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Trichloroacetic acid (CASRN 76-03-9)

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Trichloroacetic acid; CASRN 76-03-9

Health assessment information on a chemical substance is included in IRIS only after a comprehensive review of chronic toxicity data by U.S. EPA health scientists from several Program Offices and the Office of Research and Development. The summaries presented in Sections I and II represent a consensus reached in the review process. Background information and explanations of the methods used to derive the values given in IRIS are provided in the Background Documents.

STATUS OF DATA FOR Trichloroacetic acid

File First On-Line 02/01/1996

Category (section)
Status
Last Revised
Oral RfD Assessment (I.A.) no data 01/01/1994
Inhalation RfC Assessment (I.B.) no data
Carcinogenicity Assessment (II.) on-line 03/01/1996

_I.  Chronic Health Hazard Assessments for Noncarcinogenic Effects

_I.A. Reference Dose for Chronic Oral Exposure (RfD)

Substance Name — Trichloroacetic acid
CASRN — 76-03-9

Not available at this time.

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_I.B. Reference Concentration for Chronic Inhalation Exposure (RfC)

Substance Name — Trichloroacetic acid
CASRN — 76-03-9

Not available at this time.

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_II.  Carcinogenicity Assessment for Lifetime Exposure

Substance Name — Trichloroacetic acid
CASRN — 76-03-9
Last Revised — 03/01/1996

Section II provides information on three aspects of the carcinogenic assessment for the substance in question; the weight-of-evidence judgment of the likelihood that the substance is a human carcinogen, and quantitative estimates of risk from oral exposure and from inhalation exposure. The quantitative risk estimates are presented in three ways. The slope factor is the result of application of a low-dose extrapolation procedure and is presented as the risk per (mg/kg)/day. The unit risk is the quantitative estimate in terms of either risk per ug/L drinking water or risk per ug/cu.m air breathed. The third form in which risk is presented is a drinking water or air concentration providing cancer risks of 1 in 10,000, 1 in 100,000 or 1 in 1,000,000. The rationale and methods used to develop the carcinogenicity information in IRIS are described in The Risk Assessment Guidelines of 1986 (EPA/600/8-87/045) and in the IRIS Background Document. IRIS summaries developed since the publication of EPA's more recent Proposed Guidelines for Carcinogen Risk Assessment also utilize those Guidelines where indicated (Federal Register 61(79):17960-18011, April 23, 1996). Users are referred to Section I of this IRIS file for information on long-term toxic effects other than carcinogenicity.

_II.A. Evidence for Human Carcinogenicity

__II.A.1. Weight-of-Evidence Characterization

Classification — C; possible human carcinogen

Basis — The classification is based on a lack of human data and limited evidence of an increased incidence of liver neoplasms in both sexes of one strain of mice. No evidence of carcinogenicity was found in rats. Results from genotoxicity studies are mixed; trichloroacetic acid does not appear to be a point mutagen.

__II.A.2. Human Carcinogenicity Data

None. The primary source of exposure to trichloroacetic acid (TCA) in humans is as a byproduct of chlorination of drinking water. Since the early 1970s, numerous epidemiologic studies have attempted to assess the relationship between the chlorination byproducts in drinking water and several different human cancers. None of these studies has shown an association of exposure to TCA with an increased incidence of site-specific cancer.

__II.A.3. Animal Carcinogenicity Data

Limited. U.S. EPA (1994) described two separate experiments that examined the carcinogenicity of TCA in male B6C3F1 mice (50/group). Dose selection was based on the study by Herren-Freund et al. (1987). In the first study, mice were exposed to 0.05, 0.5 or 5 g/L TCA in drinking water for 60 weeks. The time-weighted mean daily doses were 8, 71 or 595 (mg/kg)/day, respectively. The control group received 2 g/L sodium chloride (NaCl) in drinking water. Animals were sacrificed at the end of the exposure period. Treatment with TCA had no effect on survival. In the high-dose group, significant depression of weight-gain (73% of control) and body-weight reduction (85% of control) were reported (DeAngelo, 1993). A dose-related increase in relative liver weight was observed, with a 69% increase in the high-dose group compared with the control group (DeAngelo, 1993). The incidences of combined hepatocellular tumors (adenoma and carcinoma) were 37.9 and 55.2% in mice receiving 0.5 and 5 g/L, respectively, compared with 13.3% in controls. The increase was statistically significant in the high-dose group compared with controls. Hyperplastic nodules (24.1%) were observed only at the 5-g/L dose level. The highest dose level tested in this study (5 g/L) was not considered excessive for assessment of the carcinogenic potential of TCA (DeAngelo, 1993).

In a second experiment reported by U.S. EPA (1991), male B6C3F1 mice were administered 4.5 g/L TCA (583 mg/kg)/day in the drinking water over a lifetime exposure (94 weeks). Body weights in the treated animals were not significantly different from controls until the end of the study (data not provided) (DeAngelo, 1993). In the treated mice, the incidences of adenomas, carcinoma, and combined hepatocellular tumors were 42, 74 (both estimated from graph) and 86.7%, respectively, compared with 0, 11 (both estimated from graph), and 10%, respectively, in control mice. All incidences reported for the treated animals were significantly different from controls.

U.S. EPA (1991) also reported on TCA-induced liver cancer in the female B6C3F1 mouse (55/group) exposed to 0, 0.5 or 4.5 g/L TCA in drinking water. The female mouse appeared to be less sensitive than the male mouse; a significantly increased incidence (60%) for combined hepatocellular adenomas/carcinomas occurred in females treated with 4.5 g/L TCA compared with controls (8%) after a 104-week exposure. A lower dose of 0.5 g/L TCA for 104 weeks resulted in a combined hepatocellular tumor incidence of 16.7% compared with control (not significant). Body weight gain was reduced by 8% and relative liver weight was increased by 47% in the high-dose group compared to the control, while survival was not affected in any group. It should be noted that the mouse studies reported in U.S. EPA (1991) did not provide adequate experimental details. For example, no information on time-to-first tumor was provided for any of the experiments and no historical control data were available. Comparison with historical control data from NTP carcinogenicity studies indicates that combined hepatocellular adenomas/carcinomas occur in approximately 30% (range 14-58%) of control male B6C3F1 mice and 8% of females (range 0-20%) (Haseman et al., 1984; Maronpot et al., 1987). The incidence of the combined hepatocellular tumors in the mice studies reported by U.S. EPA (1991) exceeded the upper end of this historical control range.

An increase in liver neoplasms has been reported in male mice receiving TCA in drinking water for 52 weeks. Bull et al. (1990) exposed groups of B6C3F1 mice (11 35 males/group, 10 females/group) to neutralized TCA (males: 0, 1 or 2 g/L; females: 0 or 2 g/L). Animals were sacrificed after the 52- week exposure period. The calculated dosage rates averaged 164 (for males) or 329 ( mg/kg )/day (for both sexes) for 52 weeks. An additional group of 11 males received 2 g/L TCA for 37 weeks, followed by a 15-week recovery period. This corresponded to a dosage rate of 309 mg/kg/day for 37 weeks. No effects of treatment on survival or body weight were obseved. Food and water consumption data were not reported. A significant increase in the relative liver weight was seen in the 1-g/L males (30% increase from control), 2-g/L males (63% increase), and 2 g/L females (25% increase) compared with controls at 52 weeks. Nonneoplastic histopathological lesions included mild intracellular swelling and glycogen accumulation in the livers of treated mice (both sexes) at 52 weeks. Male mice in the 2-g/L group had accumulation of lipofuscin near hepatoproliferative lesions (no incidence reported), and hyperplastic liver nodules (9/24). The incidences of hepatocellular adenomas in male mice were 0/35 (0%), 2/11 (18%) and 1/24 (4%), and the incidences of hepatocellular carcinomas were 0/35 (0%), 2/11 (18%), and 4/24 (17%) after exposure to 0, 1 and 2 g/L, respectively. These findings were not statistically significant at any dose level. Female mice did not develop any tumors in response to TCA treatment. Fifteen weeks after exposure to 2 g/L for 37 weeks, hepatocellular carcinomas developed in 3/11 (30%) male mice, but hepatic adenomas had not occurred by that date. Tumors were not found in any other organs. Since the total exposure duration in this study did not exceed 52 weeks, this study may not have evaluated mice for an adequate length of time to observe the full carcinogenic potential of TCA. In addition, the numbers of animals tested were inadequate. The maximum tolerated dose appears to have been reached because nonneoplastic lesions were observed.

Herren-Freund et al. (1987) investigated the initiation/promotion potential of TCA in male B6C3F1 mice (22-33/group). Mice were pretreated with a single intraperitoneal dose of 2.5 or 10 mg/kg ethylnitrosourea (ENU) at 15 days of age and then given 2 or 5 g/L TCA in drinking water [400 or 1000 (mg/kg)/day as calculated by the authors] from 4 to 65 weeks of age. The two negative control groups (66 animals) received 2 g/L NaCl in drinking water or 2.5 mg ENU/kg. Animals were sacrificed after 61 weeks of exposure. Survival data were not provided. A significant decrease of 8 10% in the final mean body weight was observed in the 5-g/L group, while a significant increase of 25-47% in the relative liver weight was found in all treatment groups compared with controls. In an uninitiated group receiving 5 g/L, the incidence was statistically significantly increased: 8/22 (36%) for hepatocellular adenomas and 7/22 (32%) for hepatocellular carcinomas compared with 2/22 and 0/22, respectively, for the NaCl controls. For the initiated groups (2.5 mg ENU/kg), the incidences of hepatocellular adenomas were also statistically significantly increased: 11/33 (33%) and 6/22 (26%) in the 2-and 5-g TCA/L groups, respectively, compared with 2/22 (9%) in the controls given 2.5 mg- ENU/kg. The incidences of hepatocellular carcinomas were 16/33 (48%) and 11/22 (50%) in the 2- and 5-g TCA/L groups, respectively, compared with 1/22 (4.5%) in the controls. Mice initiated with 10 mg ENU/kg and then administered 5 g/L TCA showed no significant increase in the incidence of hepatocellular adenomas or carcinomas and, therefore, TCA did not appear to inhibit or promote ENU-initiated hepatocarcinogenicity. Hyperplastic nodules were not observed in the treated animals and no other tumor sites were found. The authors concluded that TCA acted as a complete hepatocarcinogen in mice since ENU did not affect the ability of TCA to induce carcinogenicity. The mutation-promotion experiment could not be adequately evaluated, however since the TCA dose also produced tumors in a large number of animals.

DeAngelo et al. (1993) exposed groups of 50 male Fischer 344 rats to 0, 0.05, 0.5 and 5 g/L TCA administered in drinking water for 104 weeks. Mean daily doses were approximately 2.83, 26 and 283.9 (mg/kg)/day, respectively. The control group received 2 g/L NaCl in drinking water. No significant differences in survival were found among groups; survival rates were 88, 84, 74 and 86% for the 0, 0.05-, 0.5- or 5 g/L-groups. Body weight and body- weight gain were significantly reduced in the high-dose group (89 and 85% of control, respectively) at the end of the exposure period. A decrease of 10% in absolute liver weight was reported in the high-dose group compared with controls. Histopathology revealed an increase in cytoplasmic vacuolization (beginning at 15 weeks) and hepatocellular necrosis at the high dose but no evidence of hyperplastic nodules. At 0.5 g/L, the incidence of cytoplasmic vacuolization was lower and was not consistently observed in all interim sacrifices. No evidence of increased carcinogenicity was observed in any treatment groups compared with controls.

__II.A.4. Supporting Data for Carcinogenicity

The overall genetic toxicology database indicates that TCA is unlikely to induce point mutations in microbial systems. It did not induce gene mutations in either Escherichia coli (Andersen et al. 1972) or Salmonella typhimurium (Rapson et al., 1980). Similarly, neither point mutations nor somatic segregation resulted from exposure of Aspergillus nidulans to TCA (Bignami et al., 1977).

A significant increase in the percentage of cells with abnormal chromosome morphology was seen in Swiss-Webster mice receiving 500 mg/kg TCA by oral gavage; however, the aberration yield was approximately 4 times lower than the response when the same dose was administered intraperitoneally (Bhunya and Behera, 1987). The intraperitoneal administration of two consecutive daily doses of 125, 250 or 500 mg/kg TCA resulted in dose-related and stastisticaly significant increase in micronuclei in bone marrow polychromatic erythrocytes while administration of 5 consecutive daily doses of 25, 50 or 100 mg/kg TCA caused a dose related and statistically significant increase in the frequency of sperm-head abnormalities. Although the data from this study strongly suggest that TCA is a clastogen for both somatic and germinal mouse cells, the findings have not been confirmed.

Results are in conflict regarding the ability of TCA to cause DNA damage. In an alkaline unwinding assay, administration of oral doses of 1 10 mmol/kg TCA to B6C3F1 mice and Fischer 344 rats did not induce DNA strand breaks in a dose-related manner (Chang et al., 1992). Nelson and Bull (1988) evaluated the ability of TCA to induce single-strand DNA breaks in vivo in Sprague- Dawley rats and B6C3F1 mice. Oral gavage doses as low as 0.006 mmol/kg caused a significant increase in single-strand breaks in the hepatic DNA of mice while single-strand breaks occurred at 0.6 mmol/kg in rats. A dose of 58.5 ug/mL TCA increased DNA repair in Salmonella typhimurium TA1535 (Ono et al., 1991). The response was equivocal in the absence of exogenous metabolic activation and only weakly positive when the test material was activated by rat liver homogenates induced with phenobarbital/5,6-benzoflavone.

A whole-body half-life of 50 hours was determined for TCA in three healthy male volunteers who ingested 3 mg/kg (Mueller et al., 1974) and a half-life of 6 hours for rats and mice administered an oral dose of 100 mg/kg (Larson and Bull 1992). In a study by Fisher et al. (1991), half-lives of 9 10 hours and 2 5 hours were reported for rats and mice, respectively, after administration of 5 or 10 mg/kg TCA by intravenous infusion and intraperitoneal injection. The variations in rates of systemic clearance of TCA between species and sex may reflect differences in binding preferences of ionized TCA with proteins such as albumin or with conjugates such as glucuronides (Fisher et al., 1991). In addition, the volume of distribution (Vd) was calculated and found to be different between species (Fisher et al., 1991; Allen and Fisher, 1993). Data show that rodents have smaller Vd values than humans. Furthermore, the Vd values for humans and rats were more similar than those for humans and mice.

Dichloroacetic acid (DCA), carbon dioxide and an unidentifiable group of nonchlorinated acids are formed in Fischer 344 rats and B6C3F1 mice after administration of a single gavage dose of 20 or 100 mg/kg TCA (Bull et al., 1993; Larson and Bull, 1992). Kinetic parameters of TCA in plasma were similar in rats and mice at 20 and 100 mg/kg doses, except for a longer plasma half-life in rats than in mice at the lower dose. Systemic clearance for TCA was relatively similar between the two species, but plasma concentrations of DCA were dissimilar. Although the amount of DCA in the blood was equivalent after a 20 mg/kg TCA dose for the two species, peak concentrations of DCA after the 100 mg/kg TCA dose were about 30-fold greater than the low dose for rats, but only 5-fold greater than the low dose for mice (Bull et al., 1993; Larson and Bull, 1992). The area under the curve (AUC) values for DCA were also disproportionately increased between the two species. Unresolved nonchlorinated acids detected in the plasma had comparable concentrations and AUCs in the two species.

Larson and Bull (1992) found no species differences in urinary metabolites. A small amount of DCA (1 3%) was detected in the urine of TCA- treated animals while unresolved nonchlorinated acids represented 5-11%. About 4-8% of TCA was exhaled as carbon dioxide. Most of the administered dose (>50%) was excreted as unchanged parent compound in the urine of both rats and mice. No human data on TCA metabolism were available for comparison of metabolites in humans and rodents.

Investigators have suggested that enhanced peroxisomal proliferation by TCA in rats and mice may be involved in the induction of hepatocarcinogenicity (Bull et al., 1990; DeAngelo et al., 1989; Larson and Bull, 1992; Mather et al., 1990); however, no clear evidence to indicates an association.

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_II.B. Quantitative Estimate of Carcinogenic Risk from Oral Exposure

Not available. The Agency is exploring development of a biologically based model to accommodate the existing database and other data under development at ORD/HERL.

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_II.C. Quantitative Estimate of Carcinogenic Risk from Inhalation Exposure

None.

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_II.D. EPA Documentation, Review, and Contacts (Carcinogenicity Assessment)

__II.D.1. EPA Documentation

Source document -- U.S. EPA, 1994, 1991

The Drinking Water Criteria Document was externally peer reviewed by the Drinking Water Subcommittee of the Science Advisory Board on April 4-5, 1991. In addition, a review of this was completed by the American Water Works Association in August 1992. The comments from these reviews have been carefully evaluated and considered in the revision and finalization of this IRIS Summary. A record of the comments are included in the IRIS documentation files.

__II.D.2. EPA Review (Carcinogenicity Assessment)

Agency Work Group Review — 02/03/1993, 03/31/1993, 08/04/1993

Verification Date — 08/04/1993

Screening-Level Literature Review Findings — A screening-level review conducted by an EPA contractor of the more recent toxicology literature pertinent to the cancer assessment for Trichloroacetic acid conducted in September 2002 did not identify any critical new studies. IRIS users who know of important new studies may provide that information to the IRIS Hotline at hotline.iris@epa.gov or (202)566-1676.

__II.D.3. EPA Contacts (Carcinogenicity Assessment)

Please contact the IRIS Hotline for all questions concerning this assessment or IRIS, in general, at (202)566-1676 (phone), (202)566-1749 (FAX) or hotline.iris@epa.gov (internet address).

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_III.  [reserved]
_IV.  [reserved]
_V.  [reserved]

_VI.  Bibliography

Substance Name — Trichloroacetic acid
CASRN — 76-03-9
Last Revised — 03/01/1996

_VI.A. Oral RfD References

None

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_VI.B. Inhalation RfC References

None

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_VI.C. Carcinogenicity Assessment References

Allen, B.C. and J.W. Fisher. 1993. Pharmacokinetic modeling of trichloroethylene and trichloroacetic acid in humans. Risk Anal. 13(1): 71-86.

Andersen, K.J., E.G. Leighty and M.T. Takahashi. 1972. Evaluation of herbicides for possible mutagenic properties. J. Agric. Food Chem. 20(3): 649-656.

Bhunya, S.P. and B.C. Behera. 1987. Relative genotoxicity of trichloroacetic acid (TCA) as revealed by different cytogenetic assays: Bone marrow chromosome aberration, micronucleus and sperm-head abnormality in the mouse. Mutat. Res. 188: 215-221.

Bignami, M., G. Cardamone, P. Comba, V. Ortali, G. Morpugo and A. Carere. 1977. Relationship between chemical structure and mutagenic activity in some pesticides: The use of Salmonella typhimurium and Aspergillus nidulans. Mutat. Res. 46: 243-244.

Bull, R.J., I.M. Sanchez, M.A. Nelson, J.L. Larson and A.J. Lansing. 1990. Liver tumor induction in B6C3F1 mice by dichloroacetate and trichloroacetate. Toxicology. 63: 341-359.

Bull, R.J., M. Templin, J.L. Larson and D.K. Stevens. 1993. The role of dichloroacetate in the hepatocarcinogenicity of trichloroethylene. Toxicol. Lett. 68: 203-211.

Chang, L.W., F.B. Daniel and A.B. DeAngelo. 1992. 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. Environ. Molec. Mutagen. 20(4): 277-288.

DeAngelo, A. 1993. HERL, U.S. EPA. Personal communication to R. Cantilli, OST, U.S. EPA, regarding data from the carcinogenicity studies on trichloroacetic acid in B6C3F1 mice. July 26.

DeAngelo, A.B., F.B. Daniel, L. McMillan, P. Wernsing and R.E. Savage, Jr. 1989. Species and strain sensitivity to the induction of peroxisome proliferation by chloroacetic acids. Toxicol. Appl. Pharmacol. 101: 285-289.

DeAngelo, A.B., F.B. Daniel, J.A. Stober, G.R. Olson and N.P. Page. 1993. Carcinogen bioassays of chloroacetic acids in Fischer 344 rats. Submitted to Toxicologic Pathology. (In press)

Fisher, J.W., M.L. Gargas, B.C. Allen and M.E. Andersen. 1991. Physiologically-based pharmacokinetic modeling with trichloroethylene and its metabolite, trichloroacetic acid, in the rat and mouse. Toxicol. Appl. Pharmacol. 109: 183-195.

Haseman, J., J. Huff and G. Boorman. 1984. Use of historical control data in carcinogenicity studies in rodents. Toxicol. Pathol. 12(2): 126-135.

Herren-Freund, S.L., M.A. Pereira, M.D. Khoury and G. Olson. 1987. The carcinogenicity of trichloroethylene and its metabolites, trichloroacetic acid and dichloroacetic acid, in mouse liver. Toxicol. Appl. Pharmacol. 90: 183-189.

Larson, J.L. and R.J. Bull. 1992. Metabolism and lipoperoxidative activity of trichloroacetate and dichloroacetate in rats and mice. Toxicol. Appl. Pharmacol. 115: 268-277.

Maronpot, R.R., J. Haseman, G. Boorman, S. Eustis, G. Rao and J. Huff. 1987. Liver lesions in B6C3F1 mice: The National Toxicology Program, experience and position. Arch. Toxicol. Suppl. 10: 10-26.

Mather, G.G., J.H. Exon and L.D. Koller. 1990. Subchronic 90-day toxicity of dichloroacetic and trichloroacetic acid in rats. Toxicology. 64: 71-80.

Mueller, G., M. Spassovski and D. Henschler. 1974. Metabolism of trichloroethylene in man. II: Pharmacokinetics of metabolite. Arch. Toxicol. 32(4): 283-295.

Nelson, M.A. and R.J. Bull. 1988. Induction of strand breaks in DNA by trichloroethylene and metabolites in rat and mouse liver in vivo. Toxicol. Appl. Pharmacol. 94: 45-54.

Ono, Y., I. Somiya and M. Kawamura. 1991. The evaluation of Genotoxicity Using DNA Repairing Test for Chemicals Produced in Chlorination and Ozonation Processes. Water Sci. Technol. 23: 329-338.

Rapson, W.H., M.A. Nazar and V.V. Butsky. 1980. Mutagenicity produced by aqueous chlorination of organic compounds. Bull. Environ. Contam. Toxicol. 24: 590-596.

U.S. EPA. 1991. Toxicology of the Chloroacetic Acids, By-Products of the Drinking Water Disinfection Process. II. The Comparative Carcinogenicity of Dichloroacetic and Trichloroacetic Acid: Implication for Risk Assessment. Health Effects Research Laboratory, Research Triangle Park, NC. Document No. HERL-0820.

U.S. EPA. 1994. Drinking Water Criteria Document on Chlorinated Acids/Aldehydes/Ketones/Alcohols. Prepared by Office of Science and Technology, Office of Water, Washington, DC. PB94-179918.

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_VII.  Revision History

Substance Name — Trichloroacetic acid
CASRN — 76-03-9

Date
Section
Description
10/01/1992 I.A. Oral RfD now under review
03/01/1993 II. Carcinogenicity assessment now under review
05/01/1993 I.A. Work group review date added
05/01/1993 II. Work group review date added
07/01/1993 I.A. Work group review date added
09/01/1993 II. Work group review date added
01/01/1994 I.A. Work group review date added
08/01/1995 I.A., II. EPA's RfD/RfC and CRAVE workgroups were discontinued in May, 1995. Chemical substance reviews that were not completed by September 1995 were taken out of IRIS review. The IRIS Pilot Program replaced the workgroup functions beginning in September, 1995.
02/01/1996 II. Carcinogenicity assessment on-line
02/01/1996 VI.C. Carcinogenicity assessment references on-line
03/01/1996 II.A.3. Citation revised
03/01/1996 II.D.3. Primary contact changed
03/01/1996 VI.C. U.S. EPA, 1993 revised to DeAngelo, 1993
04/01/1997 III., IV., V. Drinking Water Health Advisories, EPA Regulatory Actions, and Supplementary Data were removed from IRIS on or before April 1997. IRIS users were directed to the appropriate EPA Program Offices for this information.
12/03/2002 II.D.2. Screening-Level Literature Review Findings message has been added.
07/30/2003 I., II. This chemical is being reassessed under the IRIS Program.

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_VIII.  Synonyms

Substance Name — Trichloroacetic acid
CASRN — 76-03-9
Last Revised — 10/01/1992

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