000". MMWR: Morbidity and Mortality Weekly Report49 (49): 1105–1108. PMID11917924.
^van Veen, MP; Fortezza F; Spaans E; Mensinga TT (2002). "Non-professional paint stripping, model prediction and experimental validation of indoor dichloromethane levels". Indoor Air12 (2): 92–7. doi:10.1034/j.1600-0668.2002.01109.x.
^Kubic VL, Anders MW (March 1975). "Metabolism of dihalomethanes to carbon monoxide. II. In vitro studies". Drug metabolism and disposition3 (2): 104–112. PMID236156.
^Dueñas A, Felipe S, Ruiz-Mambrilla M, Martín-Escudero JC, García-Calvo C (January 2000). "CO poisoning caused by inhalation of CH3Cl contained in personal defense spray". The American Journal of Emergency Medicine18 (1): 120–121. doi:10.1016/S0735-6757(00)90070-6. PMID10674554.
^Fukuhara M, Abe I, Matsumura K, Kaseda S, Yamashita Y, Shida K, Kawashima H, Fujishima M (April 1996). "Circadian variations of blood pressure in patients with sequelae of carbon monoxide poisoning". American Journal of Hypertension9 (4 Part 1): 300–305. doi:10.1016/0895-7061(95)00342-8. PMID8722431.
^Maisel, William; Roger J. Lewis (2010). "Noninvasive Measurement of Carboxyhemoglobin: How Accurate is Accurate Enough?". Annals of Emergency Medicine (Boston, MA) 56 (4): 389–391. doi:10.1016/j.annemergmed.2010.05.025.
^Brown DB, Mueller GL, Golich FC (November 1992). "Hyperbaric oxygen treatment for carbon monoxide poisoning in pregnancy: a case report". Aviation, Space, and Environmental Medicine63 (11): 1011–1014. PMID1445151.
^Juurlink DN, Buckley NA, Stanbrook MB, Isbister GK, Bennett M, McGuigan MA (January 2005). Juurlink, David N, ed. "Hyperbaric oxygen for carbon monoxide poisoning". Cochrane Database of Systematic Reviews (1): CD002041. doi:10.1002/14651858.CD002041.pub2. PMID15674890.
^Thom SR, Taber RL, Mendiguren II, Clark JM, Hardy KR, Fisher AB (April 1995). "Delayed neuropsychologic sequelae after carbon monoxide poisoning: prevention by treatment with hyperbaric oxygen". Annals of Emergency Medicine25 (4): 474–480. doi:10.1016/S0196-0644(95)70261-X. PMID7710151.
^Raphael JC, Elkharrat D, Jars-Guincestre MC, Chastang C, Chasles V, Vercken JB, Gajdos P. (August 1989). "Trial of normobaric and hyperbaric oxygen for acute carbon monoxide intoxication". Lancet2 (8660): 414–419. doi:10.1016/S0140-6736(89)90592-8. PMID2569600.
^Weaver LK, Hopkins RO, Chan KJ, Churchill S, Elliott CG, Clemmer TP, Orme JF Jr, Thomas FO, Morris AH (October 2002). "Hyperbaric oxygen for acute carbon monoxide poisoning". The New England Journal of Medicine347 (14): 1057–1067. doi:10.1056/NEJMoa013121. PMID12362006.
^Gorman DF. (June 1999). "Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: a randomised controlled clinical trial. Unfortunate methodological flaws". The Medical Journal of Australia170 (11): 563. PMID10397050.
^Buckley NA, Juurlink DN (June 2013). "Carbon monoxide treatment guidelines must acknowledge the limitations of the existing evidence". American Journal of Respiratory and Critical Care Medicine187 (12): 1390. doi:10.1164/rccm.201212-2262LE. PMID23767905.
^Tomaszewski C (January 1999). "Carbon monoxide poisoning. Early awareness and intervention can save lives". Postgraduate Medicine105 (1): 39–40, 43–48, 50. doi:10.3810/pgm.1999.01.496. PMID9924492.
^O'Donnell P, Buxton PJ, Pitkin A, Jarvis LJ (April 2000). "The magnetic resonance imaging appearances of the brain in acute carbon monoxide poisoning". Clinical Radiology55 (4): 273–280. doi:10.1053/crad.1999.0369. PMID10767186.
^Seger D, Welch L (August 1994). "Carbon monoxide controversies: neuropsychologic testing, mechanism of toxicity, and hyperbaric oxygen". Annals of Emergency Medicine24 (2): 242–248. doi:10.1016/S0196-0644(94)70136-9. PMID8037390.
^Chiang, CL; Tseng, MC (27 September 2011). "Safe use of electroconvulsive therapy in a highly suicidal survivor of carbon monoxide poisoning.". Gen Hosp Psychiatry.
^Thom SR (October 2002). "Hyperbaric-oxygen therapy for acute carbon monoxide poisoning". The New England Journal of Medicine347 (14): 1105–1106. doi:10.1056/NEJMe020103. PMID12362013.
^Partrick M, Fiesseler F, Shih R, Riggs R, Hung O (2009). "Monthly variations in the diagnosis of carbon monoxide exposures in the emergency department". Undersea & Hyperbaric Medicine: Journal of the Undersea and Hyperbaric Medical Society, Inc36 (3): 161–7. PMID19860138.
^Klein, Kelly; Herzog, Perri; Smolinske, Susan; White, Suzanne (2007). "Demand for poison control center services "surged" during the 2003 blackout.". Clinical Toxicology45 (3): 248–254. doi:10.1080/15563650601031676.
^Salameh S, Amitai Y, Antopolsky M, Rott D, Stalnicowicz R (February 2009). "Carbon monoxide poisoning in Jerusalem: epidemiology and risk factors". Clinical Toxicology (Philadelphia, Pa.)47 (2): 137–41. doi:10.1080/15563650801986711. PMID18720104.
^Liu Q, Zhou L, Zheng N, Zhuo L, Liu Y, Liu L (December 2009). "Poisoning deaths in China: type and prevalence detected at the Tongji Forensic Medical Center in Hubei". Forensic Science International193 (1–3): 88–94. doi:10.1016/j.forsciint.2009.09.013. PMID19854011.
^Wirth I, Strauch H (March–April 2007). "Suicides in East Berlin from 1980 to 1989". Archiv für Kriminologie219 (3–4): 73–88. PMID17539588.
^Thomsen AH, Gregersen M (May 21, 2007). "Carbon monoxide deaths caused by town gas in Denmark 1995–99". Ugeskrift for laeger169 (21): 2020–2024. PMID17553384.
^Skopek MA, Perkins R (Dec 1998). "Deliberate exposure to motor vehicle exhaust gas: the psychosocial profile of attempted suicide". The Australian and New Zealand Journal of Psychiatry32 (6): 830–838. doi:10.3109/00048679809073873. PMID10084348.
^Leung CM, Chung WS, So EP (May 2002). "Burning charcoal: an indigenous method of committing suicide in Hong Kong". The Journal of Clinical Psychiatry63 (5): 447–450. doi:10.4088/JCP.v63n0512. PMID12019670.
^Hunt IM, While D, Windfuhr K, Swinson N, Shaw J, Appleby L, Kapur N (May 2009). "Suicide pacts in the mentally ill: a national clinical survey". Psychiatry Research167 (1–2): 131–8. doi:10.1016/j.psychres.2008.05.004. PMID19342106.