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CHEMINFO Record Number: 516
CCOHS Chemical Name: Monochloroacetic acid solid

Chloroacetic acid
Chloracetic acid
alpha-Chloroacetic acid
Chloroethanoic acid
Monochloroacetic acid
Monochloroethanoic acid
Monochloroacetic acid (non-specific name)

CAS Registry Number: 79-11-8
UN/NA Number(s): 1751 3250
RTECS Number(s): AF8575000
EU EINECS/ELINCS Number: 201-178-4
Chemical Family: Halogenated aliphatic carboxylic acid / haloalkanoic acid / chlorinated carboxylic acid / chloroacetic acid
Molecular Formula: C2-H3-Cl-O2
Structural Formula: Cl-CH2-C(=O)-OH


Appearance and Odour:
Colourless, crystalline solid; odour of vinegar (6,17); hygroscopic (absorbs moisture from the air) (6,18)

Odour Threshold:
0.045 ppm (probably 50% recognition) (19); 6.14 ppm (23.7 mg/m3) (irritation) (6)

Warning Properties:
GOOD: The WEEL is more than 10-times the odour threshold.

Pure monochloroacetic acid (MCA) exists in 3 or 4 crystalline forms (alpha, beta, gamma and possibly the delta). The alpha form is the most stable and most important industrially. MCA may contain small amounts of dichloroacetic acid, sulfate, acetic acid, and water (less than 0.5%).(6) MCA is available as a solid or in solution. This record is for MCA solid. Refer to CHEMINFO record 767 for information on the solution.

Uses and Occurrences:
Major use as a chemical intermediate for the production of carboxymethyl cellulose (CMC), herbicides based on chlorophenoxyalkanoic acids (e.g. 2,4-D, 2,4,5-T), thioglycolic acid (mercaptoacetic acid) and glycine. Other uses include the production of glycolic acid and its esters, cyanoacetic acid used to make caffeine and barbiturates, Vitamin B6 and other pharmaceuticals, indigoid dyes, 1- and 2-naphthylacetic acids and amphoteric surfactants.(6,20)


Colourless, crystalline solid with an odour of vinegar. Hygroscopic (absorbs moisture from the air). May form explosive dust-air mixtures. Can decompose at high temperatures forming toxic phosgene and irritating/corrosive hydrogen chloride gases. VERY TOXIC. Fatal if absorbed through the skin, inhaled or swallowed. CORROSIVE to the eyes, and skin. May cause permanent eye injury and permanent scarring.


Effects of Short-Term (Acute) Exposure

Monochloroacetic acid (MCA) is a corrosive solid which absorbs water from the air and does not easily form a vapour. The dust may cause mild to severe nasal irritation, sore throat and coughing.

Skin Contact:
Solid MCA can produce redness, swelling, pain and corrosive skin damage, including permanent scarring. The severity of the effect depends on the duration of the exposure and the area of skin exposed. Even minor instances of skin contact with MCA has produced redness, swelling, and corrosive tissue damage to the affected area.(1)
Solid MCA can be quickly absorbed through the skin and may cause toxic effects and death by this route of exposure. In one fatal case, about 10% of a worker's skin surface was covered with liquid (molten) MCA. Toxic effects developed and death occurred in 10 hours, despite prompt and prolonged washing of the skin with water.(2) Toxic effects from skin absorption may include nausea, vomiting and heart beat irregularities.(30)

Eye Contact:
Solid MCA can cause moderate to severe irritation or tissue damage, depending on the duration of contact. Permanent injury, including blindness, may occur. There is no human information available, but MCA vapour is reported to have produced corrosive tissue damage in an animal test.(3)

In one fatal case of human ingestion, a 5-year-old girl was accidentally given MCA. The victim immediately vomited, collapsed and died after 6 hours due to metabolic acidosis and cardiac arrhythmias. Autopsy showed liver injury and marked irritation of the stomach.(4) Like other corrosive liquids, ingestion of MCA would cause a burning sensation in mouth and throat, abdominal pain, nausea, vomiting and, in severe cases, death. Ingestion of MCA is unlikely to occur in the workplace.

Effects of Long-Term (Chronic) Exposure

Repeated or prolonged skin contact with dusts may cause redness, dryness and itching of the skin (dermatitis).

INGESTION: No adverse effects were detected in three human volunteers who drank 300 mL of a 0.05% water solution of MCA (approximately 2 mg/kg/day) for 60 days.(5) Significant effects have been observed in animals following long-term oral administration. Ingestion is not a typical route of exposure in the workplace.


There is no human information available. MCA was not carcinogenic in animal studies.

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 designated this chemical as not classifiable as a human carcinogen (A4).

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

Teratogenicity and Embryotoxicity:
There is no human or animal information available.

Reproductive Toxicity:
There is no human or animal information available.

Negative results have been obtained in tests using live animals. Positive and negative results have been obtained in in vitro tests using mammalian cells. Negative results have been obtained in tests using fruit flies and bacteria.

Toxicologically Synergistic Materials:
There is no information available.

Potential for Accumulation:
MCA is rapidly absorbed into the body. In oral rat studies, radiolabelled MCA concentrations were greater in the liver and kidneys than in the plasma, heart and brain. At 17 hours, approximately half of the administered dose had been excreted in the urine. Most MCA is broken down; some is excreted or exhaled unchanged within 1 to 3 days. In a study with mice, metabolites found in the urine included S-carboxymethyl cysteine (which breaks down further to thiodiacetic acid), thiodiacetic acid, glycolic acid, which is oxidized to carbon dioxide, and oxalic acid. In an oral study in rats, thiodiacetic acid was identified as the major urinary metabolite, accounting for 60% of the dose; most of the remainder was excreted as S-carboxymethyl cysteine.(1,5)


If symptoms occur, remove source of contamination or have victim move to fresh air. Obtain medical advice immediately.

Skin Contact:
Avoid direct contact with this chemical. Wear chemical protective clothing, if necessary. As quickly as possible, flush contaminated area with lukewarm, gently flowing water for at least 20-30 minutes, by the clock. If irritation persists, repeat flushing. DO NOT INTERRUPT FLUSHING. If necessary, keep emergency vehicle waiting. Under running water, remove contaminated clothing, shoes, and leather goods (e.g., watchbands, belts). Transport victim to an emergency care facility immediately. Discard contaminated clothing, shoes and leather goods. DO NOT reuse.

Eye Contact:
Avoid direct contact with this chemical. Wear chemical protective gloves, if necessary. Immediately flush the contaminated eye(s) with lukewarm, gently flowing water for at least 20-39 minutes, by the clock, while holding the eyelid(s) open. Neutral saline solution may be used as soon as it is available. DO NOT INTERRUPT FLUSHING. If necessary, keep emergency vehicle waiting. Take care not to rinse contaminated water into the non-affected eye or onto the face. If irritation persists, repeat flushing. Quickly transport victim to an emergency care facility.

NEVER give anything by mouth if victim is rapidly losing consciousness, is unconscious or is convulsing. Have victim rinse mouth thoroughly with water. DO NOT INDUCE VOMITING. Have victim drink 240 to 300 mL (8 to 10 oz.) of water to dilute material in stomach. If milk is available, it may be administered AFTER the water has been given. If vomiting occurs naturally, rinse mouth and repeat administration of water. Quickly transport victim to an emergency care facility.

First Aid Comments:
Provide general supportive measures (comfort, warmth, rest). Consult a doctor and/or the nearest Poison Control Centre for all exposures except minor instances of inhalation or skin contact.
All first aid procedures should be periodically reviewed by a doctor familiar with the material and its conditions of use in the workplace.


Flash Point:
126 deg C (259 deg F) (closed cup) (6)

Lower Flammable (Explosive) Limit (LFL/LEL):
8% (17)

Upper Flammable (Explosive) Limit (UFL/UEL):
Not available

Autoignition (Ignition) Temperature:
470 deg C (878 deg F) (6); greater than 500 deg C (932 deg F) (17)

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

Sensitivity to Static Charge:
Under certain conditions, airborne dust of monochloroacetic acid (MCA) can explode when ignited by an electrostatic spark or other ignition source.(21,22,23)

Combustion and Thermal Decomposition Products:
May decompose to form irritating/toxic phosgene and hydrogen chloride gases. (17,18,24)

Fire Hazard Summary:
MCA can burn if strongly heated. During a fire, irritating/corrosive hydrogen chloride gas may be generated. Closed containers may explode in the heat of a fire. Under certain conditions, a dust cloud of MCA may explode when ignited by a spark or flame. See references 22 and 23 for a list of the main ignition sources of sufficient energy to cause a dust explosion. When evaluating the explosion hazard of a specific process or sample of material, the important factors to consider include: particle size and shape, dust concentration, the nature of any impurities, oxygen concentration, humidity, and extent of containment.(23) MINIMUM IGNITION TEMPERATURE: 620 deg C (1148 deg F) (cloud) (21,22)

Extinguishing Media:
Dry chemical powder, carbon dioxide, polymer foam, alcohol foam, water spray or fog.(17,18)

Fire Fighting Instructions:
Evacuate area and fight fire from a safe distance or a protected location. Approach fire from upwind to avoid toxic decomposition products.
If possible, isolate materials not involved in the fire, if this can be done without risk, and protect personnel. Avoid generating dust to minimize risk of explosion. Water or foam may cause frothing. The frothing may be violent and could endanger personnel close to the fire. However, a water spray or fog that is carefully applied to the surface of the material, preferably with a fine spray or fog nozzle, will cause frothing that will blanket and extinguish the fire. In addition, water can be used in the form of spray or fog to prevent dust formation, keep fire-exposed containers cool and absorb heat to help prevent rupture. Water spray may also be used to knock down irritating/toxic combustion products which may be produced in a fire. Apply water from as far a distance as possible.
MCA decomposition products, such as phosgene and hydrogen chloride, are hazardous to health. Do not enter without wearing specialized protective equipment suitable for the situation. Firefighter's normal protective equipment (Bunker Gear) will not provide adequate protection. A full-body encapsulating chemical resistant suit with positive pressure self-contained breathing apparatus (MSHA/NIOSH approved or equivalent) may be necessary.


NFPA - Health: 4 - Very short exposure could cause death or major residual injury.
NFPA - Flammability: 1 - Must be preheated before ignition can occur.
NFPA - Instability: 0 - Normally stable, even under fire conditions, and not reactive with water.


Molecular Weight: 94.50

Conversion Factor:
1 ppm = 3.86 mg/m3; 1 mg/m3 = 0.259 ppm at 25 deg C (calculated)

Physical State: Solid
Melting Point: 62-63 deg C (144-145 deg F) (alpha form) (6); 61-63 deg C (commercial product) (5)
Boiling Point: 189 deg C (372 deg F) (5,19,20)
Relative Density (Specific Gravity): 1.404 at 25 deg C (20) (water = 1)
Solubility in Water: Extremely soluble (421 g/100 g at 20 deg C) (6)
Solubility in Other Liquids: Very soluble in acetone; soluble in ethanol, methanol, diethyl ether, benzene, chloroform, carbon disulfide and methylene chloride.(7,20)
Coefficient of Oil/Water Distribution (Partition Coefficient): Log P(oct) = -0.53 to +0.48 (calculated) (26)
pH Value: 1.93 (0.1 M solution (9.45 g/L)) (calculated); 3.8 (500 mg/L) (19)
Vapour Density: 3.25 (air = 1) (19)
Vapour Pressure: 0.1 kPa (0.75 mm Hg) at 20 deg C (18)
Saturation Vapour Concentration: 1000 ppm (0.1%) at 20 deg C (calculated)
Evaporation Rate: Not available
Critical Temperature: Not available

Other Physical Properties:
ACIDITY: Moderate to weak acid; pKa = 2.85-2.86 (5,20)
VISCOSITY-DYNAMIC: 2.16 mPa.s (2.16 centipoises) at 70 deg C (6)
SURFACE TENSION: 35.17 mN/m (35.17 dynes/cm) at 100 deg C (6,20)



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.

STRONG OXIDIZING AGENTS (e.g. chromium trioxide, perchlorates, peroxides) - may react violently or explosively. Increased risk of fire.(18)
STRONG BASES (e.g. sodium hydroxide) - violent reaction may occur, producing heat and pressure.(18,24)
STRONG REDUCING AGENTS - may react violently.(18)
REACTIVE METALS (e.g. aluminum, zinc) - may produce flammable hydrogen gas.

Hazardous Decomposition Products:
None reported

Conditions to Avoid:
Temperatures above 126 deg C

Corrosivity to Metals:
Corrosive to cast iron, steel, some stainless steels, copper, brass, aluminum, silver and lead.(27)


LC50 (rat): 47 ppm (reported as 180 mg/m3) (no duration given) (6,7)

LD50 (oral, rat): 55 mg/kg (7, unconfirmed)
LD50 (oral, rat): 76 mg/kg (31)
LD50 (oral, mouse): 165 mg/kg (32)
LD50 (oral, guinea pig): 80 mg/kg (9,32)
Symptoms in LD50 studies have included stomach pain, loss of appetite, nausea and vomiting.(9) Convulsions and respiratory depression have been observed in mice given single lethal doses of MCA.(5)

LD50 (skin, rabbit): 650 mg/kg (closed patch test) (10); 178 mg/kg (dry MCA) (2, unconfirmed)

Eye Irritation:

Monochloroacetic acid (MCA) vapour produced tissue damage to the cornea in one instance (species unspecified).(3)

Skin Irritation:

Application of a 4.3% solution (dose of 100 mg/kg) produced redness and swelling in rabbits. A 43% solution (dose of 1000 mg/kg) produced corrosive tissue damage and death in most animals.(10)

Effects of Short-Term (Acute) Exposure:

Short-term inhalation of high concentrations of MCA by rats produced lung irritation.(6)

Rats were orally administered up to 120 mg/kg/day in their drinking water for 16 days. Male mice were administered doses up to 240 mg/kg/day and female mice up to 480 mg/kg/day for 16 days. Clear nasal discharge and/or lacrimation (tearing) were observed in rats. At 120 mg/kg/day, 1/5 male rats and at 240 mg/kg/day and above all mice died. Central nervous system (CNS) effects such as impaired grasping reflex, muscular incoordination, prostration and slow breathing were observed in the rat and mice that died. No compound-related gross lesions were observed in mice at autopsy.(5) Mice were orally administered 80-800 mg/kg MCA. A small number of mice surviving 260 mg/kg or 380 mg/kg exhibited neurological damage to their front paws and hind legs which caused difficulty in walking. In the most severe cases, many of the mice had arched backs, severe tremors and convulsions and died within 48 hours after MCA treatment. The damage appeared to be permanent in the survivors and there was no improvement up to 6 months after treatment. Further studies indicate that the lethal effects of MCA and the physical deficits observed in survivors may be associated with impairment of the brain-blood barrier function.(8)

Effects of Long-Term (Chronic) Exposure:

Doses of up to 150 mg/kg/day (rats) or 200 mg/kg/day (mice) MCA were administered orally for up to 13 weeks. Deaths occurred at the four highest doses in rats (60-150 mg/kg/day) and at the highest dose (200 mg/kg/day) in mice. A dose-related increase in the incidence and severity of cardiomyopathy (degeneration of the heart muscle) was observed in rats. Relative liver and kidney weights of rats exposed at 60 mg/kg/day and relative liver weights of female mice exposed at 200 mg/kg/day were significantly increased. No compound related lesions were observed in mice.(11) In 2-year oral studies, rats were given 0, 15 or 30 mg/kg/day, while mice were given 0, 50 or 100 mg/kg MCA. At the high doses, the body weights of male rats and female mice were reduced. The body weights of low-dose female mice were also significantly reduced. Survival of high-dose male rats and mice was significantly reduced, as was survival of all dosed female rats. No significant degenerative lesions of the heart, similar to those seen in the 13-week studies, were observed. This lack of cardiac effects may be due to the lower doses used in the 2-year studies. Nonneoplastic lesions of the nasal mucosa, olfactory epithelium and the forestomach were observed in mice.(5) No exposure-related effects were observed in mice given 0.05% to 0.55% MCA in their drinking water for 44 weeks.(5)

MCA applied to or injected under the skin of mice was not carcinogenic in two studies.(7,12) Oral doses of 18-46 mg/kg for 18 months did not cause cancer in mice.(13) There was no evidence of carcinogenic activity for MCA in rats given 0, 15 or 30 mg/kg or in mice given 0, 50 or 100 mg/kg in 2-year oral studies.(5)

Negative results (DNA strand breakage) were obtained in the liver, spleen and epithelial cells of mice and rats administered a single oral dose (1-10 mmol) of MCA salt.(14)
Positive and negative results have been obtained in cultured mammalian cells. A dose-related increase in sister chromatid exchanges (SCEs) was observed in cultured Chinese hamster ovary (CHO) cells, without metabolic activation. No significant increase in chromosomal aberrations was observed in CHO cells, with and without metabolic activation. No significant chromosomal aberrations or SCEs were observed in Chinese hamster lung fibroblast cells, with or without metabolic activation.(5) Positive results were obtained in the L5178Y mouse lymphoma cell forward mutation assay, with (15) and without (16) metabolic activation. DNA strand breaks were not induced in human or rodent cells.(14) MCA was not mutagenic in Salmonella typhimurium, with and without metabolic activation.(5)
Negative results were obtained in the sex-linked recessive lethal mutations test in germ cells of male Drosophila melanogaster (fruit flies) fed MCA.(5)


Selected Bibliography:
(1) Dancer, G.H., et al. A case of skin contamination with carbon-14 labelled chloroacetic acid. Health Physics. Vol. 11, no. 10 (1965). p. 1055-1058
(2) Accident Case Histories. Monochloroacetic acid skin contact fatality. Case history no. 1708. Manufacturing Chemists Association, Dec. 1970
(3) Grant, W.M. Toxicology of the eye. 4th ed. Charles C. Thomas, 1993. p. 1013
(4) Rogers, D.R. Accidental fatal monochloroacetic acid poisoning. The American Journal of Forensic Medicine and Pathology. Vol. 16, no. 2 (1995). p. 115-116
(5) National Toxicology Program. NTP technical report on the toxicology and carcinogenesis studies of monochloroacetic acid (CAS no. 79-11-8) in F344/N rats and B6C3F1 mice (gavage studies). NTP TR 396. US Department of Health and Human Services, Jan. 1992
(6) Koenig, G., et al. Chloroacetic acids. In: Ullmann's encyclopedia of industrial chemistry. 5th completely revised ed. Vol. A 6. VCH Verlagsgesellschaft, 1986. p. 537-552
(7) RTECS record for acetic acid, chloro-. Last updated: 9603
(8) Beradi, M.R., et al. Monochloroacetic acid toxicity in the mouse associated with blood-brain barrier damage. Fundamental and Applied Toxicology. Vol. 9, no. 3 (Oct. 1987). p. 469-479
(9) Dalgaard-Mikkelsen, S., et al. Toxic effects of monobromacetic acid on pigs. Acta Pharmacologica et Toxicologica. Vol. 11, no. 1 (1955). p. 13-32
(10) Harton, E., et al. Toxicological and skin corrosion testing of selected hazardous materials. (Final report 1973-1974). US Department of Transportation, Apr. 1976. p. 1, 5-10, 23-28
(11) Bryant, B.J., et al. Toxicity of monochloroacetic acid administered by gavage to F344 rats and B6C3F1 mice for up to 13 weeks. Toxicology. Vol. 72, no. 1 (1992). p. 77-87
(12) Van Duuren, B.L., et al. Carcinogenic activity of alkylating agents. Journal of the National Cancer Institute. Vol. 53, no. 3 (Sept. 1974). p. 695-700
(13) Innes, J.R.M., et al. Bioassay of pesticides and industrial chemicals for tumorigenicity in mice: a preliminary note. Journal of the National Cancer Institute. Vol. 42, no. 6 (June, 1969). p. 1101-1114
(14) Chang, L.W., et al. Analysis of DNA strand breaks induced in rodent liver in vivo, hepatocytes in primary culture, and a human cell line by chlorinated acetic acids and chlorinated acetaldehydes. Environmental and Molecular Mutagenesis. Vol. 20, no. 4 (1992). p. 277-288
(15) Amacher, D. E., et al. Mutagenic evaluation of carcinogens and non-carcinogens in the L5178Y/TK assay utilizing postmitochondrial fractions (S9) from normal rat liver. Mutation Research. Vol. 97, no. 1 (1982). p. 49-65
(16) McGregor, D. B., et al. Responses of the L5178Y tk+/tk- mouse lymphoma cell forward mutation assay to coded chemicals. 1. Results for nine compounds. Environmental Mutagenesis. Vol. 9, no. 2 (1987). p. 143-160
(17) Fire protection guide to hazardous materials. 13th ed. Edited by A.B. Spencer, et al. National Fire Protection Association, 2002. NFPA 325; NFPA 49
(18) The Sigma-Aldrich library of chemical safety data. Ed. II. Vol. 1. Sigma-Aldrich, 1988. p. 726C
(19) Verschueren, K. Handbook of environmental data on organic chemicals. 3rd ed Van Nostrand Reinhold, 1996. p. 447-449
(20) Morris, E.D., et al. Acetic acid and derivatives: halogenated derivatives. In: Kirk-Othmer encyclopedia of chemical technology. 4th ed. Vol. 1. John Wiley and Sons, 1991. p. 165-168, 173-175
(21) Field, P. Explosibility assessment of industrial powders and dusts. Building Research Establishment, 1983
(22) Grossel, S.S. Safety considerations in conveying of bulk solids and powders. Journal of Loss Prevention in the Process Industries. Vol. 1 (Apr. 1988). p. 62-74
(23) Schwab, R.F. Dusts. In: Fire protection handbook. Edited by A.E. Cote. 18th ed. National Fire Protection Association, 1991. p. 4-174 to 4-181
(24) Chemical safety sheets: working safely with hazardous chemicals. Kluwer Academic Publishers, 1991. p. 620
(26) Leo, A., et al. Partition coefficients and their uses. Chemical Reviews. Vol. 71, no. 6 (Dec. 1971). p. 557
(27) Corrosion data survey: metals section. 6th ed. National Association of Corrosion Engineers, 1985. p. 36-1 to 37-1
(28) European Economic Community. Commission Directive 93/72/EEC. Sept. 1, 1993
(29) Forsberg, K., et al. Quick selection guide to chemical protective clothing. 4th ed. Van Nostrand Reinhold, 2002
(30) Kusch, G.D., et al. Monochloroacetic acid exposure: A case report. Polish Journal of Occupational Medicine. Vol. 3, no. 4 (1990). p. 409-414
(31) Morrison, J.L. Toxicity of certain halogen substituted aliphatic acids for white mice. J. of Pharm. Exp. Therap. Vol. 86 (Apr. 1946). p. 336-338
(32) Woodard, G., et al. The acute oral toxicity of acetic acid, chloroacetic acid, dichloroacetic acid and trichloroacetic acids. Journal of Industrial Hygiene and Toxicology. Vol. 23, no. 2 (Feb. 1941). p. 78-82
(33) Mason, D.W., et al. Sampling and analytical methods for the determination of monochloroacetic acid in air. American Industrial Hygiene Association Journal. Vol. 47, no. 1 (1986). p. 14-21.
(34) National Institute for Occupational Safety and Health (NIOSH). Chloroacetic Acid. In: NIOSH Manual of Analytical Methods (NMAM(R)). 4th ed. Edited by M.E. Cassinelli, et al. DHHS (NIOSH) Publication 94-113. Aug. 1994. Available at: <>

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: 1996-12-23

Revision Indicators:
US transport 1998-03-01
WHMIS health effects 2002-04-24
NFPA (health) 2003-04-16
Personal hygiene 2003-05-05
Resistance of materials for PPE 2004-04-05
WEEL STEL 2004-07-02
WEEL TWA 2004-07-02
Passive Sampling Devices 2005-03-12
Bibliography 2005-03-13
Sampling/analysis 2005-03-13
TLV-TWA 2006-02-14
TLV basis 2006-02-14
TLV comments 2006-02-14
TLV proposed changes 2006-02-14
Carcinogenicity 2006-02-15
WHMIS detailed classification 2006-02-15

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