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Carbon monoxide poisoning occurs after the inhalation of carbon monoxide gas. Carbon monoxide (CO) is a product of combustion of organic matter under conditions of restricted oxygen supply, which prevents complete oxidation to carbon dioxide (CO2). Carbon monoxide is colorless, odorless, tasteless, and non-irritating, making it difficult for people to detect.
Carbon monoxide is a significantly toxic gas with poisoning being the most common type of fatal poisoning in many countries. Symptoms of mild poisoning include headaches and flu-like effects; larger exposures can lead to significant toxicity of the central nervous system and heart. Following poisoning, long-term sequelae often occur. Carbon monoxide can also have severe effects on the fetus of a pregnant woman.
The mechanisms by which carbon monoxide produces toxic effects are not yet fully understood, but hemoglobin, myoglobin, and mitochondrial cytochrome oxidase are thought to be compromised. Treatment largely consists of administering 100% oxygen or hyperbaric oxygen therapy, although the optimum treatment remains controversial. Domestic carbon monoxide poisoning can be prevented by the use of household carbon monoxide detectors.
Common sources of CO that may lead to poisoning include house fires, furnaces or heaters, wood-burning stoves, motor vehicle exhaust, and propane-fueled equipment such as portable camping stoves, ice resurfacers, forklifts, and engine-driven generators. CO poisoning can also occur in scuba diving due to faulty or badly sited diving air compressors. (See Effects of relying on breathing equipment while underwater for more information) Another source is exposure to the organic solvent methylene chloride, which is metabolized to CO by the body.
Carbon monoxide poisoning is the most common type of fatal poisoning in France and the United States. It has been estimated that more than 40,000 people per year seek medical attention for carbon monoxide poisoning in the United States. In many industrialized countries, carbon monoxide may be the cause of greater than 50% of fatal poisonings. In the U.S., about 200 people die each year from carbon monoxide poisoning associated with home fuel-burning heating equipment. The CDC reports, "Each year, more than 500 Americans die from unintentional CO poisoning, and more than 2,000 commit suicide by intentionally poisoning themselves."
As other poisons such as cyanide and arsenic were placed under increasingly stringent legal restrictions, the carbon monoxide in town gas became the principal method of suicide by poisoning.[How to reference and link to summary or text] Suicide was also often committed by inhaling exhaust fumes of running car engines. In the past, motor car exhaust may have contained up to 25% carbon monoxide. However, newer cars have catalytic converters, which can eliminate over 99% of carbon monoxide produced. However, even cars with catalytic converters can produce substantial carbon monoxide if an idling car is left in an enclosed space. This is due to reduced oxygen availability, and therefore, less efficient combustion.
As carbon monoxide poisoning via car exhaust has become less of a suicide option, there has been an increase in new methods of carbon monoxide poisoning such as burning charcoal or other fossil fuels within a confined space, such as a small room, tent, or car. Such incidents have occurred mostly in connection with group suicide pacts in both Japan and Hong Kong, but are starting to occur in western countries as well, such as the 2007 suicide of Boston lead singer Brad Delp.
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, and migraine or other headaches. This often makes the diagnosis of carbon monoxide poisoning difficult. If suspected, the diagnosis can be confirmed by measurement of blood carboxyhemoglobin.
The main manifestations of poisoning develop in the organ systems most dependent on oxygen use: the central nervous system and the heart. The clinical manifestations include tachycardia and hypertension, and central nervous system symptoms such as headache, dizziness, confusion, convulsions, and unconsciousness. CO poisoning may also produce myocardial ischemia, atrial fibrillation, pneumonia, pulmonary edema, hyperglycemia, muscle necrosis, acute renal failure, skin lesions, visual and auditory problems, and respiratory arrest.
One of the major concerns following CO poisoning is the severe neurological manifestations that may occur days or even weeks after an acute poisoning. Common problems encountered are difficulty with higher intellectual functions and short-term memory, dementia, irritability, gait disturbance, speech disturbances, parkinson-like syndromes, cortical blindness, and depression (depression can occur in those accidentally exposed). These delayed sequelae occur in approximately 15 percent of severely poisoned patients after an interval of 2 to 28 days. It is difficult to predict who may develop delayed sequelae; however, advancing age, loss of consciousness while poisoned, and initial neurological abnormalities may indicate a greater chance of developing delayed symptoms. According to the Philadelphia poison control hotline, sequelae are generally not anticipated when exposure is not severe enough to result in loss of consciousness.
Long term, repeat exposures present a greater risk to persons with coronary heart disease and in pregnant patients. Chronic exposure may increase the incidence of cardiovascular symptoms in some workers, such as motor vehicle examiners, firefighters, and welders. Patients often complain of persistent headaches, lightheadedness, depression, confusion, and nausea. Upon removal from exposure, the symptoms usually resolve themselves.
Carbon monoxide is a significantly toxic gas, although patients may demonstrate varied clinical manifestations with different outcomes, even under similar exposure conditions. Toxicity is also increased by several factors, including: increased activity and rate of ventilation, pre-existing cerebral or cardiovascular disease, reduced cardiac output, anemia or other hematological disorders, decreased barometric pressure, and high metabolic rate.
Under ordinary conditions, it is less dense than air, but during fires, it accumulates on the ground, so that if poisoning causes loss of consciousness, the amount of carbon monoxide inhaled increases and the possibility of fatality is radically increased.
Carbon monoxide is life-threatening to humans and other forms of air-breathing life, as inhaling even relatively small amounts of it can lead to hypoxic injury, neurological damage, and possibly death. A concentration of as little as 0.04% (400 parts per million) carbon monoxide in the air can be fatal. The gas is especially dangerous because it is not easily detected by human senses. Early symptoms of carbon monoxide poisoning include drowsiness and headache, followed by unconsciousness, respiratory failure, and death. First aid for a victim of carbon monoxide poisoning requires access to fresh air; administration of artificial respiration and, if available, oxygen; and, as soon as possible, medical attention.
When carbon monoxide is inhaled, it takes the place of oxygen in hemoglobin, the red blood pigment that normally carries oxygen to all parts of the body. Because carbon monoxide binds to hemoglobin several hundred times more strongly than oxygen, its effects are cumulative and long-lasting, causing oxygen starvation throughout the body. Prolonged exposure to fresh air (or pure oxygen) is required for the CO-tainted hemoglobin (carboxyhemoglobin) to clear.
The effects of carbon monoxide in parts per million are listed below:
- 35 ppm (0.0035%) Headache and dizziness within six to eight hours of constant exposure
- 100 ppm (0.01%) Slight headache in two to three hours
- 200 ppm (0.02%) Slight headache within two to three hours
- 400 ppm (0.04%) Frontal headache within one to two hours
- 800 ppm (0.08%) Dizziness, nausea, and convulsions within 45 minutes. Insensible within two hours.
- 1,600 ppm (0.16%) Headache, dizziness, and nausea within 20 minutes. Death in less than two hours.
- 3,200 ppm (0.32%) Headache, dizziness and nausea in five to ten minutes. Death within 30 minutes.
- 6,400 ppm (0.64%) Headache and dizziness in one to two minutes. Death in less than 20 minutes.
- 12,800 ppm (1.28%) Death in less than three minutes.
Levels of carbon monoxide bound in the blood can be determined by measuring carboxyhemoglobin, which is a stable complex of carbon monoxide and hemoglobin that forms in red blood cells. Carbon monoxide is produced normally in the body, establishing a low background carboxyhemoglobin saturation. Carbon monoxide also functions as a neurotransmitter. Normal carboxyhemoglobin levels in an average person are less than 5%, whereas cigarette smokers (two packs/day) may have levels up to 9%.
Serious toxicity is often associated with carboxyhemoglobin levels above 25%, and the risk of fatality is high with levels over 70%. Still, no consistent dose response relationship has been found between carboxyhemoglobin levels and clinical effects. Therefore, carboxyhemoglobin levels are more guides to exposure levels than effects as they do not reliably predict clinical course or short- or long-term outcome.
The precise mechanisms by which toxic effects are induced by CO are not fully understood.
Carbon monoxide has a significant affinity to the iron sites in hemoglobin, the principal oxygen-carrying compound in blood. The affinity between carbon monoxide and hemoglobin is 240 times stronger than the affinity between hemoglobin and oxygen.
CO binds to hemoglobin, producing carboxyhemoglobin (COHb) - the traditional belief is that carbon monoxide toxicity arises from the formation of carboxyhemoglobin, which decreases the oxygen-carrying capacity of the blood. This inhibits the transport, delivery, and utilization of oxygen.  Because hemoglobin is a tetramer with four oxygen binding sites, binding of CO at one of these sites also increases the oxygen affinity of the remaining 3 sites, which interferes with normal release of oxygen. This causes hemoglobin to retain oxygen that would otherwise be delivered to the tissue. 
Levels of oxygen available for tissue use are decreased. This situation is described as CO shifting the oxygen dissociation curve to the left. Blood oxygen content is actually increased in the case of carbon monoxide poisoning; because all the oxygen is in the blood, none is being given to the tissues, and this causes tissue hypoxic injury. However, despite CO affecting oxygen availability, other mechanisms may contribute to the crucial effects of CO poisoning.
A sufficient exposure to carbon monoxide can reduce the amount of oxygen taken up by the brain to the point that the victim becomes unconscious, and can suffer brain damage or even death from hypoxia. The brain regulates breathing based upon carbon dioxide levels in the blood, rather than oxygen levels, so a victim can succumb to hypoxia without ever noticing anything up to the point of collapse. Hallmark pathological change following CO poisoning is bilateral necrosis of the pallidum.
Hemoglobin acquires a bright red color when converted to carboxyhemoglobin, so a casualty of CO poisoning is described in textbooks as looking pink-cheeked and healthy. However, this "classic" cherry-red appearance is not always seen — in one study it was noted in only 2% of cases — so care should be taken not to overlook the diagnosis even if this color is not present.
Carbon monoxide also has a high affinity for myoglobin. CO bound to myoglobin may impair cardiac output and result in cerebral ischemia. A delayed return of symptoms has been reported and appears to result following a recurrence of increased carboxyhemoglobin levels; this effect may be due to late release of CO from myoglobin, which subsequently binds to hemoglobin.
A second mechanism involves co-effects on the mitochondrial respiratory enzyme chain that is responsible for effective tissue utilization of oxygen. CO does not bind to cytochrome oxidase with the same affinity as oxygen, so it likely requires significant intracellular hypoxia before binding. This binding interferes with aerobic metabolism and efficient adenosine triphosphate (ATP) synthesis. Cells respond by switching to anaerobic metabolism, causing anoxia, lactic acidosis, and eventual cell death.
Another mechanism that is thought to have a significant influence on delayed effects involves formed blood cells and chemical mediators, which cause brain lipid peroxidation.
CO causes endothelial cell and platelet release of nitric oxide, and the formation of oxygen free radicals including peroxynitrite. In the brain, this causes further mitochondrial dysfunction, capillary leakage, leukocyte sequestration, and apoptosis. The end result is lipid peroxidation (degradation of unsaturated fatty acids), which causes delayed reversible demyelinization of white matter in the central nervous system, and can lead to edema and focal areas of necrosis within the brain.
This brain damage occurs mainly during the recovery period and results in cognitive defects (especially affecting memory and learning) and movement disorders. The movement disorders are related to a predilection of CO to damage the basal ganglia. These delayed neurological effects may develop over days following the initial acute poisoning.
Carbon monoxide poisoning can have significant fetal effects. CO causes fetal tissue hypoxia by decreasing the release of maternal oxygen to the fetus, and by carbon monoxide crossing the placenta and combining with fetal hemoglobin, which has a 10 to 15% higher affinity for CO than adult hemoglobin. Elimination of carbon monoxide is also slower in the fetus, leading to an accumulation of CO. The level of fetal morbidity and mortality in acute carbon monoxide poisoning is significant, so despite maternal wellbeing, severe fetal poisoning can still occur. Due to these effects, pregnant patients are treated with normal or hyperbaric oxygen for longer periods of time than non-pregnant patients.
First aid for carbon monoxide poisoning is to immediately remove the victim from the exposure without endangering oneself, call for help, and apply CPR if needed. The main medical treatment for carbon monoxide poisoning is 100% oxygen by a tight fitting oxygen mask. Oxygen hastens the dissociation of carbon monoxide from hemoglobin, improving tissue oxygenation by reducing its biological half-life. Hyperbaric oxygen is also used in the treatment of CO poisoning; hyperbaric oxygen also increases carboxyhemoglobin dissociation and does so to a greater extent than normal oxygen. Hyperbaric oxygen may also facilitate the dissociation of CO from cytochrome oxidase.
A significant controversy in the medical literature is whether or not hyperbaric oxygen actually offers any extra benefits over normal high flow oxygen in terms of increased survival or improved long term outcomes. There have been clinical trials 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 recent robust review of all the literature on carbon monoxide treatment concluded that the role of hyperbaric oxygen is unclear and the available evidence neither confirms nor denies a clinically meaningful benefit. The authors suggested a large, well designed, externally audited, multicentre trial to compare normal oxygen with hyperbaric oxygen.
Further specific treatment for other complications such as seizure, cardiac abnormalities, pulmonary edema, and acidosis may be required. The delayed development of neuropsychiatric impairment is one of the most serious complications of poisoning, with extensive follow up and treatment often being required.
Prevention remains a vital public health issue, requiring public education on the safe operation of appliances, heaters, fireplaces, and internal-combustion engines, as well as increased emphasis on the installation of carbon monoxide detectors. Carbon monoxide alarms are usually installed in homes around heaters and other equipment. If a high level of CO is detected, the device sounds an alarm, giving people in the area a chance to ventilate the area or safely leave the building. Unlike smoke detectors, they do not need to be placed near ceiling level. The Consumer Product Safety Commission says that "carbon monoxide detectors are as important to home safety as smoke detectors are," and recommends that each home should have at least one carbon monoxide detector.
The devices, which retail for USD$20-$60 and are widely available, can either be battery-operated or AC powered (with or without a battery backup). Since CO is colorless and odorless (unlike smoke from a fire), detection in a home environment is impossible without such a warning device. Some state and municipal governments, including those of Ontario, Canada, and New York City, require installation of CO detectors in new units. Massachusetts and Illinois began to require a detector in all residences on January 1, 2007.
The carbon monoxide can be easily detected by the filtering paper impregnated by the solution of the palladium chloride. Carbon monoxide reduces the palladium monoxide to the black metallic palladium. This reaction is very sensitive.
- ↑ 1.0 1.1 1.2 1.3 Omaye ST. (2002). Metabolic modulation of carbon monoxide toxicity. Toxicology 180 (2): 139-50. PMID 12324190.
- ↑ 2.0 2.1 Buckley NA, Isbister GK, Stokes B, Juurlink DN. (2005). Hyperbaric oxygen for carbon monoxide poisoning : a systematic review and critical analysis of the evidence. Toxicol Rev 24 (2): 75-92. PMID 16180928.
- ↑ Johnson C, Moran J, Paine S, Anderson H, Breysse P (1975). Abatement of toxic levels of carbon monoxide in Seattle ice-skating rinks. Am J Public Health 65 (10): 1087-90. PMID 1163706.
- ↑ Fawcett T, Moon R, Fracica P, Mebane G, Theil D, Piantadosi C (1992). Warehouse workers' headache. Carbon monoxide poisoning from propane-fueled forklifts. J Occup Med 34 (1): 12-5. PMID 1552375.
- ↑ Non-fire carbon monoxide deaths associated with the use of consumer products
- ↑ Kubic VL, Anders MW. (1975). Metabolism of dihalomethanes to carbon monoxide. II. In vitro studies. Drug Metab Dispos 3 (2): 104-12. PMID 236156.
- ↑ Hampson NB. (1998). Emergency department visits for carbon monoxide poisoning in the Pacific Northwest. J Emerg Med 16 (5): 695-8. PMID 9752939.
- ↑ 
- ↑ 
- ↑ Vossberg B, Skolnick J. (1999). The role of catalytic converters in automobile carbon monoxide poisoning: a case report. Chest 115 (2): 580-1. PMID 10027464.
- ↑ Chung WS, Leung CM. (2001). Carbon monoxide poisoning as a new method of suicide in Hong Kong. Psychiatr Serv 52 (6): 836-7. PMID 11376237.
- ↑ Police Report On Delp's Death Reveals His Final Message. WMUR. URL accessed on 2007-04-30.
- ↑ Ilano AL, Raffin TA. (1990). Management of carbon monoxide poisoning. Chest 97 (1): 165-9. PMID 2403894.
- ↑ Choi IS. (2001). Carbon monoxide poisoning: systemic manifestations and complications. J Korean Med Sci 16 (3): 253-61. PMID 11410684.
- ↑ Roohi F, Kula RW, Mehta N. (2001). Twenty-nine years after carbon monoxide intoxication. Clin Neurol Neurosurg 103 (2): 92-5. PMID 11516551.
- ↑ Allred EN, Bleecker ER, Chaitman BR, Dahms TE, Gottlieb SO, Hackney JD, Pagano M, Selvester RH, Walden SM, Warren J. (1989). Short-term effects of carbon monoxide exposure on the exercise performance of subjects with coronary artery disease. N Engl J Med 321 (21): 1426-32. PMID 2682242.
- ↑ Fawcett TA, Moon RE, Fracica PJ, Mebane GY, Theil DR, Piantadosi CA. (1992). Warehouse workers' headache. Carbon monoxide poisoning from propane-fueled forklifts. J Occup Med 34 (1): 12-5. PMID 1552375.
- ↑ Raub JA, Mathieu-Nolf M, Hampson NB, Thom SR. (2000). Carbon monoxide poisoning-a public health perspective. Toxicology 145 (1): 1-14. PMID 10771127.
- ↑ Henry CR, Satran D, Lindgren B, Adkinson C, Nicholson CI, Henry TD, MD (2006). Myocardial Injury and Long-term Mortality Following Moderate to Severe Carbon Monoxide Poisoning. JAMA 295: 398-402. Abstract
- ↑ (2001) Ford MD, Delaney KA, Ling LJ, Erickson T. Clinical toxicology, WB Saunders Company. ISBN 0-7216-5485-1.
- ↑ 21.0 21.1 Hardy KR, Thom SR. (1994). Pathophysiology and treatment of carbon monoxide poisoning. J Toxicol Clin Toxicol 32 (6): 613-29. PMID 7966524.
- ↑ 22.0 22.1 Scheinkestel CD, Bailey M, Myles PS, Jones K, Cooper DJ, Millar IL, Tuxen DV. (1999). Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: a randomised controlled clinical trial. Med J Aust 170 (5): 203-10. PMID 10092916.
- ↑ Haldane J. (1895). The action of carbonic oxide on man. J Physiol 18: 430-62.
- ↑ 24.0 24.1 Gorman D, Drewry A, Huang YL, Sames C. (2003). The clinical toxicology of carbon monoxide. Toxicology 187 (1): 25-38. PMID 12679050.
- ↑ Brooks DE, Lin E, Ahktar J. (2002). What is cherry red, and who cares?. J Emerg Med 22 (2): 213-4. PMID 11858933.
- ↑ Alonso JR, Cardellach F, Lopez S, Casademont J, Miro O. (2003). Carbon monoxide specifically inhibits cytochrome c oxidase of human mitochondrial respiratory chain. Pharmacol Toxicol 93 (3): 142-6. PMID 12969439.
- ↑ 27.0 27.1 Blumenthal I. (2001). Carbon monoxide poisoning. J R Soc Med 94 (6): 270-2. PMID 11387414.
- ↑ Thom SR, Taber RL, Mendiguren II, Clark JM, Hardy KR, Fisher AB. (1995). Delayed neuropsychologic sequelae after carbon monoxide poisoning: prevention by treatment with hyperbaric oxygen. Ann Emerg Med 25 (4): 474-80. PMID 7710151.
- ↑ Raphael JC, Elkharrat D, Jars-Guincestre MC, Chastang C, Chasles V, Vercken JB, Gajdos P. (1989). Trial of normobaric and hyperbaric oxygen for acute carbon monoxide intoxication. Lancet 2 (8660): 414-9. PMID 2569600.
- ↑ Ducasse JL, Celsis P, Marc-Vergnes JP. (1995). Non-comatose patients with acute carbon monoxide poisoning: hyperbaric or normobaric oxygenation?. Undersea Hyperb Med 22 (1): 9-15. PMID 7742714.
- ↑ Mathieu D, Mathieu-Nolf M, Durak C, Wattel F, Tempe JP, Bouachour G, Sainty JM. (1996). Randomized prospective study comparing the effect of HBO vs 12 hours NBO in non-comatose CO-poisoned patients: results of the preliminary analysis. Undersea Hyperb Med 23: 7.
- ↑ Weaver LK, Hopkins RO, Chan KJ, Churchill S, Elliott CG, Clemmer TP, Orme JF Jr, Thomas FO, Morris AH. (2002). Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med 347 (14): 1057-67. PMID 12362006.
- ↑ Gorman DF. (1999). Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: a randomised controlled clinical trial. Unfortunate methodological flaws. Med J Aust 170 (11): 563. PMID 10397050.
- ↑ Scheinkestel CD, Jones K, Myles PS, Cooper DJ, Millar IL, Tuxen DV. (2004). Where to now with carbon monoxide poisoning?. Emerg Med Australas 16 (2): 151-4. PMID 15239731.
- ↑ Isbister GK, McGettigan P, Harris I. (2003). Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med 348 (6): 557-60. PMID 12572577.
- ↑ 
- ↑ Massachusetts General Laws, Chapter 148, Section 26F 1/2. Also known as "Nicole's Bill". Enacted November 4, 2005.
- ↑ Illinois Public Act 094-0741. Effective 01/01/2007.
- Carbonmonoxidekills.com: Carbon Monoxide Poisoning Protection Video
- Carbonmonoxide.net: Carbon Monoxide Poisoning Support Forum
- COALERT: Carbon monoxide poisoning information, co detectors, co detector placement
- 2003 report of a group suicide via charcoal-produced carbon monoxide poisoning, in Japan
- 2005 report of a group suicide via charcoal-produced carbon monoxide poisoning, in the UK
- COSUPPORT: Carbon monoxide study from UK carbon monoxide poisoning victims support group
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