1-9 A-D E-G H-M N-P Q-S T-Z


CAS No : 76-03-9


76-03-9; Acetic acid; Ethanoic acid; Trichloracetic acid; Triklorik asit; Asit; Triklorik; Trichloroacetic acid; Asetik asit; Etanoik asit;Trichloroethanoic acid; Aceto-caustin; Trichloracetic acid; Acetic acid, trichloro-; Trichloressigsaeure; Konesta; Acide trichloracetique; Acido tricloroacetico; Amchem grass killerTrichloorazijnzuur; TCA; Trichloroacetate; 2,2,2-trichloroacetic acid; Tecane; Kyselina trichloroctova; Acetic acid, trichloro- (solid); CCl3COOH; Caswell No. 870;Trichloorazijnzuur [Dutch]; TKhU; Trichloressigsaeure [German]; Trichloroacetic acid solution; UNII-5V2JDO056X; TKhUK; Trichloroacetic acid (IUPAC); Trichloromethanecarboxylic acid; Varitox; Dow sodium inhibited; NSC 215204; trichloro acetic acid; CCRIS 4015; Acide trichloracetique [French]; Acido tricloroacetico [Italian]; Kyselina trichloroctova [Czech]HSDB 1779; Acetic acid, 2,2,2-trichloro-; EINECS 200-927-2; MFCD00004177; UN1839; UN2564; TCA [BSI:ISO]; EPA Pesticide Chemical Code 081002; BRN 0970119;AI3-24157; 5V2JDO056X; CHEBI:30956; YNJBWRMUSHSURL-UHFFFAOYSA-N; NCGC00091021-02; WLN: QVXGGG; Trichloroacetic acid solid; DSSTox_CID_1378; Trichloorazijnzuur (DUTCH);DSSTox_RID_76121; DSSTox_GSID_21378; Trichloressigsaeure (GERMAN); Acide trichloracetique (FRENCH); Acido tricloroacetico (ITALIAN); Trichloroacetic acid, 99%, extra pure;CAS-76-03-9; SMR000059159; C2HCl3O2; Trichloroacetic acid [USP]; TCA solution; Trichloressigsaure; Trichloroacetic acid [USP XXI]; Tricloroacetic acid; perchloroacetic acidsNplJqDJHtQdTaeTp@; TCAA; trichloro-acetic acid; Varitox (Salt/Mix); CCl3CO2H; NA TA (Salt/Mix); AC1L1MHU; ACMC-1BK0N; EC 200-927-2; AC1Q71RA; Acido tricloroacetico (TN)SCHEMBL3220; NCIOpen2_000772; 4-02-00-00508 (Beilstein Handbook Reference); KSC377I7P; MLS001066365; MLS001336033; MLS001336034; UN 2564 (Salt/Mix); CHEMBL14053;Trichloroacetic acid, solution; 2,2,2-Trichloro-Acetic acid; AC1Q71R9; Aceticacid, 2,2,2-trichloro-; DTXSID1021378; CTK2H7477; TRICHLOROACETIC ACID, ACS; Trichloroacetic acid solid (DOT);MolPort-001-770-628; s221; Trichloroacetic acid, >=99.5%; Trichloroacetic acid, ACS reagent; HMS2233M06; HMS3374M09; NSC77363; Trichloroacetic acid, 99% 250g; ZINC3791092Tox21_111060; Tox21_201632; Tox21_300187; Trichloroacetic acid solution (DOT); ANW-13593; BBL012209; NSC-77363; NSC215204; STL163550;AKOS000118939;Trichloroacetic acid (ACD/Name 4.0);Trichloroacetic acid solution, 0.6 N;Trichloroacetic acid solution, 6.1 N; Trichloroacetic acid, reagent grade, 98%;Trichloroacetic acid, 99+%, ACS reagent;Trichloroacetic acid, BioXtra, >=99.0%AB1003175; TR-024396; FT-0645145; T0369; Trichloroacetic acid [UN1839] [Corrosive]; Trichloroacetic acid, >=99.0% (titration);Trichloroacetic acid [UN1839] [Corrosive];Trichloroacetic acid, 5% w/v aqueous solution; Trichloroacetic acid, 80% (w/v) in solution; Trichloroacetic acid, ACS reagent, >=99.0%;TCA Deblock, 3 % (w/v) in methylene chlorideTrichloroacetic acid, BioUltra, >=99.5% (T); Trichloroacetic acid, purum p.a., >=99.0% (T); I04-1163; J-525058; Trichloroacetic acid, JIS special grade, >=99.0%;Trichloroacetic acid, solution [UN2564] [Corrosive]; F1908-0096; Trichloroacetic acid, PESTANAL(R), analytical standard;Trichloroacetic acid, solution [UN2564] [Corrosive]Z1270446580; InChI=1/C2HCl3O2/c3-2(4,5)1(6)7/h(H,6,7; TRICHLOROACETIC ACID (SEE ALSO DICHLOROACETIC ACID); Trichloroacetic acid solution, ~6.25 % (w/v), 0.38 N;Trichloroacetic acid solution, 6.1 N (approx. 100% w/v);Trichloroacetic acid, biotech. grade, redistilled, >=99%; Trichloroacetic acid, puriss. p.a., ACS reagent, >=99.5%Deblock trichloroacetic acid solution, 3 % (w/v) in methylene chloride;Trichloroacetic acid solution, certified reference material, 1000 mug/mL in methyl tert-butyl ether;Trichloroacetic acid, ACS reagent, for the determination of Fe in blood according to Heilmeyer, >=99.5%;Trichloroacetic acid, for electrophoresis, suitable for fixing solution (for IEF and PAGE gels), >=99%;Trichloroacetic acid, puriss., meets analytical specification of Ph. Eur., USP 21, 99-100.5% (calc. to the dried substance)Validated by Experts, Validated by Users, Non-Validated, Removed by Users;2,2,2-trichloroacetic acid; 200-927-2 [EINECS]; 5V2JDO056X; 650-51-1 [RN]; Acetic acid, 2,2,2-trichloro- [ACD/Index Name] acetic acid, trichloro-; Acide trichloroacétique [French] [ACD/IUPAC Name]; NATA; TCA; Trichloressigsaeure [German]; Trichloressigsäure [German] [ACD/IUPAC Name];Trichloroacetic acid [ACD/IUPAC Name] [Wiki]; Trichloro-acetic acid; trichloroacetic-acid; Trichloroethanoic acid; Trichloromethanecarboxylic acid;TRICHLOROACETIC ACID;Trichloorazijnzuur; Trichloorazijnzuur (DUTCH);Trichloorazijnzuur [Dutch]trichloracetic acid; Trichloressigsaeure (GERMAN); Trichloressigsaeure [German]; Trichloressigsaure; Trichloro acetic acid; TRI-CHLORO-ACETALDEHYDE; tri-chloroacetic acidTrichloroacetic acid [UN1839] [Corrosive]; Trichloroacetic acid, solution [UN2564] [Corrosive];tri; chloro; acatic; acid; tri; kloro; asetik; asit; acetic;tri chloro acetic acid; trichloro acetic acid; trichloro aceticacid; trikloro asetikasit; trikloroasetikasit; trichloroaceticacid; trıchloroacetıcacıd; trı chloro acetıc acıd; trı; chloroacetıc; acıd; trichloroacetic acid; trikloroasetik asit;TRıCHLOROACETİC ACıD, SOLUTİON [UN2564] [CORROSİVE];TRı; CHLORO; ACATıC; ACıD; TRİ; KLORO; ASETİK; ASİT; ACETıC;TRİ CHLORO ACETİC ACİD; TRICHLORO ACETIC ACID; TRICHLORO ACETICACID; TRİKLORO ASETİKASİT; TRİKLOROASETİKASİT; TRICHLOROACETICACID; TRICHLOROACETICACID; TRI CHLORO ACETIC ACID; TRI; CHLOROACETIC; ACID; TRİCHLOROACETİC ACİD; TRİKLOROASETİK ASİT;


Molecular Formula: C2HCl3O2 or CCl3COOH or C2Cl3NaO2 or CCl3CO2Na
Molecular Weight: 163.378 g/mol
state of matter Solid 
Density 1.63 kg/l (20°C) 
Solubility (20°C) 1600 g/L (H2O) 
Melting point 52 - 58°C 
Formula CCl3COOH 
M 163.39 g/mol 
CAS-No.: 76-03-9 
HS-No.: 29154000 
EC-No.: 200-927-2



For definition of Groups, see Preamble Evaluation. VOL.: 84 (2004) (p. 403) CAS No.: 76-03-9
5. Summary of Data Reported and Evaluation 5.1 Exposure data Trichloroacetic acid is mainly used as a selective herbicide. It also finds use in the metal, plastics and textile industries and as an analytical reagent. It is used in the topical treatment of warts, cervical lesions and other dermatological conditions. Trichloroacetic acid is a major end metabolite of trichloroethylene and tetrachloroethylene. Wider exposure to trichloroacetic acid occurs at microgram-per-litre levels in drinking-water and swimming pools as a result of chlorination or chloramination.
5.2 Human carcinogenicity data Several studies analysed risk with respect to one or more measures of exposure to complex mixtures of disinfection by-products that are found in most chlorinated and chloraminated drinking-water. No data specifically on trichloroacetic acid were available to the Working Group.
5.3 Animal carcinogenicity data In four studies, neutralized trichloroacetic acid, when administered in the drinking-water to female and/or male mice, increased the incidences of hepatocellular adenomas and carcinomas. In a study in male rats, trichloroacetic acid did not increase the incidence of liver tumours or tumours at any other site. When administered in the drinking-water, trichloroacetic acid promoted the induction of hepatocellular adenomas and/or carcinomas in carcinogen-initiated male and female mice and of kidney tumours in male mice.
5.4 Other relevant data The half-life of trichloroacetic acid, given orally or formed as a metabolite of trichloroethylene or trichloroethanol, is longer in humans than in rodents. Trichloroacetic acid may be reduced in vivo to dichloroacetic acid, but the artefactual conversion of trichloroacetic acid to dichloroacetic acid hinders any clear conclusions. A fraction of trichloroacetic acid is metabolized to carbon dioxide.
Trichloroacetic acid induces peroxisome proliferation in the livers of mice at doses within the same range as those that induce hepatic tumours. A brief stimulation of cell division is observed in the liver during the first days of treatment, but depressed cell replication results from chronic treatment. The initial increase in cell proliferation was correlated with decreased methylation of the promoter regions of the c-jun and c-myc proto-oncogenes and increased expression of these genes.
Effects of trichloroacetic acid on reproduction and development in rats have been reported, but were not confirmed in a subsequent study. In-vitro results suggest that trichloroacetic acid can produce teratogenic effects at high doses.
In male mice, trichloroacetic acid modified neither the incidence of mutations in exon 2 of H-ras in carcinomas, nor the mutational spectrum observed in tumours that bore a mutation in exon 2. In female mice, 27% of tumours promoted by trichloroacetic acid exhibited loss of heterozygosity at a minimum of two loci on chromosome 6.
In mouse liver in vivo, measurements of trichloroacetic acid-induced 8-hydroxydeoxyguanosine DNA adducts gave different results depending on the route of administration. Trichloroacetic acid induced abnormal sperm in mice in vivo in one study and chromosomal aberrations in mouse and chicken bone marrow in vivo. The results of in-vivo studies in rodents on the induction of DNA strand breaks and micronuclei were inconsistent. It induced the formation of micronuclei in newt larvae in vivo.
In human cells in vitro, trichloroacetic acid did not induce chromosomal aberrations or DNA strand breaks in single studies. In single studies on cultured rodent cells, trichloroacetic acid was weakly mutagenic; no effect was observed in a DNA strand-break assay or a single-cell gel assay. It also inhibited intercellular communication in cultured rodent cells. Trichloroacetic acid caused neither mutation in bacteria nor SOS repair. 
5.5 Evaluation There is inadequate evidence in humans for the carcinogenicity of trichloroacetic acid.There is limited evidence in experimental animals for the carcinogenicity of trichloroacetic acid.
Overall evaluation Trichloroacetic acid is not classifiable as to its carcinogenicity to humans (Group 3). For definition of the italicized terms, see Preamble Evaluation. 
Previous evaluation: Vol. 63 (1995)
·TCA (acid)
·Trichloracetic acid
·Trichloroethanoic acid
·Trichloromethane carboxylic acid



Trichloroacetic acid is a chemical that is commonly used for cosmetic skin peels and removal of warts, skin tags, moles, and tattoos. It works by removing the top few layers of skin, allowing new skin cells to appear. Peels with this acid are considered medium-deep, as compared to alpha-hydroxy acids with are more shallow and phenol peels which are much deeper.
Cosmetic skin peels with trichloroacetic acid are generally performed by dermatologists or plastic surgeons because the solution is too caustic to be safe for home or salon use. After several weeks of pre-treatment with alpha-hydroxy gels and anti-viral medications, the doctor performs the peel during a one-hour visit. Following the peel, the skin looks severely sunburned, and crusts and scabs may form. The recovery time for a peel is at least two weeks, though it might be longer for some people.
Chemical skin peels are cheaper and less invasive than plastic surgery, but they can yield similar results. Fine wrinkles, age spots, and discoloration caused by sun exposure or other environmental factors are removed in a chemical peel. Trichloroacetic acid peels can also remove many types of pre-cancerous lesions on the face. Many patients opt to have this treatment done every two or three years to maintain its effects.



Wart, mole and skin tag removal are another common uses of trichloroacetic acid. For these blemishes, a doctor applies a 50% solution of the acid directly to the area. In general, the blemish comes off within a week. For genital warts and HPV, doctors regularly use trichloroacetic acid to treat external outbreaks of warts that are suspected of being pre-cancerous. This type of treatment is less painful than freezing or cutting off the warts, but some patients require several treatments to completely remove an outbreak. Trichloroacetic acid can't be used on internal genital warts.
Trichloroacetic acid might also be used to remove or fade tattoos, although there are no clinical standards for this use. The concentration of acid used for tattoo removal is higher than that used for the face. In order for this treatment to be effective, it should be performed by a physician. Home treatment kits are available, but these can be ineffective at best, or damaging to the skin at worst. A chemical peel may not be able to remove a very large or deep tattoo, but in most cases, the tattoo significantly fades after several treatments.
One of the primary goals of WHO and its member states is that "all people, whatever their stage of development and their social and economic conditions, have the right to have access to an adequate supply of safe drinking water." A major WHO function to achieve such goals is the responsibility "to propose ... regulations, and to make recommendations with respect to international health matters ...."



The first WHO document dealing specifically with public drinking-water quality was published in 1958 as International Standards for Drinking-water. It was subsequently revised in 1963 and in 1971 under the same title. In 1984-1985, the first edition of the WHO Guidelines for Drinking-water Quality (GDWQ) was published in three volumes: Volume 1, Recommendations; Volume 2, Health criteria and other supporting information; and Volume 3, Surveillance and control of community supplies. Second editions of these volumes were published in 1993, 1996 and 1997, respectively. Addenda to Volumes 1 and 2 of the second edition were published in 1998, addressing selected chemicals. An addendum on microbiological aspects reviewing selected microorganisms was published in 2002. 
The GDWQ are subject to a rolling revision process. Through this process, microbial, chemical and radiological aspects of drinking-water are subject to periodic review, and documentation related to aspects of protection and control of public drinkingwater quality is accordingly prepared/updated. 
Since the first edition of the GDWQ, WHO has published information on health criteria and other supporting information to the GDWQ, describing the approaches used in deriving guideline values and presenting critical reviews and evaluations of the effects on human health of the substances or contaminants examined in drinkingwater. 
For each chemical contaminant or substance considered, a lead institution prepared a health criteria document evaluating the risks for human health from exposure to the particular chemical in drinking-water. Institutions from Canada, Denmark, Finland, France, Germany, Italy, Japan, Netherlands, Norway, Poland, Sweden, United Kingdom and United States of America prepared the requested health criteria documents. 
Under the responsibility of the coordinators for a group of chemicals considered in the guidelines, the draft health criteria documents were submitted to a number of scientific institutions and selected experts for peer review. Comments were taken into consideration by the coordinators and authors before the documents were submitted for final evaluation by the experts meetings. A "final task force" meeting reviewed the health risk assessments and public and peer review comments and, where appropriate, decided upon guideline values. During preparation of the third edition of the GDWQ, it was decided to include a public review via the world wide web in the process of development of the health criteria documents. 
During the preparation of health criteria documents and at experts meetings, careful consideration was given to information available in previous risk assessments carried out by the International Programme on Chemical Safety, in its Environmental Health Criteria monographs and Concise International Chemical Assessment Documents, the International Agency for Research on Cancer, the joint FAO/WHO Meetings on Pesticide Residues and the joint FAO/WHO Expert Committee on Food Additives (which evaluates contaminants such as lead, cadmium, nitrate and nitrite, in addition to food additives). 
Further up-to-date information on the GDWQ and the process of their development is available on the WHO internet site and in the current edition of the GDWQ.



The first draft of Trichloroacetic Acid in Drinking-water, Background document for development of WHO Guidelines for Drinking-water Quality, was prepared by Dr D. Wong, US Environmental Protection Agency, to whom special thanks are due. 
The work of the following working group coordinators was crucial in the development of this document and others in the third edition: 
Mr J.K. Fawell, United Kingdom (Organic and inorganic constituents) Dr E. Ohanian, Environmental Protection Agency, USA (Disinfectants and disinfection by-products) Ms M. Giddings, Health Canada (Disinfectants and disinfection by-products) Dr P. Toft, Canada (Pesticides) Prof. Y. Magara, Hokkaido University, Japan (Analytical achievability) Mr P. Jackson, WRc-NSF, United Kingdom (Treatment achievability) 
The contribution of peer reviewers is greatly appreciated. The draft text was posted on the world wide web for comments from the public. The revised text and the comments were discussed at the Final Task Force Meeting for the third edition of the GDWQ, held on 31 March to 4 April 2003, at which time the present version was finalized. The input of those who provided comments and of participants in the meeting is gratefully reflected in the final text. 
The WHO coordinators were as follows: Dr J. Bartram, Coordinator, Water Sanitation and Health Programme, WHO Headquarters, and formerly WHO European Centre for Environmental Health Mr P. Callan, Water Sanitation and Health Programme, WHO Headquarters Mr H. Hashizume, Water Sanitation and Health Programme, WHO Headquarters 
Ms C. Vickers provided a liaison with the International Chemical Safety Programme, WHO Headquarters.Ms Marla Sheffer of Ottawa, Canada, was responsible for the scientific editing of the document. 
Many individuals from various countries contributed to the development of the GDWQ. The efforts of all who contributed to the preparation of this document and in particular those who provided peer or public domain review comment are greatly appreciated. 
Acronyms and abbreviations used in the text CAS Chemical Abstracts Service CoA coenzyme A DNA deoxyribonucleic acid EPA Environmental Protection Agency (USA) IARC International Agency for Research on Cancer IUPAC International Union of Pure and Applied Chemistry LD50 median lethal dose LOAEL lowest-observed-adverse-effect level NOAEL no-observed-adverse-effect level TDI tolerable daily intake USA United States of America 
Table of contents



1 1.1 Identity
1 1.2 Physicochemical properties
1 1.3 Organoleptic properties
1 1.4 Major uses




2 3.1 Air
2 3.2 Water
2 3.3 Food
2 3.4 Estimated total exposure and relative contribution of drinking-water



4 5.1 Acute exposure







1.1 Identity


CAS No.: 76-03-9 Molecular formula: Cl3CCOOH


The IUPAC name for trichloroacetic acid is trichloroethanoic acid. 
1.2 Physicochemical properties1(Verschueren, 1977; Weast, 1988; Budavari et al., 1989; HSDB, 2001) 
Property Value Boiling point (°C) 197.5 Melting point (°C) 58.0 Density (g/cm3) 1.62 at 25 °C Vapour pressure (kPa) 0.02 at 25 °C 0.133 at 51 °C pKa at 25 °C 
0.512-0.70 Water solubility (g/litre) 13 Log octanol-water partition coefficient 1.33-1.7



1.3 Organoleptic properties 
No information is available on the taste or odour threshold of trichloroacetic acid in water.



1.4 Major uses 
Trichloroacetic acid is used as a soil sterilizer and a laboratory intermediate or reagent in the synthesis of a variety of medicinal products and organic chemicals.
Medical uses of trichloroacetic acid include application as an antiseptic and a peeling agent. Trichloroacetic acid is also used industrially as an etching and 
pickling agent for the surface treatment of metals and as a solvent in the plastics industry (Verschueren, 1977; Hawley, 1981; Budavari et al., 1989; Meister, 1989;
HSDB, 2001).



The chloroacetic acids can be detected in water by EPA Method 552.1, EPA Method 552.2 or Standard Method 6251B (APHA et al., 1998). In EPA Method 552.1, the haloacetic
acids are extracted on a miniature anion exchange column and converted to methyl esters in the eluant prior to analysis. EPA Method 552.2 involves a liquid- liquid
extraction procedure, after which the acetic acids are converted to methyl esters (US EPA, 1995). Both EPA methods use gas chromatography and electron capture 
detection. Standard Method 6251B uses a micro liquid-liquid extraction procedure 1 Conversion factor in air: 
1 ppm = 6.68 mg/m3. 
TRICHLOROACETIC ACID IN DRINKING-WATER combined with gas chromatography and electron capture detection. Method detection limits range from <0.1 to 0.4 µg/litre 
The practical quantification level for trichloroacetic acid is approximately 1 µg/litre (P. Fair, personal communication, 2002).



3.1 Air 
Trichloroacetic acid can be formed as a combustion by-product of organic compounds in the presence of chlorine (Juuti & Hoekstra, 1998). Stack gases of municipal
waste incinerators have been reported to contain trichloroacetic acid at concentrations in the range 0.37-3.7 µg/m3 (Mower & Nordin, 1987). Trichloroacetic acid 
could be a photooxidation product of tetrachloroethylene and 1,1,1-trichloroethane in the atmosphere (Reimann et al., 1996; Sidebottom & Franklin, 1996; Juuti & 
Hoekstra, 1998). However, Sidebottom & Franklin (1996) suggested that atmospheric degradation of chlorinated solvents contributes only a minor amount of 
trichloroacetic acid to the atmosphere, based on mechanistic and kinetic evidence as well as the observed global distribution of trichloroacetic acid in precipitation. 
The US National Air Toxics Information Clearinghouse reported that the annual, 8-h and 24-h time-weighted average ambient air concentrations of trichloroacetic acid in
the USA were 7, 73.24 and 58.14 µg/m3, respectively, when averaged across seven representative states (NATICH, 1993). Reimann et al. (1996) reported that levels of 
trichloroacetic acid in rainwater ranged from 0.01 to 1 µg/litre. It can be assumed that the chlorinated acetic acids detected in rainwater are from the atmosphere. 
Rainwater in Germany contained 0.1-20 µg of trichloroacetic acid per litre (IARC, 1995). Sidebottom & Franklin (1996) reported that trichloroacetic acid concentrations
in rainwater in remote areas (Antarctic, Arctic and sub-Arctic regions) generally ranged from 10 to 100 ng/litre.



3.2 Water 
Chlorinated acetic acids are formed from organic material during water chlorination (Coleman et al., 1980; IPCS, 2000). Concentrations of trichloroacetic acid measured
in various water sources have been summarized by IARC (1995): in Japan, chlorinated drinking-water contained 7.5 µg of trichloroacetic acid per litre; in Germany, 
groundwater contained 0.05 µg of trichloroacetic acid per litre; in Australia, a maximum concentration of 200 µg/litre was found for trichloroacetic acid in 
chlorinated water; and chlorinated water in Switzerland contained 3.0 µg of trichloroacetic acid per litre. Data for drinking-water supplies in the USA
(US EPA, 2001, 2002a) indicate that trichloroacetic acid was detected in groundwater and surface water distribution systems at mean concentrations of 5.3 and 
16 µg/litre, respectively; detected 
TRICHLOROACETIC ACID IN DRINKING-WATER concentrations range from <1.0 to 174 µg/litre in surface water distribution systems and from <1.0 to 80 µg/litre in groundwater
systems (US EPA, 2001, 2002a). Trichloroacetic acid has also been detected in swimming pool water. In a German study of 15 indoor and 3 outdoor swimming pools 
(Clemens & Scholer, 1992), trichloroacetic acid concentrations averaged 6.2 µg/litre and 94.1 µg/litre in indoor and outdoor pools, respectively. By contrast, the 
highest concentration of trichloroacetic acid measured in an outdoor pool was 871 µg/litre, with a mean concentration of 420 µg/litre (Kim & Weisel, 1998). 
The difference between this study and the lower levels reported in the German study may have been due to differences in the amounts of chlorine used to disinfect 
swimming pools, sample collection time relative to chlorination of the water or addition or exchanges of water in the pools.



3.3 Food 
As chlorine is used in food production and processing - including disinfection of chicken in poultry plants; processing seafood, poultry and red meats; sanitizing 
equipment and containers; cooling heat-sterilized foods; and oxidizing and bleaching in the flour industry (US EPA, 1994) - trichloroacetic acid is likely to be found 
as a disinfection by-product in meat and other food products (US EPA, 2002a). Trichloroacetic acid can also be taken up from cooking water (Raymer et al., 2001). In 
addition, there is evidence that trichloroacetic acid may be taken up by plants via the roots or by leaves via uptake from the air (Schroll et al., 1994; Sutinen et 
al., 1995). Reimann et al. (1996) examined the concentrations of trichloroacetic acid and other chlorinated acetic acids in a limited number of samples from several
vegetables, fruits, grains and beer. Trichloroacetic acid concentrations ranged from <0.2 to 5.9 µg/kg in vegetables and from <1.6 to 4.1 µg/kg in grains. 
Trichloroacetic acid was below the detection limit of 1.5 µg/kg in breads and 0.6 µg/kg in wheat flours. It was not detected in fruits or tomatoes.



3.4 Estimated total exposure and relative contribution of drinking-water 
Although the available data for trichloroacetic acid are sufficient to demonstrate that food and air are relevant exposure sources in addition to drinking-water, the 
data are not adequate to quantify the contributions of each source for an overall assessment of exposure.



Trichloroacetic acid is rapidly absorbed from the gastrointestinal tract in rats (Schultz et al., 1999) and by both the dermal and oral routes in humans (Kim & Weisel,
1998). Following oral and intravenous administration in rats, trichloroacetic acid appears to bind significantly to plasma proteins (Templin et al., 1993; Schultz et
al., 1999; Yu et 
al., 2000) and also distributes to the liver. A relatively small proportion of trichloroacetic acid is metabolized in the liver. The formation of carbon dioxide, 
glyoxylic acid, oxalic acid, glycolic acid and dichloroacetic acid was observed in rats and mice following oral administration of 20 or 200 mg of radiolabelled 
trichloroacetic acid per kg of body weight. The authors suggested that trichloroacetic acid was metabolized by reductive dehalogenation to dichloroacetic acid 
(Larson & Bull, 1992). Further reductive dehalogenation of dichloroacetic acid to monochloroacetic acid and ultimately to thiodiglycolate has been proposed as a 
metabolic pathway (Bull, 2000).



Other investigators have suggested that metabolism to dichloroacetic acid may have been over-reported in earlier studies due to analytical artefacts (Lash et al., 2000).
In F344 rats given intravenous injections of radiolabelled trichloroacetic acid at doses of 0, 6.1, 61 or 300 µmol/kg of body weight (approximately 0, 1, 10 or 
50 mg/kg of body weight), as much as 84% of the administered radioactivity was excreted in the urine within 24 h of dosing; high-performance liquid chromatographic 
analyses of plasma, urine and liver homogenate did not detect any oxalate, glyoxalate, glycolate or dichloroacetic acid, suggesting that trichloroacetic acid was 
poorly metabolized by the rats (Yu et al., 2000). The primary route of excretion is via the urine (Templin et al., 1993; Schultz et al., 1999; Yu et al., 2000). 
Approximately 40% of the clearance of trichloroacetic acid from blood following a single intravenous dose of 500 µmol/kg of body weight (approximately 80 mg/kg of
body weight) to male F344 rats was accounted for by renal clearance; excretion in faeces was negligible (Schultz et al., 1999). In light of the minimal metabolism 
observed, the authors suggested that the remaining 54% of the trichloroacetic acid dose was removed from blood primarily by tissue sequestration. In rats exposed to
82 mg/kg of body weight via the intravenous route, the elimination half-life of trichloroacetic acid was 8 h (Schultz et al., 1999). Some limited data on comparative 
excretion rates in rats and humans are available, based on a study of the inhalation of tetrachloroethylene, which is metabolized to trichloroacetic acid
(Volkel et al., 1998). The mean elimination half-life of trichloroacetic acid in urine was 45.6 h in humans, compared with 11.0 h in rats, suggesting that elimination
of trichloroacetic acid in rats is more rapid. It is possible, however, that the observed differences may be due to differences in tetrachloroethylene metabolism.



5.1 Acute exposure 
Oral LD50s of 3320 and 4970 mg/kg of body weight for trichloroacetic acid have been reported in rats and mice, respectively (Woodard et al., 1941). Dosed animals 
quickly passed into a state of narcosis or semi-narcosis and, within 36 h, either recovered completely or died in the narcotic state. 



5.2 Short-term exposure 
Groups of male B6C3F1 mice were given 0, 0.1, 0.5 or 2.0 g of trichloroacetic acid per litre in drinking-water (0, 25, 125 or 500 mg/kg of body weight per day) 
3 or 10 weeks and evaluated for oxidative DNA damage in the liver. After 3 weeks, liver weight was increased in the two highest dose groups, accompanied by increased 
12hydroxylation of lauric acid. After 10 weeks, effects included increased absolute and relative liver weights in the two highest dose groups, a dose-related increase
in cyanide-insensitive palmitoyl-coenzyme A (CoA) oxidase activity, increased 12hydroxylation of lauric acid and increased peroxisome proliferation. Based on these 
liver effects, the NOAEL was 25 mg/kg of body weight per day (Parrish et al., 1996). 
Groups of male Sprague-Dawley rats were exposed to trichloroacetate in drinkingwater at a concentration of 5 g/litre (about 312 mg/kg of body weight per day) for 10,
20 or 30 days. No treatment-related changes in body weight, organ weights, gross necropsy or histopathology were found. The NOAEL for this study was 312 mg/kg of body
weight per day (Parnell et al., 1988). Six male F344 rats and eight male B6C3F1 mice were given trichloroacetic acid by gavage at 500 mg/kg of body weight per day
for 10 days. In both species, relative liver weights and cyanide-insensitive palmitoyl-CoA oxidation were increased. There was no effect on relative kidney weights.
The LOAEL for liver effects in this study was 500 mg/kg of body weight per day for both rats and mice (Goldsworthy & Popp, 1987). Male Sprague-Dawley rats (10 per
dose) received trichloroacetic acid in drinkingwater at 0, 0.05, 0.5 or 5.0 g/litre (0, 4.1, 36.5 or 355 mg/kg of body weight per day) for 90 days. At the two highest
dose levels, decreased absolute spleen weight and increased relative liver and kidney weights were observed. At the highest dose, there was focal hepatocellular 
enlargement, intracellular hepatic swelling, hepatic glycogen accumulation and increased hepatic peroxisomal β-oxidation activity. The NOAEL for this study was 
36.5 mg/kg body weight per day (Mather et al., 1990). Male B6C3F1 mice were given trichloroacetic acid in their drinking-water at 0, 0.3, 1.0 or 2.0 g/litre
(0, 75, 250 or 500 mg/kg of body weight per day, based on strainspecific default values for water intake and body weight) for 14 days. A dose-related increase in
liver weight was observed, beginning at 0.3 mg/litre and becoming statistically significant at 1.0 g/litre. Based on these effects, the NOAEL was 75 mg/kg of body
weight per day (Sanchez & Bull, 1990). Male Wistar rats (5-6 per dose) were given water containing 0 or 0.025 g of trichloroacetic acid per litre (0 or 3.8 mg/kg of
body weight per day) for 10 weeks. Effects included decreased body weight, changes in serum markers of lipid and carbohydrate metabolism (increased succinate
dehydrogenase activity, increased glycogen accumulation and decreased liver triglyceride and cholesterol levels) and decreased kidney glutathione levels. No changes
in relative liver weight, serum liver enzyme activity or liver glutathione levels were observed (Acharya et al., 1995). In a 
follow-up study using the same experimental protocol and dose level, mild liver and kidney histopathology were noted (Acharya et al., 1997). Based on these effects, the single dose tested, 3.8 mg/kg of body weight per day, was a minimal LOAEL (Acharya et al., 1995, 1997). 
5.3 Long-term exposure 
Decreased body weight and increased relative liver weights were associated with administration of trichloroacetic acid to female B6C3F1 mice in drinking-water at concentrations of 0, 0.33, 1.1 or 3.3 g/litre (0, 78, 262 or 784 mg/kg of body weight per day, based on US EPA [1988] conventions for drinking-water intake and body weight for B6C3F1 mice) for 51 or 82 weeks. Based on significantly increased relative liver weights at 262 mg/kg of body weight per day and above, the NOAEL for this study is 78 mg/kg of body weight per day (Pereira, 1996). 
Groups of male F344 rats were given trichloroacetate in drinking-water at 0, 0.05, 0.5 or 5.0 g/litre (0, 3.6, 32.5 or 364 mg/kg of body weight per day) for 2 years. At 364 mg/kg of body weight per day, effects observed included decreased body weight, decreased absolute (but not relative) liver weight, increased serum alanine aminotransferase activity, increased cyanide-insensitive palmitoyl-CoA oxidase activity and increased severity of hepatic necrosis. No changes in kidney, spleen or testis weights were observed. There was no evidence of increased hepatocellular proliferation, as measured by radiolabelled thymidine incorporation rates. At 32.5 mg/kg of body weight per day, a significant decrease in serum aspartate aminotransferase activity was observed. This effect was not considered by the authors to be adverse. Based on non-neoplastic effects, the NOAEL for this study was 32.5 mg/kg of body weight per day (DeAngelo et al., 1997).


5.4 Reproductive and developmental toxicity


Groups of pregnant Long-Evans rats were given trichloroacetic acid by gavage at doses of 0, 330, 800, 1200 or 1800 mg/kg of body weight per day on gestation days 6-15. At 800 mg/kg of body weight per day and higher, effects included decreased maternal body weight gain, dose-related increases in maternal spleen and kidney (but not liver) weights and increased resorptions. At 330 mg/kg of body weight per day and higher, fetal weight and length were significantly reduced, and an increase in the incidence of soft tissue malformations, primarily involving the cardiovascular and renal systems, was observed. Skeletal malformations of the orbit and hydronephrosis were also noted. The maternal LOAEL was 330 mg/kg of body weight per day, based on decreased body weight gain. The developmental LOAEL was 330 mg/kg of body weight per day, based on teratogenic and fetal growth effects; no developmental NOAEL was identified (Smith et al., 1989). Pregnant Sprague-Dawley rats were given trichloroacetic acid in drinking-water at concentrations of 0 or 2.73 g/litre (0 or 290 mg/kg of body weight per day) on gestation days 1-22. A significant decrease in body weight gain was observed in treated dams relative to controls. Reproductive effects included increased resorptions 
and increased cardiac soft tissue malformations. Based on decreased maternal weight gain, the LOAEL for maternal toxicity is the only dose tested, 290 mg/kg of body weight per day, which is also a LOAEL for reproductive and developmental toxicity (Johnson et al., 1998). 
Trichloroacetic acid was not observed to exhibit teratogenic potential in a nonmammalian developmental toxicity screening assay with Hydra attenuata (Fu et al., 1990).


5.5 Mutagenicity and related end-points


Trichloroacetic acid was not mutagenic in Salmonella typhimurium strain TA100 without metabolic activation (Rapson et al., 1980), but it gave positive results in three in vivo chromosomal aberration assays in mice: the bone marrow assay, the micronucleus test and the sperm head abnormality assay (Bhunya & Behera, 1987); the results were time- and route-dependent (oral gavage or intraperitoneal injection) but did not demonstrate a dose-response. In modified Ames S. typhimurium assays, mixed results have been reported (DeMarini et al., 1994; Giller et al., 1997). In the SOS chromotest (an inducible error-prone repair system), trichloroacetic acid did not show evidence of genotoxicity with or without metabolic activation (Giller et al., 1997). Trichloroacetic acid showed weakly positive mutagenic activity in a mouse lymphoma cell assay and was considered to be one of the least potent mutagens among a range of chemical compounds evaluated in this test system (HarringtonBrock et al., 1998). Mixed results were observed in DNA strand break tests (Nelson & Bull, 1988; Chang et al., 1991), and no chromosomal damage was noted in cultured human peripheral lymphocytes (Mackay et al., 1995). Recent evidence suggests that trichloroacetic acid-induced clastogenicity is secondary to pH changes and not a direct effect of trichloroacetic acid exposure (Mackay et al., 1995). 
Although the data are somewhat conflicting, the weight of evidence suggests that trichloroacetic acid has neither significant mutagenic potential nor any structural alerts for mutagenicity. This conclusion is supported by the results from carcinogenicity bioassays in two species (negative in rats, liver tumours only in mice), discussed in the next section.


5.6 Carcinogenicity


Male B6C3F1 mice received trichloroacetic acid in drinking-water at concentrations of 0, 1.0 or 2.0 g/litre (approximately 0, 178 or 319 mg/kg of body weight per day, based on the study authors' calculations) for 37 or 52 weeks. An increase in the incidence of hepatocellular carcinomas was seen in males in both dose groups. No increases in tumours were noted in females in either dose group (Bull et al., 1990). 
Male B6C3F1 mice (50 per dose group) received 0, 0.05, 0.5 or 5 g of trichloroacetic acid per litre (0, 8, 71 or 595 mg/kg of body weight per day) in drinking-water for 60 weeks. At the two highest doses, a significant increase in the incidences of combined hepatocellular tumours (adenomas and carcinomas) was observed relative to controls 
(37.9% and 55.2% in mice receiving 71 and 595 mg/kg of body weight per day, respectively, compared with 13.3% in controls) (US EPA, 1991). In a second experiment, a significantly increased incidence of combined hepatocellular adenomas/carcinomas was also observed in male and female B6C3F1 mice (50 males and 55 females) given 4.5 g of trichloroacetic acid per litre (583 mg/kg of body weight per day) in drinking-water for 94 weeks (US EPA, 1991). 
No evidence of carcinogenicity was observed in groups of male F344 rats (50 per dose group) administered trichloroacetic acid in their drinking-water at concentrations of 0, 0.05, 0.5 or 5.0 g/litre (0, 3.6, 32.5 or 364 mg/kg of body weight per day) for 104 weeks (DeAngelo et al., 1997). 
Female B6C3F1 mice were given trichloroacetate in drinking-water at concentrations of 0, 0.3, 1.1 or 3.3 g/litre (approximately 0, 78, 262 or 784 mg/kg of body weight per day) for 51 or 82 weeks. After 51 weeks at 784 mg/kg of body weight per day, 25% of animals had liver carcinomas, compared with none in the other groups. After 82 weeks, mice in this group exhibited significantly increased incidences of altered hepatocellular foci, adenomas and carcinomas. After 82 weeks at 262 mg/kg of body weight, significant increases in altered foci and carcinomas were also observed. Staining showed that these lesions were predominantly basophilic or mixed basophilic/eosinophilic, lacked expression of glutathione-S-transferase-pi and were consistent with peroxisome proliferation involvement in tumorigenesis (Pereira, 1996). 
No treatment-related effects on the mutation patterns of the K- and H-ras protooncogenes were observed in trichloroacetic acid-induced liver tumours in male B6C3F1 mice, suggesting to the authors that trichloroacetic acid is a tumour promoter, not a tumour initiator (Ferreira-Gonzalez et al., 1995). In a number of recent mechanistic studies, trichloroacetic acid promoted liver tumours in mice pretreated with N-methyl-N-nitrosourea, a tumour-initiating agent (Pereira & Phelps, 1996; Tao et al., 1996; Latendresse & Pereira, 1997).




Trichloroacetic acid has been used clinically in chemical skin-peeling treatments for years, at concentrations of 16.9-50%. This procedure results in a slight erythema and swelling for the first few days post-operatively and is followed by exfoliation of dead skin. Histologically, trichloroacetic acid-induced skin damage is characterized by epidermal loss, early inflammatory response and collagen degeneration (Moy et al., 1996; Tse et al., 1996). Marked erythema and tenderness in the vulvar vestibule area, lasting for 2-15 weeks, have been reported in two cases in which trichloroacetic acid was used for the topical treatment of genital warts (Nunns & Mandal, 1996). 




Trichloroacetic acid has been shown to induce tumours in the liver of mice. It has given mixed results in in vitro assays for mutations and chromosomal aberrations and has been reported to cause chromosomal aberrations in in vivo studies. IARC (2002) has classified trichloroacetic acid in Group 3, not classifiable as to its carcinogenicity to humans. US EPA (1994) classified trichloroacetic acid as C, possible human carcinogen, in accordance with the 1986 EPA Guidelines for Carcinogen Risk Assessment (US EPA, 1986). Under the 1999 US EPA Draft Guidelines for Carcinogen Risk Assessment (US EPA, 1999), there is suggestive evidence of trichloroacetic acid carcinogenicity, but the data are not sufficient to assess human carcinogenicity (US EPA, 2002a). 
The weight of evidence indicates that trichloroacetic acid is not a genotoxic carcinogen. A TDI of 32.5 µg/kg of body weight was calculated, based on a NOAEL of 32.5 mg/kg of body weight per day from a study in which decreased body weight, increased liver serum enzyme activity and liver histopathology were seen in rats exposed to trichloroacetate in drinking-water for 2 years (DeAngelo et al., 1997), and incorporating an uncertainty factor of 1000 (100 for intra- and interspecies variation and 10 for database deficiencies, including the absence of a multigeneration reproductive study, the lack of a developmental study in a second species and the absence of full histopathological data in a second species). On the basis of the TDI of 32.5 µg/kg of body weight per day, and assuming a 60-kg body weight, drinking-water consumption of 2 litres/day and an allocation of 20% of the TDI to drinking-water, a guideline value of 200 µg/litre (rounded figure) can be calculated for trichloroacetic acid. This guideline value is achievable using commonly available analytical methods. 
It is noted that this guideline value is the same as would have been calculated from the TDI established by IPCS (2000), based on the Pereira (1996) study. The DeAngelo et al. (1997) study used to establish the guideline value has better dose definition, evaluated more non-cancer end-points and conducted a full histopathological examination of tissues.



APHA, AWWA, WPCF (1998) Standard methods for the examination of water and wastewater, 20th ed. Washington, DC, American Public Health Association/American Water Works Association/Water Pollution Control Federation. 
Trichloroacetic Acid TCA instructions
Determine if you are a suitable candidate for a Trichloroacetic Acid. TCA peels can have positive impacts on your skin by removing signs of aging and acne. However, there are certain instances when you should not apply a TCA peel. Do not use a TCA peel if you:
Have cuts, broken skin, or received a recent facial surgical procedure.
Have a sunburn.
Have active Herpes simplex 1 sores.
Are pregnant or breastfeeding.
Have taken Accutane in the last year.
Have recently received chemotherapy or radiation treatment.
Use products that contain alpha hydroxy acids 5-7 days before the peel. In order to prepare your skin for a TCA peel and make the treatment more effective, you should use a face product that contains AHAs, such as glycolic or lactic acids. There are a variety of creams, lotions, and toners available for your skin. Begin using this product approximately five to seven days before applying the peel.
Test the TCA on a small patch of skin. This way you will be able to determine if the acid solution is too strong or if you are allergic to the solution. For example, if you want to apply a TCA peel to your face, you should test a small patch of skin under your ear. This area is out of the way and will not be overly visible if you have a negative reaction. Always test the skin near the area you want to treat.
Rinse the test patch of skin once it starts to burn.
Wait 48 hours to apply the peel. This way you will know how the peel will react on your skin. If the spot that was tested becomes itchy, red, or bumpy, you should not apply the peel to your skin. This is likely a sign that you are experiencing an allergic reaction.
Applying a TCA Peel
Cleanse your skin. Immediately before you apply a TCA peel, you need to completely clean your skin. If you are applying the TCA peel to your face, you should remove all of your make up. Washing your face will help to remove any surface oils allowing the TCA solution to peel away a layer of skin.
Remove surface oils using a prep solution. Some TCA peels will come with a prep solution that should be applied to your skin prior to administering the peel. These solutions help to fully dry out your skin and remove any lingering surface oils.
If you did not purchase a prep solution, you can apply witch hazel or diluted rubbing alcohol to your skin using gauze.
Apply petroleum jelly around the eyes, mouth, and nose. If you are applying a TCA peel to your face, you want to protect some sensitive areas from the acid. In order to do this, use a cotton swab to apply a bit of petroleum jelly to your lips, and the skin around your eyes and nostrils. This will prevent the acid from damaging these sensitive areas.
You may want to wear safety goggles to prevent any TCA solution from dripping into your eyes. You will still have to apply petroleum jelly to your nose and mouth, however.
Put on latex gloves. While working with the TCA solution, you want to be careful that the acid does not touch other areas of skin. As a result, you should always wear latex gloves to protect your hands from the acid. This is especially important if you are applying the TCA using gauze because it will likely come into contact with your fingers.
Pour the TCA solution into a small dish. Place a small dish on your counter and pour some of the TCA solution into the dish. This will make it easy for you to dip your brush or gauze into the solution while you are applying the TCA to your skin.
Use gauze to apply TCA to your skin. Dip a piece of gauze into the TCA solution. Then squeeze the gauze gently. You want the gauze to be wet, but not dripping. This will prevent the solution from running into your eyes. Then apply a thin layer of TCA to the desired area of skin. If you are applying the TCA to your face, you may want to divide the area into sections.
For example, start by applying the TCA solution to the right side of your face, then the left side, and do the forehead last. This will help prevent you from overlapping the solution.
You can also apply TCA using a makeup brush, but a brush is more likely to cause dripping.
Wait 2-5 minutes. Once the solution has been applied to your skin, you should wait approximately two to five minutes. The time will vary depending on the strength of the solution, the number of peels you have performed, and your own skin type. It is normal for your skin to turn red and sting a bit while the peel is on your face.
If your skin begins to frost (i.e. turn white) or sting uncomfortably, you should begin neutralizing immediately by washing the solution off with water.
This is more likely to occur when using a stronger TCA of 15% or higher.
Apply a post-peel neutralizer to your skin. If you begin to experience frosting, you should apply a post-peel neutralizer to your skin. This typically comes with the TCA peel kit. Apply the neutralizer to your skin using a gauze or a soft cloth dipped in the neutralizer.
You can also make your own neutralizer by mixing 2 tablespoons of baking soda with 1 and a half cups (355 ml) of water.
Wash your face with water. After the peel has been on for five minutes, you should wash it off by splashing water onto your face. You can also apply water by dabbing your skin with a wet cloth. This will help to remove the TCA from your skin and will help to neutralize the area.
Apply a healing ointment. Once your skin is dry, apply a healing ointment to the skin. For example, try using emu oil or Bacitracin to help heal your skin following a TCA peel. You should re-apply this solution a few times a day for at least 48 hours following the peel.



Recovering from a TCA Peel
Use SPF 30 sunscreen to protect your skin. Your skin will likely peel for approximately five to seven days following the procedure and during this time you should avoid exposing your skin to the sun. Make sure to use a sunscreen with an SPF of 30 or higher during this time.
Avoid picking at your skin. If you used a stronger TCA solution, you skin will likely peel for a few days following the treatment. Do not pick at your skin. Instead, let it peel on its own. Picking the skin can lead to skin damage.
Wait 10-14 days for the final results to appear. Do not apply another peel during this time. Although your skin may stop peeling prior to 14 days, the solution is still working on your face and the results will not fully appear for 10-14 days. Once the results are visible, you can determine if another treatment is necessary. TCA peels are quite strong, so if you notice positive results after the first peel, you likely do not need to perform another peel.
Replacement Information
In North America 100807.1000 replaces, has a superior specification, but a different pack size to TX1045-5
In North America 100807.0100 replaces, but has a superior specification and a slightly smaller pack size to TX1045-3



Key Spec Table
EC Number
Hill Formula
Chemical Formula
Molar Mass
Grade Value
163.38 g/mol 
ACS,Reag. Ph Eur 
Pricing & Availability
Catalogue Number



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100 g
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Glass bottle 250 g
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Add To Favorites Add To Cart Description Catalogue Number100807 Replaces TX1045; TX1045-5; TX1045-3 Description Trichloroacetic acid Product Information 
CAS number 76-03-9 EC index number 607-004-00-7 EC number 200-927-2 Grade ACS,Reag. Ph Eur Hill Formula C₂HCl₃O₂ Chemical formula CCl₃COOH Molar Mass 163.38 g/mol
HS Code 2915 40 00 Structure formula Image Physicochemical Information Density 1.63 g/cm3 (20 °C) Flash point >110 °C Ignition temperature 711 °C Melting Point
54 - 56 °C pH value <1 (50 g/l, H₂O, 20 °C) Vapor pressure 1 hPa (20 °C) Bulk density 900 kg/m3 Solubility 1300 g/l Toxicological Information LD 50 oral LD50 Rat 3320 mg/kg
Safety Information according to GHS Hazard Pictogram(s)



Hazard Statement(s) H314: Causes severe skin burns and eye damage. H335: May cause respiratory irritation. H410: Very toxic to aquatic life with long lasting effects.
Precautionary Statement(s) P273: Avoid release to the environment. P280: Wear protective gloves/ protective clothing/ eye protection/ face protection. P301 + P330 + P331: IF SWALLOWED: Rinse mouth. Do NOT induce vomiting.
P305 + P351 + P338: IF IN EYES: Rinse cautiously with water for several minutes. Remove contact lenses, if present and easy to do. Continue rinsing. P308 + P310: IF exposed or concerned: immediately call a POISON CENTER or doctor/ physician. Signal Word
Danger RTECS AJ7875000 Storage class 8B Non-combustible, corrosive hazardous materials WGK WGK 2 obviously hazardous to water Disposal 3 Relatively unreactive organic 
reagents should be collected in container A. If halogenated, they should be collected in container B. For solid residues use container C. Safety Information Hazard 
Symbols Dangerous for the environment Corrosive Categories of danger corrosive, dangerous for the environment R Phrase R 35-50/53 Causes severe burns.Very toxic to 
aquatic organisms, may cause long-term adverse effects in the aquatic environment.
S Phrase S 26-36/37/39-45-60-61 In case of contact with eyes, rinse immediately with plenty of water and seek medical advice.Wear suitable protective clothing, gloves 
and eye/face protection.In case of accident or if you feel unwell, seek medical advice immediately (show the label where possible).This material and its container must
be disposed of as hazardous waste.Avoid release to the environment. Refer to special instructions/ Safety data sheets.
Storage and Shipping Information Storage Store at +15°C to +25°C. Transport Information Declaration (railroad and road) ADR, RID UN 1839 , 8, II Declaration (transport by air) IATA-DGR
UN 1839 , 8, II Declaration (transport by sea) IMDG-Code UN 1839 , 8, II, Segregation Group: 1 (Acids) Specifications Assay (alkalimetric) ≥ 99.5 % Identity (IR-spectrum)
passes test Appearance colorless, deliquescent crystals Appearance of solution (200 g/l; water) clear and colorless In water insoluble matter ≤ 0.01 % Chloride (Cl)
≤ 10 ppm Nitrate (NO₃) ≤ 20 ppm Phosphate (PO₄) ≤ 5 ppmSulphate (SO₄) ≤ 200 ppm Heavy metals (as Pb) ≤ 20 ppm Cu (Copper) ≤ 5 ppm Fe (Iron) ≤ 10 ppm Readily carbonisable substance
passes test Sulfated ash (600 °C) ≤ 300 ppm Trichloroacetic acid ingilizcede ne demek, Trichloroacetic acid nerede nasıl kullanılır? Acid : Bir çözeltiye h+ iyonu (proton) çıkaran madde. Ekşi. Asit gibi. Suda çözündüğünde hidronyum yükünü h3o+ veren kimyasalözdek. (yapısındaki hidrojenleri, baz kökleri ya da metallerle yer değiştirerek tuzları oluşturur, ph ölçeğinde 0-7 arasında değer gösterirler.) (bronsted) proton verme yatkınlığı olan kimyasal bileşik. (lewis) ortaklanmamış elektron çifti ya da çiftlerini almaya yatkın olan kimyasal özdek. Bir çözeltiye hidrojen iyonu veren, suda çözündüğü zaman hidrojen iyonları açığa çıkaran, bileşimindeki hidrojenin yerine herhangi bir mineral alarak tuz meydana getirebilen ve turnusolün mavi rengini kırmızıya çevirme özelliği olan hidrojenli bileşim. Akü elektroliti. Asitli. Asit çeliği. Alkali maddenin tersi özellikler taşıyan, turnusolün mavi rengini kırmızıya çeviren, suda eridiği zaman hidrojen iyonları meydana getiren hidrojenli bileşik. Dokunaklı.
Abietic acid : Çam asidi. Reçine asidi. Abiyetik asit. Abscisic acid : (biyokimya) yaprak çıkarmayı teşvik eden çimlenmeyi ise basılayan bitki hormonu. Absisik asit. Yaprak asidi.
Accumulator acid : Akümülatör asidi. Kaynak: https://nedir.ileilgili.org/trichloroacetic+acid



Evaluation of Drinking Water Disinfectant Byproducts Compliance Data as an Indirect Measure for Short-Term Exposure in Humans OPEN International journal of
environmental research and public health Published about 2 years ago Discuss In the absence of shorter term disinfectant byproducts (DBPs) data on regulated 
Trihalomethanes (THMs) and Haloacetic acids (HAAs), epidemiologists and risk assessors have used long-term annual compliance (LRAA) or quarterly...
Concepts: Acid, Trichloroacetic acid, Term, Regulation, Water supply network, United States Environmental Protection Agency, Drinking water, Water



Universal Trichloroacetic Acid Peel Technique for Light and Dark Skin JAMA facial plastic surgery Published over 2 years ago Discuss Despite their great potential, 
medium and deep trichloroacetic acid peels are underused in light-skinned patients and are rarely used in darker-skinned patients because of the widespread fear of
pigmentary complications... Concepts: Trichloroacetic acid, Chemical peel



Palladium-Catalyzed Regioselective C-H Functionalization of Arenes Substituted by Two N-Heterocycles and Application in Late-Stage Functionalization The Journal of
organic chemistry Published over 1 year ago Discuss Reported herein is a Pd-catalyzed regioselective C-H activation method that is used for C-H deuteration, 
carbonylation, halogenation, and oxidation of arene substrates substituted by two N-heterocycles. When conducted in acetic...
Concepts: Cativa process, Vinegar, Trichloroacetic acid, Oxygen, Base, Trifluoroacetic acid, Carboxylic acid, Acetic acid



Trifluoroacetic acid: Three times the fluoride, three times the toxicity?
The American journal of emergency medicine Published over 1 year ago Discuss 
Trifluoroacetic acid (TFAA) is a carboxylic acid, similar to acetic acid, used industrially and in laboratories. There is a paucity of data regarding exposure and the concern is that toxicity...
Concepts: Organic acid, Formic acid, Carboxylic acids, Trichloroacetic acid, Trifluoroacetic acid, Burn, Carboxylic acid, Acetic acid



Organocatalyzed Decarboxylative Trichloromethylation of Morita-Baylis-Hillman Adducts in Batch and Continuous Flow
Chemistry (Weinheim an der Bergstrasse, Germany) Published over 1 year ago Discuss 
Two protocols for the organocatalyzed decarboxylative trichloromethylation of Morita-Baylis-Hillman (MBH) substrates have been developed. Applying simple sodium trichloroacetate, as the trichloromethyl anion precursor, in combination with an organocatalyst, and acetylated...
Concepts: Trichloroacetic acid, Redox, Acetic acid, Sodium, Catalysis, Enzyme, Chemical reaction, Method acting



Proposal of a flow scheme for the chemicalform-based quantitative analysis of chlorine compounds in pulp for sanitary products and verification of safety
OPEN Regulatory toxicology and pharmacology : RTP Published over 1 year ago Discuss 
To determine the amounts and chemical forms of chlorine compounds in elemental chlorine-free (ECF) bleached pulp for sanitary products, a chemical-form-based quantitative analysis flow scheme was created. The scheme involves...
Concepts: Trichloroacetic acid, Sodium chloride, Hydrochloric acid, Chloroacetic acid, Hydrogen chloride, Chloroacetic acids, Chloride, Chlorine



Randomized controlled trial comparing 35% trichloroacetic acid peel and 5-aminolevulinic acid photodynamic therapy for the treatment of multiple actinic keratosis
The British journal of dermatology Published over 2 years ago Discuss 
Photodynamic therapy (PDT) and chemical peels with trichloroacetic acid (TCA) can be applied to larger skin areas and thus are suitable treatment options for patients with multiple actinic keratosis (AK)....
Concepts: Peel, Actinic keratosis, Randomized controlled trial, Trichloroacetic acid, Chemical peel



Detection of genotoxic effects of drinking water disinfection by-products using Vicia faba bioassay
Environmental science and pollution research international Published over 2 years ago Discuss 
Plant-based bioassays have gained wide use among the toxicological and/or ecotoxicological assessment procedures because of their simplicity, sensitivity, low cost, and reliability. The present study describes the use of Vicia...
Concepts: Water, Chloroacetic acid, Dichloroacetic acid, Vicia, Vicia faba, Trichloroacetic acid, Carboxylic acids, Chloroacetic acids



Transport of haloacids across biological membranes
Biochimica et biophysica acta Published over 2 years ago Discuss 
Haloacids are considered to be environmental pollutants, but some of them have also been tested in clinical research. The way that haloacids are transported across biological membranes is important for...
Concepts: Carboxylic acids, Evolution, Chloroacetic acid, Trichloroacetic acid, Dichloroacetic acid, Carboxylic acid, Chloroacetic acids, Transport



In vitro bioacessibility and transport across Caco-2 monolayers of haloacetic acids in drinking water
Chemosphere Published almost 3 years ago Discuss 
Water disinfection plays a crucial role in water safety but it is also a matter of concern as the use of disinfectants promotes the formation of disinfection by-products (DBPs). Haloacetic...
Concepts: Chlorine, Acetic acid, Water, Dichloroacetic acid, Trichloroacetic acid, Chloroacetic acid, Carboxylic acids, Chloroacetic acids



The Formation of 7-Membered Heterocycles under Mild Pictet-Spengler Conditions: A Route to Pyrazolo[3,4]benzodiazepines
The Journal of organic chemistry Published about 3 years ago Discuss 
Reported is a method for the synthesis of 7-membered heterocycles via a Pictet-Spengler condensation reaction under very mild conditions. High substrate scope allows for use of aldehydes using catalytic amounts...
Concepts: Oxygen, Amino acid, Functional group, Ethanol, Acetic acid, Carboxylic acid, Condensation reaction, Trichloroacetic acid



Natural Organic Matter Exposed to Sulfate Radicals Increases its Potential to Form Halogenated Disinfection By-products
Environmental science & technology Published about 3 years ago Discuss 
Sulfate radical-based advanced oxidation processes (SR-AOPs) are considered as viable technologies to degrade a variety of recalcitrant organic pollutants. This study demonstrates that o-phthalic acid (PA) could lead to the...
Concepts: Carboxylic acid, Organic chemistry, Chlorine, Organic matter, Bromine, Halogen, Natural organic matter, Trichloroacetic acid



Combination of microneedling and 10% trichloroacetic acid peels in the management of infraorbital dark circles
Journal of cosmetic and laser therapy : official publication of the European Society for Laser Dermatology Published over 3 years ago Discuss 
Dark circles (DC), seen in the periorbital area, are defined as bilateral, round, homogeneous pigmented macules whose aetiology is thought to be multifactorial. Available treatments include bleaching creams, topical retinoic...
Concepts: Light, Plastic surgery, Retinoic acid receptor, Retinoic acid, Tretinoin, Chemical peel, Trichloroacetic acid



Effect of dissolved oxygen concentration on iron efficiency: Removal of three chloroacetic acids
Water research Published over 4 years ago Discuss 
The monochloroacetic, dichloroacetic and trichloroacetic acid (MCAA, DCAA and TCAA) removed by metallic iron under controlled dissolved oxygen conditions (0, 0.75, 1.52, 2.59, 3.47 or 7.09 mg/L DO) was investigated...
Concepts: Oxygen, Carbon dioxide, Iron, Hydrogen, Carbon, Acetic acid, Chloroacetic acids, Trichloroacetic acid.


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