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1,1-Dichloroethylene
CASRN 75-35-4
(02/01/1998)
Contents
0039
1,1-Dichloroethylene; CASRN 75-35-4 (02/01/1998)
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 1,1-Dichloroethylene
File On-Line 01/31/1987
Category (section) Status Last Revised
----------------------------------------- -------- ------------
Oral RfD Assessment (I.A.) on-line 04/01/1989
Inhalation RfC Assessment (I.B.) no data
Carcinogenicity Assessment (II.) on-line 02/01/1998
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=========
_I. CHRONIC HEALTH HAZARD ASSESSMENTS FOR NONCARCINOGENIC EFFECTS
__I.A. REFERENCE DOSE FOR CHRONIC ORAL EXPOSURE (RfD)
Substance Name -- 1,1-Dichloroethylene
CASRN -- 75-35-4
Primary Synonym -- Vinylidene Chloride
Last Revised -- 04/01/1989
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.
NOTE: The Oral RfD for 1,1,-dichloroethylene may change in the near future
pending the outcome of a further review now being conducted by the Oral RfD
Work Group.
___I.A.1. ORAL RfD SUMMARY
Critical Effect Experimental Doses* UF MF RfD
-------------------- ----------------------- ----- --- ---------
Hepatic lesions NOAEL: none 1000 1 9E-3
mg/kg/day
Rat Chronic Oral LOAEL: 50 ppm (con-
Bioassay verted to 9 mg/kg/day)
Quast et al., 1983
*Conversion Factors: Doses were calculated by the authors.
___I.A.2. PRINCIPAL AND SUPPORTING STUDIES (ORAL RfD)
Quast, J.F., C.G. Humiston, C.E. Wade, et al. 1983. A chronic toxicity and
oncogenicity study in rats and subchronic toxicity study in dogs on ingested
vinylidene chloride. Fund. Appl. Toxicol. 3: 55-62.
Groups of 48 each male and female Sprague-Dawley rats (Spartan SUBSTrain) were
administered 50, 100, or 200 ppm 1,1-dichloroethylene in drinking water for a
period of 2 years. Control groups of 80 animals/sex were maintained for the
same period. Daily intake was calculated by the authors to be 7, 10, or 20
mg/kg bw/day for males and 9, 14, or 30 mg/kg bw/day for females. There were
no treatment-related effects on mortality, body or organ weight, clinical
chemistry, urinalysis, hematology, or numbers of tumors. The only pathologic
findings were of hepatic lesions, generally characterized by minimal mid-zonal
hepatocellular fatty change and hepatocellular swelling. These findings were
noted in rats of all female treatment groups. In male rats, only the 200 ppm
treatment group showed a statistically significant increase in the incidence
of hepatocellular swelling, but this trend was also observed in animals
receiving 100 ppm 1,1-dichloroethylene.
As part of this same study, beagle dogs (4/sex/group) were administered 6.25,
12.5, or 25 mg/kg bw/day in gelatin capsules. Treatment for 97 days had no
effect.
This study, as well as a review of the available data, indicate that the liver
is the most sensitive target organ and, futhermore, that rats are the most
sensitive species. The drinking water exposure reported by Quast et al.
(1983) offers a more suitable model for potential human exposure to 1,1-
dichloroethylene than does the NTP bioassay wherein animals were gavaged. It
is, therefore, appropriate to set an RfD based on the LOAEL of 9 mg/kg bw/day
for hepatic lesions in female rats.
___I.A.3. UNCERTAINTY AND MODIFYING FACTORS (ORAL RfD)
UF -- A factor of 10 each was used for use of a LOAEL, for interspecies
variation, and for protection of sensitive human subpopulations.
MF -- None
___I.A.4. ADDITIONAL COMMENTS (ORAL RfD)
1,1-Dichloroethylene has been shown to be fetotoxic, but not teratogenic to
rodents after exposure in drinking water or by inhalation (Short et al., 1977;
Murray et al., 1979).
___I.A.5. CONFIDENCE IN THE ORAL RfD
Study -- Medium
Data Base -- Medium
RfD -- Medium
The study by Quast et al. (1983) was conducted using appropriate numbers of
animals of two species, measured several endpoints, and was of chronic
duration (rats). Since there are corroborative chronic and subchronic oral
bioassays, confidence in the study, data base, and RfD are considered medium.
___I.A.6. EPA DOCUMENTATION AND REVIEW OF THE ORAL RfD
Source Document -- U.S. EPA, 1985
This document has received a lengthy internal review and has undergone public
comments.
Other EPA Documentation -- None
Agency Work Group Review -- 01/22/1985
Verification Date -- 01/22/1985
___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 -- 1,1-Dichloroethylene
CASRN -- 75-35-4
Primary Synonym -- Vinylidene Chloride
Not available at this time.
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=========
_II. CARCINOGENICITY ASSESSMENT FOR LIFETIME EXPOSURE
Substance Name -- 1,1-Dichloroethylene
CASRN -- 75-35-4
Primary Synonym -- Vinylidene Chloride
Last Revised -- 02/01/1998
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 -- C; possible human carcinogen
Basis -- Tumors observed in one mouse strain after inhalation exposure is the
basis for this classification. Other studies were of inadequate design.
Vinylidene chloride is mutagenic, and a metabolite is known to alkylate and to
bind covalently to DNA. It is structurally related to the known human
carcinogen, vinyl chloride.
___II.A.2. HUMAN CARCINOGENICITY DATA
Inadequate. An epidemiologic study of 138 workers showed no carcinogenic
effect associated with vinylidene chloride exposure (Ott et al., 1976). Based
on power considerations, this study is inadequate for assessing cancer risk in
humans.
___II.A.3. ANIMAL CARCINOGENICITY DATA
Limited. Eighteen animal studies have been reported, which provide
information about the carcinogenic potential of vinylidene chloride. Eleven
of the studies involved inhalation exposure, five were oral, and one each
was by skin application and subcutaneous injection. Most were not designed
for maximum sensitivity to detect carcinogenic effects. None of the 11
inhalation exposures were for lifetime; all were 12 months or less. Three
of the five oral studies were of lifetime exposures. Of all the studies, only
one inhalation study produced a response as a complete carcinogen.
In the inhalation study by Maltoni et al. (1985) both sexes of Swiss
mice were exposed to 10 and 25 ppm (MTD) for 4-5 days/week for 12 months. A
statistically significant increase in kidney adenocarcinoma was noted in
male mice. Although statistically significant increases in mammary carcinomas
in female mice and pulmonary adenomas in both sexes were reported, dose-
response relationships were unclear. A second Maltoni study exposed Sprague-
Dawley rats to 10, 25, 50, 100, or 150 ppm, 4-5 days/week for 12 months and
observed them until spontaneous death. A statistically significant increase
in total mammary tumors, but not carcinomas alone, was seen only at 10 and 100
ppm. No dose-response relationship was apparent, and the overall
interpretation of the mammary tumor incidence is inconclusive.
Four gavage studies (in rats and mice) and one drinking water study in
rats have been negative (Maltoni et al., 1985; Quast et al., 1983; Humiston et
al., 1978; NTP, 1982; Ponomarkov and Tomatis, 1980). Only the NTP (1982) corn
oil gavage study in Fischer 344 rats and female B6C3F1 mice and the drinking
water study in Sprague-Dawley rats were undertaken for 2 years dosing. The
NTP study was apparently not conducted at the MTD and the drinking water study
did not achieve a maximum dose of metabolite. All other oral studies were
limited in design and, thus, lacking in sensitivity sufficient to detect a
response.
Vinylidene chloride did not act as a complete carcinogen when applied
topically or s.c. to ICR/Ha mice but did serve as an initiator when followed
by phorbol myristate acetate treatment (Van Duuren et al., 1979).
___II.A.4. SUPPORTING DATA FOR CARCINOGENICITY
Vinylidene chloride has been shown to be mutagenic for Salmonella
typhimurium in multiple assays. This activity is largely dependent on the
presence of microsomal enzymes. It has been used as a positive control in
studies of chemicals that are gases at or near room temperature. Both
conventional and host-mediated assays of Saccharomyces cerevisiae have been
positive for mitotic gene conversion (Bronzetti et al., 1981). Vinylidene
chloride was not mutagenic for V79 cells exposed to vapor in vitro (Drevon and
Kuroki, 1979), nor did it produce chromosomal aberrations in bone marrow cells
of ICR mice given single or repeated i.p. treatment in vivo (Cerna and
Kypenova, 1977). CD-1 mice and Sprague-Dawley rats treated in vivo with
labeled vinylidene chloride showed evidence of DNA alkylation and subsequent
repair which was specific to liver and kidney. Kidney in rat and mouse had
higher alkylation than liver (Reitz et al., 1980). Covalent binding of
vinylidene chloride closely correlates with metabolite formation. McKenna et
al. (1977) observed greater binding in kidney than liver, and greater binding
in mice than in rats. Vinylidene chloride failed to induce dominant lethal
mutations in mice (Anderson et al., 1977) or rats (Short et al., 1977).
Vinylidene chloride is structurally related to the known carcinogen, vinyl
chloride.
__II.B. QUANTITATIVE ESTIMATE OF CARCINOGENIC RISK FROM ORAL
EXPOSURE
___II.B.1. SUMMARY OF RISK ESTIMATES
Oral Slope Factor -- 6E-1 per (mg/kg)/day
Drinking Water Unit Risk -- 1.7E-5 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) 6E+0 ug/L
E-5 (1 in 100,000) 6E-1 ug/L
E-6 (1 in 1,000,000) 6E-2 ug/L
___II.B.2. DOSE-RESPONSE DATA (CARCINOGENICITY, ORAL EXPOSURE)
Tumor Type -- adrenal pheochromocytomas
Test Animals -- rat/F344, male
Route -- drinking water
Reference -- NTP, 1982
Administered Human Equivalent Tumor
Dose (mg/kg-day) Dose (mg/kg-day) Incidence
---------------- ---------------- ---------
0 0 6/50
0.71 0.120 5/48
3.57 0.603 13/47
Human equivalent doses were determined by adjusting the administered
animal dose by the cube root of the ratio of the weight of the animal
(estimated 0.43 kg) to human weight (70 kg), and adjusting for length of
exposure and length of the experiment.
The unit risk estimate chosen was derived from the highest of four slope
factors calculated from two studies that did not show a statistically
significant increase in tumor incidence attributable to oral exposure of
vinylidene chloride. The drinking water study in rats (Quast et al., 1983)
produced the lowest slope factor of 0.2 per (mg/kg)/day. The highest slope
factor [0.6 per (mg/kg)/day] was based on male rat adrenal tumors from NTP
(1982). Use of data from this study wherein there were no statistically
significant increases in tumor incidence appears justified, since the slope
factor derived is within a factor of 2 of the slope factor based on data from
the inhalation study of Maltoni et al. (1977, 1985).
___II.B.3. ADDITIONAL COMMENTS (CARCINOGENICITY, ORAL EXPOSURE)
Animal pharmacokinetic data show that metabolite elimination is dose-
dependent and saturable at inhalation concentrations of 150-200 ppm, or
approximately 50 mg/kg oral ingestion. Vinylidene chloride is rapidly
absorbed, has limited solubility, and is not stored in body tissues.
Pharmacokinetics and metabolism data indicate that the available assays were
not of adequate design. The positive Maltoni inhalation study comes
closest to achieving a maximum dose of metabolite, albeit less than lifetime
exposure, but less than maximum dosing vis-a-vis metabolites. The water
unit risk based on incidence data from a drinking water study was chosen
because route of administration is appropriate to oral risk estimation.
The unit risk should not be used if the water concentration exceeds 6E+2
ug/L, since above this concentration the unit risk may not be appropriate.
___II.B.4. DISCUSSION OF CONFIDENCE (CARCINOGENICITY, ORAL EXPOSURE)
The estimate is based on a data set in which there is no significant
increase in tumor incidence. The confidence that the upper limit is not
greater than 0.6 per (mg/kg)/day is high, since it is the largest value by a
factor of 3 from four rat data sets in two studies. If drinking water
exposure alone is considered the estimates might be reduced by a factor of 3.
The slope factors for the oral quantitative estimate based on data from
inhalation exposure and based on the negative oral data are within a factor
of 2.
__II.C. QUANTITATIVE ESTIMATE OF CARCINOGENIC RISK FROM INHALATION
EXPOSURE
___II.C.1. SUMMARY OF RISK ESTIMATES
Inhalation Unit Risk -- 5.0E-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) 2E+0 ug/cu.m
E-5 (1 in 100,000) 2E-1 ug/cu.m
E-6 (1 in 1,000,000) 2E-2 ug/cu.m
___II.C.2. DOSE-RESPONSE DATA FOR CARCINOGENICITY, INHALATION
EXPOSURE
Tumor Type -- kidney adenocarcinoma
Test Animals -- Mouse/Swiss, male
Route -- inhalation
Reference -- Maltoni et al., 1977, 1985
Dose Tumor
Administered Human Equivalent Incidence
(ppm) (mg/kg/day)
------------ ---------------- ---------
0 0 0/56
0 0 0/70
10 0.078 0/25
25 0.195 3/21
25 0.195 25/98
___II.C.3. ADDITIONAL COMMENTS (CARCINOGENICITY, INHALATION
EXPOSURE)
Within each same dose pair there were no statistically significant
differences between incidences in the two control and the 25 ppm groups.
These groups were combined for modeling. The number of animals surviving to
appearance of the first kidney adenocarcinoma was used as the denominator for
incidence. Human equivalent doses were determined assuming 0.035 kg as the
average weight of the male mice, adjusting for continuous lifetime exposure in
the mice, accounting for metabolism and pharmacokinetics for mice, and using
70 kg weight and with 1.85 sq.m surface area for humans (U.S. EPA, 1985). A
slope factor of 0.2E+0 per (mg/kg)/day was calculated using estimated animal
administered doses.
The unit risk should not be used if the air concentration exceeds 2E+2
ug/cu.m, since above this concentration the unit risk may not be appropriate.
___II.C.4. DISCUSSION OF CONFIDENCE (CARCINOGENICITY, INHALATION
EXPOSURE)
Sufficient numbers of animals were used for treatment and control groups.
Treatment was for approximately 50% of lifetime. Only two dose points
provided data suitable for modeling.
__II.D. EPA DOCUMENTATION, REVIEW, AND CONTACTS (CARCINOGENICITY
ASSESSMENT)
___II.D.1. EPA DOCUMENTATION
Source Document -- U.S. EPA, 1985
The values in the 1985 Health Assessment Document for Vinylidene Chloride
received extensive peer and public review.
___II.D.2. REVIEW (CARCINOGENICITY ASSESSMENT)
Agency Work Group Review -- 12/04/1986, 01/07/1987
Verification Date -- 01/07/1987
___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).
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=========
_VI. BIBLIOGRAPHY
Substance Name -- 1,1-Dichloroethylene
CASRN -- 75-35-4
Primary Synonym -- Vinylidene Chloride
Last Revised -- 08/01/1991
__VI.A. ORAL RfD REFERENCES
Murray, F.J., K.D. Nitschke, L.W. Rampy and B. Schwetz. 1979. Embryotoxicity
and fetotoxicity of inhaled or ingested vinylidene chloride in rats and
rabbits. Toxicol. Appl. Pharmacol. 49: 189-202.
Quast, J.F., C.G. Humiston, C.E. Wade, et al. 1983. A chronic toxicity and
oncogenicity study in rats and subchronic toxicity study in dogs on ingested
vinylidene chloride. Fund. Appl. Toxicol. 3: 55-62
Short, R.D., J.M. Winston, J.L. Minor, J. Seifter and C.C. Lee. 1977. Effect
of various treatments on toxicity of inhaled vinylidene chloride. Environ.
Health Perspect. 21: 125-129.
U.S. EPA. 1985. Drinking Water Criteria Document for 1,1-Dichloroethylene
(Vinylidene Chloride). Prepared by the Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH for
the Office of Drinking Water, Washington, DC.
__VI.B. INHALATION RfC REFERENCES
None
__VI.C. CARCINOGENICITY ASSESSMENT REFERENCES
Anderson, M.W., T.E. Eling, R.J. Lutz, R.L. Dedrick and H.B. Matthews. 1977.
The construction of a pharmacokinetic model for the disposition of
polychlorinated biphenyls in the rat. Clin. Pharmacol. Therap. 22(5.2):
765-773.
Bronzetti, G., C. Bauer, C. Corsi, C. Leporini, R. Nieri and R. Del Carratore.
1981. Genetic activity of vinylidene chloride in yeast. Mutat. Res. 89:
179-185.
Cerna, M. and H. Kypenova. 1977. Mutagenic activity of chloroethylenes
analyzed by screening system tests. Mutat. Res. 46(3): 214-215.
Drevon, C. and Kuroki, T. 1979. Mutagenicity of vinyl chloride, vinylidene
chloride and chloroprene in V79 Chinese-hamster cells. Mutat. Res. 67(20):
173-182.
Humiston, C.G., J.F. Quast, C.E. Wade, J. Ballard, J.E. Beyer and R.W. Lisowe.
1978. Results of a two-year toxicity and oncogenicity study with vinylidene
chloride incorporated in the drinking water of rats. MCA Report No. VCD 1.3-
Tox-Orl-Dow. Toxicology Research Laboratory Health and Environmental Research,
Dow Chemical U.S.A., Midland, MI.
Maltoni, C., G. Cotti, L. Morisi and P. Chieco. 1977. Carcinogenicity
bioassays of vinylidene chloride. Research plan and early results. Med. Lav.
68(4): 241-262.
Maltoni, C., G. Lefemine, P. Chieco, G. Cotti and V. Patella. 1985.
Experimental reSEARCH on vinylidene chloride carcinogenesis. In: Archives of
Research on Industrial Carcinogenesis. Vol. 3. Maltoni, C. and M.A. Mehlman,
ed. Princeton Scientific Publishers, Princeton, NJ.
McKenna, M.J., P.G. Watanabe and P.G. Gehring. 1977. Pharmacokinetics of
vinylidene chloride in the rat. Environ. Health Perspect. 21: 99-105.
NTP (National Cancer Institute/National Toxicology Program). 1982. NTP
Technical Report on the Carcinogenesis Bioassay of Vinylidene Chloride (CAS
No. 75-35-4) in F344/N Rats and B6CF1/Mice (Gavage Study). NPT No. 80-82. NIH
Pub. No. 82-1784. NTP Research Triangle Park, NC. and Bethesda, MD. U.S.
Department of Health and Human Services, Public Health Services, National
Institute of Health.
Ott, M.G., W.A. Fishbeck, J.C. Townsend and E.J. Schneider. 1976. A Health
study of employees exposed to vinylidene chloride. J. Occup. Med. 18(11):
735-738.
Ponomarkov, V. and L. Tomatis. 1980. Long-term testing of vinylidene
chloride and chloroprene for carcinogenicity in rats. Oncology. 37: 136-141.
Quast, J.F., C.G. Humiston, C.E. Wade, et al. 1983. A chronic toxicity and
oncogenicity study in rats and subchronic toxicity study in dogs on ingested
vinylidene chloride. Fund. Appl. Toxicol. 3: 55-62
Reitz, R.H., P.G. Watanabe, M.J. McKenna, J.F. Quast and P.J. Gehring. 1980.
Effects of vinylidene chloride on DNA synthesis and DNA repair in the rat and
mouse: A comparative study with dimethylnitrosamine. Toxicol. Appl.
Pharmacol. 52: 357-370.
Short, R.D., J.M. Winston, J.L. Minor, J. Seifter and C-C. Lee. 1977. Effect
of various treatments on toxicity of inhaled vinylidene chloride. Environ.
Health Perspect. 21: 125-129.
U.S. EPA. 1985. Health Assessment Document for Vinylidene Chloride. Prepared
by the Office of Health and Environmental Assessment, Environmental Criteria
and Assessment Office, Research Triangle Park, NC. EPA 600/8-83-031F.
Van Duuren, B., B.M. Goldschmidt, G. Loewengert, A.C. Smith, S. Melchionne, I.
Seidman and D. Roth. 1979. Carcinogenicity of halogenated olefinic and
aliphatic hydrocarbons in mice. J. Natl. Cancer Inst. 63(6): 1433-1439.
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=========
_VII. REVISION HISTORY
Substance Name -- 1,1-Dichloroethylene
CASRN -- 75-35-4
Primary Synonym -- Vinylidene Chloride
-------- -------- --------------------------------------------------------
Date Section Description
-------- -------- --------------------------------------------------------
03/31/1987 II. Carcinogenicity Section added
03/01/1988 I.A.1. Dose conversion clarified
03/01/1988 I.A.7. Contact changed
03/01/1988 II.A.2. Text added
03/01/1988 II.B.3. Text revised
03/01/1988 II.B.4. Confidence statement revised
03/01/1988 II.C.3. Text added
03/01/1988 II.C.4. Confidence statement revised
06/30/1988 I.A.7. Changed primary contact's telephone number
12/01/1988 II.A.3. van Durren et al. citation year corrected
04/01/1989 I.A. Oral RfD summary noted as pending change
12/01/1989 I.B. Inhalation RfD now under review
03/01/1990 II. Clarified NTP, 1982 citation
03/01/1990 VI. Bibliography on-line
01/01/1991 II. Text edited
01/01/1991 II.C.1. Inhalation slope factor removed (global change)
02/01/1991 II.C.3. Information on extrapolation process included
08/01/1991 VI.A. References clarified
08/01/1991 VI.C. References clarified
01/01/1992 IV. Regulatory actions updated
02/01/1998 II.C.3. Slope factor corrected from 1.2 to 0.2E+0
=====================================================================
=========
VIII. SYNONYMS
Substance Name -- 1,1-Dichloroethylene
CASRN -- 75-35-4
Primary Synonym -- Vinylidene Chloride
Last Revised -- 01/31/1987
75-35-4
CHLORURE DE VINYLIDENE
1,1-DCE
1,1-DICHLOROETHENE
Dichloroethylene, 1,1-
ETHENE, 1,1-DICHLORO-
ETHYLENE, 1,1-DICHLORO-
NCI-C54262
RCRA WASTE NUMBER U078
SCONATEX
UN 1303
VDC
Vinylidene Chloride
VINYLIDENE DICHLORIDE
VINYLIDINE CHLORIDE
Last updated: 5 May 1998
URL: http://www.epa.gov/iris/SUBST/0039.HTM
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