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SECTION 1. CHEMICAL IDENTIFICATION

CHEMINFO Record Number: 57
CCOHS Chemical Name: Carbon monoxide

Synonyms:
Carbonic oxide
Carbon oxide
CO
Oxyde de carbone

Chemical Name French: Monoxyde de carbone
Chemical Name Spanish: Monóxido de carbono
CAS Registry Number: 630-08-0
UN/NA Number(s): 1016
RTECS Number(s): FG3500000
Chemical Family: Inorganic carbon compound / carbon oxide / carbon monoxide / inorganic gas
Molecular Formula: C-O
Structural Formula: C=O

SECTION 2. DESCRIPTION

Appearance and Odour:
Colourless, odourless gas

Odour Threshold:
Odourless.

Warning Properties:
None - Compound is odourless and non-irritating

Uses and Occurrences:
A reducing agent in metallurgical operations; manufacture of many chemicals including metal carbonyls, methanol, acetic acid, phosgene and oxo alcohols; fuel; constituent of syngas (CO+H2). By-product of combustion of organic materials.
Metabolite of methylene chloride.


SECTION 3. HAZARDS IDENTIFICATION

POTENTIAL HEALTH EFFECTS

Effects of Short-Term (Acute) Exposure

Inhalation:
Short-term exposures below 50 ppm normally do not cause adverse effects in healthy people.(24)
In two studies, healthy subjects exposed to either 50 ppm for 5 minutes or 100 ppm for 1 hour tired more quickly during exercise than unexposed controls. Other effects were not observed.(7)
In some studies, task performance (alertness) was poorer in people exposed to carbon monoxide (50 ppm or greater) for 1 1/2 to 4 hours.(7)
Carbon monoxide causes increasingly severe toxic effects as the concentration and duration of exposure increase. The effects include mild headache (50 ppm and above) to severe headache (above 200 ppm); weakness, dizziness, nausea, fainting (above 400 ppm); increased heartbeat, irregular heartbeat (above 1200 ppm); loss of consciousness and death (above 2000 ppm). At concentrations above 5000 ppm, death may occur in minutes.(24)
These symptoms are usually seen sooner or at lower concentrations if there is a heavy workload (increased breathing rate and increased blood flow) or if the exposed person has heart disease.
Tobacco smokers have elevated levels of carbon monoxide in their bodies and may therefore be more sensitive than non-smokers to occupational exposures.
At high altitudes, people may be more susceptible to carbon monoxide.
When poisoning is serious but not fatal, the victim may suffer the following effects during recovery; headache and dizziness, vision problems, loss of memory, confusion and mental problems. Permanent damage to the brain has been reported, and, in these cases, total recovery is not possible.(23)
Carbon monoxide combines with hemoglobin in the blood to form carboxyhemoglobin, and this reduces the blood's ability to supply oxygen to the tissues, particularly the brain and heart. The observed effects are related to this tissue hypoxia (low oxygen).

Skin Contact:
Carbon monoxide gas does not cause irritation.

Eye Contact:
Carbon monoxide gas does not cause irritation.

Ingestion:
Not applicable to gases.

Effects of Long-Term (Chronic) Exposure

EFFECTS ON THE HEART: Studies show a relationship between exposure to carbon monoxide in specific occupations (firefighters, foundry workers, motor vehicle examiners) and an increased incidence of cardiovascular problems.(8)

Carbon monoxide can aggravate some diseases of the cardiovascular system, such as coronary artery disease and angina pectoris.(9)

Carcinogenicity:

No human or animal information is available.

The International Agency for Research on Cancer (IARC) has not evaluated the carcinogenicity of this chemical.

The American Conference of Governmental Industrial Hygienists (ACGIH) has not assigned a carcinogenicity designation to this chemical.

The US National Toxicology Program (NTP) has not listed this chemical in its report on carcinogens.

Teratogenicity and Embryotoxicity:
ACUTE EXPOSURES: Severe exposures to carbon monoxide during pregnancy have caused adverse effects and death of the fetus. In general, maternal symptoms are an indicator of the potential risk to the fetus since carbon monoxide is toxic to the mother before it becomes toxic to the fetus.(10,11)
CHRONIC EXPOSURES: No specific human information. Carbon monoxide in cigarette smoke is thought to contribute to the delayed development observed in babies of smoking mothers.(7)
Animal studies suggest that repeated exposure to relatively high levels of carbon monoxide during pregnancy may cause developmental effects without causing maternal toxicity.

Reproductive Toxicity:
No human or animal information available.

Mutagenicity:
Human information is not available. In the one animal study available, carbon monoxide gas increased chromosomal damage in blood cells of mice.(5)

Toxicologically Synergistic Materials:
Animal studies indicate that a combination of carbon dioxide and carbon monoxide causes an increase in the rate of carbon monoxide-binding to hemoglobin.(12)

Potential for Accumulation:
Carbon monoxide is excreted from the body in exhaled air. Elimination may be quite rapid during the first few hours after exposure, but complete elimination of CO may require 1-2 days.


SECTION 4. FIRST AID MEASURES

Inhalation:
Take proper precautions to ensure your own safety before attempting rescue; e.g., wear appropriate protective equipment, use the "buddy" system. Remove source of contamination or move victim to fresh air. If breathing has stopped, trained personnel should begin artificial respiration or, if the heart has stopped, cardiopulmonary resuscitation (CPR) immediately. If exposure is severe, oxygen should be administered by a person trained in its use, preferably on a physician's advice. Transport victim to an emergency facility immediately.

Skin Contact:
Not applicable

Eye Contact:
Not applicable

Ingestion:
Not applicable

First Aid Comments:
Provide general supportive measures (comfort, warmth, rest). Minimize physical activity.
Some recommendations in the above sections, including administration of oxygen, may be considered medical acts in some jurisdictions. These recommendations should be reviewed with a physician and appropriate delegation of authority obtained, as required.
All first aid procedures should be periodically reviewed by a physician familiar with the material and its conditions of use in the workplace.



SECTION 5. FIRE FIGHTING MEASURES

Flash Point:
Flammable gas.

Lower Flammable (Explosive) Limit (LFL/LEL):
12.5% (3,4)

Upper Flammable (Explosive) Limit (UFL/UEL):
74.2% (3,4)

Autoignition (Ignition) Temperature:
607 deg C (1125 deg F) (3); 652 deg C (1206 deg F) (4); 700 deg C (1292 deg F) (2)

Sensitivity to Mechanical Impact:
Probably not sensitive. Stable material.

Sensitivity to Static Charge:
Concentrations of carbon monoxide gas in the flammable range can be readily ignited by static discharge of sufficient energy.

Combustion and Thermal Decomposition Products:
Decomposes into carbon and carbon dioxide between 400 and 700 deg C.(2)

Fire Hazard Summary:
Gas can form flammable or explosive mixtures with air. Carbon monoxide gas is about the same density as air and mixes readily with air. The gas can travel a considerable distance to a source of ignition and flash back to a leaking container.

Extinguishing Media:
Stop flow of gas before extinguishing fire. Use water spray. (6) Do not extinguish burning gas if flow cannot be shut off immediately. Extinguish secondary fires with appropriate materials.

Fire Fighting Instructions:
Move cylinders from fire area if without risk. Use water to keep fire-exposed containers cool.



NATIONAL FIRE PROTECTION ASSOCIATION (NFPA) HAZARD IDENTIFICATION

NFPA - Health: 2 - Intense or continued (but not chronic) exposure could cause temporary incapacitation or possible residual injury.
NFPA - Flammability: 4 - Will rapidly or completely vaporize at atmospheric pressure and normal ambient temperature, or readily disperse in air and burn readily.
NFPA - Instability: 0 - Normally stable, even under fire conditions, and not reactive with water.

SECTION 9. PHYSICAL AND CHEMICAL PROPERTIES

Molecular Weight: 28.01

Conversion Factor:
1 ppm = 1.14 mg/m3; 1 mg/m3 = 0.87 ppm at 25 deg C

Physical State: Gas
Melting Point: -205 deg C (-337 deg F) (2,4)
Boiling Point: -192 deg C (-313 deg F) (2,18)
Relative Density (Specific Gravity): Not applicable (gas)
Solubility in Water: Sparingly soluble (30 mg/L at 20 deg C) (2)
Solubility in Other Liquids: Appreciably soluble in some organic solvents, such as ethyl acetate, chloroform, acetic acid, methanol, ethanol, acetone and ether.(2,3)
Coefficient of Oil/Water Distribution (Partition Coefficient): Not available
pH Value: Probably neutral
Vapour Density: 0.967 (air = 1)
Vapour Pressure: Not applicable (cannot be liquified at 25 deg C)
Vapour Pressure at 50 deg C: Greater than 7000 kPa (69 atm) (estimated from graph) (18b)
Saturation Vapour Concentration: Not applicable
Evaporation Rate: Not applicable
Critical Temperature: -140.2 deg C (-220.4 deg F) (18)
Critical Pressure: 3496 kPa (34.5 atm) (18b)

SECTION 10. STABILITY AND REACTIVITY

Stability:
Normally stable.

Hazardous Polymerization:
Does not occur

Incompatibility - Materials to Avoid:

NOTE: Chemical reactions that could result in a hazardous situation (e.g. generation of flammable or toxic chemicals, fire or detonation) are listed here. Many of these reactions can be done safely if specific control measures (e.g. cooling of the reaction) are in place. Although not intended to be complete, an overview of important reactions involving common chemicals is provided to assist in the development of safe work practices.


METAL OXIDES (e.g. iron oxide, nickel oxide) - reduced to lower metal oxides, metals or metal carbides at elevated temperatures.(18)

SOME HEAVY METALS (e.g. nickel, iron, chromium) - formation of explosive metal carbonyls.(18)

ALKALI & ALKALINE EARTH METALS (e.g. sodium, potassium, magnesium) - react to produce salts.(18)

ALUMINUM POWDER - ignition can occur

IODINE HEPTAFLUORIDE - ignition can occur

SULFUR - carbon monoxide reacts slowly with the liquid and rapidly with the vapour to give carbonyl sulfide.(18)

CHLORINE - can form phosgene in the presence of light or a charcoal catalyst.(18)

BROMINE - can form carbonyl bromide in the presence of light or a charcoal catalyst.(18)

BROMINE TRIFLUORIDE, BROMINE PENTAFLUORIDE, CHLORINE DIOXIDE OR PEROXODISULFURYL DIFLUORIDE - react explosively.

OXIDIZING MATERIALS - increased risk of fire and explosion.

Hazardous Decomposition Products:
None

Corrosivity to Metals:
Mildly corrosive to nickel and iron.(18)

Stability and Reactivity Comments:
Natural rubber and neoprene are attacked by carbon monoxide.(3)


SECTION 11. TOXICOLOGICAL INFORMATION

LC50 (rat): 2070 mg/m3 (1811 ppm) (4-hour exposure) (1)
LC50 (mouse): 2800 mg/m3 (2450 ppm) (4-hour exposure) (1)
LC50 (guinea pig): 6550 mg/m3 (5731 ppm) (4-hour exposure) (1)

NOTE: The above toxicity values are based on deaths which occurred during the 4-hour exposure. There was not a subsequent observation period.

LC50 (rat): 4600 ppm (0.5-hour exposure; 14-day observation period) (12)

REPRODUCTIVE EFFECTS: In some experiments, animals continuously exposed to carbon monoxide (90 ppm and greater) for several days during pregnancy (or throughout pregnancy) exhibited increased resorptions, and gave birth to offspring with adverse effects which included: increased resorptions, decreased viability, lower birthweights, lower rate of weight gain and minor skeletal abnormalities.
Effects were observed at doses that were not toxic to the mother.(14,15,16)

Offspring of animals exposed to 150 ppm for several days during pregnancy exhibited subtle behavioral effects. There is limited evidence that these effects can be persistent.(17)

MUTAGENICITY: Groups of mice were exposed to 1500, 2500 or 3500 ppm carbon monoxide for 10 minutes on either day 5, 11 or 16 of pregnancy. There were dose-dependent increases in chromosomal damage (micronuclei and sister-chromatid exchanges) in both maternal and fetal blood cells.(5)

Other groups of mice were exposed to 500 ppm carbon monoxide for 1 hour/day for several days during pregnancy. Increases in chromosome damage were observed in both maternal and fetal blood cells.(5)


SECTION 16. OTHER INFORMATION

Selected Bibliography:
(1) Rose, C.S., et al. The acute hyperbaric toxicity of carbon monoxide. Toxicology and Applied Pharmacology. Vol. 17 (1970). p. 752-760
(2) The Merck index: an encyclopedia of chemicals, drugs, and biologicals. 10th ed. Merck, 1983. p. 252
(3) Ullmann's encyclopedia of industrial chemistry. 5th rev. ed. Vol. A5. VCH Verlagsgesellschaft, 1986. p. 203-216
(4) Kirk-Othmer encyclopedia of chemical technology. Vol. 4. 3rd ed. John Wiley & Sons, 1978. p. 772-791
(5) Kwak, H.M., et al. Cytogenetic effects on mouse fetus of acute and chronic transplacental in vivo exposure to carbon monoxide : induction of micronuclei and sister chromatid exchanges. Yonsei Medical Journal. Vol. 27, no. 3 (1986). p. 205-212
(6) Fire protection guide to hazardous materials. 13th ed. Edited by A.B. Spencer, et al. National Fire Protection Association, 2002. NFPA 325; NFPA 49; NFPA 491
(7) Rylander, R., et al. Carbon monoxide criteria: with reference to effects on the heart, central nervous system and fetus. Scandinavian Journal of Work, Environment and Health. Vol. 7, supplement 1, (1981). p. 1-39
(8) Carbon monoxide : rules and regulations. Federal Register. Vol. 54, no. 12 (January 19, 1989). p. 2648-2649, 2651-2652
(9) Atkins, E.H., et al. Exacerbation of coronary artery disease by occupational carbon monoxide exposure : a report of two fatalities and a review of the literature. American Journal of Industrial Medicine. Vol. 7, no. 1 (1985). p. 73-79
(10) Caravati, E.M., et al. Fetal toxicity associated with maternal carbon monoxide poisoning. Annals of Emergency Medicine. Vol. 17, no. 7 (July 1988). p. 714-717
(11) Ginsberg, M.D., et al. Fetal brain injury after maternal carbon monoxide intoxication: clinical and neuropathologic aspects. Neurology. Vol. 26 (1976). p. 15-23
(12) Levin, B.C., et al. Toxicological interactions between carbon monoxide and carbon dioxide. Toxicology. Vol. 47 (1987). p. 135-164
(13) Documentation of the threshold limit values and biological exposure indices. 5th ed. ACGIH, 1986. p. 106-107
(14) Astrup, P., et al. Effect of moderate carbon-monoxide exposure on fetal development. The Lancet. (December 9, 1972). p. 1220-1222
(15) Schwetz, B.A., et al. Teratogenic potential of inhaled carbon monoxide in mice and rabbits. Teratology. Vol. 19 (1979). p. 385-391
(16) Singh, J. et al. Threshold for carbon monoxide induced fetotoxicity. Teratology. Vol. 30, no. 2 (1984). p. 253-257
(17) Fechter, L.D., et al. Carbon monoxide and brain development. Neurotoxicology. Vol. 7, no. 2 (1986). p. 463-474
(18a) Braker, W., et al. Matheson gas data book. 6th ed. Matheson Gas Products, 1980. p. 130-138
(18b) Yaws, C.L. Matheson gas data book. 7th ed. McGraw-Hill, 2001. p. 135-138
(19) Regulation respecting control of exposure to biological or chemical agents made under the Occupational Health and Safety Act. R.S.O. 1980, c. 321. p. 43
(20) NIOSH pocket guide to chemical hazards. NIOSH, June 1994. p. 54-55
(21) Carbon monoxide. IN : Environmental health criteria 13. Geneva, Switzerland : World Health Organization, 1979
(22) Ratney, R.S.; Wegman, D.H.; Elkins, H.B. In vivo conversion of methylene chloride to carbon monoxide. Archives of Environmental Health. Vol. 28 (1974). p. 223-226
(23) Stewart, R.D. The effect of carbon monoxide on humans. Annual Review of Pharmacological Toxicology. Vol. 15 (1975). p. 409-423
(24) Carbon monoxide (guidance note EH 43). U.K. : Health and Safety Executive, 1984
(25) Kuller, L.H.; Radford, E.P.; Swift, D.; Perper, J.A.; Fisher, R. Carbon monoxide and heart attacks. Archives of Environmental Health. Vol. 30 (1975). p. 477-482
(26) Hernberg, S.; Karava, R.; Koskela, R.-S.; Luoma, K. Angina pectoris, ECG findings and blood pressure of foundry workers in relation to carbon monoxide exposure. Scandinavian Journal of Work, Environment and Health. Vol. 2, suppl. 1 (1976). p. 54-63
(27) Davies, D.M.; Smith, D.J. Electrocardiographic changes in health men during continuous low-level carbon monoxide exposure. Environmental Research. Vol. 21 (1980). p. 197-206
(28) European Economic Community. Commission Directive 94/69/EC. December 19, 1994.
(29) Forsberg, K., et al. Quick selection guide to chemical protective clothing. 4th ed. Van Nostrand Reinhold, 2002

Information on chemicals reviewed in the CHEMINFO database is drawn from a number of publicly available sources. A list of general references used to compile CHEMINFO records is available in the database Help.


Review/Preparation Date: 1989-09-28

Revision Indicators:
TLV-TWA 1993-01-01
TLV-STEL 1993-01-01
TLV comments 1993-01-01
PEL-TWA 1993-03-01
PEL-C 1993-03-01
NFPA (health) 1993-03-01
NFPA (flammability) 1993-03-01
NFPA (reactivity) 1993-03-01
REGULATORY INFORMATION 1993-03-01
Trans PEL-TWA 1993-04-01
WHMIS (detailed class) 1994-03-01
WHMIS (effects) 1994-03-01
Sampling 1995-08-01
Respiratory guidelines 1995-08-01
Protective equipment 1995-08-01
EU number 1995-08-01
EU risk 1995-08-01
EU safety 1995-08-01
EU comments 1995-08-01
US transport 1998-03-01
Resistance of materials 1998-05-01
ERPG 2001-03-01
TDG 2002-06-04
US transport 2002-12-03
NFPA (health) 2003-03-26
WHMIS disclosure list 2003-07-07
Carcinogenicity 2003-07-24
PEL transitional comments 2003-10-28
PEL-TWA final 2003-10-28
PEL-C final 2003-10-28
EU classification 2005-02-06
Bibliography 2006-01-18
Vapour pressure at 50 deg C 2006-01-18
Critical pressure 2006-01-18



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