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Carbon tetrachloride
CASRN 56-23-5
Contents
0020
Carbon tetrachloride; CASRN 56-23-5
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 Carbon tetrachloride
File On-Line 01/31/1987
Category (section) Status Last Revised
----------------------------------------- -------- ------------
Oral RfD Assessment (I.A.) on-line 06/01/1991
Inhalation RfC Assessment (I.B.) no data
Carcinogenicity Assessment (II.) on-line 06/01/1991
_I. CHRONIC HEALTH HAZARD ASSESSMENTS FOR NONCARCINOGENIC EFFECTS
__I.A. REFERENCE DOSE FOR CHRONIC ORAL EXPOSURE (RfD)
Substance Name -- Carbon tetrachloride
CASRN -- 56-23-5
Last Revised -- 06/01/1991
The oral Reference Dose (RfD) is based on the assumption that thresholds exist
for certain toxic effects such as cellular necrosis. It is expressed in units
of mg/kg-day. In general, the RfD is an estimate (with uncertainty spanning
perhaps an order of magnitude) of a daily exposure to the human population
(including sensitive subgroups) that is likely to be without an appreciable
risk of deleterious effects during a lifetime. Please refer to the Background
Document for an elaboration of these concepts. RfDs can also be derived for
the noncarcinogenic health effects of substances that are also carcinogens.
Therefore, it is essential to refer to other sources of information concerning
the carcinogenicity of this substance. If the U.S. EPA has evaluated this
substance for potential human carcinogenicity, a summary of that evaluation
will be contained in Section II of this file.
___I.A.1. ORAL RfD SUMMARY
Critical Effect Experimental Doses* UF MF RfD
-------------------- ----------------------- ----- --- ---------
Liver lesions NOAEL: 1 mg/kg/day 1000 1 7E-4
(converted to 0.71 mg/kg/day
Subchronic Rat Gavage mg/kg/day)
Study
LOAEL: 10 mg/kg/day
Bruckner et al., 1986 (converted to 7.1
mg/kg/day)
*Conversion Factors: 1 mg/kg/day (NOAEL) x 5/7 = 0.71 mg/kg/day (5 day/week
dosing regimen)
___I.A.2. PRINCIPAL AND SUPPORTING STUDIES (ORAL RfD)
Bruckner, J.V., W.F. MacKenzie, S. Muralidhara, R. Luthra, G.M. Kyle and D.
Acosta. 1986. Oral toxicity of carbon tetrachloride: Acute, subacute and
subchronic studies in rats. Fund. Appl. Toxicol. 6(1): 16-34.
Male Sprague-Dawley rats were given 1, 10, or 33 mg carbon
tetrachloride/kg/day by corn oil gavage, 5 days/week for 12 weeks. Liver
lesions, as evidenced by mild centrilobular vacuolization and statistically
significant increases in serum sorbitol dehydrogenase activity, were observed
at the 10 and 33 mg/kg/day dosesm in a dose-related manner. Therefore, the
LOAEL was established at 10 mg/kg/day (converted to 7.1 mg/kg/day) and the
NOAEL was 1 mg/kg/day (converted to 0.71 mg/kg/day).
___I.A.3. UNCERTAINTY AND MODIFYING FACTORS (ORAL RfD)
UF -- UF allows for interspecies and intrahuman variability and extrapolation
from subchronic to chronic duration of exposure.
MF -- None
___I.A.4. ADDITIONAL COMMENTS (ORAL RfD)
A 1983 draft of the Bruckner et al. (1986) study was used as the basis for the
RfD by the RfD Work Group at a 05/20/1985 verification meeting. When this study
was subsequently published (Bruckner et al., 1986), no change to the verified
value was required.
Subchronic studies in mice gavaged with carbon tetrachloride in corn oil
(Condie et al., 1986; Hayes et al., 1985) support the critical effect and the
magnitude of the NOAEL and LOAEL found in the rat studies. Additional studies
(Alumot et al., 1976; NCI, 1976) in rats lend moderate support to the choice
of a NOAEL in the chosen rat study.
___I.A.5. CONFIDENCE IN THE ORAL RfD
Study -- High
Data Base -- Medium
RfD -- Medium
The principal study was well conducted and good dose-response was observed
in the liver, which is the target organ for carbon tetrachloride toxicity;
thus, high confidence was assigned. Four additional subchronic studies
support the RfD, but reproductive and teratology endpoints are not well
investigated; thus, the data base rates a medium confidence. Medium
confidence in the RfD follows.
___I.A.6. EPA DOCUMENTATION AND REVIEW OF THE ORAL RfD
Source Document -- U.S. EPA, 1985
Public review of RfD following ODW proposal of RMCL in June 1984.
Science Advisory Board review of RfD on January 14, 1986.
Other EPA Documentation -- None
Agency Work Group Review -- 05/20/1985
Verification Date -- 05/20/1985
___I.A.7. EPA CONTACTS (ORAL RfD)
Please contact the Risk Information Hotline for all questions concerning this
assessment or IRIS, in general, at (513)569-7254 (phone), (513)569-7159 (FAX)
or RIH.IRIS@EPAMAIL.EPA.GOV (internet address).
__I.B. REFERENCE CONCENTRATION FOR CHRONIC INHALATION EXPOSURE (RfC)
Substance Name -- Carbon tetrachloride
CASRN -- 56-23-5
Not available at this time.
_II. CARCINOGENICITY ASSESSMENT FOR LIFETIME EXPOSURE
Substance Name -- Carbon tetrachloride
CASRN -- 56-23-5
Last Revised -- 06/01/1991
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 CLASSIFICATION AS TO HUMAN CARCINOGENICITY
___II.A.1. WEIGHT-OF-EVIDENCE CLASSIFICATION
Classification -- B2; probable human carcinogen
Basis -- Carcinogenicity in rats, mice, and hamsters
___II.A.2. HUMAN CARCINOGENICITY DATA
Inadequate. There have been three case reports of liver tumors developing
after carbon tetrachloride exposure. Several studies of workers (Milham,
1976; Blair et al., 1979) who may have used carbon tetrachloride have
suggested that these workers may have an excess risk of cancer.
___II.A.3. ANIMAL CARCINOGENICITY DATA
Sufficient. Carbon tetrachloride has produced hepatocellular carcinomas
in rats, mice, and hamsters, the species evaluated to date.
Hepatocellular carcinomas developed in Osborne-Mendel, Japanese, and
Wistar rats, but not Sprague-Dawley or Black rats, following s.c. injection of
carbon tetrachloride. Hyperplastic nodules were noted in Buffalo rats
treated s.c. (Reuber and Glover, 1967a,b, 1970). Sensitivity varied among
strains, and trends in incidence appeared inversely related to severity of
cirrhosis.
Fifty Osborne-Mendel rats/sex were administered carbon tetrachloride by
corn oil gavage at 47 and 94 mg/kg/injection for males and 80 and 159 mg/kg
for females 5 times/week for 78 weeks. At 110 weeks, only 7/50 high-dose
males and 14/50 high-dose females survived; 14/50 low-dose males and 20/50
low-dose females survived. The incidence of hepatocellular carcinomas was
increased in animals exposed to carbon tetrachloride as compared with pooled
colony controls. The apparent decrease in the incidence of hepatocellular
carcinomas in high-dose female rats compared with the low-dose females (1/14
vs. 4/20, respectively) was attributed by the authors to increased lethality
before tumors could be expressed (NCI, 1976a,b, 1977).
In this same study, using the same dosing schedule, male and female B6C3F1
mice received 1250 or 2500 mg/kg carbon tetrachloride. The incidences of
hepatocellular carcinomas in males were 5/77, 49/49, and 47/48 in the control,
low- and high-dose groups, respectively, and 1/80, 40/40, and 43/45 in the
control, low- and high-dose groups, respectively.
Carbon tetrachloride administered by gavage has also been shown to produce
neoplastic changes in livers of five additional strains of mice (C3H, A, Y, C,
and L) (Andervont, 1958; Edwards, 1941; Eschenbrenner and Miller 1943; Edwards
and Dalton, 1942; Edwards et al., 1942). In the last study, 56 male and 19
female L mice, which have a low incidence of spontaneous hepatomas, were
treated with 0.1 mL of 40% carbon tetrachloride 2 or 3 times/week over 4
months, for a total of 46 treatments. Animals were killed 3 to 3.5 months
after the last treatment. The combined hepatoma incidence of treated male
mice was 47% (7/15 vs. 2/71 in the untreated male controls); treated females
showed and incidence of 38% (3/8 vs. 0/81 in the untreated female controls).
As part of a larger study of liver carcinogens, Della Porta et al. (1961)
treated Syrian golden hamsters (10/sex/dose) with carbon tetrachloride by
gavage, weekly for 30 weeks. For the first 7 weeks, 0.25 mL of 0.05% carbon
tetrachloride in corn oil was administered; this dose was halved for the
remainder of the exposure period. All animals were observed for an additional
25 weeks. All of the 10 hamsters that were killed or dying between weeks 43
and 55 had liver cell carcinomas, compared with 0 in controls.
___II.A.4. SUPPORTING DATA FOR CARCINOGENICITY
Carbon tetrachloride was not mutagenic to either S. typhimurium or E.
coli (McCann et al., 1975; Simmon et al., 1977; Uehleke et al., 1976). At low
concentrations, carbon tetrachloride did not produce chromatid or chromosomal
aberrations in an epithelial cell line derived from rat liver (Dean and
Hodson-Walker, 1979). In vivo unscheduled DNA synthesis assays have likewise
been negative in male Fischer 344 rats (Mirsalis and Butterworth, 1980;
Mirsalis et al., 1982). Carbon tetrachloride produced mitotic recombination
and gene conversion in S. cerevisiae, but only at concentrations which reduced
viability to 10% (Callen et al., 1980). Carbon tetrachloride may be
metabolized to reactive intermediates capable of binding to cellular
nucleophilic macromolecules. Negative responses in bacterial mutagenicity
assays may have been due to inadequate metabolic activation in the test
systems.
__II.B. QUANTITATIVE ESTIMATE OF CARCINOGENIC RISK FROM ORAL EXPOSURE
___II.B.1. SUMMARY OF RISK ESTIMATES
Oral Slope Factor -- 1.3E-1 per (mg/kg)/day
Drinking Water Unit Risk -- 3.7E-6 per (ug/L)
Extrapolation Method -- Linearized multistage procedure, extra risk
Drinking Water Concentrations at Specified Risk Levels:
Risk Level Concentration
-------------------- -------------
E-4 (1 in 10,000) 3E+1 ug/L
E-5 (1 in 100,000) 3E+0 ug/L
E-6 (1 in 1,000,000) 3E-1 ug/L
___II.B.2. DOSE-RESPONSE DATA (CARCINOGENICITY, ORAL EXPOSURE)
Tumor Type -- Hepatocellular carcinomas/hepatomas
Test Animals -- various, see table
Route -- gavage
Reference -- several, see table
Administered Human Equivalent Tumor Unit Risk
Dose (mg/day) Dose (mg/kg)/day Incidence per (ug/L) Reference
------------- ---------------- --------- ---------- ----------
Hamster/Syrian, male and female
0 0 0/80 3.4E-5 Della
0.95 1.02 10/19 Porta et
al., 1961
Mouse/L, male and female
0 0 2/152 9.4E-6 Edwards
15 2.3 34/73 et al.,
1942
Mouse/B6C3F1, male and female
0 0 6/157 1.8E-6 NCI,
21 55.4 89/89 1976a,b,
42 110.8 90/93 1977
Rat/Osborne-Mendel:
M, F 0 0 0/37 3.1E-7 NCI,
M 11 4.5 2/45 1976a,b,
F 18 7.4 4/46 1977
M 21 8.7 2/47
F 36 14.9 1/30
___II.B.3. ADDITIONAL COMMENTS (CARCINOGENICITY, ORAL EXPOSURE)
A geometric mean was calculated from the unit risks derived from the
four data sets above. Della Porta et al. (1961) did not report controls in
this study, but did give incidence rate for vehicle controls in an earlier
study. Animal doses are TWA.
The unit risk should not be used if the water concentration exceeds 3E+3
ug/L, since above this concentration the unit risk may not be appropriate.
___II.B.4. DISCUSSION OF CONFIDENCE (CARCINOGENICITY, ORAL EXPOSURE)
The studies used were all deficient in some respect, precluding the choice
of any one study as most appropriate. For all studies, data from males and
females were combined because of the small sample sizes. In the first and
second studies (Della Porta et al., 1961; Edwards et al., 1942) one dose was
tested. Della Porta et al. (1961) did not report concurrent control
incidence. In the NCI (1976a,b) studies, tumor incidence in the mice was
virtually 100%, and goodness-of-fit criteria were not satisfied for the
multistage model. Tumor incidence in rats in these studies was higher at low
doses, presumably because early mortality at higher doses precluded tumor
formation. The studies lacked pharmacokinetic data. However, a common
biological mechanism, cell death and regeneration, leading to development of
the same tumor type, was suggested by observations in all the studies. Since
the risk estimates from these data (across 3-4 species and strains)
only vary by 2 orders of magnitude, a geometric mean was derived as the risk
estimate to accommodate the several study deficiencies.
__II.C. QUANTITATIVE ESTIMATE OF CARCINOGENIC RISK FROM INHALATION EXPOSURE
___II.C.1. SUMMARY OF RISK ESTIMATES
Inhalation Unit Risk -- 1.5E-5 per (ug/cu.m)
Extrapolation Method -- Linearized multistage procedure, extra risk
Air Concentrations at Specified Risk Levels:
Risk Level Concentration
-------------------- ---------------
E-4 (1 in 10,000) 7E+0 ug/cu.m
E-5 (1 in 100,000) 7E-1 ug/cu.m
E-6 (1 in 1,000,000) 7E-2 ug/cu.m
___II.C.2. DOSE-RESPONSE DATA FOR CARCINOGENICITY, INHALATION EXPOSURE
The inhalation risk estimates were calculated from the oral exposure data
in Section II.B.2.
___II.C.3. ADDITIONAL COMMENTS (CARCINOGENICITY, INHALATION EXPOSURE)
Inhalation risk was calculated assuming an air intake of 20 cu.m/day and
40% absorption rate by humans (U.S. EPA, 1984). This absorption coefficient
was based on 30% inhalation in monkeys, and 30% and 57-65% inhalation in
humans. A range of estimates of unit risk for inhalation exposures for the
four studies cited above was determined, with 1.5E-5 per (ug/cu.m) calculated
as the geometric mean for the unit risk.
The unit risk should not be used if the air concentration exceeds 7E+2
ug/cu.m, since above this concentration the unit risk may not be appropriate.
___II.C.4. DISCUSSION OF CONFIDENCE (CARCINOGENICITY, INHALATION EXPOSURE)
See II.B.4.
__II.D. EPA DOCUMENTATION, REVIEW, AND CONTACTS (CARCINOGENICITY ASSESSMENT)
___II.D.1. EPA DOCUMENTATION
Source Document -- U.S. EPA, 1984
The 1984 Health Assessment Document for Carbon Tetrachloride received Agency
and external review.
___II.D.2. REVIEW (CARCINOGENICITY ASSESSMENT)
Agency Work Group Review -- 11/12/1986, 12/04/1986
Verification Date -- 12/04/1986
___II.D.3. U.S. EPA CONTACTS (CARCINOGENICITY ASSESSMENT)
Please contact the Risk Information Hotline for all questions concerning this
assessment or IRIS, in general, at (513)569-7254 (phone), (513)569-7159 (FAX)
or RIH.IRIS@EPAMAIL.EPA.GOV (internet address).
_VI. BIBLIOGRAPHY
Substance Name -- Carbon tetrachloride
CASRN -- 56-23-5
Last Revised -- 10/01/1992
__VI.A. ORAL RfD REFERENCES
Alumot E., E. Nachtomi, E. Mandel and P. Holstein. 1976. Tolerance and
acceptable daily intake of chlorinated fumigants in the rat diet. Food
Cosmet. Toxicol. 14: 105-110.
Bruckner, J.V., S. Muralidhara, R. Luthra, G.M. Kyle, W.F. MacKenzie and D.
Acosta. 1983. Oral toxicity of carbon tetrachloride: Acute, subacute and
subchronic studies in rats. University of Georgia, Athens, GA. (Draft)
Bruckner, J.V., W.F. MacKenzie, S. Muralidhara, R. Luthra, G.M. Kyle and D.
Acosta. 1986. Oral toxicity of carbon tetrachloride: Acute, subacute and
subchronic studies in rats. Fund. Appl. Toxicol. 6(1): 16-34.
Condie, L.W., R.D. Laurie, T. Mills, M. Robinson and J.P. Bercz. 1986.
Effect of gavage vehicle on hepatotoxicity of carbon tetrachloride in CD-1
mice: Corn oil versus Tween-60 aqueous emulsion. Fund. Appl. Toxicol. 7(2):
199-206.
NCI (National Cancer Institute). 1976. Report on the Carcinogenesis Bioassay
of Chloroform. Carcinogenesis Program, Division of Cancer Cause and
Prevention. March 1.
U.S. EPA. 1985. Drinking Water Criteria Document for Carbon Tetrachloride.
Office of Drinking Water, Washington, DC. PB86-118155.
__VI.B. INHALATION RfC REFERENCES
None
__VI.C. CARCINOGENICITY ASSESSMENT REFERENCES
Andervont, H.B. 1958. Induction of hepatomas in strain C3H mice with 4-o-
tolylazo-o-toluidine and carbon tetrachloride. J. Natl. Cancer Inst. 20(2):
431-438.
Blair, A., P. Decoufle and D. Grauman. 1979. Causes of death among laundry
and dry cleaning workers. Am. J. Public Health. 69(5): 508-511.
Callen, D.F., C.R. Wolf and R.M. Philpot. 1980. Cytochrome P-450 mediated
genetic activity and cytoxicity of seven halogenated aliphatic hydrocarbons in
Saccharomyces cerevisiae. Mutat. Res. 77: 55-63.
Dean, B.J. and G. Hodson-Walker. 1979. An in vitro chromosome assay using
cultured rat-liver cells. Mutat. Res. 64: 329-337.
Della Porta, G., B. Terracini and P. Shubik. 1961. Induction with carbon
tetrachloride of liver cell carcinomas in hamsters. J. Natl. Cancer Inst.
26(4): 855-863.
Edwards, J.E. and H.A. Dalton. 1942. Induction of cirrhosis of the liver
and of hepatomas in mice with carbon tetrachloride. J. Natl. Cancer Inst. 3:
19-41.
Edwards, J.E., W.E. Heston and H.A. Dalton. 1942. Induction of the carbon
tetrachloride hepatoma in strain L. mice. J. Natl. Cancer Inst. 3: 297-301.
Eschenbrenner, A.B. and E. Miller. 1943. Studies on hepatomas size and
spacing of multiple doses in the induction of carbon tetrachloride hepatomas.
J. Natl. Cancer Inst. 4: 385-388.
McCann, J., E. Choi, E. Yamasaki and B.N. Ames. 1975. Detection of
carcinogens as mutagens in the Salmonella/microsome test: Assay of 300
chemicals. Proc. Natl. Acad. Sci. 72: 5135-5139.
Milham, S. 1976. Neoplasia in the wood and pulp industry. Ann. New York
Acad. Sci. 271: 294-300.
Mirsalis, J.C. and B.E. Butterworth. 1980. Detection of unscheduled DNA
synthesis in hepatocytes isolated from rats treated with genotoxic agents:
An in vivo-in vitro assay for potential carcinogens and mutagens.
Carcinogenesis. 1: 621-625.
Mirsalis, J.C., C.K. Tyson and B.E. Butterworth. 1982. Detection of
genotoxic carcinogens in the in vivo-in vitro hepatocyte DNA repair assay.
Environ. Mutagen. 4: 553-562.
NCI (National Cancer Institute). 1976a. Report on the Carcinogenesis
Bioassay of Chloroform. National Cancer Institute, Bethesda, MD. March.
NCI (National Cancer Institute). 1976b. Carcinogenesis Bioassay of
Trichloroethylene. National Cancer Institute Carcinogenesis Technical Report
Series, No. 2. NCI-CG-TR-2. February.
NCI (National Cancer Institute). 1977. Bioassay of 1,1,1-Trichlorethane for
Possible Carcinogenicity. National Cancer Institute Carcinogenesis Technical
Report Series, No. 3. NCI-CG-TR-3. January.
Reuber, M.D. and E.L. Glover. 1967a. Hyperplastic and early neoplastic
lesions of the liver in buffalo strain rats of various ages given subcutaneous
carbon tetrachloride. J. Natl. Cancer Inst. 38(6): 891-899.
Reuber, M.D. and E.L. Glover. 1967b. Cholangiofibrosis in the liver of
Buffalo strain rats injected with carbon tetrachloride. Br. J. Exp. Pathol.
48(3): 319-322.
Reuber, M.D. and E.L. Glover. 1970. Cirrhosis and carcinoma of the liver in
male rats given subcutaneous carbon tetrachloride. J. Natl. Cancer Inst.
44(2): 419-427.
Simmon, V.F., K. Kauhanen and R.G. Tardiff. 1977. Mutagenic activity of
chemicals identified in drinking water. In: Progress in Genetic Toxicology, D.
Scott, B.A Bridges and F.H. Sobels, Ed. Elsevier/North-Holland Biomedical
Press, New York. p. 249-258.
Uehleke, H., H. Greim, M. Kramer and T. Werner. 1976. Covalent binding of
haloalkanes to liver constituents, but absence of mutagenicity on bacteria in
a metabolizing test system mutation. Research. 38: 114.
U.S. EPA. 1984. Health Assessment Document for Carbon Tetrachloride.
Prepared by the Office of Health and Environmental Assessment, Environmental
Criteria and Assessment Office, Cincinnati, OH. EPA 600/8/82-001F.
_VII. REVISION HISTORY
Substance Name -- Carbon tetrachloride
CASRN -- 56-23-5
-------- -------- --------------------------------------------------------
Date Section Description
-------- -------- --------------------------------------------------------
03/01/1988 I.A.1. Dose conversion clarified
03/01/1988 I.A.2. Principal study corrected
03/01/1988 I.A.4. Text added
03/01/1988 I.A.4. Text revised
03/01/1988 I.A.6. Verification and meeting dates changed
03/01/1988 II.A.2. Text corrected
03/01/1988 II.B.4 Confidence statement revised
03/01/1988 II.C.4. Confidence statement revised
03/01/1988 III.A. Health Advisory added
06/30/1988 I.A.7. Primary contact changed
12/01/1989 I.A.4. Corrected citation year for Condie et al.
12/01/1989 VI. Bibliography on-line
06/01/1990 IV.A.1. Area code for EPA contact corrected
06/01/1990 IV.F.1. EPA contact changed
08/01/1990 III.A.2. Uncertainty factor text corrected
08/01/1990 III.A.10 Primary contact changed
01/01/1991 II. Text edited
01/01/1991 II.C.1. Inhalation slope factor removed (global change)
03/01/1991 I.A.7. Primary contact changed
06/01/1991 I.A. Text edited
06/01/1991 II. Text edited
06/01/1991 IV.B.1. EPA contact changed
06/01/1991 IV.B.2. EPA contact changed
08/01/1991 VI.C. Blair et al., 1979 and Milham, 1976 references added
01/01/1992 IV. Regulatory actions updated
04/01/1992 IV.A.1. CAA regulatory action withdrawn
10/01/1992 VI.C. Missing reference added
VIII. SYNONYMS
Substance Name -- Carbon tetrachloride
CASRN -- 56-23-5
Last Revised -- 01/31/1987
56-23-5
Acritet
Benzinoform
Carbona
Carbon chloride
Carbon tet
Carbon tetrachloride
Carbo tetrachloride
Czterochlorek wegla
ENT 4,705
Fasciolin
Flukoids
Freon 10
Halon 104
Mecatorina
Methane tetrachloride
Methane, tetrachloro-
Necatorina
Necatorine
Perchloromethane
R 10
Tetrachloorkoolstof
Tetrachloormetaan
Tetrachlorkohlenstoff, tetra
Tetrachlormethan
Tetrachlorocarbon
Tetrachloromethane
Tetrachlorure de carbone
Tetrachorkohlenstoff uvasol
Tetraclorometano
Tetracloruro di carbonio
Tetrafinol
Tetraform
Tetrasol
Univerm
Ventox
Vermoestricid
WLN: GXGGG.
Last updated: 5 May 1998
URL: http://www.epa.gov/iris/SUBST/0020.HTM
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