| GHS-Einstufung | DangerH220: Extremely flammable gas [Danger Flammable gases]P203, P210, P222, P260, P261, P264, P270, P271, P280, P304+P340, P316, P318, P319, P321, P377, P381, P403, P403+P233, P405, and P501 (click each P-code to see the statement)H220 (87.3%): Extremely flammable gas [Danger Flammable gases]P203, P210, P222, P260, P261, P264, P270, P271, P280, P304+P340, P316, P318, P319, P321, P377, P381, P403, P403+P233, P405, P410+P403, and P501 (click each P-code to see the statement) |
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| Hazards Identification | Toxic/poison by inhalation (TIH/PIH) |
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| Regulatorische Informationen | Chemical: Carbon monoxideHazard Traits - Cardiovascular ToxicityDevelopmental ToxicityNeurotoxicityReproductive ToxicityCarbon monoxide is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of Carbon monoxide are required to report information about their production and use of this chemical to the EPA under the Toxic Substances Control Act (TSCA). (40 eCFR Part 711)2008/967Status: Active Update: 27-04-2023 https://echa.europa.eu/registration-dossier/-/registered-dossier/15368Carbon monoxide: HSNO Approval: HSR001056 Approved with controls |
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| Weitere Sicherheitsinformationen | IMAP assessments - Carbon monoxide: Human health tier II assessment |
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| DOT-Kennzeichnung | Poison Gas Flammable Gas |
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| Brandgefahren | Special Hazards of Combustion Products: Asphyxiation due to carbon dioxide production may result.Excerpt from ERG Guide 168 [Carbon Monoxide (Refrigerated Liquid)]:· EXTREMELY FLAMMABLE.· Flammablemay be ignited by heat, sparks or flames.Extremely flammable. Heating will cause rise in pressure with risk of bursting. Gas/air mixtures are explosive. |
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| Brandpotenzial | Flammable gas. |
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| Gesundheitsgefahren | Inhalation causes headache, dizziness, weakness of limbs, confusion, nausea, unconsciousness, and finally death. 0.04% conc., 2-3 hr. or 0.06% conc., 1 hr.- headache and discomfortwith moderate exercise, 0.1-0.2% will produce throbbing in the head in about 1/2 hr., a tendency to stagger in about 1 1/2 hr., and confusion of the mind, headache, and nausea in about 2 hrs. 0.20-25% usually produces unconsciousness in about 1/2 hr. Inhalation of a 0.4% conc. can prove fatal in less than 1 hr. Inhalation of high concentrations can cause sudden, unexpected collapse. Contact of liquid with skin will cause frostbite. (USCG, 1999)Excerpt from ERG Guide 168 [Carbon Monoxide (Refrigerated Liquid)]:· TOXICExtremely Hazardous.may be fatal if inhaled or absorbed through skin. Some may cause severe skin burns and eye damage. |
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| Gefahrenübersicht | Carbon monoxide is a colorless, nonirritating, odorless, and tasteless gas. It is found in both outdoor and indoor air.Carboxyhemoglobin 1/2 life in the body = 4 hours in room air and 60-90 minutes in 100% oxygenNonsmoker normal = 2%Smoker = 5-7%Neurological symptoms = 30%Death = 40-50%Carbon monoxide is the most common cause of chemical asphyxia. There is limited positive data that carbon monoxide causes low birth weight and fetal death in humans. In animals, there is strong positive data that it causes birth defects and neonatal mortality and limited positive data that it causes testicular damage. [ATSDR Case Studies, #29] Decreased exercise time to onset of angina or ischemia was observed at COHb levels as low as 3% and increased ventricular arrhythmias at COHb levels of 6%. [ACGIH] Early on, symptoms include headache, dizziness, and disorientation. More prolonged or severe hypoxia is accompanied by a varying combination of tremor, chorea, spasticity, dystonia, rigidity, and bradykinesia. Recovery from the hypoxia may be incomplete. Residual dementia, spasticity, cortical blindness, and parkinsonian features are relatively common. [Ladou, p. 430] |
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| DOT-Nummer und Handbuch | 9202 1681016 1199202 168(cryogenic liquid) |
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| Reaktive Gruppe | Reducing Agents, Weak |
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| EG-Einstufung | Symbol: F+, TR: 12-23-48/23-61S: 53-45Note: E |
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| UN-Einstufung | UN Hazard Class: 2.3UN Subsidiary Risks: 2.1 |
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| Brandbekämpfung | Excerpt from ERG Guide 119 [Gases - Toxic - Flammable]:Excerpt from ERG Guide 168 [Carbon Monoxide (Refrigerated Liquid)]:Shut off supplyif not possible and no risk to surroundings, let the fire burn itself out. In other cases extinguish with carbon dioxide, water spray, powder. In case of fire: keep cylinder cool by spraying with water. Combat fire from a sheltered position. |
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| Erste-Hilfe-Maßnahmen | Fresh air, rest. Administration of oxygen may be needed. Artificial respiration may be needed. Refer immediately for medical attention. |
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| Freisetungsmaßnahmen | · CALL 911. Then call emergency response telephone number on shipping paper. If shipping paper not available or no answer, refer to appropriate telephone number listed on the inside back cover.· ELIMINATE all ignition sources (no smoking, flares, sparks or flames) from immediate area. |
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| Erste Hilfe | Excerpt from NIOSH Pocket Guide for Carbon monoxide:General First Aid:(General first aid procedures) |
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| Sichere Lagerung | Fireproof. Cool. Keep in a well-ventilated room. |
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| Firefighting Hazards | Flame has very little color. Containers may explode in fire.Carbon monoxide is the most frequent cause of immediate fire deaths, and carbon monoxide poisoning should be suspected in every fire victim. Carbon monoxide levels at fires may reach 10%, which can raise carboxyhemoglobin levels in active firefighters without respiratory protection to 75% within 1 minute.Asphyxiation due to carbon dioxide production may result /from combustion/. |
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| Expositionsschutz und Persönliche Schutzausrüstung | · Wear positive pressure self-contained breathing apparatus (SCBA).Biological Exposure Indices (BEI) [ACGIH] - Carboxyhemoglobin in blood = 3.5% of hemoglobin at end of shiftcarbon monoxide in end-exhaled air = 20 ppm at end of shift30.0 [ppm] |
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| Brandbekämpfungsverfahren | Stop flow of gas before extinguishing fire. Use water spray to keep fire-exposed containers cool. Fire situation may require evacuation.Use powder or carbon dioxide.If material on fire or involved in fire: Do not extinguish fire unless flow can be stopped. Use water in flooding quantities as fog. Cool all affected containers with flooding quantities of water. Apply water from as far a distance as possible.Let fire burnshut off flow of gas and cool adjacent exposures with water. Extinguish (only if wearing self-contained breathing apparatus) with dry chemicals or carbon dioxide. |
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| Lagerbedingungen | Store in a cool, dry, well-ventilated location.Remove the sources of ignition. Electric installation should be explosion-proof construction. Protect container against sunlight, and store in well-ventilated, safe areas. |
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| Reinigungsverfahren | 1. Ventilate area of leak or release to disperse gas. 2. Stop flow of gas. If source of leak is a cylinder and the leak cannot be stopped in place, remove the leaking cylinder to a safe place in the open air and repair the leak or allow the cylinder to empty.Use water spray to cool and disperse vapors and protect personnel. With cryogenic liquids, releases may require isolation or evacuation.Gas leakage: By forced ventilation, maintain concentration of gas below the range of explosive mixture. Remove the tank or cylinder to an open area. Leave to bleed off in the atmosphere. |
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| Freisetung ohne Brand | Excerpt from ERG Guide 119 [Gases - Toxic - Flammable]:Excerpt from ERG Guide 168 [Carbon Monoxide (Refrigerated Liquid)]: |
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| Entsorgungsverfahren | SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air qualitypotential migration in soil or watereffects on animal and plant lifeand conformance with environmental and public health regulations.Incineration: Remove leaky cylinders to remote area to emptythen return to supplier with label indicating that repairs are needed. The waste carbon monoxide can be piped to an approved incinerator or the cylinder can be placed in a pit to burn carbon monoxide to carbon dioxide under controlled conditions. |
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| Toxikologische Informationen | CDC-ATSDR Toxicological Profile |
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| Treatment | Carbon monoxide poisoning is first treated by immediate removal from the source of exposure. High-flow or 100% oxygen should then be administered by a nonrebreather reservoir oxygen mask. Oxygen hastens the dissociation of carbon monoxide from hemoglobin, improving tissue oxygenation by reducing carbon monoxides biological half-life. Hyperbaric oxygen may also be used, as it increases carboxyhemoglobin dissociation to a greater extent than normal oxygen. (L961) |
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| Wechselwirkungen | Combined exposure to carbon monoxide plus hydrogen cyanide had an additive effect in rats, as evidenced by increases in mortality rate. Results from this series of experiments showed that the exposed animals died at lower carbon monoxide concentrations as the levels of hydrogen cyanide increased. In the presence of hydrogen cyanide, carboxyhemoglobin at equilibrium was less than that measured in the absence of hydrogen cyanidehowever, the initial rate of carboxyhemoglobin formation was the same. This apparent depressive effect of hydrogen cyanide on carboxyhemoglobin formation may explain the reason for the low carboxyhemoglobin levels (<50%) seen in some people who died in a fire.Combined exposure of rats to carbon monoxide plus nitric oxide for 3 hr caused a significant (P < 0.01) increase in mean methemoglobin levels when compared with methemoglobin levels in rats exposed to nitric oxide alone. No significant changes were observed in blood carboxyhemoglobin levels compared with exposure to carbon monoxide alone or to carbon monoxide plus nitric oxide. Combined exposure also caused significant behavioral changes..In the study of interactions of intraperitoneal carbon monoxide administration with psychoactive drugs on operant behavior of mice, d-amphetamine, chlorpromazine, nicotine, diazepam and morphine were studied in addition to alcohol and pentobarbital. As with alcohol, a suggestion of greater than additive effects was obtained from combinations of carbon monoxide with both d-amphetamine and chlorpromazinehowever, in these cases, the differences from additivity did not reach statistical significance. Effects of carbon monoxide in combination with nicotine, caffeine and morphine were additive.A large interaction of carbon monoxide exposure and alcohol administration /was observed/ on operant behavior in animals. Mice, trained to lever press for water reinforcement, were tested with 1.1 g alcohol/kg body weight and various doses of carbon monoxide, alone and in combination. An unusual feature of this study was that both alcohol and carbon monoxide were administered by intraperitoneal injection. A dose of alcohol that had little effect on rates of lever pressing when given alone resulted in large rate-decreasing effects when given in combination with doses of carbon monoxide that also had no effects when given alone. Typically, behavioral effects of carbon monoxide alone were not seen under these test conditions until carboxyhemoglobin saturations greater than 40-50% were obtained. Thus, alcohol about doubled the acute toxicity of carbon monoxide in this study.For more Interactions (Complete) data for Carbon monoxide (12 total), please visit the HSDB record page. |
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| Zielorgane | Cardiovascular (Heart and Blood Vessels), Death, Developmental (effects while organs are developing), Hematological (Blood Forming), Neurological (Nervous System), Respiratory (From the Nose to the Lungs)cardiovascular system, lungs, blood, central nervous system |
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| Gesundheitliche Auswirkungen | Chronic exposure to low levels of carbon monoxide may cause persistent headaches, lightheadedness, depression, confusion, memory loss, and nausea and vomiting. (L961) |
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| Umweltverhalten | ATMOSPHERIC FATE: A photochemical model was used to quantify the sensitivity of the tropospheric oxidants ozone (O3) and OH to changes in methane (CH4), carbon monoxide (CO), and NO emissions and to perturbations in climate and stratospheric chemistry. In most cases, incr CH4 and CO emissions will suppress OH (neg coefficients) in incr O3 (pos coefficients) except in areas where NO and O3 influenced by pollution are sufficient to incr OH. In most regions, NO, CO, and CH4 emission incr will suppress OH and incr O3, but these trends may be opposed by stratospheric O3 depletion and climate change. |
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| Unerwünschte Wirkungen | Neurotoxin - Parkinsonism |
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| Expositionspfade | The substance can be absorbed into the body by inhalation.inhalation, skin and/or eye contact (liquid)Inhalation (L960) |
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| Toxizitätsübersicht | It is a product of the incomplete combustion of carbon-containing fuels and is also produced by natural processes or by biotransformation of halomethanes within the human body. With external exposures to additional carbon monoxide, subtle effects can begin to occur, and exposure to higher levels can result in death. The health effects of carbon monoxide are largely the result of the formation of carboxyhemoglobin (COHb), which impairs the oxygen carrying capacity of the blood ... During typical daily activities, people encounter carbon monoxide in a variety of microenvironments - while travelling in motor vehicles, working at their jobs, visiting urban locations associated with combustion sources, or cooking or heating with domestic gas, charcoal or wood fires - as well as in tobacco smoke. ... Studies of human exposure have shown that motor vehicle exhaust is the most important source for regularly encountered elevated carbon monoxide levels ... The workplace is another important setting for carbon monoxide exposures ... Certain industrial processes can expose workers to carbon monoxide produced directly or as a byproduct ... Carbon monoxide is absorbed through the lungs, and the concentration of carboxyhemoglobin will depend ... mainly on the concentrations of inspired carbon monoxide and oxygen ... and will also depend on the duration of exposure, pulmonary ventilation, and the concentration of carboxyhemoglobin originally present ... In addition to its reaction with hemoglobin, carbon monoxide combines with myoglobin, cytochromes, and metalloenzymes such as cytochromoe c oxidase and cytochrome P-450 ... The binding of carbon monoxide to hemoglobin, producing carboxyhemoglobin and decreasing the oxygen carrying capacity of blood, appears to be the principal mechanism of action underlying the induction of toxic effects of low-level carbon monoxide exposures. The precise mechanisms by which toxic effects are induced ... are not understood fully but likely include the induction of a hypoxic state in many tissues of diverse organ systems ... A unique feature of carbon monoxide exposure, therefore, is that the blood carboxyhemoglobin level represents a useful biological marker of the dose that the individual has received ... The formation of carboxyhemoglobin is a reversible processhowever, because of the tight binding of carbon monoxide to hemoglobin, the elimination half-time is quite long, ranging from 2 to 6.5 hr ... The level of carboxyhemoglobin in the blood may be determined directly by blood analysis or indirectly by measuring carbon monoxide in exhaled breath ... Decreased oxygen uptake and the resultant decreased work capacity under maximal exercise conditions have clearly been shown to occur ... However, of greater concern at more typical ambient carbon monoxide exposure levels are certain cardiovascular effects (i.e., aggravation of angina symptoms during exercise) likely to occur in a smaller, but sizeable, segment of the general population. This group, chronic angina patients, is currently viewed as the most sensitive risk group for carbon monoxide exposure effects ... The adverse health consequences of low level carbon monoxide exposure to patients with ischemic heart disease are very difficult to predict in the at-risk population of individuals with heart disease ... At high carbon monoxide concentrations, excessive increases in hemoglobin and hematocrit may impose an additional workload on the heart and compromise blood flow to the tissues ... It is unlikely that carbon monoxide has any direct effects on lung tissue except for extremely high concentrations associated with carbon monoxide poisoning ... Occupational or accidental exposure to the products of combustion and pyrolysis, particularly indoors, may lead to acute decrements in lung function if the carboxyhemoglobin levels are high. It is difficult, however, to separate the potential effects of carbon monoxide from those due to other respiratory irritants in the smoke and exhaust ... Of special note are those individuals who are taking drugs with primary or secondary depressant effects that would be expected to exacerbate carbon monoxide-related neurobehavorial decrements. Other groups at possible increased risk for carbon monoxide-induced neurobehavorial effects are the aged and ill ... Under normal circumstances, the brain can increase blood flow or tissue oxygen extraction to compensate for the hypoxia caused by exposure to carbon monoxide ...... Studies in several laboratory animal species provide strong evidence that maternal carbon monoxide exposures ... produce reductions of birth weight, cardiomegaly, delays in behavorial development and disruptions in cognitive function ... Laboratory animal studies suggest that enzyme metabolism of xenobiotic compounds may be affected by carbon monoxide exposure ... The decreases in xenobiotic metabolism shown with carbon monoxide exposure might be important to individuals receiving treatment with drugs ... Tissues of highly active oxygen metabolism, such as heart, brain, liver, kidney, and muscle, may be particularly sensitive to carbon monoxide poisoning. There are reports ... of effects on liver, kidney, bone and the immune capacity of the lung and spleen. It is generally agreed that the severe tissue damage occurring during acute carbon monoxide poisoning is due to one of more of the following: (1) ischemia resulting from the formation of carboxyhemoglogin, (2) inhibition of oxygen release from oxyhemoglobin, (3) inhibition of oxygen release from oxyhemoglobin, (3) inhibition of cellular cytochrome function (e.g., cytochrome oxidases) and (4) metabolic acidosis ... Whereas certain data also suggest that perinatal effects (e.g., reduced birth weight, slowed post-natal developments, sudden infant death syndrome) are associated with carbon monoxide exposure, insufficient evidence exists by which to either qualitatively confirm such an association in humans or establish any pertinent exposure-effect relationships ... There remains little direct information on the possible enhancement of carbon monoxide toxicity by concomitant drug use or abuse ... The greatest evidence for a potentially important interaction of carbon monoxide comes from studies with alcohol in both laboratory animals and humans, where at least additive effects have been obtained. The significance of this is augmented by the high probable incidence of combined alcohol use and carbon monoxide exposure ... Besides being a source of carbon monoxide for smokers as well as non-smokers, tobacco smoke is also a source of other chemicals with which environmental carbon monoxide could interact ... On the basis of known effects described, patients with reproducible exercise-induced ischemia appear to be the best established as a sensitive group within the general population that is at increased risk for experiencing health effects of concern (i.e., decreased exercise duration due to exacerbation of cardiovascular symptoms) at ambient or near-ambient carbon monoxide concentrations ... Decrements in exercise duration in the healthy population would therefore be of concern mainly to competing athletes, rather than to ordinary people carrying out the common activities of daily life. It can be hypothesized, however, from both clinical and theoretical work and from experimental research on laboratory animals, that certain other groups in the population may be at probable risk from exposure to carbon monoxide. Identifiable probable risk groups can be categorized by gender differencesby age ...by genetic variations ...by pre-existing diseases ...or by the use of medications, recreational drugs or alterations in environment ... Unfortunately, little empirical evidence is currently available by which to specify health effects associated with ambient or near-ambient carbon monoxide exposure to these probable risk groups ...... Carbon monoxide is responsible for a large percentage of the accidental poisonings and deaths reported throughout the world each year ... Outdoors, concentrations of carbon monoxide are highest near street intersections, in congested traffic, near exhaust gases from internal combustion engines and from industrial sources, and in poorly ventilated areas such as parking garages and tunnels. Indoors, carbon monoxide concentrations are highest in workplaces or in homes that have faulty or poorly vented combustion appliances or downdrafts or backdrafts. The symptoms and signs of acute carbon monoxide poisoning correlate poorly with the level of carboxyhemoglobin measured at the time of arrival at the hospital ... Neurological symptoms of carbon monoxide poisoning can ocur, such as headache, dizziness, weakness, nausea, confusion, disorientation and visual disturbances. Exertional dyspnea, increases in pulse and respiratory rates and syncope are observed with continuous exposure ... When carboxyhemoglobin levels are higher than 50%, convulsions and cardiopulmonary arrest may occur. Complications occur frequently in carbon monoxide poisoning (immediate death, myocardial impairment, hypotension, arrhythmias, pulmonary edema). Perhaps the most insidious effect of carbon monoxide poisoning is the delayed development of neuropyschiatric impairment ... and the neurobehavioral consequences, especially in children. Carbon monoxide poisoning during pregnancy results in high risk for the mother, by increasing the short-term complications rate and for the fetus by causing fetal death, developmental disorders, and cerebral anoxic lesions. Furthermore, the severity of fetal intoxication cannot be assessed by the maternal rate. Carbon monoxide poisoning occurs frequently, has severe consequences, including immediate death, involves complications and late sequelae and is often overlooked ...Carbon monoxide possesses a higher affinity than oxygen for hemoglobin, leading to the formation of carboxyhemoglobin, this provoking anoxemia. Carbon monoxide also binds to myoglobin, impairing its ability to utilize oxygen. It can also bind to cytochrome c oxidase, though with a lesser affinity than oxygen. This interferes with aerobic metabolism and efficient ATP synthesis. As a result, cells switch to anaerobic metabolism, causing anoxia, lactic acidosis, and eventual cell death. Carbon monoxide also causes endothelial cell and platelet release of nitric oxide, and the formation of oxygen free radicals. This results in lipid peroxidation, leading to edema and necrosis within the brain. (L961) |
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| Ökotoxizitätsauszüge | /AQUATIC SPECIES/ At concentrations of 28-350 mg/L in the air and a light intensity of 18 klux, carbon monoxide had no effect on growth of Chlorella cultures. However, at 4.5 klux, the lowest concentration of CO inhibited the algal growth rate./OTHER TERRESTRIAL SPECIES/ Ladybirds and stick insects exposed to high levels of carbon monoxide (80% CO, 20% O) for < 10 days, all survived. When exposed for > 10 days, they died./OTHER TERRESTRIAL SPECIES/ At levels of 100 ppm (50%), CO had negligible effects on the behavior of Enchytraeus species, Arion fasciatus, Tracheoniscus rathkei, Diploiulus species, Liobunum calcar, and several other forest litter invertebrates. Also, it had no effect on the health and biological functions of the various organisms./PLANTS/ Leaves of 35 species of temperate and tropical plants absorbed CO in light from air containing 6 ppm CO at an average rate of 190 nL/kg of fresh wt. CO uptake by 9 species, having widely different rates of absorption, was proportional to CO concn in the range 0 to 100 ppm. Absorbed CO was metabolized either by oxidation to carbon dioxide and fixation as such or by reduction and incorporation into serine. CO had various effects on the photosynthesis of leaves of different species, acting like an inhibitory at concn as low as 65 ppm, or exerting no influence, or even permitting an increase in net CO2 fixation at 99% CO because of the absence of oxygen. |
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| Signs and Symptoms | Shortness of breath. Headache. Weakness. Irregular heartbeat. Chest pain. Nausea. Dizziness. Unconsciousness.headache, tachypnea, nausea, lassitude (weakness, exhaustion), dizziness, confusion, hallucinationscyanosisdepressed S-T segment of electrocardiogram, angina, syncopeEarly symptoms of acute carbon monoxide poisoning are nonspecific and include headaches, nausea, and fatigue. Symptoms may progress to tachycardia and hypertension. The central nervous system is one of the organ systems most sensitive to poisoning and symptoms displayed include dizziness, ataxia, confusion, convulsions, unconsciousness, respiratory arrest, and even death. (L961) |
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| Medical Surveillance | This clinical policy focuses on critical issues concerning the management of adult patients presenting to the emergency department (ED) with acute symptomatic carbon monoxide (CO) poisoning. The subcommittee reviewed the medical literature relevant to the questions posed. The critical questions are: Should hyperbaric oxygen (HBO(2)) therapy be used for the treatment of patients with acute CO poisoningand Can clinical or laboratory criteria identify CO-poisoned patients who are most or least likely to benefit from this therapy? Recommendations are provided on the basis of the strength of evidence of the literature. Level A recommendations represent patient management principles that reflect a high degree of clinical certaintyLevel B recommendations represent patient management principles that reflect moderate clinical certaintyand Level C recommendations represent other patient management strategies that are based on preliminary, inconclusive, or conflicting evidence, or based on committee consensus. This clinical policy is intended for physicians working in hospital-based EDs. .Patients with acute carbon monoxide poisoning commonly have cognitive sequelae. ... A double-blind, randomized trial /was conducted/ to evaluate the effect of hyperbaric-oxygen treatment on such cognitive sequelae. METHODS: ... Patients with symptomatic acute carbon monoxide poisoning /were randomly assigned/ in equal proportions to three chamber sessions within a 24-hour period, consisting of either three hyperbaric-oxygen treatments or one normobaric-oxygen treatment plus two sessions of exposure to normobaric room air. Oxygen treatments were administered from a high-flow reservoir through a face mask that prevented rebreathing or by endotracheal tube. Neuropsychological tests were administered immediately after chamber sessions 1 and 3, and 2 weeks, 6 weeks, 6 months, and 12 months after enrollment. The primary outcome was cognitive sequelae six weeks after carbon monoxide poisoning. RESULTS: The trial was stopped after the third of four scheduled interim analyses, at which point there were 76 patients in each group. Cognitive sequelae at six weeks were less frequent in the hyperbaric-oxygen group (19 of 76 [25.0 percent]) than in the normobaric-oxygen group (35 of 76 [46.1 percent], P=0.007), even after adjustment for cerebellar dysfunction and for stratification variables (adjusted odds ratio, 0.45 [95 percent confidence interval, 0.22 to 0.92]P=0.03). The presence of cerebellar dysfunction before treatment was associated with the occurrence of cognitive sequelae (odds ratio, 5.71 [95 percent confidence interval, 1.69 to 19.31]P=0.005) and was more frequent in the normobaric-oxygen group (15 percent vs. 4 percent, P=0.03). Cognitive sequelae were less frequent in the hyperbaric-oxygen group at 12 months, according to the intention-to-treat analysis (P=0.04). CONCLUSIONS: Three hyperbaric-oxygen treatments within a 24-hour period appeared to reduce the risk of cognitive sequelae 6 weeks and 12 months after acute carbon monoxide poisoning.The aim of this study was to make a retrospective descriptive analysis of the features of children with acute carbon monoxide poisoning (COP). We evaluated 74 children (43 girls, 31 boysage range 1 to 17.8 years) who were consecutively admitted to our emergency unit and hospitalized with accidental acute COP between June 2003 and June 2005. All patients received normobaric oxygen therapy until their carboxyhemoglobin (COHb) levels were decreased below 2% and their symptoms resolved. Thirty-eight of 74 patients (51.4%) also received hyperbaric oxygen (HBO) therapy as indicated by signs and symptoms or COHb levels. COHb levels were significantly higher and hospitalization period was longer in the children who had abnormal neurological findings (p<0.05 for both). All patients showed complete recovery without neurological sequelae except one who had visual impairment at discharge, and antiepileptic therapy was started because of epilepsy after seven months...Clinical studies suggest that all patients admitted to hospital with moderate to severe CO poisoning should routinely undergo ECG and serial evaluation of cardiac markers, and that those with positive signs of myocardial cytonecrosis or preexisting ischemic heart disease should also undergo echocardiography. A finding of myocardial damage in patients with CO poisoning seems to indicate an unfavorable long-term prognosis, although it needs further confirmation.For more Medical Surveillance (Complete) data for Carbon monoxide (7 total), please visit the HSDB record page. |
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| Alarmwort | Achtung |
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| Gefahrenhinweise | Code Gefahrenhinweise Gefahrenklasse Abteilung Alarmwort Symbol P-Code H220 |
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