March 31, 1987
820K90100
CIS-1,2-DICHLOROETHYLENE
Health Advisory
Office of Drinking Water
U.S. Environmental Protection Agency
I. INTRODUCTION
The Health Advisory (HA) Program, sponsored by the Office of Drinking
Water (ODW), provides information on the health effects, analytical method-
ology and treatment technology that would be useful in dealing with the
contamination of drinking water. Health Advisories describe nonregulatory
concentrations of drinking water contaminants at which adverse health effects
would not be anticipated to occur over specific exposure durations. Health
Advisories contain a margin of safety to protect sensitive members of the
population.
Health Advisories serve as informal technical guidance to assist Federal,
State and local officials responsible for protecting public health when
emergency spills or contamination situations occur. They are not to be
construed as legally enforceable Federal standards. The HAs are subject to
change as new information becomes available.
Health Advisories are developed for One-day, Ten-day, Longer-term
(approximately 7 years, or 10% of an individual's lifetime) and Lifetime
exposures based on data describing noncarcinogenic end points of toxicity.
Health Advisories do not quantitatively incorporate any potential carcinogenic
risk from such exposure. For those substances that are known or probable
human carcinogens, according to the Agency classification scheme (Group A or
B), Lifetime HAs are not recommended. The chemical concentration values for
Group A or B carcinogens are correlated with carcinogenic risk estimates by
employing a cancer potency (unit risk) value together with assumptions for
lifetime exposure and the consumption of drinking water. The cancer unit
risk is usually derived from the linear multistage model with 95% upper
confidence limits. This provides a low-dose estimate of cancer risk to
humans that is considered unlikely to pose a carcinogenic risk in excess
of the stated values. Excess cancer risk estimates may also be calculated
using the One-hit, Weibull, Logit or Probit models. There is no current
understanding of the biological mechanisms involved in cancer to suggest that
any one of these models is able to predict risk more accurately than another.
Because each model is based on differing assumptions, the estimates that are
derived can differ by several orders of magnitude.
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cis-1,2-Dichloroethylene
March 31, 1987
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This Health Advisory is based on information presented in the Office
of Drinking Water's Health Effects Criteria Document (CD) for the Dichloro-
ethylenes (U.S. EPA, 1984a). The HA and CD formats are similar for easy
reference. Individuals desiring further information on the toxicological
data base or rationale for risk characterization should consult the CD. The
CD is available for review at each EPA Regional Office of Drinking Water
counterpart (e.g., Water Supply Branch or Drinking Water Branch), or for a
fee from the National Technical Information Service, U.S. Department of
Commerce, 5285 Port Royal Rd., Springfield, VA 22161, PB #86-117785/AS.
The toll-free number is (800) 336-4700; in the Washington, D.C. area: (703)
487-4650.
II. GENERAL INFORMATION and PROPERTIES
CAS No. 156-59-2
Chemical Structure
Cl Cl
H-C=C-H
1,2-DCE; cis-1,2-DCE; 1, 2-dichloroethene
Synonyms
Uses
In a mixture with the trans-1,2- isomer, as a captive intermediate
in the manufacture of other chlorinated solvents
Properties (Irish, 1963; Windholz et al., 1976)
C2H2C12
96.95
clear, colorless liquid
-80.5°C
60°C
Chemical Formula
Molecular Weight
Physical State
Freezing Point
Boiling Point
Melting Point
Density —
Vapor Pressure 208 mm Hg (25°C)
Specific Gravity 1.27 (25°C)
Water Solubility 3500 ug/L (20°C)
Log Octanol/Water Partition
Coefficient
Taste Threshold Not available
Odor Threshold Not available
Conversion Factor
Occurrence
The 1,2-dichloroethylenes are synthetic chemicals with no known natural
sources (U.S. EPA, 1983).
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0 There is little information on the current production and use of the
1,2-dichloroethylenes. The production volume for 1,2-dichloroethylene
(mixed isomers) was 1,000 Ibs or less in 1978 (U.S. EPA, '1978).
0 The major releases of the 1,2-dichloroethylenes are from the manufac-
turing plants in the Gulf Coast region of the U.S., where they are used
as a captive intermediate. Releases are expected to be small. The 1,2-
dichloroethylenes, particularly the cis- isomer, have been identified
as the degradation products of trichloroethylene and tetrachloroethylene
in ground water (Parsons et al., 1984; Vogel and McCarty, 1985).
0 There is little direct information on the fate of the 1,2-dichloro-
ethylenes in the environment. However, the behavior of the compounds
has been estimated based upon the information on similar chlorinated
compounds (U.S. EPA 1979). 1,2-Dichloroethylenes released to the
atmosphere are expected to chemically degrade in a matter of hours;
when released to surface waters, they are expected to volatilize
rapidly to air. 1,2-Dichloroethylenes are chemically stable in water
and mobile in soils. Once released to land the 1,2-dichloroethylenes
are expected to migrate with ground water. 1,2-Dichloroethylenes
have been shown to biologically degrade to vinyl chloride in some
groundwaters. These compounds are not expected to bioaccumulate in
plants or animals. Based upon their similar physical properties,
the two isomers of 1,2-dichloroethylene are not expected to behave
differently in the environment.
8 Monitoring studies have found that the 1,2-dichloroethylenes occur as
widespread but relatively rare contaminants of ground water. The
cis- isomer has been reported to occur at higher levels than the
trans- isomer. The majority of the 1,2-dichloroethylenes has been
found to co-occur with trichloroethylene. Levels of the 1,2-dichloro-
ethylenes in approximately 1 % of all ground waters are greater than
0.5 ug/L. Levels as high as 300 ug/L have been reported for the
trans- isomer, while levels of 800 ug/L have been reported for the
cis- isomer. The 1,2-dichloroethylenes occur in surface water at
lower amounts. Levels of 1,2-dichloroethylenes in air are in the ppt
range except near production sites where they may reach levels in the
low ppb range. Based upon these compounds' volatility and limited
use, levels of 1,2-dichloroethylenes in food are expected to be
negligible (U.S. EPA, 1983).
0 The major source of exposure to the 1,2-dichloroethylenes is from
contaminated water except in the areas near production sites where
air exposures may dominate.
III. PHARMACOKINETICS
Absorption
0 cis-1,2-Dichloroethylene is a neutral, low molecular weight, lipid
soluble material which would be expected to be readily absorbed
following exposure by any route (oral, inhalation, dermal) at the
levels expected to be encountered in contamination incidents (U.S.
EPA, 1984a).
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Distribution
0 Kinetic data to define the tissue distribution of cis-1,2-dichloro-
ethylene after oral exposure are not available. If this isomer,
however, follows the same absorption and distribution pattern as
observed for 1,1-dichloroethylene, the highest concentrations would
be expected to be found in the liver and kidney (McKenna et al.,
1978).
Metabolism
0 The metabolic end products of chlorinated ethylenes are predominantly
alcohols and carboxylic acids. Perfusion of cis-1,2-dichloroethylene
through isolated rat liver yielded dichloroethanol and dichloro-
acetic acid, possibly indicating the initial formation of dichloro-
acetaldehyde (Bonse et al., 1975).
0 The position of the chlorine moeity on the chlorinated ethylenes appears
to play an important role in their metabolism. Cis-1,2-dichloroethylene
was metabolized at a faster rate than trans-1,2-dichloroethylene
(which possesses a relatively greater degree of asymmetry) in an
in vitro hepatic microsomal system (Costa, 1983).
0 Using isolated rat liver microsomes, Freundt and Macholz (1978)
reported that cis-1,2-dichloroethylene showed competitive and
reversible interaction with the mixed function oxygenase system,
resulting in decreased drug metabolism.
Excretion
No data concerning the excretion of cis-1,2-dichloroethylene are
available. If it is similar to 1,1-dichloroethylene, then the rate
of elimination would be expected to be relatively rapid, with most of
a single dose being excreted in the urine within 24 to 72 hours after
cessation of exposure (Jaeger et al., 1977).
IV. HEALTH EFFECTS
Humans
At high concentrations, the dichloroethylenes, like other chlorinated
ethylenes, possess anesthetic properties, cis-1,2-Dichloroethylene
was used as an anesthetic with some success prior to introduction of
newer anesthetic gases, and appeared to be safe (Irish, 1963).
Animals
Short-term Exposure
No cis- isomer-specific LD50s have been reported. An oral
of 770 mgAg of the isomer mixture was reported for rats
(NIOSH, 1978).
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0 At high exposure levels, general anesthetic and narcotic effects
are observed (Irish, 1963).
0 Administration of a. single dose of cis-1,2-dichloroethylene at 400
mg/kg to rats caused a significant elevation of liver alkaline
phosphatase (Jenkins et al., 1972).
Long-term Exposure
0 No information was found in the available literature on the effects
of long-term exposures to cis-1,2-dichloroethylene.
Reproductive Effects
0 No information was found in the available literature on the potential
of cis-1,2-dichloroethylene to produce reproductive effects.
Developmental Effects
0 No information was found in the available literature on the potential
of cis-1,2-dichloroethylene to produce developmental effects.
Mutagenicity
0 cis-1,2-Dichloroethylene was not mutagenic, with or without metabolic
activation, when assayed in E_. coli K12 at a medium concentration of
2.9 mM (Greim et al., 1975)
0 Galli et al. (1982a) reported that cis-1,2-dichloroethylene did not
induce point mutation, mitotic gene conversion or mitotic recombination
in yeast. In addition, they (1982b) reported that cis-1,2-dichloro-
ethylene was not mutagenic in an in vivo (intravenous host-mediated
assay) test. (Both manuscripts are in Italian.)
Carcinogenicity
0 No information was found in the available literature on the carcinogenic
potential of cis-1,2-dichloroethylene.
V. QUANTIFICATION OF TOXICOLOGICAL EFFECTS
Health Advisories (HAs) are generally determined for One-day, Ten-day,
Longer-term (approximately 7 years) and Lifetime exposures if adequate data
are available that identify a sensitive noncarcinogenic end point of toxicity.
The HAs for noncarcinogenic toxicants are derived using the following formula:
HA = (NOAEL or LOAEL) x (BW) = mg/L ( ug/L)
(UF) x ( L/day)
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where:
NOAEL or LOAEL = No- or Lowest-Observed-Adverse-Effect-Level
in mg/kg bw/day.
BW = assumed body weight of a child (10 kg) or
an adult (70 kg).
UF = uncertainty factor (10, 100 or 1,000), in
accordance with NAS/ODW guidelines.
L/day = assumed daily water consumption of a child
(1 L/day) or an adult (2 L/day).
One-day Health Advisory
There are few animal studies which provide dose-response data on the
effects of cis-1,2-dichloroethylene (Irish, 1963; Jenkins et al., 1972;
Freundt and Macholz, 1978). Only the study by Jenkins et al. provides
sufficient information from which a One-day Health Advisory can be calculated.
These authors monitored levels of liver glucose-6-phosphatase, liver alkaline
phosphatase, liver tyrosine transaminase, plasma alkaline phosphatase and
plasma alkaline transaminase and observed that a single, oral dose of 400 mg/kg
to the rat produced a significant change only in liver alkaline phosphatase.
The LOAEL of 400 mg/kg reported by Jenkins et al. (1972) will be used for the
one-day calculations.
The One-day Health Advisory for the 10 kg child is calculated as follows:
One-day HA = (400 mg/kg/day) (10 kg) = 4 m /L (4 000 ug/L)
(1,000) (1 L/day)
where:
400 mg/kg/day = LOAEL based on increase in liver alkaline phosphatase.
10 kg = assumed body weight of a child.
1,000 = uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a LOAEL from an animal study.
1 L/day * assumed daily water consumption of a child.
Ten-day Health Advisory
Appropriate studies for the calculation of a Ten-day Health Advisory
are not available. Evaluation of the available toxicological data on cis-1,2-
dichloroethylene and 1,1-dichloroethylene suggests that the Longer-term
Health Advisory of 1 mg/L should provide adequate protection over a 10-day
exposure period as well.
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Longer-term Health Advisory
A Longer-term HA for cis-1,2-dichloroethylene cannot be derived directly
from compound-specific data since appropriate data do not exist at this time.
The available information from shorter-term exposure to 1,1-dichloroethylene
and cis- and trans 1,2-dichloroethylene suggests that the non-carcinogenic
effects induced by the 1,2- isomers is likely to be no more, and conceivably
less, severe than those induced by 1,1-dichloroethylene. Since the non-carcin-
ogenic end-points of toxicity for all three isomers appear to be essentially
identical, adopting the Longer-term HA derived for 1,1-dichloroethylene for
use as the Longer-term HA for cis-1 ,2-dichloroethylene may even result in an
added margin of safety.
The Longer-term HA will be derived from a 90-day subchronic study in which
rats of both sexes were administered 1,1-dichloroethylene at nominal concen-
trations of 0, 50, 100 or 200 ppm (0-25.6 mg/kg/day) in their drinking water
(Rampy et al., 1977). Except for a decreased kidney:body weight ratio in
males at the low dose, there were no statistically significant differences in
organ weights or organ:body weight ratios at the end of the study. The only
histopathology noted was an increased cytoplasmic vacuolization of hepatocytes
in the livers of both sexes exposed to the highest dose. A NOAEL of 100 ppm
(10 to 12.6 mg/kg) was identified.
The Longer-term HA for the 10-kg child is calculated as follows:
Longer-term HA = (10 mg/kg/day) (10 kg) = ., » (1000 /L)
(100) (1 L/day)
where:
10 mg/kg/day = NOAEL based on the absence of liver effects.
10 kg = assumed body weight of a child.
100 = uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a NOAEL from an animal study.
1 L/day = assumed daily water consumption of a child.
The Longer-term HA for the 70-kg adult is calculated as follows:
Longer-term HA = (10 mg/kg/day) (70 kg) = 3 5 mg/L (3500 ug/L)
(100) (2 L/day)
where:
10 mg/kg/day = NOAEL based on the absence of liver effects.
70 kg = assumed body weight of an adult.
100 = uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a NOAEL from an animal study.
2 L/day = assumed daily water consumption of an adult.
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Lifetime Health Advisory
The Lifetime HA represents that portion of an individual's total exposure
.that is attributed to drinking water and is considered protective of noncar-
cinogenic adverse health effects over a lifetime exposure. The Lifetime HA
is derived in a three step process. Step 1 determines the Reference Dose
(RfD), formerly called the Acceptable Daily Intake (ADI). The RfD is an esti-
mate of a daily exposure to the human population that is likely to be without
appreciable risk of deleterious effects over a lifetime, and is derived from
the NOAEL (or LOAEL), identified from a chronic (or subchronic) study, divided
by an uncertainty factor(s). From the RfD, a Drinking Water Equivalent Level
(DWEL) can be determined (Step 2). A DWEL is a medium-specific (i.e., drinking
water) lifetime exposure level, assuming 100% exposure from that medium, at
which adverse, noncarcinogenic health effects would not be expected to occur.
The DWEL is derived from the multiplication of the RfD by the assumed body
weight of an adult and divided by the assumed daily water consumption of an
adult. The Lifetime HA is determined in Step 3 by factoring in other sources
of exposure, the relative source contribution (RSC). The RSC from drinking
water is based on actual exposure data or, if data are not available, a
value of 20% is assumed for synthetic organic chemicals and a value of 10%
is assumed for inorganic chemicals. If the contaminant is classified as a
Group A or B carcinogen, according to the Agency's classification scheme of
carcinogenic potential (U.S. EPA, 1986), then caution should be exercised in
assessing the risks associated with lifetime exposure to this chemical.
Lifetime toxicity data for cis-1,2-dichloroethylene do not exist.
Data from the chronic drinking water study in rats as used for the Lifetime
Health Advisory for 1,1-dichloroethylene will be used instead. The same
caveats and assumptions as were described above for the Longer-term HA also
apply here.
The Lifetime HA can be calculated from the 2-year chronic study in rats
(Quast et al., 1983). 1,1-Dichloroethylene, at nominal concentrations of 0,
50, 100 or 200 ppm (0 to 20 mg/kg/day) in drinking water, was administered
to animals of both sexes. No consistent treatment-related changes were
observed in any parameter measured. The only histopathology observed was in
the livers of both sexes receiving the highest dose, changes characterized
by a minimal amount of mid-zonal fatty accumulation. No liver degeneration was
noted. A LOAEL of 100 ppm (10 mg/kg) was identified, based upon a trend
towards increased fatty deposition in the liver.
A Drinking Water Equivalent Level (OWED and Lifetime HA for the 70-kg
adult are calculated as follows:
Step 1: Determination of the Reference Dose (RfD)
RfD = (10 mg/kg/day) = 0.01 mg/kg/day
(1,000)
where:
10 mg/kg/day = LOAEL based on adverse liver effects.
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1,000 = uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a LOAEL from an animal study.
Step 2: Determination of the Drinking Water Equivalent Level (DWEL)
DWEL » (0-01 mg/kg/day) (70 kg) = 0>35 mg/L (350 u /L)
(2 L/day)
where:
0.01 mgAg/day = RfD.
70 kg = assumed body weight of an adult.
2 L/day = assumed daily water consumption of an adult.
Step 3: Determination of Lifetime Health Advisory
Lifetime HA = (0.35 mg/L) (20%) = 0.07 mg/L (70 ug/L)
where:
0.35 mg/L = DWEL.
20% = assumed relative source contribution from water.
Evaluation of Carcinogenic Potential
0 There are no data available on the carcinogenic potential of cis-1,2-
dichloroethylene.
0 Applying the criteria described in EPA's guidelines for assessment
of carcinogenic risk (U.S. EPA, 1986), cis-1,2-dichloroethylene is
classified in Group D: Not classified. This category is for agents
with inadequate animal evidence of carcinogenicity.
VI. OTHER CRITERIA, GUIDANCE AND STANDARDS
0 The Threshold Limit Value (TLV) in the occupational setting for the
1,2-dichloroethylene isomer mixture is 200 ppm (790 mg/m3) (ACGIH, 1982).
VII. ANALYTICAL METHODS
Analysis of cis-1,2-dichloroethylene is by a purge-and-trap gas
chromatographic procedure used for the determination of volatile
organohalides in drinking water (U.S. EPA, 1984b). This method calls
for the bubbling of an inert gas through the sample and trapping
1,2-dichloroethylene on an adsorbant material. The adsorbant material
is heated to drive off the 1,2-dichloroethylene onto a gas chromato-
graphic column. This method will differentiate between the two
isomers of 1,2-dichloroethylene. This method is applicable to the
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measurement of 1,2-dichloroethylene over a concentration range of
0.03 to 1500 ug/L. Confirmatory analysis for 1,2-dichloroethylene is
by mass spectrometry (U.S. EPA, 1985a). The detection limit for
confirmation by mass spectometry 0.2 ug/L.
VIII. TREATMENT TECHNOLOGIES
0 Treatment technologies which will remove cis-1 ,2-dichloroethylene
from water include granular activated carbon (GAC) adsorption,
aeration and boiling.
0 Dobbs and Cohen -(1980) developed adsorption isotherms for cis-1,2-
dichloroethylene It was reported that Filtrasorb® 300 carbon exhibited
adsorptive capacities of 1.3 mg and 0.26 mg cis-1,2-dichloroethylene/gm
carbon at equilibrium concentrations of 100 and 10 ug/L, respectively.
0 USEPA-DWRD installed pilot-scale adsorption columns at three locations
in New England (U.S. EPA, 1985b,c). Cis-1,2-dichloroethylene was
present in the contaminated groundwater at concentrations ranging from
2 to 18 ug/L. The raw water was passed through a Filtrasorb ® 400 GAC
column until breakthrough concentration of 0.1 ug/L was achieved
which after approximately 10 weeks of continuous operation.
0 cis-1,2-Dichloroethylene is amenable to removal by aeration on the
basis of its Henry's Law Constant of 225 atm (U.S. EPA, 1985b,c). In
a pilot-scale diffused air aeration column, removal efficiency of 85%
was achieved from original concentrations of 18 to 118 ug/L at an
air-to-water ratio of 30:1. At an air-to-water ratio of 5:1 and the
same operating conditions, 58% of cis-1,2-dichloroethylene was removed
from the same source water (Love, 1983). In another pilot-scale
study, a countercurrent diffused air aeration column removed 80% of
cis-1,2-dichloroethylene from well water with 0.5 ug/L, at an air-to-
water ratio of 4:1 (Love and Eilers, 1982). Numerous packed column
air stripping plant studies have been performed by EPA. All of the
studies (using identical column size) indicated that packed column
aeration is effective in removing cis-1,2-dichloroethylene from
drinking water supplies at different concentrations. The best removal,
i.e., 99%+, was achieved at an optimum air-to-water ratio of 80-85:1
(U.S. EPA, 1985b,c; ESE, 1985).
0 Boiling also is effective in eliminating cis-1,2-dichloroethylene
from water on a short-term, emergency basis. Studies have shown that
five minutes of vigorous boiling will remove 96% of cis-1,2-dichloro-
ethylene present in the water (Love and Eilers, 1982).
0 Air stripping is an effective, simple and relatively inexpensive
process for removing cis-1,2-dichloroethylene and other volatile
organics from water. However, this process transfers the contaminant
directly into the air stream. When considering this method as a
treatment process, it is suggested that careful consideration be
given to the overall environmental occurrence, fate, route of exposure
and various hazards associated with the chemical.
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cis-1,2-Dichloroethylene • March 31, 1987
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IX. REFERENCES
ACGIH. 1982. American Council of Governmental Industrial Hygienists. TLVs.
Threshold limit values for chemical substances and physical agents in the
workroom environment. Cincinnati, Ohio. p.
Bonse, G., T. Urban, R. Montessano and L. Tomatis. 1975. Chemical reactivity,
metabolic oxirane formation and biological reactivity of chlorinated
ethylenes in the isolated perfused rat liver preparation. Biochem.
Pharmacol. 24:1829-1834.
Costa, A.K. 1983. The chlorinated ethylenes: Their hepatic metabolism and
carcinogenicity. Diss. Abst. Int [B]. 44(6):1791-B.
Dobbs, R.A. and J.M. Cohen. 1980. Carbon adsorption isotherms for toxic
chemicals. Cincinnati, Ohio. EPA-600/8-80-023.
ESE. 1985. Environmental Science and Engineering. Technologies and costs
for the removal of volatile organic chemicals from potable water supplies.
ESE No. 84-912-300. Prepared for U.S. EPA Science and Technology Branch,
CSD, PDW, Washington, DC.
Freundt, J.J., and J. Macholz. 1978. Inhibition of mixed function oxidases
in rat liver by trans-and cis-1,2-dichloroethylene. Toxicology.
10:131-139.
Galli, A., C. Bauer, G. Brenzetti, C. Corsi, R. Del Carratore, R. Nieri and
M. Paolini. 1982a. (a) Studio in vitro. Attivita genetica dell1
1,2-dichloroetilene. Boll. Soc. It. Biol. Sper. 58:860-863.
Galli, A., C. Bauer, G. Brenzetti, C. Corsi, R. Del Carratore, R. Nieri and
M. Paolini. 1982b. (a) Studio in vivo. Attivita genetica dell'
1,2-dichloroetilene. Boll. Soc. It. Biol. Sper. 58:864-869.
Greim, H., G. Bonse, Z. Radwan, D. Reichert and D. Henschler. 1975.
Mutagenicity in vitro and potential carcinogenicity of chlorinated
ethylenes as a function of metabolic oxirane formation. Biochem.
Pharmacol. 24:2013-2017.
Irish, D.D. 1963. Vinylidene chloride. In: F.A. Patty (ed), Industrial
Hygiene and Toxicology. 2nd ed. Vol. II. John Wiley and Sons, Inc.,
New York. pp. 1305-1309.
Jaeger, R.J., L.G. Shoner and L.J. Coffman. 1977. 1,1-Dichloroethylene
hepatotoxicity: Proposed mechanism of action of distribution and binding
of 14c radioactivity following inhalation exposure in rats. Environ.
Health Perspect. 21:113-119.
Jenkins, L.J., Jr., M.J. Trabulus and S.D. Murphy. 1972. Biochemical effects
of 1,1-dichloroethylene in rats: Comparison with carbon tetrachloride
and 1,2-dichloroethylene. Toxicol. Appl. Pharmacol. 23:501-510.
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cis-1,2-Dichloroethylene March 31, 1987
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Love, D.T., Jr. 1983. Treatment of volatile organic compounds in drinking
water. U.S. Dept. of Commerce. NTIS.
Love, D.T., Jr., and R.G. Eilers. 1982. Treatment of drinking water containing
trichloroethylene and related industrial solvents. J.A.W.W.A. 74:413-425.
McKenna, M.J., J.A. Zempel, E.O. Madrid and P.J. Gehring. 1978. The pharmaco-
kinetics of (14C) vinylidene chloride in rats following inhalation
exposure. Toxic si. Appl. Pharmacol. 45:599-610.
NIOSH. 1978. National Institute for Occupational Safety and Health.
1,2-Dichloroethylene. Registry of toxic effects of chemical substances.
p. 563.
Parsons, P., P.R. Wood and J. DeMarco. 1984. Transformation of tetrachloro-
ethene and trichloroethene in microcosms and groundwater. J.A.W.W.A.
76:56.
Quast, J.P., C.G. Humiston, C.E. Wade, J. Ballard, J.E. Beyer, R.W. Schwetz
and J.M. Norris. 1983. A chronic toxicity and oncogenicity study in rats
and subchronic toxicity study in dogs on ingested vinylidine chloride.
Fund. Appl. Toxicol. 3:55-62.
Rampy, L.W., J.F. Quast, C.G. Humiston, M.F. Blamer and B.A. Schwetz. 1977.
Interim results of two-year toxicological studies in rats of vinylidene
chloride incorporated in the drinking water or administered by repeated
inhalation. Environ. Health Perspect. 21:33-43.
U.S. EPA. 1978. U.S. Environmental Protection Agency. TSCA Inventory-
Non-confidential portion. Office of Toxic Substances.
U.S. EPA. 1979. U.S. Environmental Protection Agency. Water related environ-
mental fate of 129 priority pollutants. Office of Water Planning and
Standards. EPA-440/4-79-029. December.
U.S. EPA. 1983. U.S. Environmental Protection Agency. 1,2-Dichloroethylene
occurrence in drinking water, food, and air. Office of Drinking Water.
U.S. EPA. 1984a. U.S. Environmental Protection Agency. Draft health effects
criteria document for the dichloroethylenes. Criteria and Standards
Division, Office of Drinking Water. Washington, DC. December.
U.S. EPA. 1984b. U.S. Environmental Protection Agency. Method 502.1.
Volatile halogenated organic compounds in water by purge and trap gas
chromatography. Environmental Monitoring and Support Laboratory,
Cincinnati, Ohio 45268. June.
U.S. EPA. 1985a. U.S. Environmental Protection Agency. Method 524.1.
Volatile halogenated organic compounds in water by purge and trap gas
chromatography/mass spectrometry. Environmental Monitoring and Support
Laboratory, Cincinnati, Ohio 45268. June.
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U.S. EPA. 1985b. U.S. Environmental Protection Agency. Office of Drinking
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