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CHEMINFO Record Number: 766
CCOHS Chemical Name: Trichloroacetic acid solutions

Trichloracetic acid
Trichloroethanoic acid
Trichloromethanecarboxylic acid
Acide trichloracetique (solutions)
Trichloroacetic acid (non-specific name)

Chemical Name French: Acide trichloroacétique (solutions)
CAS Registry Number: 76-03-9
UN/NA Number(s): 2564
RTECS Number(s): AJ7875000
EU EINECS/ELINCS Number: 200-927-2
Chemical Family: Halogenated aliphatic carboxylic acid / haloalkanoic acid / chlorinated carboxylic acid / chloroacetic acid
Molecular Formula: C2-H-Cl3-O2
Structural Formula: CCl3-C(=O)-OH


Appearance and Odour:
Colourless to slightly yellow solution with a sharp, pungent odour (4,21)

Odour Threshold:
0.24 to 0.375 ppm (1.6 to 2.5 mg/m3) (recognition) (21)

Warning Properties:
NOT RELIABLE - odour threshold about the same magnitude as TLV.

Dichloroacetic acid may be present as an impurity (1.2-2.5%); other impurities may include sulfuric acid, sulfated ash and/or water.(4) TCA is sold as a solid and as a 90% aqueous solution. This record provides information for TCA solutions. For information on the solid refer to CHEMINFO record 539 for information.

Uses and Occurrences:
The main use is in the production of its sodium salt, which is used as a herbicide; also used as a pickling or etching agent in metal surface finishing; a swelling agent and solvent in the plastics industry; auxiliary in textile finishing; decalcifier and fixative in microscopy; protein precipitating agent in laboratories; additive in mineral lubricating oils; polymerization catalyst; intermediate in the chemical synthesis of esters; medical agent in treating skin disorders, to remove genital warts and as an astringent and antiseptic.(4,13)


Colourless to slightly yellow solution with a sharp, pungent odour. Deliquescent. Does not burn or support combustion. Can decompose upon heating, forming irritating/toxic phosgene and chlorinated hydrocarbons, such as chloroform, and hydrogen chloride. TOXIC. Fatal if swallowed. CORROSIVE to the eyes, skin and respiratory tract. May cause permanent eye injury and permanent scarring. May cause lung injury--effects may be delayed.


Effects of Short-Term (Acute) Exposure

Trichloroacetic acid (TCA) is corrosive and mists from solutions can cause mild to severe irritation or corrosive tissue damage. The degree of injury increases with the concentration of the acid and the duration of the exposure. Early symptoms may include sore throat, irritation of the nose and coughing. Extreme exposures may cause shortness of breath, difficult breathing and a life threatening build-up of fluid in the lungs (pulmonary edema). Symptoms of pulmonary edema, such as shortness of breath may not appear until several hours after exposure and are aggravated by physical exertion.

Skin Contact:
Contact with solutions can produce redness, swelling, pain and corrosive skin damage, based on the acidity of TCA. The severity of injury increases with the concentration of the acid and the duration of exposure. Limited animal evidence has only shown mild irritation following contact with TCA.
TCA is not readily absorbed through the skin.(1)

Eye Contact:
Contact with solutions or mists can cause mild to severe irritation or corrosive injury. The severity of injury increases with the concentration of the acid and the degree and duration of contact. Permanent eye damage or blindness could result.
In two accidents which occurred during the medical treatment of cataract-like eye tissue, TCA (10% or saturated solutions) contacted healthy tissue and caused pain, redness, swelling and serious corrosive injury. One report describes a very slow recovery from this type of injury.(2) Severe irritation has also been observed following contact with TCA in one animal test.

TCA is a corrosive material. Ingestion of concentrated solutions of TCA can produce severe burns to the lips, mouth and throat. Other symptoms may include salivation, vomiting of blood, burning sensation in mouth and throat, diarrhea, and pain. Permanent digestive tract damage could result. In severe cases, shock, severe respiratory effects, and death may result.(3) Ingestion is not a typical route of occupational exposure.

Effects of Long-Term (Chronic) Exposure

SKIN CONTACT: There is no specific information available for TCA, but repeated or prolonged skin contact with dilute acid solutions may cause redness, drying and itching (dermatitis).

INHALATION: There is no specific information available for TCA, but workers exposed to sodium trichloroacetate mists daily for 5 1/2 months experienced cough, sore throat, chest pains, and burning, irritated eyes. Many of these symptoms worsened at night. One worker exposed to these mists for 2 1/2 years (exposed 5 1/2 months/year) also had symptoms of shortness of breath and fatigue.(3)

EYE CONTACT: One worker exposed to sodium trichloroacetate mists for 2 1/2 years (exposed 5 1/2 months/year) also had itchy, swollen eyes.(3)


There is inadequate evidence for the carcinogenicity of trichloroacetic acid in humans. There is no specific human available. There is limited evidence for the carcinogenicity of trichloroacetic acid in animal studies. Increased liver tumours were seen in two animal studies following oral administration of neutralized trichloroacetic acid.(4,31)

The International Agency for Research on Cancer (IARC) has concluded that this chemical is not classifiable as to its carcinogenicity to humans (Group 3).

The American Conference of Governmental Industrial Hygienists (ACGIH) has designated this chemical as an animal carcinogen (A3).

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

Teratogenicity and Embryotoxicity:
There is no specific human or animal information available for TCA. Developmental effects have been observed in rats following oral administration of maternally toxic doses of neutralized TCA.

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

There are no reports of human in vivo studies. TCA, neutralized to avoid the effects of low pH, did not induce chromosomal aberrations in cultured human lymphocytes.(5) TCA was mutagenic when a large dose was injected into mice. However, this positive effect was probably caused by the low pH, rather than a genotoxic effect. Similar effects were not observed following the oral administration of neutralized TCA. Positive and negative results have been observed in bacteria and cultured mammalian cells.

Toxicologically Synergistic Materials:
There is no specific information available for TCA. Neutralized TCA increased the toxicity of chloroform to the kidneys of rats.(6)

Potential for Accumulation:
Probably does not accumulate. Ingestion of 3 mg/kg of sodium trichloroacetate by humans resulted in very slow excretion of unchanged trichloroacetate. About one half of the ingested dose was excreted by 50 hours.(7) Animal evidence indicates that TCA and its metabolites are mostly excreted in the urine (60-70% of administered dose, of which 60% appears to be unchanged TCA). After oral administration, TCA is metabolized in rats and mice to dichloroacetic acid, which in turn gives oxalate and carbon dioxide, or monochloroacetic acid, which is then further metabolized to thiodiacetic acid. The major urinary products, are unchanged TCA, and oxalic and thiodiacetic acids.(4)


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 is difficult, oxygen may be beneficial if administered by trained personnel, preferably on a doctor's advice. DO NOT allow victim to move about unnecessarily. Symptoms of pulmonary edema can be delayed up to 48 hours after exposure. Immediately transport victim to an emergency care facility.

Skin Contact:
Avoid direct contact with this chemical. Wear chemical protective gloves, 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. Completely decontaminate clothing, shoes and leather goods before re-use or discard.

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 20-30 minutes, by the clock, 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 unaffected 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, or is unconscious or 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 the 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.
Some recommendations in the above sections may be considered medical acts in some jurisdictions. These recommendations should be reviewed with a doctor and appropriate delegation of authority obtained, as required.
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:
Aqueous solutions are not combustible.

Lower Flammable (Explosive) Limit (LFL/LEL):
Not applicable

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

Autoignition (Ignition) Temperature:
Not applicable

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

Sensitivity to Static Charge:
Aqueous solutions will not accumulate static charge.

Combustion and Thermal Decomposition Products:
Ignition may be possible, if the water has evaporated. Under fire conditions, trichloroacetic acid (TCA) can decompose to form irritating/toxic phosgene and chlorinated hydrocarbons, such as chloroform, and irritating/corrosive hydrogen chloride gas, as well as carbon dioxide and carbon monoxide.(13,22,23)

Fire Hazard Summary:
Aqueous solutions do not burn or support combustion. However, ignition may be possible if the water has evaporated. During a fire, TCA can decompose upon heating, forming irritating/toxic phosgene and chlorinated hydrocarbons, such as chloroform, and irritating/corrosive hydrogen chloride. Closed containers may explode in the heat of a fire.

Extinguishing Media:
Aqueous solutions of TCA do not burn or support combustion. Use fire extinguishing media appropriate to the surrounding fire conditions. Extinguishing media which have basic properties (such as dry chemical powder) may react violently with TCA.

Fire Fighting Instructions:
Evacuate area and fight fire from a safe distance or protected location. Approach fire from upwind to avoid toxic decomposition products.
Move containers from fire area if it can be done without risk. Otherwise, use water in flooding quantities as a spray or fog to 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.
TCA 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 - Comments:
NFPA has no listing for this chemical in Codes 49 or 325.


Molecular Weight: 163.39

Conversion Factor:
1 ppm = 6.67 mg/m3; 1 mg/m3 = 0.150 ppm at 25 deg C (calculated)

Physical State: Liquid
Melting Point: Not available
Boiling Point: Not available
Relative Density (Specific Gravity): Not available
Solubility in Water: Completely soluble
Solubility in Other Liquids: Very soluble in acetone; soluble in ethanol and methanol.
Coefficient of Oil/Water Distribution (Partition Coefficient): Log P(oct) = 0.10 to 1.96 (calculated) (24)
pH Value: 1.2 (0.1 M solution)
Acidity: Strong acid; pKa = 0.70 (Ka = 0.2) at 25 deg C (13,25) NOTE: Trichloroacetic acid is as strong an acid as hydrochloric acid.(26)
Vapour Density: 5.6 (air = 1) (22)
Vapour Pressure: Not available; probably very low. 0.133 kPa (1 mm Hg) at 51 deg C (solid TCA) (21,25)
Saturation Vapour Concentration: Low; 1300 ppm (0.13%) at 51 deg C (calculated)
Evaporation Rate: Not available


Normally stable. Decomposes above the boiling point (197.5 deg C). Dilute solutions of trichloroacetic acid (TCA) in water may decompose slowly depending on the temperature, giving off chloroform and carbon dioxide.(4,13,22)

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.(23)
ORGANIC BASES (e.g. amines) or INORGANIC BASES (e.g. sodium hydroxide) - may react violently producing heat and pressure, forming chloroform and carbon dioxide. Facilitate thermal decomposition of water solutions, forming chloroform.(13,26)
DIMETHYL SULFOXIDE AND COPPER WOOL - mixture reacted violently and explosively.(23,27)
REACTIVE METALS (eg. aluminum, zinc) - highly reactive; may produce flammable and explosive hydrogen gas.

Hazardous Decomposition Products:
Chloroform, carbon dioxide.

Conditions to Avoid:
Heat, generation of mist.

Corrosivity to Metals:
Corrosive to cast iron, stainless steels, copper, brass, bronze, aluminum, zinc and lead.(28)


LD50 (oral, rat): 400 mg/kg (8)

Eye Irritation:

Application of 3.5 mg trichloroacetic acid for 5 seconds produced severe irritation in rabbits.(9, unconfirmed)

Skin Irritation:

Application of 0.21 mg in a standard Draize test produced mild irritation on rabbit skin.(9, unconfirmed) A single application of trichloroacetic acid to the tail of a rat apparently caused no change, but repeated application produced severe tissue death (necrosis).(3)

Effects of Short-Term (Acute) Exposure:

Oral administration of 30 or 300 mg/kg/day of neutralized trichloroacetic acid in the drinking water of rats for 7 days resulted in reduced weight and severe toxicity, at the high dose. Oral administration of 24 or 240 mg/kg/day of neutralized trichloroacetic acid in the drinking water of rats for 14 days caused reduced weight gain only, at the high dose.(10)

Effects of Long-Term (Chronic) Exposure:

Administration of trichloroacetic acid or neutralized trichloroacetic acid at doses as low as 350 mg/kg/day for 90 days have produced decreased body weight and liver and kidney effects in male rats.(11,12) Male rats given trichloroacetic acid in the drinking water for 90 days, at a concentration providing daily doses of about 4, 35 or 350 mg/kg, had decreased body weights. At the high dose, increased liver and kidney weights and increased liver enzyme activity was also observed.(11) In another study, male rats given approximately 780 mg/kg/day of neutralized trichloroacetic acid in their drinking water had decreased body weight (approximately 17%) and liver weight (approximately 14%) after 90 days. Minimal to mild changes were seen in the liver and the lungs.(12) Administration of neutralized trichloroacetic acid at levels of 2000 mg/kg and greater in the diet produced body weight loss, lesions to mouth and gums, change in white blood cell count, lesions to liver and heart, skeletal muscle atrophy and impaired sperm formation. The nontoxic effect level was 500 mg/kg.(13) Study details are not available.

The International Agency for Research on Cancer (IARC) has determined that there is limited evidence in experimental animals for the carcinogenicity of trichloroacetic acid.(4,31)
Neutralized trichloroacetic acid was tested for carcinogenicity by oral administration in two studies using male mice. In both studies, the incidence of liver tumours (hepatocellular adenomas and carcinomas) was increased.(4,14)

Teratogenicity, Embryotoxicity and/or Fetotoxicity:
There is no specific information available for trichloroacetic acid. In one study, oral administration of neutralized trichloroacetic acid cause developmental effects, but only at maternally toxic doses (low dose 330 mg/kg/day).(15)

Reproductive Toxicity:
Injection of 500 mg/kg trichloroacetic acid into the body cavity of mice produced a slight increase in abnormal sperm head shape.(16) This route of exposure is not considered relevant to an occupational setting.

Positive results (chromosomal aberrations and micronucleus tests in bone marrow cells) have been obtained in mice following the injection of trichloroacetic acid.(16) This positive effect was probably due to the pH of the injected solution, rather than a genotoxic effect. In a follow-up injection study with mice, a ten-fold higher dose of neutralized trichloroacetic acid did not cause similar mutagenic effects.(17) Reversible positive effects (DNA strand breaks) were observed in the liver cells of rats and mice treated orally with neutralized trichloroacetic acid.(18,19) In another study, negative results (DNA strand breaks) were observed in the liver, spleen and epithelial cells from the stomach and duodenum of mice or rats following the oral administration of neutralized trichloroacetic acid.(20)
DNA strand breaks were not induced in human or rodent cells in vitro.(20) Trichloroacetic acid was not mutagenic to Salmonella typhimurium strains, in the presence or absence of metabolic activation (Ames test). However, trichloroacetic acid was mutagenic in a bacterial test when combined with the solvent DMSO.(4,16)


Selected Bibliography:
(1) Trichloroacetic acid. In: Documentation of the threshold limit values and biological exposure indices. 6th ed. American Conference of Governmental Industrial Hygienists, 1991. p. 1602-1604
(2) Grant, W.M., et al. Toxicology of the eye. 4th ed. Charles C. Thomas, 1993. p. 1446-1447
(3) Hayes, W.J. Pesticides studied in man. Williams and Wilkins, 1982. p. 537
(4) Trichloroacetic acid. In: IARC Monographs on the evaluation of the carcinogenic risk of chemicals to humans. Vol. 63. Dry cleaning, some chlorinated solvents and other industrial chemicals. International Agency for Research on Cancer, 1995. p. 291-314
(5) Mackay, J.M., et al. Trichloroacetic acid: investigation into the mechanism of chromosomal damage in the in vitro human lymphocyte cytogenetic assay and the mouse bone marrow micronucleus test. Carcinogenesis. Vol. 16, no. 5 (May 1995). p. 1127-1133
(6) Davis, M.E. Effect of chloroacetic acids on the kidneys. Environmental Health Perspectives. Vol. 69 (1986). p. 209-214
(7) Muller, G., et al. Metabolism of trichloroethylene in man II: pharmacokinetics of metabolites. Archives of Toxicology. Vol. 32 (1974). p. 283-295
(8) The pesticide manual: a world compendium. 7th ed. The British Crop Protection Council, 1983. p. 11170
(8) Woodard, G., et al. The acute oral toxicity of acetic, chloracetic, dichloracetic, and trichloracetic acids. Journal of Industrial Hygiene and Toxicology. Vol. 23 (1941). p. 78-82
(9) RTECS record for acetic acid, trichloro-. Last updated: 9603
(10) Davis, M.E. Effect of chloroacetic acids on the kidneys. Environmental Health Perspectives. Vol. 69 (1986). p. 209-214
(11) Mather, G.G., et al. Subchronic 90 day toxicity of dichloroacetic and trichloroacetic acid in rats. Toxicology. Vol. 64, no. 1 (Oct. 1990). p. 71-80
(12) Bhat, H.K., et al. Ninety day toxicity study of chloroacetic acid in rats. Fundamental and Applied Toxicology. Vol. 17, no. 2 (Aug. 1991). p. 240-253
(13) Koenig, G., et al. Chloroacetic acids. In: Ullmann's encyclopedia of industrial chemistry. 5th completely revised ed. Volume A 6. VCH Verlagsgesellschaft, 1986. p. 537-552
(14) Herren-Freund, S.L., et al. The carcinogenicity of trichloroethylene and its metabolites, trichloroacetic acid and dichloroacetic acid, in mouse liver. Toxicology and Applied Pharmacology. Vol. 90 (1987). p. 183-189
(15) Smith, M.K., et al. Teratogenic activity of trichloroacetic acid in the rat. Teratology. Vol. 40 (1989). p. 445-451
(16) Bhunya, S.P., et al. Relative genotoxicity of trichloroacetic acid (TCA) as revealed by different cytogenetic assays: bone marrow chromosome aberration, micronucleus and sperm-head abnormality in the mouse. Mutation Research. Vol. 188 (1987). p. 215-221
(18) Nelson, M.A., et al. Induction of strand breaks in DNA by trichloroethylene and metabolites in rat and mouse liver in vivo. Toxicology and Applied Pharmacology. Vol. 94, no. 1 (June 1988). p. 45-54
(19) Nelson, M.A., et al. Dichloroacetic acid and trichloroacetic acid-induced DNA strand breaks are independent of peroxisome proliferation. Toxicology. Vol. 58, no. 3 (Oct. 1989). p. 239-248
(20) 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
(21) Verschueren, K. Handbook of environmental data on organic chemicals. 3rd ed. Van Nostrand Reinhold, 1996. p. 1758-1759
(22) Chemical safety sheets: working safely with hazardous chemicals. Kluwer Academic Publishers, 1991. p. 873
(23) The Sigma-Aldrich library of chemical safety data. Ed. II. Vol. 2. Sigma-Aldrich, 1988. p. 3402C
(24) Leo, A., et al. Partition coefficients and their uses. Chemical Reviews. Vol. 71, no. 6 (Dec. 1971). p. 556
(25) Weast, R.C., ed. Handbook of chemistry and physics. 66th ed. CRC Press, 1985-1986. p. C-530, D-162, D-197
(26) 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. 169-170, 173-175
(27) Urben, P.G., ed. Bretherick's handbook of reactive chemical hazards. 5th ed. Vol. 1. Butterworth-Heinemann Ltd., 1995. p. 254
(28) Corrosion data survey: metals section. 6th ed. National Association of Corrosion Engineers, 1985. p. 128-9 to 129-9
(29) European Communities (EC). Commission Directive 2004/73/EC. Apr. 29, 2004
(30) Forsberg, K., et al. Quick selection guide to chemical protective clothing. 4th ed. Van Nostrand Reinhold, 2002
(31) International Agency for Research on Cancer (IARC). IARC monographs on the evaluation of carcinogenic risks to humans. Vol. 84. Some Drinking-water Disinfectants and Contaminants, including Arsenic. {Summary}. World Health Organization, Dec. 2002. Available on the World Wide Web: <>
(32) Occupational Safety and Health Administration (OSHA). 2,2-Dichloropropionic Acid and Trichloroacetic Acid. In: OSHA Analytical Methods Manual. Revision Date: Oct. 31, 2001. 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
TLV-TWA 1998-06-01
TLV comments 1998-06-01
Toxicological Info 1998-06-01
Storage 1998-06-01
Engineering controls 1998-06-01
Emergency overview 1999-03-01
Handling 1999-03-01
WHMIS (proposed class) 1999-03-01
WHMIS (detailed class) 1999-03-01
WHMIS (effects) 1999-03-01
WHMIS (disclosure list) 1999-03-01
EU risks 2002-02-12
EU safety 2002-02-12
TDG 2002-05-29
PEL-TWA final 2003-12-04
Resistance of materials for PPE 2004-04-05
Carcinogenicity 2004-08-25
Bibliography 2005-01-05
EU classification 2005-01-05
EU comments 2005-01-05
Bibliography 2005-03-13
Passive Sampling Devices 2005-03-13
Sampling/analysis 2005-03-13

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