English Safety Data Sheet Database 中文版 MSDS

Carbon Monoxide

CAS No. 630-08-0 | PubChem CID 281
Section 1. Identification
Chemical NameCarbon Monoxide CAS No.630-08-0
Synonymsfluegas; carbonmonoxide Chinese Name一氧化碳
Molecular FormulaCO Molecular Weight28.01
UN No.1016 Data SourcePubChem (NIH/NLM)
GHS Hazard Classification
Signal Word DANGER
Pictograms GHS02 · Flammable GHS04 · Compressed Gas GHS06 · Acute Toxic GHS08 · Health Hazard
Hazard Statements H220H331H372H221H280H360H370H373
Precautionary Statements P203P210P222P260P261P264P270P271P280P304+P340P316P318P319P321P377P381P403P403+P233P405P501P410+P403P308+P316

Section 2. Hazards Identification

H220: Extremely flammable gas [Danger Flammable gases]

H331: Toxic if inhaled [Danger Acute toxicity, inhalation]

H360D ***: May damage the unborn child [Danger Reproductive toxicity]

H372 **: Causes damage to organs through prolonged or repeated exposure [Danger Specific target organ toxicity, repeated exposure]

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]

H221 (12.9%): Flammable gas [Danger Flammable gases]

H280 (77.8%): Contains gas under pressure; may explode if heated [Warning Gases under pressure]

H331 (99%): Toxic if inhaled [Danger Acute toxicity, inhalation]

H360 (63.1%): May damage fertility or the unborn child [Danger Reproductive toxicity]

H360D (37.2%): May damage the unborn child [Danger Reproductive toxicity]

H372 (100%): Causes damage to organs through prolonged or repeated exposure [Danger Specific target organ toxicity, repeated exposure]

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)

Aggregated GHS information provided per 613 reports by companies from 30 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown. For more detailed information, please visit ECHA C&L website.

H220 (100%): Extremely flammable gas [Danger Flammable gases]

H280 (100%): Contains gas under pressure; may explode if heated [Warning Gases under pressure]

H331 (100%): Toxic if inhaled [Danger Acute toxicity, inhalation]

H360 (100%): May damage fertility or the unborn child [Danger Reproductive toxicity]

Aggregated GHS information provided per 38 reports by companies from 1 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

P203, P210, P222, P280, P377, P381, and P403 (click each P-code to see the statement)

H280: Contains gas under pressure; may explode if heated [Warning Gases under pressure]

H360: May damage fertility or the unborn child [Danger Reproductive toxicity]

H370: Causes damage to organs [Danger Specific target organ toxicity, single exposure]

H373: May causes damage to organs through prolonged or repeated exposure [Warning Specific target organ toxicity, repeated exposure]

P203, P210, P222, P260, P261, P264, P270, P271, P280, P304+P340, P308+P316, P316, P318, P319, P321, P377, P381, P403, P403+P233, P405, P410+P403, and P501 (click each P-code to see the statement)

H360D: May damage the unborn child [Danger Reproductive toxicity]

H372: Causes damage to organs through prolonged or repeated exposure [Danger Specific target organ toxicity, repeated exposure]

Section 4. First-Aid Measures

Fresh air, rest. Administration of oxygen may be needed. Artificial respiration may be needed. Refer immediately for medical attention.

Excerpt from NIOSH Pocket Guide for Carbon monoxide:

Eye: FROSTBITE - If eye tissue is frozen, seek medical attention immediately; if tissue is not frozen, immediately and thoroughly flush the eyes with large amounts of water for at least 15 minutes, occasionally lifting the lower and upper eyelids. If irritation, pain, swelling, lacrimation, or photophobia persist, get medical attention as soon as possible.

Skin: FROSTBITE - If frostbite has occurred, seek medical attention immediately; do NOT rub the affected areas or flush them with water. In order to prevent further tissue damage, do NOT attempt to remove frozen clothing from frostbitten areas. If frostbite has NOT occurred, immediately and thoroughly wash contaminated skin with soap and water.

Breathing: RESPIRATORY SUPPORT - If a person breathes large amounts of this chemical, move the exposed person to fresh air at once. If breathing has stopped, perform artificial respiration. Keep the affected person warm and at rest. Get medical attention as soon as possible. (NIOSH, 2024)

General First Aid:

· Call 911 or emergency medical service.

· Ensure that medical personnel are aware of the material(s) involved, take precautions to protect themselves and avoid contamination.

· Move victim to fresh air if it can be done safely.

· Administer oxygen if breathing is difficult.

· If victim is not breathing:

-- DO NOT perform mouth-to-mouth resuscitation; the victim may have ingested or inhaled the substance.

-- If equipped and pulse detected, wash face and mouth, then give artificial respiration using a proper respiratory medical device (bag-valve mask, pocket mask equipped with a one-way valve or other device).

-- If no pulse detected or no respiratory medical device available, provide continuous compressions. Conduct a pulse check every two minutes or monitor for any signs of spontaneous respirations.

· Remove and isolate contaminated clothing and shoes.

· For minor skin contact, avoid spreading material on unaffected skin.

· In case of contact with substance, remove immediately by flushing skin or eyes with running water for at least 20 minutes.

· For severe burns, immediate medical attention is required.

· Effects of exposure (inhalation, ingestion, or skin contact) to substance may be delayed.

· Keep victim calm and warm.

· Keep victim under observation.

· For further assistance, contact your local Poison Control Center.

· Note: Basic Life Support (BLS) and Advanced Life Support (ALS) should be done by trained professionals.

Specific First Aid:

· In case of contact with liquefied gas, only medical personnel should attempt thawing frosted parts.

· In case of burns, immediately cool affected skin for as long as possible with cold water. Do not remove clothing if adhering to skin.

In Canada, an Emergency Response Assistance Plan (ERAP) may be required for this product. Please consult the shipping paper and/or the "ERAP" section.

(General first aid procedures)

Eye: Frostbite - If eye tissue is frozen, seek medical attention immediately; if tissue is not frozen, immediately and thoroughly flush the eyes with large amounts of water for at least 15 minutes, occasionally lifting the lower and upper eyelids. If irritation, pain, swelling, lacrimation, or photophobia persist, get medical attention as soon as possible.

Skin: Frostbite - Compressed gases may create low temperatures when they expand rapidly. Leaks and uses that allow rapid expansion may cause a frostbite hazard. Wear appropriate personal protective clothing to prevent the skin from becoming frozen.

Breathing: Respiratory support

Section 5. Fire-Fighting Measures

Excerpt from ERG Guide 119 [Gases - Toxic - Flammable]:

DO NOT EXTINGUISH A LEAKING GAS FIRE UNLESS LEAK CAN BE STOPPED.

SMALL FIRE: Dry chemical, CO2, water spray or alcohol-resistant foam.

LARGE FIRE: Water spray, fog or alcohol-resistant foam. FOR CHLOROSILANES, DO NOT USE WATER; use alcohol-resistant foam. If it can be done safely, move undamaged containers away from the area around the fire. Damaged cylinders should be handled only by specialists.

FIRE INVOLVING TANKS: Fight fire from maximum distance or use unmanned master stream devices or monitor nozzles. Cool containers with flooding quantities of water until well after fire is out. Do not direct water at source of leak or safety devices; icing may occur. Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank. ALWAYS stay away from tanks in direct contact with flames. (ERG, 2024)

Excerpt from ERG Guide 168 [Carbon Monoxide (Refrigerated Liquid)]:

CAUTION: Flame can be invisible. Use an alternate method of detection (thermal camera, broom handle, etc.) DO NOT EXTINGUISH A LEAKING GAS FIRE UNLESS LEAK CAN BE STOPPED.

SMALL FIRE: Dry chemical, CO2 or water spray.

LARGE FIRE: Water spray, fog or regular foam. If it can be done safely, move undamaged containers away from the area around the fire.

Shut off supply; if 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.

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 burn; shut off flow of gas and cool adjacent exposures with water. Extinguish (only if wearing self-contained breathing apparatus) with dry chemicals or carbon dioxide.

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/.

Section 6. Accidental Release Measures

· 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.

· Keep unauthorized personnel away.

· Stay upwind, uphill and/or upstream.

· Many gases are heavier than air and will spread along the ground and collect in low or confined areas (sewers, basements, tanks, etc.).

· Ventilate closed spaces before entering, but only if properly trained and equipped.

· ELIMINATE all ignition sources (no smoking, flares, sparks or flames) from immediate area.

· All equipment used when handling the product must be grounded.

· Do not touch or walk through spilled material.

· Stop leak if you can do it without risk.

· Use water spray to reduce vapors or divert vapor cloud drift. Avoid allowing water runoff to contact spilled material.

· Do not direct water at spill or source of leak.

· If possible, turn leaking containers so that gas escapes rather than liquid.

· Prevent entry into waterways, sewers, basements or confined areas.

· Isolate area until gas has dispersed.

· FOR CHLOROSILANES, use alcohol-resistant foam to reduce vapors.

Excerpt from ERG Guide 119 [Gases - Toxic - Flammable]:

IMMEDIATE PRECAUTIONARY MEASURE: Isolate spill or leak area for at least 100 meters (330 feet) in all directions.

SPILL: See ERG Table 1 - Initial Isolation and Protective Action Distances on the UN/NA 1016 datasheet.

FIRE: If tank, rail tank car or highway tank is involved in a fire, ISOLATE for 1600 meters (1 mile) in all directions; also, consider initial evacuation for 1600 meters (1 mile) in all directions. (ERG, 2024)

Excerpt from ERG Guide 168 [Carbon Monoxide (Refrigerated Liquid)]:

SPILL: See ERG Table 1 - Initial Isolation and Protective Action Distances on the UN/NA 9202 datasheet.

FIRE: If tank, rail tank car or highway tank is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. (ERG, 2024)

Immediate precautionary measure

· Isolate spill or leak area for at least 100 meters (330 feet) in all directions.

· See Table 1 - Initial Isolation and Protective Action Distances.

· If tank, rail tank car or highway tank is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions.

Small spill:

- ISOLATE in all directions: 30 m (100 ft)

Large spill:

- ISOLATE in all directions: 200 m (600 ft)

- PROTECT people from downwind during DAY time: 0.1 km (0.1 mi)

- PROTECT people from downwind during NIGHT time: 0.2 km (0.1 mi)

- PROTECT people from downwind during DAY time: 1.2 km (0.7 mi)

- PROTECT people from downwind during NIGHT time: 3.9 km (2.4 mi)

· For highlighted materials: see Table 1 - Initial Isolation and Protective Action Distances.

· For non-highlighted materials: increase the immediate precautionary measure distance, in the downwind direction, as necessary.

· If tank, rail tank car or highway tank is involved in a fire, ISOLATE for 1600 meters (1 mile) in all directions; also, consider initial evacuation for 1600 meters (1 mile) in all directions.

Evacuate danger area! Consult an expert! Personal protection: self-contained breathing apparatus. Remove all ignition sources. Ventilation.

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.

Section 7. Handling and Storage

Excerpt from ERG Guide 119 [Gases - Toxic - Flammable]:

ELIMINATE all ignition sources (no smoking, flares, sparks or flames) from immediate area. All equipment used when handling the product must be grounded. Do not touch or walk through spilled material. Stop leak if you can do it without risk. Do not direct water at spill or source of leak. Use water spray to reduce vapors or divert vapor cloud drift. Avoid allowing water runoff to contact spilled material. FOR CHLOROSILANES, use alcohol-resistant foam to reduce vapors. If possible, turn leaking containers so that gas escapes rather than liquid. Prevent entry into waterways, sewers, basements or confined areas. Isolate area until gas has dispersed. (ERG, 2024)

Excerpt from ERG Guide 168 [Carbon Monoxide (Refrigerated Liquid)]:

ELIMINATE all ignition sources (no smoking, flares, sparks or flames) from immediate area. All equipment used when handling the product must be grounded. Do not touch or walk through spilled material. Stop leak if you can do it without risk. Use water spray to reduce vapors or divert vapor cloud drift. Avoid allowing water runoff to contact spilled material. Do not direct water at spill or source of leak. If possible, turn leaking containers so that gas escapes rather than liquid. Prevent entry into waterways, sewers, basements or confined areas. Isolate area until gas has dispersed. (ERG, 2024)

Fireproof. Cool. Keep in a well-ventilated room.

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.

Section 8. Exposure Controls / Personal Protection

· Wear positive pressure self-contained breathing apparatus (SCBA).

· Wear chemical protective clothing that is specifically recommended by the manufacturer when there is NO RISK OF FIRE.

· Structural firefighters' protective clothing provides thermal protection but only limited chemical protection.

· Always wear thermal protective clothing when handling refrigerated/cryogenic liquids.

Biological Exposure Indices (BEI) [ACGIH] - Carboxyhemoglobin in blood = 3.5% of hemoglobin at end of shift; carbon monoxide in end-exhaled air = 20 ppm at end of shift;

TIH (Toxic Inhalation Hazard) - Term used to describe gases and volatile liquids that are toxic when inhaled. Some are TIH materials themselves, e.g., chlorine, and some release TIH gases when spilled in water, e.g., chlorosilanes. [ERG 2016].

30.0 [ppm]

AEGL 1: Notable discomfort, irritation, or certain asymptomatic non-sensory effects. However, the effects are not disabling and are transient and reversible upon cessation of exposure (Unit: ppm)

AEGL 2: Irreversible or other serious, long-lasting adverse health effects or an impaired ability to escape (Unit: ppm)

AEGL 3: Life-threatening health effects or death (Unit: ppm)

NR = Not recommended due to insufficient data

AEGLs Status: Final

75 [ppm]

83 [ppm]

330 [ppm]

35 ppm (40 mg/m³)

200 ppm (229 mg/m³)

TWA 35 ppm (40 mg/m3) C 200 ppm (229 mg/m3)

50.0 [ppm]

50 ppm (55 mg/m³)

TWA 50 ppm (55 mg/m3) See Appendix G

1200 ppm (NIOSH, 2024)

1200.0 [ppm]

Excerpts from Documentation for IDLHs: Other human data: It has been stated that a 1­hour exposure to 1,000 to 1,200 ppm would cause unpleasant but no dangerous symptoms, but that 1,500 to 2,000 ppm might be a dangerous concentration after 1 hour [Henderson et al. 1921a, 1921b]. In general, a carboxyhemoglobin (COHb) level of 10­20% will only cause slight headaches [NIOSH 1972] and a COHb of 11­13% will have no effect on hand and foot reaction time, hand steadiness, or coordination [Stewart and Peterson 1970]. At a COHb of 35%, manual dexterity is impaired [Stewart 1975]. At 40% COHb, mental confusion, added to increasing incoordination, precludes driving an automobile [Stewart 1975]. A 30­minute exposure to 1,200 ppm will produce a COHb of 10­13% [NIOSH 1972].

1200 ppm

See: 630080

25.0 [ppm]

8 hr Time Weighted Avg (TWA): 25 ppm.

Excursion Limit Recommendation: Excursions in worker exposure levels may exceed 3 times the TLV-TWA for no more than a total of 30 minutes during a work day, and under no circumstances should they exceed 5 times the TLV-TWA, provided that the TLV-TWA is not exceeded.

Biological Exposure Index (BEI): Determinant: carboxyhemoglobin in blood; Sampling Time: end of shift; BEI: 3.5% of hemoglobin. Determinant: carbon monoxide in end-exhaled air; Sampling Time: end of shift; BEI: 20 ppm. The determinant may be present in biological specimens collected from subjects who have not been occupationally exposed, at a concentration which could affect interpretation of the result. Such background concentrations are incorporated in the BEI value. The determinant is nonspecific, since it is also observed after exposure to other chemicals.

25 ppm as TWA; BEI issued.

CAUTION: Flame can be invisible. Use an alternate method of detection (thermal camera, broom handle, etc.)

· DO NOT EXTINGUISH A LEAKING GAS FIRE UNLESS LEAK CAN BE STOPPED.

Small Fire

· Dry chemical, CO2 or water spray.

Large Fire

· Water spray, fog or regular foam.

· If it can be done safely, move undamaged containers away from the area around the fire.

Fire Involving Tanks

· Fight fire from maximum distance or use unmanned master stream devices or monitor nozzles.

Section 9. Physical and Chemical Properties

Carbon monoxide is a colorless, odorless gas. Prolonged exposure to carbon monoxide rich atmospheres may be fatal. It is easily ignited. It is just lighter than air and a flame can flash back to the source of leak very easily. Under prolonged exposure to fire or intense heat the containers may violently rupture and rocket.

Carbon monoxide, refrigerated liquid (cryogenic liquid) appears as a colorless cryogenic liquid. Prolonged exposure to carbon monoxide rich atmospheres may be fatal. Contact with the liquid can cause severe frostbite. Less dense than air. Easily ignited and a flame can flash back to the source of a leak very easily. Burns with a violet flame. Under prolonged exposure to fire or intense heat the containers may rupture violently and rocket. It is used in organic synthesis, metallurgy, and a fuel.

CBI; Gas Vapor

Colorless, odorless gas. [Note: Shipped as a nonliquefied or liquefied compressed gas.] [NIOSH]

ODOURLESS TASTELESS COLOURLESS COMPRESSED GAS.

Colorless, odorless gas.

Colorless, odorless gas. [Note: Shipped as a nonliquefied or liquefied compressed gas.]

Colorless gas [Note: Shipped as a nonliquefied or liquefied compressed gas].

Odorless

Tasteless

-312.7 °F at 760 mmHg (USCG, 1999)

-313 °F at 760 mmHg (NIOSH, 2024)

-191.5 °C

-191.5 °C @760 [mm Hg]

-326 °F (USCG, 1999)

-337 °F (NIOSH, 2024)

-205.02 °C

-56.5 °C

Flammable gas

NA (Gas)

2 % (NIOSH, 2024)

Soluble in benzene

Freely absorbed by a concentrated solution of cuprous chloride in hydrochloric acid or ammonium hydroxide; Appreciably soluble in some organic solvents, such as ethyl acetate, chloroform, acetic acid; solubility in methanol and ethanol about 7 times as great as in water.

Sparingly soluble in water: 3.3 ml/100 ml at 0 °C, 2.3 ml/100 ml at 20 °C

1.48 mg/mL at 25 °C

Solubility in water, ml/100ml at 20 °C: 2.3 (sparingly soluble)

0.791 at -312.7 °F (USCG, 1999) - Less dense than water; will float

1.250 g/L at 0 °C/4 °C

Density at critical point = 301.0 kg/cu m

Density of liquid = 788.6 kg/cu m at 81.63 K

Density of solid, hexagonal = 929 kg/cu m at 65 K

0.791 at -312.7 °F

1.145 g/L

0.97(relative gas density)

0.97 (NIOSH, 2024) - Lighter than air; will rise (Relative to Air)

0.968 (Air = 1)

Relative vapor density (air = 1): 0.97

greater than 35 atm (NIOSH, 2024)

1.55X10+8 mm Hg at 25 °C

Henry's Law constant = 1.04 atm-cu m/mol at 25 °C (reported as 57978.5 atm/mol fraction)

Section 10. Stability and Reactivity

Highly flammable.

Reducing Agents, Weak

Highly Flammable

Bromine trifluoride and carbon monoxide react explosively at high temperatures or concentrations [Mellor 2 Supp. 1:166 1956]. The same is true for various oxidizers such as: chlorine dioxide, oxygen (liquid), peroxodisulfuryl difluoride. The product of the reaction between lithium and carbon monoxide, lithium carbonyl, detonates violently with water, igniting the gaseous products [Mellor 2, Supp. 2:84 1961]. Potassium and sodium metals behave similarly. Cesium oxide, iron(III) oxide, and silver oxide all react, in the presence of moisture, at ambient temperatures with carbon monoxide causing ignition, [Mellor, 1941, vol. 2, 487]. Contact of very cold liquefied gas with water may result in vigorous or violent boiling of the product and extremely rapid vaporization due to the large temperature differences involved. If the water is hot, there is the possibility that a liquid "superheat" explosion may occur. Pressures may build to dangerous levels if liquid gas contacts water in a closed container [Handling Chemicals Safely 1980].

Contact of very cold liquefied gas with water may result in vigorous or violent boiling and extremely rapid vaporization. If the water is hot, a liquid "superheat" explosion may occur. Pressures may build to dangerous levels if the liquid contacts water in a closed container [Handling Chemicals Safely 1980]. Reacts explosively with bromine trifluoride at high temperatures or concentrations [Mellor 2, Supp. 1:166 1956]. The same is true for various oxidizers such as: chlorine dioxide, oxygen (liquid), peroxodisulfuryl difluoride. Reacts with lithium to give lithium carbonyl, which detonates violently with water, igniting the gaseous products [Mellor 2, Supp 2:84 1961]. Potassium and sodium metals behave similarly. Cesium oxide, iron(III) oxide, and silver oxide all react, in the presence of moisture, at ambient temperatures with carbon monoxide causing ignition, [Mellor, 1941, vol. 2, 487].

May react vigorously with oxygen, acetylene, chlorine, fluorine, nitrous oxide.

Strong oxidizers, bromine trifluoride, chlorine trifluoride, lithium.

... Explosion /occurred/ during reduction of iron oxide with carbon monoxide /due to/ formation of pentacarbonyliron at temperatures between 0 and 150 °C.

Carbon monoxide is exothermically oxidized over silver oxide, and the temperature may attain 300 °C.

For more Hazardous Reactivities and Incompatibilities (Complete) data for Carbon monoxide (8 total), please visit the HSDB record page.

Strong oxidizers, bromine trifluoride, chlorine trifluoride, lithium

Section 11. Toxicological Information

CDC-ATSDR Toxicological Profile

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 process; however, 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 differences; by 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)

No indication of carcinogenicity to humans (not listed by IARC).

Chronic exposure to low levels of carbon monoxide may cause persistent headaches, lightheadedness, depression, confusion, memory loss, and nausea and vomiting. (L961)

The substance can be absorbed into the body by inhalation.

inhalation, skin and/or eye contact (liquid)

Inhalation (L960)

Shortness of breath. Headache. Weakness. Irregular heartbeat. Chest pain. Nausea. Dizziness. Unconsciousness.

headache, tachypnea, nausea, lassitude (weakness, exhaustion), dizziness, confusion, hallucinations; cyanosis; depressed S-T segment of electrocardiogram, angina, syncope

Early 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)

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

Neurotoxin - Parkinsonism

Other Poison - Chemical Asphyxiant

Reproductive Toxin - A chemical that is toxic to the reproductive system, including defects in the progeny and injury to male or female reproductive function. Reproductive toxicity includes developmental effects. See Guidelines for Reproductive Toxicity Risk Assessment.

LC50 (rat) = 1,807 ppm/4H

LC50 Rat inhalation 1807 ppm/4 hr

LC50 Rat inhalation 4600-5000 ppm 30 min

LC50 Mouse inhalation 2444 ppm/4 hr

LC50 ICR Mouse inhalation ca. 8000 ppm for 30 min

For more Non-Human Toxicity Values (Complete) data for Carbon monoxide (6 total), please visit the HSDB record page.

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)

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 cyanide; however, 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 chlorpromazine; however, 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.

Treatment includes 100% oxygen and, in severe cases, hyperbaric oxygen. The half-life of carboxyhemoglobin is 6 hours at room air, 1.5 hours with 100% oxygen, and 23 minutes at three atmospheres of pressure.

The prompt administration of oxygen is critical to maternal and fetal survival. In gestationally appropriate pregnancies, it is reasonable to use indicators of adequate fetal oxygenation central nervous system responsiveness (heart rate and variability), in addition to responses of the mother and her laboratory findings, in adjusting or terminating oxygen therapy. To ensure adequate treatment of the fetus, it has been recommended that the mother receive oxygen therapy for five times as long as it is expected to require to return her carbon monoxide concentrations to normal; this is how long it may take for fetal levels to normalize. The maternal carboxyhemoglobin elimination rate can be increased from a half-life of 2 to 3 hours to 3/4 of an hour by breathing 100% oxygen; fetal carboxyhemoglobin half-lives are expected to decrease from 6 to 7 hours to 2 to 4 hours by the use of maternal oxygen therapy. The fetal rate of elimination remains slower than that of the mother.

Immediate first aid: Remove patient from contact with the material. Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand-valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR as necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Carbon Monoxide and Related Compounds/

Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if necessary. Administer 100% oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for shock and treat if necessary ... . Monitor for signs of an acute myocardial infarction and treat if necessary. Monitor for pulmonary edema and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . /Carbon Monoxide and Related Compounds/

For more Antidote and Emergency Treatment (Complete) data for Carbon monoxide (8 total), please visit the HSDB record page.

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 poisoning; and 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 certainty; Level B recommendations represent patient management principles that reflect moderate clinical certainty; and 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 boys; age 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.

Section 12. Ecological Information

/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.

NATURAL SOURCES SUCH AS ATMOSPHERIC OXIDN OF METHANE, FOREST FIRES, TERPENE OXIDN & OCEAN (WHERE MICROORGANISMS PRODUCE CARBON MONOXIDE) ARE RESPONSIBLE FOR ABOUT 90% OF ATMOSPHERIC CARBON MONOXIDE; HUMAN ACTIVITY PRODUCES ABOUT 10%.

A small amount of carbon monoxide is produced normally in the body. This endogenous carbon monoxide is sufficient in amount to maintain a carbon monoxide hemoglobin saturation of about 0.4 to 0.7 percent. In some persons with blood disease, such as hemolytic anemia, the carbon monoxide saturation may reach 6 percent

WATER HEATERS ARE A COMMON SOURCE OF CARBON MONOXIDE.

MOTOR VEHICLES ACCOUNT FOR ABOUT 55 TO 60% OF GLOBAL MAN-MADE EMISSIONS OF CARBON MONOXIDE.

SINCE MOST...POLYMERIC MATERIALS CONTAIN CARBON, CARBON MONOXIDE IS ONE OF THE PRIMARY GASES GENERATED FROM THE HEATING AND BURNING OF THESE MATERIALS /PLASTICS/.

Concentrations as high as 30% have been measured in automobile exhaust gas, although 7% is more common. Pyrolysis of some vinyl plastics results in the production of appreciable concentrations of carbon monoxide. Natural gas associated with petroleum deposits has no carbon monoxide but in processing natural gas (e.g., cracking), carbon monoxide may be produced. As distributed, manufactured gas commonly has a carbon monoxide content between 2 and 15% (by volume)

For more Artificial Pollution Sources (Complete) data for Carbon monoxide (8 total), please visit the HSDB record page.

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.

Unblended non filter cigarettes were made of the leaf and cutter of 5 kinds of bright tobacco cultivars and smoked to a 30 mm butt length on a smoking machine. Large variations were observed in the rates of formation of CO among the different kinds of tobacco. Leaf cigarette CO values ranged from 15.7 to 22.9 mg/cigarette, while cutter CO values ranged from 13.9 to 19.4 mg/cigarette. The CO formation rate was a more influential factor determining the amount of CO in mainstream smoke than the wt loss of the cigarette during puffs. Correlation coefficients were calculated for rate of CO formation and ethanol benzene extract, hexane extract, nicotine, or potassium. The highest was with potassium (-0.95). The rate of formation of CO was mainly dependent on the potassium content of the tobacco and could be estimated from the amounts of potassium, total carbon, and lignin. The rates of formation of CO increased with a rise in combustion temperature, which in turn rose as the potassium content of the tobacco decr.

Environmental tobacco smoke was analyzed after smoking of research cigarettes by a machine in an experimental chamber 13.6 cu m in volume. The ventilation rate was 3.55 air changes per hour. Air removed for sampling added about 0.5 air changes per hour. One cigarette was lit every 30 min and was smoked with a 35 ml puff of 2 sec every minute until extinguished after about 12 min. Mainstream smoke was vented to the outside of the chamber. Additional tests were performed with one cigarette smoked every 15 min and with several commercial cigarette brands. Carbon monoxide concentrations averaged 2.48 + or - 0.2 mg/cu m in the first series of 9 tests and 1.79 + or - 0.81 mg/cu m in a similar series. With one cigarette every 15 min the carbon monoxide concentrations averaged 4.76 + or - 0.21 mg/cu m. The airborne yield per cigarette was 67 mg of carbon monoxide. Concentrations of carbon monoxide varied in a saw toothed form with the pattern of smoking one cigarette every 30 min. The ratio of the average maximum to the minimum concentration was about 3. The average concentration of carbon monoxide was about 65 to 70% of the maximum concentration. The ventilation time of carbon monoxide corresponded to the predetermined air exchange rate of about 4 per hour. Concentrations of carbon monoxide using commercial brands of cigarettes in the chamber and in a tavern setting were similar to those produced by the research cigarettes.

...LARGE QUANTITIES OF CARBON MONOXIDE GAS RELEASED BY BURNING CHARCOAL CAN RESULT IN SEVERE POISONING OR DEATH. HIBACHIS SHOULD NEVER BE USED AS A SOURCE OF HEAT IN SLEEPING QUARTERS.

CAR EXHAUST CONTAINS 1 TO 7% CARBON MONOXIDE. THIS IS WELL INTO...TOXIC RANGE...

Occupational exposure to increased ambient carbon monoxide has been a major /concern/ to firefighters, traffic police, coal miners, coke oven and smelter workers, caisson workers, toll both attendants, and transportation mechanics. As commuting distances increase, workers driving to and from work are exposed to more ambient carbon monoxide.

Section 13. Disposal Considerations

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 quality; potential migration in soil or water; effects on animal and plant life; and conformance with environmental and public health regulations.

Incineration: Remove leaky cylinders to remote area to empty; then 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.

Section 14. Transport Information

If ... THERE IS NO FIRE, go directly to the Table of Initial Isolation and Protective Action Distances /(see table below)/ ... to obtain initial isolation and protective action distances. IF THERE IS A FIRE, or IF A FIRE IS INVOLVED, go directly to the appropriate guide /(see guide(s) below)/ and use the evacuation information shown under PUBLIC SAFETY. /Carbon monoxide; Carbon monoxide, compressed; Carbon monoxide, refrigerated liquid (cryogenic liquid)/

Table: Table of Initial Isolation and Protective Action Distances for Carbon monoxide; Carbon monoxide, compressed; Carbon monoxide, refrigerated liquid (cryogenic liquid) [Table#2376]

/GUIDE 119: GASES - TOXIC - FLAMMABLE/ Health: TOXIC; may be fatal if inhaled or absorbed through skin. Contact with gas or liquefied gas may cause burns, severe injury and/or frostbite. Fire will produce irritating, corrosive and/or toxic gases. Runoff from fire control may cause pollution. /Carbon monoxide; Carbon monoxide, compressed/

/GUIDE 119: GASES - TOXIC - FLAMMABLE/ Fire or Explosion: Flammable; may be ignited by heat, sparks or flames. May form explosive mixtures with air. Those substances designated with a "P" may polymerize explosively when heated or involved in a fire. Vapors from liquefied gas are initially heavier than air and spread along ground. Vapors may travel to source of ignition and flash back. Some of these materials may react violently with water. Cylinders exposed to fire may vent and release toxic and flammable gas through pressure relief devices. Containers may explode when heated. Ruptured cylinders may rocket. Runoff may create fire or explosion hazard. /Carbon monoxide; Carbon monoxide, compressed/

/GUIDE 119: GASES - TOXIC - FLAMMABLE/ Public Safety: CALL Emergency Response Telephone Number ... As an immediate precautionary measure, isolate spill or leak area for at least 100 meters (330 feet) in all directions. Keep unauthorized personnel away. Stay upwind. Many gases are heavier than air and will spread along ground and collect in low or confined areas (sewers, basements, tanks). Keep out of low areas. Ventilate closed spaces before entering. /Carbon monoxide; Carbon monoxide, compressed/

For more DOT Emergency Guidelines (Complete) data for Carbon monoxide (17 total), please visit the HSDB record page.

9202 168(cryogenic liquid)

IMO 2.3; Carbon monoxide, compressed; Carbon monoxide, refrigerated liquid (cryogenic liquid)

NA 9202; Carbon monoxide, refrigerated liquid (cryogenic liquid)

UN 1016; Carbon monoxide, compressed

49 201 90; Carbon monoxide

No person may /transport,/ offer or accept a hazardous material for transportation in commerce unless that person is registered in conformance ... and the hazardous material is properly classed, described, packaged, marked, labeled, and in condition for shipment as required or authorized by ... /the hazardous materials regulations (49 CFR 171-177)./

The International Air Transport Association (IATA) Dangerous Goods Regulations are published by the IATA Dangerous Goods Board pursuant to IATA Resolutions 618 and 619 and constitute a manual of industry carrier regulations to be followed by all IATA Member airlines when transporting hazardous materials.

The International Maritime Dangerous Goods Code lays down basic principles for transporting hazardous chemicals. Detailed recommendations for individual substances and a number of recommendations for good practice are included in the classes dealing with such substances. A general index of technical names has also been compiled. This index should always be consulted when attempting to locate the appropriate procedures to be used when shipping any substance or article.

Poison Gas Flammable Gas

Symbol: F+, T; R: 12-23-48/23-61; S: 53-45; Note: E

UN Hazard Class: 2.3; UN Subsidiary Risks: 2.1

Source: PubChem CID 281 (NIH/NLM, public domain). Retrieved from PubChem, a public-domain chemistry database maintained by the U.S. National Library of Medicine. Last updated: 2026-08-02 09:28:50.
Disclaimer: This information is compiled for reference only and does not replace the manufacturer's official Safety Data Sheet. Always consult the supplier's SDS before handling any chemical.