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DISCLAIMER
This report Is an external draft for review purposes only and does not
constitute Agency policy. Mention of trade names or commercial products
does not constitute endorsement or recommendation for use.
11
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PREFACE
Health and Environmental Effects Documents (HEEDs) are prepared for the
Office of Solid Waste and Emergency Response (OSWER). This document series
Is Intended to support listings under the Resource Conservation and Recovery
Act (RCRA) as well as to provide health-related limits and goals for
emergency and remedial actions under the Comprehensive Environmental
Response, Compensation and Liability Act (CERCLA). Both published
literature and information obtained for Agency Program Office files are
evaluated as they pertain to potential human health, aquatic life and
environmental effects of hazardous waste constituents. The literature
searched for In this document and the dates searched are Included In
"Appendix: Literature Searched." Literature search material Is current up
to 8 months previous to the final draft date listed on the front cover.
Final draft document dates (front cover) reflect the date the document Is
sent to the Program Officer (OSWER).
Several quantitative estimates are presented provided sufficient data
are available. For systemic toxicants, these Include: Reference doses
(RfDs) for chronic and subchronlc exposures for both the Inhalation and oral
exposures. The subchronlc or partial lifetime RfO, Is an estimate of an
exposure level which would not be expected to cause adverse effects when
exposure occurs during a limited time Interval I.e., for an Interval which
does not constitute a significant portion of the llfespan. This type of
exposure estimate has not been extensively used, or rigorously defined as
previous rlsfc assessment efforts have focused primarily on lifetime exposure
scenarios. Animal data used for subchronlc estimates generally reflect
exposure durations of 30-90 days. The general methodology for estimating
subchronlc RfDs 1s the same as traditionally employed for chronic estimates,
except that subchronlc data are utilized when available.
In the case of suspected carcinogens, a carcinogenic potency factor, or
q-j* (U.S. EPA, 1980), 1s provided. These potency estimates are derived
for both oral and Inhalation exposures where possible. In addition, unit
risk estimates for air and drinking water are presented based on Inhalation
and oral data, respectively. An,.RfD may also be derived for the noncarclno-
genlc health effects of compounds that are also carcinogenic.
Reportable quantities (RQs) based on both chronic toxlclty and
carclnogenldty are derived. The RQ Is used to determine the quantity of a
hazardous substance for which notification Is required In the event of a
release as specified under the Comprehensive Environmental Response,
Compensation and Liability Act (CERCLA). These two RQs (chronic toxlclty
and cardnogenlclty) represent two of six scores developed (the remaining
four reflect IgnltabllUy, reactivity, aquatic toxlclty, and acute mammalian
toxlclty). Chemical-specific RQs reflect the lowest of these six primary
criteria. The methodology for chronic toxlclty and cancer based RQs are
defined In U.S. EPA, 1984 and 1986a, respectively.
111
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EXECUTIVE SUMMARY
ds-l,2-D1chloroethy1ene Is a volatile, colorless liquid and 1s soluble
In water and common polar or nonpolar organic solvents. In 1977, between 1
and 11 million pounds of cls-1,2-d1chloroethylene was produced by PPG
Industries at their production facilities In Lake Charles, LA, and Ponce,
Puerto R1co (TSCAPP, 1989). Recent production volume data are not avail-
able. ds-1,2-D1chloroethylene 1s produced by the partial chlorlnatlon of
acetylene, and 1t 1s separated from the trans-1somer by fractional distilla-
tion (Stevens, 1979). ds-1,2-D1chloroethylene 1s also produced during the
manufacture of other chlorinated solvents. Most cls-1,2-D1chloroethylene
produced commercially Is used directly In the synthesis of other chlorinated
solvents. It Is also used as a low temperature extraction solvent, a
solvent for organic synthesis and as a solvent for specialty applications
(Sax and Lewis, 1987; Stevens, 1979).
ds-1,2-D1chloroethylene Is expected to exist almost entirely 1n the
vapor phase 1n the atmosphere. Its atmospheric fate 1s expected to be
dominated by the gas phase destruction by photochemlcally produced hydroxyl
radicals; the half-life for this process can be estimated at 8.3 days based
on an experimentally determined rate constant. Wet deposition of ds-1,2-
dlchloroethylene may occur; however, any compound removed from the atmo-
sphere by this process Is expected to volatilize again quickly. Neither
direct photochemical degradation nor gas phase destruction by ozone or other
chemical oxldants Is expected to occur to any significant extent In the
atmosphere.
The fate of ds-1,2-d1chloroethylene In surface water Is expected to be
dominated by rapid volatilization to the atmosphere. The half-life for the
volatilization of ds-1,2-d1chloroethylene from a model river Is ~3 hours.
1v
-------
Although m1crob1al degradation of ds-1,2-d1chloroethylene under anaerobic
conditions Is known to occur, H occurs at a slow rate. There are conflict-
ing data regarding the degradation of this compound under aerobic condi-
tions. It appears that some organisms are capable of degrading cls-1,2-dl-
chloroethylene under aerobic conditions If suitable nutritional sources are
present. The destruction of ds-1,2-d1chloroethylene 1n water by direct
photolysis or by abiotic chemical degradation Is not expected to be signifi-
cant. c1s-l,2-D1chloroethylene 1s not expected to bloconcentrate signifi-
cantly In fish and aquatic organisms nor 1s 1t expected to adsorb to
sediment and suspended organic matter.
Limited experimental data on the fate of cls-1,2-d1chloroethylene In
soil were located 1n the available literature. It may be highly mobile 1n
soil and leach Into groundwater. c1s-l,2-D1chloroethylene will volatilize
readily from the soil surface to the atmosphere. It Is expected to undergo
slow microblal degradation 1n anoxlc soils and groundwater. A recent
experiment Indicated that this process may also occur under aerobic
conditions with certain microorganisms 1f secondary nutritional sources are
available.
ds-1,2-D1chloroethylene may be released to the atmosphere 1n emissions
from Us production and use and from the volatilization from contaminated
wastewater or from waste disposal sites, ds-1,2-Dlchloroethylene may also
be released to the environment as a result of the combustion of poly(vlnyl)-
chlor.lde polymers or as a result of the biological breakdown of other
chlorinated solvents.
Occupational exposure to c1s-l,2-dlchloroethylene may occur by Inhala-
tion or dermal contact during Us manufacture, transportation or use as a
solvent or chemical Intermediate. Exposure by Inhalation 1s also likely 1n
areas, such as landfills, where cls-1,2-d1chloroethylene Is discarded.
-------
c1s-1,2-D1ch1oroethylene has been detected In surface water, ground-
water, rainwater and drinking water. Consequently, exposure to the general
population can occur by drinking contaminated water. Since ds-l,2-d1-
chloroethylene has been detected In tap water, exposure to the general
population may occur by dermal contact or Inhalation while bathing or
showering, ds-1,2-D1chloroethylene has also been detected In urban air
samples. Based on an analysis of urban air levels of ds-l,2-d1chloro-
ethylene (Shah and Heyerdahl, 1988), a median dally Inhalation Intake can be
calculated as 3.96 yg/day. Sufficient data are not available to
accurately estimate human exposure to l,2--d1chloroethylene by other routes
of exposure.
Pertinent data regarding the environmental toxldty of ds-l,2-d1chloro-
ethylene were not located 1n the available literature cited 1n Appendix A.
Pharmacok1net1c data for ds-l,2-d1chloroethylene are limited. Gas
uptake studies Indicate that c1s-l,2-d1chloroethylene Is absorbed readily
from the respiratory tract of rats (FUser and Bolt, 1979). Because the
compound 1s neutral, low molecular weight and UpophlUc, It Is expected to
be readily absorbed by any natural route of exposure (U.S. EPA, 1987a).
Although tissue distribution data were not located, the highest tissue
levels would be expected In the liver and kidneys (U.S. EPA, 1987a), 1f this
compound behaves similarly to 1 ,l-d1chloroethylene (McKenna et al., 1978).
ds-1,2-D1chloroethylene Is metabolized by hepatic cytochrome P-450
oxldases, with the formation of dlchloroacetaldehyde and dlchloroethanol
(Costa and Ivanetlch, 1982). The Initial step In the metabolism probably
Involves formation of a chloroethylene epoxlde that undergoes rearrangement
to dlchloroacetaldehyde (Henschler, 1977; Lelbman and Ortiz, 1977).
v1
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Metabolic elimination of ds-1,2-d1chloroethylene was described as a satur-
able process, changing from a first-order to a zero-order process at 20 ppm
(Fllser and Bolt, 1979).
Pertinent data regarding the excretion of ds-1,2-dlchloroethylene
following oral, Inhalation or dermal exposure were not located 1n the
available literature dted In Appendix A.
Acute Inhalation exposure of animals or humans to high concentrations of
ds-1,2-d1chloroethylene vapors can produce anesthesia and narcosis (Smyth,
1937-1955; ACGIH, 1986). In rats, exposure to 16,000 ppm ds-1,2-dlchloro-
ethylene for 4 hours resulted 1n death (Smyth, 1937-1955).
The results of an acute oral toxlclty rat study provided biochemical
evidence that ds-1,2-d1chloroethylene 1s hepatotoxlc (Jenkins et al.,
1972). ds-l,2-01chloroethylene significantly elevated the activity of
liver alkaline phosphatase at the 400 and 1500 mg/kg dose levels. The
activities of liver glucose-6-phosphatase, liver tyroslne transamlnase and
plasma alanlne transamlnase decreased at the 1500 mg/kg dose level.
The systemic toxlclty resulting from subchronlc or chronic exposure to
ds-l,2-d1chloroethylene, either by Inhalation or oral administration, has
not been examined.
Pertinent data regarding the carclnogenlclty or developmental toxlclty
of ds-1,2-d1chloroethylene to animals or humans exposed by any route to
this chemical were not located 1n the available literature cited In Appendix
A. cls-1,2-D1chloroethylene yielded a positive result In a host-mediated
assay using £. cerlvlslae 07 strains In mice (Bronzettl et al., 1984) but
did not cause chromosomal aberrations or sister chromatid exchanges In
Chinese hamster cells 1n vitro (Sawada et al., 1987).
-------
Because of the lack of cancer data In either humans or animals, ds-1,2-
dlchloroethylene was assigned to U.S. EPA we1ght-of-ev1dence group D: cannot
be classified as to cardnogenldty to humans. Data were not available from
which to estimate potency slope factors or to assign an RQ for cardno-
genldty.
Sufficient chemlcal-spedf 1c subchronlc or chronic noncancer toxlclty
data were not available for derivation of RfD values for ds-l,2-d1chloro-
ethylene. The RfO of 0.009 mg/kg/day for chronic oral exposure to I,l-d1-
chloroethylene was adopted for subchronlc and chronic oral exposure to
ds-1,2-d1chloroethylene. The Agency had previously determined that the
metabolism and effects of exposure to the dlchloroethylenes are similar
(U.S. EPA, 1987a,b). Using similar logic, a previously derived chronic
toxlclty RQ of 1000 derived for 1,1-dlchloroethylene was adopted for
ds-1,2-d1chloroethylene.
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TABLE OF CONTENTS
Page
1. INTRODUCTION 1
1.1. STRUCTURE AND CAS NUMBER 1
1.2. PHYSICAL AND CHEMICAL PROPERTIES 1
1.3. PRODUCTION DATA 2
1.4. USE DATA 2
1.5. SUMMARY 2
2. ENVIRONMENTAL FATE AND TRANSPORT 4
2.1. AIR 4
2.1.1. Reaction with Hydroxyl Radicals 4
2.1.2. Reaction with Ozone and Other Oxldants 4
2.1.3. Photolysis 4
2.1.4. Physical Removal Processes 5
2.2. WATER .- 5
2.2.1. Hydrolysis 5
2.2.2. Oxidation 5
2.2.3. Photolysis 5
2.2.4. M1crob1al Degradation 5
2.2.5. Bloconcentratlon 6
2.2.6. Adsorption 6
2.2.7. Volatilization 6
2.3. SOIL 7
2.3.1. M1crob1al Degradation 7
2.3.2. Adsorption 7
2.3.3. Volatilization 7
2.4. SUMMARY 8
3. EXPOSURE 10
3.1. WATER 10
3.2. FOOD 11
3.3. INHALATION 11
3.4. DERMAL 11
3.5. OTHER 11
3.6. SUMMARY 12
1x
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TABLE OF CONTENTS (cent.)
Page
4. ENVIRONMENTAL TOXICOLOGY 13
4.1. AQUATIC TOXICOLOGY 13
4.1.1. Acute Toxic Effects on Fauna 13
4.1.2. Chronic Effects on Fauna 13
4.1.3. Effects on Flora 13
4.1.4. Effects on Bacteria ^_ 13
4.2. TERRESTRIAL TOXICOLOGY 13
4.2.1. Effects on Fauna 13
4.2.2. Effects on Flora 14
4.3. FIELD STUDIES 14
4.4. AQUATIC RISK ASSESSMENT 14
4.5. SUMMARY 14
5. PHARMACOKINETCS 15
5.1. ABSORPTION 15
, 5.2. DISTRIBUTION 15
5.3. METABOLISM 15
5.4. EXCRETION 16
5.5. SUMMARY 16
6. EFFECTS 19
6.1. SYSTEMIC TOXICITY 19
6.1.1. Inhalation Exposure 19
6.1.2. Oral Exposure 19
6.1.3. Other Relevant Information 20
6.2. CARCINOGENICITY 21
6.2.1. Inhalation 21
6.2.2. Oral 21
6.2.3. Other^ Relevant Information 21
6.3. GENOTOXICITY 21
6.4. DEVELOPMENTAL TOXICITY 25
6.5. OTHER REPRODUCTIVE EFFECTS 25
6.6. SUMMARY 25
7. EXISTING GUIDELINES AND STANDARDS 27
7.1. HUMAN 27
7.2. AQUATIC 27
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TABLE OF CONTENTS (cont.)
Page
8. RISK ASSESSMENT 28
8.1. CARCINOGENICITY 28
8.1.1. Inhalation 28
8.1.2. Oral 28
8.1.3. Other Routes 28
8.1.4. Weight of Evidence 28
8.1.5. Quantitative Risk Estimates 28
8.2. SYSTEMIC TOXICITY 28
8.2.1. Inhalation Exposure ... 28
8.2.2. Oral Exposure 29
9. REPORTABLE QUANTITIES 31
9.1. BASED ON SYSTEMIC TOXICITY 31
9.2. BASED ON CARCINOGENICITY 33
10. REFERENCES 34
APPENDIX A: LITERATURE SEARCHED 46
APPENDIX B: SUMMARY TABLE FOR ds-1,2-DICHLCIROETHYLENE 49
APPENDIX C: DOSE/DURATION RESPONSE GRAPH(S) FOR EXPOSURE TO
C1S-1.2-DICHLOROETHYLENE 50
x1
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LIST OF ABBREVIATIONS
AEL Adverse-effect level
BCF Bloconcentratlon factor
CAS Chemical Abstract Service
CS Composite score
PEL Frank effect level
HA Health advisory
HID Highest Ineffective dose
Koc Son sorptlon coefficient
Kow Octanol/water partition coefficient
L05Q Dose lethal to 50% of recipients
LOU Log dose unit
LEO Lowest effective dose
LOAEL Lowest-observed-adverse-effect level
MED Minimum effective dose
ppb Parts per billion
ppm Parts per million
RfD Reference dose
RQ Reportable quantity
RV(j Dose-rating value
RVe Effect-rating value
STEL Short-term exposure level
TLV Threshold limit value
TWA Time-weighted average
UV Ultraviolet
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1. INTRODUCTION
1.1. STRUCTURE AND CAS NUMBER
ds-l,2-D1ch1oroethylene 1s known by the synonyms els-acetylene
dkhlorlde, Z-acetylene dlchlorlde, ds-1,2-d1chlorethylene and Z-l,2-d1-
chlorethylene (Chemllne, 1989). The structure, CAS number, empirical
formula and molecular weight are as follows:
H
H
\
C=C
\
Cl
Cl
CAS Registry number: 156-59-2
Empirical formula: C-HpCl-
Molecular weight: 96.94
1.2. PHYSICAL AND CHEMICAL PROPERTIES
ds-1,2-D1chloroethylene Is a colorless; liquid at room temperature and
1s soluble 1n water and common polar or nonpolar organic solvents (Sax and
Lewis, 1987; Weast et al., 1988). It has a slight ether-Uke odor (Wlndholz
et al., 1983). Selected physical and chemical properties for ds-l,2-d1-
chloroethylene are given below:
Melting point: -80.5°C
Boiling point: 60.3°C
Water solubility at 25°C: 3500 mg/a.
Vapor pressure at 25°C: 215 mm Hg
Log Kow: 1.86
Flash point: 6°C
Conversion factors at 25°C: 1 ppm = 3.96 mg/m3;
1 mg/m3 =0.25 ppm
Weast et al., 1988
Weast et al., 1988
Horvath, 1982
Stevens, 1979
Hansch and Leo, 1985
Stevens, 1979
0267d
-1-
12/19/89
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1.3. PRODUCTION DATA
Between 1 and 11 million pounds of ds-1,2-dlchloroethylene was produced
In 1977 by PPG Industries at their production facilities 1n Lake Charles,
LA, and Ponce, Puerto R1co (TSCAPP, 1989). Production at the Lake Charles
plant was listed as site-limited. More recent production volume data are
not available.
cls-1,2-D1chloroethylene Is produced by the partial chlorlnatlon of
acetylene at 40°C. Separation from the trans-1somer 1s performed by
fractional distillation, ds-1,2-D1chloroethylene Is also produced as a
by-product of the manufacture of other chlorinated compounds (Stevens, 1979).
1.4. USE DATA
ds-1,2-D1chloroethylene Is used primarily as a chemical Intermediate In
the synthesis of other commercially significant chlorinated solvents.
ds-1,2-D1chloroethylene Is also used as a low-temperature extraction
solvent for organic materials such as dyes, perfumes, lacquers and thermo-
plastics, and as a solvent for organic synthesis (Stevens, 1979; Sax and
Lewis, 1987).
1.5. SUMMARY
cls-1,2-D1chloroethylene 1s a volatile, colorless liquid and Is soluble
In water and common polar or nonpolar organic solvents. In 1977, between 1
and 11 million pounds of cls-1,2-dlchloroethylene was produced by PPG
Industries at their production facilities In Lake Charles, LA, and Ponce,
Puerto R1co (TSCAPP, 1989). Recent production volume data are not avail-
able. ds-1,2-D1chloroethylene 1s produced by the partial chloMnation of
acetylene, and 1t 1s separated from the trans-lsomer by fractional distilla-
tion (Stevens, 1979). c1s-l,2-D1chloroethylene Is also produced during the
manufacture of other chlorinated solvents. Most ds-1,2-dlchloroethylene
0267d -2- 02/07/90
-------
produced commercially Is used directly In the synthesis of other chlorinated
solvents. It Is also used as a low temperature extraction solvent, a
solvent for organic synthesis and as a solvent for specialty applications
(Sax and Lewis, 1987; Stevens, 1979).
0267d -3- 12/19/89
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2. ENVIRONMENTAL FATE AND TRANSPORT
2.1. AIR
The vapor pressure of ds-1,2-d1chloroethylene (215 mm Hg) at 25°C
(Stevens, 1979) suggests that this compound will exist almost entirely In
the vapor phase 1n the atmosphere (Elsenrelch et al., 1981).
2.1.1. Reaction with Hydroxyl Radicals. The dominant atmospheric fate
process for ds-1,2-d1chloroethylene 1s expected to be destruction by the
gas phase reaction with photochemlcally produced hydroxyl radicals. Experi-
mental rate constants for this reaction have been determined at 2.0xlO"12
cmVmolecule-sec at 25°C (Goodman et al., 1986), Indicating a half-life of
8.3 days at an average atmospheric hydroxyl radical concentration of 5xl05
molecules/cm3.
2.1.2. Reaction with Ozone and Other Oxldants. Experimental data on the
gas phase reaction of ds-1,2-d1chloroethylene with ozone, nitrate radicals
or singlet oxygen Indicate that these reactions are too slow to be environ-
mentally significant (Atkinson and Carter, 1984; Atkinson et al., 1987;
Sanhueza and Helcklen 1975a,b). N1k1 et al. (1983) reported that the gas
phase reaction of ds-1,2-dlchloroethylene with ozone was a relatively rapid
reaction under controlled experimental conditions, but concluded that since
free radical scavengers drastically reduce the rate of this reaction, 1t 1s
not significant under atmospheric conditions.
2.1.3. Photolysis. The primary UV band for c1s-l ,2-d1chloroethylene
extends from -190-240 nm (Ausubel and Wljnen, 1975). Since this compound
does not adsorb significant amounts of radiation at wavelengths >290 nm,
atmospheric removal by direct photolytlc degradation Is not expected to be a
significant process.
0267d -4- 02/07/90
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2.1.4. Physical Removal Processes. 1,2-D1chloroethylene has been found
In rainwater (Kawamura and Kaplan, 1983). Wet depostlon from the atmosphere
Is a likely atmospheric removal process. Any 1,2-d1chloroethylene removed
from the atmosphere by this process, however, is expected to revolatHIze
rapidly to the atmosphere.
2.2. WATER
2.2.1. Hydrolysis. Hydrolysis of 1,2-d1chloroethylene 1n water Is
expected to be slow and should not be an environmentally significant fate
process (Jaber et al., 1984; Mabey et al., 1981).
2.2.2. Oxidation. Data specific to the chemical oxidation of ds-l,2-d1-
chloroethylene 1n water were not located In the available literature dted
In Appendix A. By analogy to other chlorinated ethylenes, H Is not
expected to be a significant process (DllUng et al., 1975).
2.2.3. Photolysis, ds-1,2-D1chloroethylene does not adsorb light 1n the
environmentally significant range >290 nm (Ausubel and Wljnen, 1975);
therefore, direct photochemical degradation 1n water Is not expected to be a
significant fate process.
2.2.4. M1crob1al Degradation. cls-1,2-D1chloroethylene undergoes slow
reductive dechlorlnatlon under anaerobic conditions. ds-1,2-D1chloro-
ethylene, when Incubated with methanogenlc aquifer material obtained near a
landfill, underwent mlcroblal degradation under anaerobic conditions. After
16 weeks, >98X of this compound had been removed by biological degradation
(Wilson et al., 1986). When 5 mg/a of ds-1,2-dlchloroethene was added to
anoxlc microcosms containing water and sediment, the half-life for removal
was 88-339 days. This compound degraded to chloroethane and vinyl chloride
(Barr1o-Lage et al., 1986).
0267d -5- 12/19/89
-------
c1s-l,2-D1chloroethylene has been found to resist mlcroblal attack under
aerobk conditions (Fogel et al., 1986). Tabak et al. (1981), however.,
determined that ds-1,2-dlchloroethylene was susceptible to biological
degradation, using a settled domestic wastewater Inoculum. In sediment
samples obtained from a cattail marsh, 660 ppb cls-1,2-dlchloroethylene
completely degraded after 50 hours under aerobic conditions with methane as
a secondary nutrient source (Fogel et al., 1986). It appears that aerobic
blodegradatlon of ds-1,2-dlchloroethylene may occur In the presence of
suitable microorganisms and nutrients.
2.2.5. B1oconcentrat1on. A BCF of 15 can be obtained for ds-l,2-dl-
chloroethylene using the linear regression equation log BCF - 0.76 log K
- 0.23 (Bysshe, 1982) and the KQW reported 1n Section 1.2. This value
suggests that bloaccumulatlon In fish and aquatic organisms 1s not expected
to be a significant fate process.
2.2.6. Adsorption. Soil adsorption coefficients ranging from 49-254 can
be estimated for ds-1,2-dlchloroethylene (Section 2.3.2.). These values
suggest that this compound will not adsorb strongly to soil, therefore, It
1s not expected to adsorb significantly to sediment and suspended organic
matter In aquatic systems.
2.2.7. Volatilization. An experimental Henry's Law constant of
4.08xlO~3 atm-mVmol at 24.8°C has been determined for cls-1,2-dlchloro-
ethylene (Gossett, 1987). Based on this value, the estimated volatilization
half-life from a model river 1 m deep, flowing at 1 m/sec with a wind
velocity of 3 m/sec Is ~3 hours (Thomas, 1982). In the laboratory, the
volatilization rate of ds-l,2-d1chloroethylene from a rapidly stirred
solution was determined and the author estimated that the corresponding
volatilization half-life from a body of water 1 m deep would be 5 hours
0267d -6- 12/19/89
-------
(D1ll1ng, 1977). It Is expected that volatilization from water to the
atmosphere will be a dominant fate process.
2.3. SOIL
2.3.1. M1crob1al Degradation. Limited data on the mlcroblal degradation
of ds-1,2-dlchloroethylene In soil were located 1n the available literature
dted 1n Appendix A. Experimental studies have shown that cls-1,2-dlchloro-
ethylene can undergo mlcroblal degradation using Inocula from groundwater
microcosms (Barr1o-Lage et a!., 1986; Wilson et al., 1986); therefore, this
compound may undergo biological degradation under anaerobic conditions In
soil. Henson et al. (1989) reported that a mixed culture of soil organisms
acclimated to chlorinated hydrocarbons completely degraded ds-1,2-dlchloro-
ethylene 1n 8 days under aerobic conditions using methane gas as a nutrient.
The biological degradation of ds-1,2-d1chloroethylene 1n soil, therefore,
appears to be a likely fate process under both aerobic and anaerobic
conditions.
2.3.2. Adsorption. A soil adsorption coefficient of 245 can be obtained
using the linear regression equation log K = 0.544 log K + 1.377
(Lyman, 1982) and the K reported In Section 1.2. Using the water
solubility reported In Section 1.2. 1n the regression equation log K =
-0.55 log S * 3.64 {Lyman, 1982), a K of 49 Is obtained. These values
suggest that ds-1,2-dlchloroethylene will be highly to moderately mobile In
soil (Swann et al., 1983); therefore, cls-1,2-dlchloroethylene has the
potential to leach Into groundwater.
2.3.3. Volatilization. The relatively high vapor pressure of cls-1,2-dl-
chloroethylene, 215 mm Hg (Stevens, 1979), and the expectation that this
compound will not adsorb strongly to soil (see Section 2.3.2.) suggest that
It will readily volatilize from the soil surface to the atmosphere.
0267d -7- 02/07/90
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2.4. SUMMARY
ds-1,2-01chloroethylene 1s expected to exist almost entirely In the
vapor phase In the atmosphere. Its atmospheric fate Is expected to be
dominated by the gas phase destruction by photochemlcally produced hydroxyl
radicals; the half-life for this process can be estimated at 8.3 days based
on an experimentally determined rate constant. Wet deposition of cls-1,2-
dlchloroethylene may occur; however, any compound removed from the atmo-
sphere by this process Is expected to volatilize again quickly. Neither
direct photochemical degradation nor gas phase destruction by ozone or other
chemical oxldants Is expected to occur to any significant extent In the
atmosphere.
The fate of cls-1,2-d1chloroethylene In surface water 1s expected to be
dominated by rapid volatilization to the atmosphere. The half-life for the
volatilization of ds-1,2-d1chloroethylene from a model river Is -3 hours.
Although mlcroblal degradation of ds-1,2-d1chloroethylene under anaerobic
conditions \s known to occur. It occurs at a slow rate. There are conflict-
ing data regarding the degradation of this compound under aerobic condi-
tions. It appears that some organisms are capable of degrading cls-1,2-d1-
chloroethylene under aerobic conditions If suitable nutritional sources are
present. The destruction of cls-1,2-dlchloroethylene In water by direct
photolysis or by abiotic chemical degradation 1s not expected to be signifi-
cant. cls-1,2-Olchloroethylene 1s not expected to bloconcentrate signifi-
cantly In fish and aquatic organisms nor Is It expected to adsorb to
sediment and suspended organic matter.
Limited experimental data on the fate of cls-1,2-d1chloroethylene In
soil were located 1n the available literature. It may be highly mobile In
soil and leach Into groundwater. cls-1,2-D1chloroethylene will volatilize
0267d -8- 12/19/89
-------
readily from the soil surface to the atmosphere. It Is expected to undergo
slow mlcroblal degradation 1n anoxlc soils and groundwater. A recent
experiment Indicated that this process may also occur under aerobic
conditions with certain microorganisms if secondary nutritional sources are
available.
0267d -9- 12/19/89
-------
3. EXPOSURE
1,2-D1chloroethylene may be released to the atmosphere 1n emissions from
Us production and use and by the volatilization from contaminated
wastewater or from waste disposal sites. It can be formed from the pyroly-
sls or combustion of poly(v1nyl)chlor1des and some vinyl copolymers (Mkhal,
1976; Shen, 1982). 1,2-01chloroethylene Is known to enter the environment
as a result of the anaerobic breakdown of other chlorinated solvents, most
notably tetrachloroethane and 1,1,2-trlchloroethylene (CUne and V1ste,
1985; Hallen et a!., 1986; Parsons et al., 1984).
According to an occupational survey conducted by NIOSH (1989), 215
people are potentially exposed to 1,2-d1chloroethylene In the workplace.
Occupational exposure may occur by Inhalation of 1,2-d1chloroethylene vapors
or dermal contact during Us production or use.
3.1. WATER
ds-1,2-D1chloroethylene has been detected 1n drinking water, ground-
water and surface water. It has been qualitatively detected In the drinking
water of Philadelphia, PA (Suffet et al., 1980). In a survey of drinking
water supplies conducted throughout the United States, ds-1,2-d1chloro-
ethylene was found 1n 16 of 466 random sites at a maximum concentration of
2.0 ppb, and 1n 38 of 479 nonrandom sites at a maximum concentration of 120
i
ppb (WestMck et al., 1984). It was detected 1n samples taken from the
Indian River, FL, at a concentration of 4.0-48.1 ppb {Wang et al., 1985).
In groundwater surveys, ds-1,2-dlchloroethylene was detected In Nebraska
(2.9 ppb maximum concentration) and Wisconsin (Goodenkauf and Atkinson,
1986; KM11 and Sonzognl, 1986). cls-1,2-D1chloroethylene has also been
detected In groundwater samples obtained near sites of chlorinated organic
0267d -10- 02/07/90
-------
solvent use or hazardous waste sites (Cllne and V1ste, 1985; S1lka and
Wallen, 1988; Wang et al., 1985) and In the leachate from landfills (Sabel
and Clark, 1984).
3.2. FOOD
Pertinent data regarding human exposure to ds-1,2-d1chloroethylene In
food were not located 1n the available literature dted 1n Appendix A.
3.3. INHALATION
In a recent compilation and analysis of ambient levels of volatile
organic compounds In the atmosphere, Shah and Heyerdahl (1988) determined
that the median dally urban level of ds-1,2-d1chloroethylene was 0.050 ppb,
based on an analysis of 124 data points. The levels were below the limits
of detection 1n suburban or rural areas. Given the above value, and using
the average volume of air Inhaled by an adult human (20 m3), the median
dally Inhalation Intake of cls-1,2-d1chloroethylene by the urban population
can be calculated at 3.96 wg/day. Since ds-1,2-d1chloroethylene has been
found In tap water, human exposure may occur by Inhalation of vapors that
have volatilized from the water during showers and other uses of household
water.
/
3.4. DERMAL
Pertinent data regarding dermal exposure to ds-1,2-dlchloroethylene
were not located 1n the available literature, dted in Appendix A. Since
ds-l,2-d1chloroethylene has been detected 1n tap water, 1t Is likely that
the general population may be dermally exposed to this compound while
showering or bathing with contaminated water.
3.5. OTHER
Pertinent data regarding other routes of exposure to ds-1,2-dlchloro-
ethylene were not located In the available literature cited 1n Appendix A.
0267d -11- 12/19/89
-------
3.6. SUMMARY
ds-l,2-D1chloroethylene may be released to the atmosphere 1n emissions
from Us production and use and from the volatilization from contaminated
wastewater or from waste disposal sites, ds-1,2-D1chloroethylene may also
be released to the environment as a result of the combustion of poly(vlnyl)-
chloMde polymers or as a result of the biological breakdown of other
chlorinated solvents.
Occupational exposure to ds-1,2-d1chloroethylene may occur by Inhala-
tion or dermal contact during Us manufacture, transportation or use as a
solvent or chemical Intermediate. Exposure by Inhalation 1s also likely 1n
areas, such as landfills, where ds-1,2-d1chloroethylene 1s discarded.
ds-1,2-01chloroethylene has been detected 1n surface water, ground-
water, rainwater and drinking water. Consequently, exposure to the general
population can occur by drinking contaminated water. Since ds-l,2-d1-
chloroethylene has been detected 1n tap water, exposure to the general
population may occur by dermal contact or Inhalation while bathing or
showering. ds-1,2-D1chloroethylene has also been detected 1n urban air
samples. Based on an analysis of urban air levels of ds-1,2-d1chloro-
ethylene (Shah and Heyerdahl, 1988), a median dally Inhalation Intake can be
calculated as 3.96 pg/day. Sufficient data are not available to
accurately estimate human exposure to 1,2-d1chloroethylene by other routes
of exposure.
0267d -12- 02/07/90
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4. ENVIRONMENTAL TOXICOLOGY
4.1. AQUATIC TOXICOLOGY
4.1.1. Acute Toxic Effects on Fauna. Pertinent data regarding the
effects of acute exposure of aquatic fauna to ds-1,2-d1ch1oroethylene were
not located 1n the available literature cited 1n Appendix A.
4.1.2. Chronic Effects on Fauna.
4.1.2.1. TOXICITY — Pertinent data regarding the effects of chronic
exposure of aquatic fauna to ds-1,2-d1chloroethylene were not located 1n
the available literature dted 1n Appendix A.
4.1.2.2. BIOACCUMULATION/BIOCONCENTRATION — Pertinent data regarding
the b1oaccumulat1on/b1oconcentrat1on potential of cls-1,2-dlchloroethylene
In aquatic fauna were not located In the available literature cited 1n
Appendix A.
4.1.3. Effects on Flora.
4.1.3.1. TOXICITY — Pertinent data regarding the toxic effects of
exposure of aquatic flora to ds-1,2-dlchloroethylene were not located In
the available literature cited 1n Appendix A.
4.1.3.2. BIOCONCENTRATION — Pertinent data regarding the bloconcen-
tratlon potential of ds-1,2-dlchloroethylene In aquatic flora were not
located 1n the available literature dted In Appendix A.
4.1.4. Effects on Bacteria. Pertinent data regarding the effects of
exposure of aquatic bacteria to ds-l,2-d1c:hloroethylene were not located In
the available literature dted In Appendix A.
4.2. TERRESTRIAL TOXICOLOGY
4.2.1. Effects on Fauna. Pertinent data regarding the effects of
exposure of terrestrial fauna to ds-1,2-dlchloroethylene were not located
In the available literature dted 1n Appendix A.
0267d -13- 12/19/89
-------
4.2.2. Effects on Flora. Pertinent data regarding the effects of
exposure of terrestrial flora to ds-l,2-d1chloroethylene were not located
In the available literature cited In Appendix A.
4.3. FIELD STUDIES
Pertinent data regarding the effects of ds-1,2-d1chloroethylene on
flora and fauna In the field were not located In the available literature
cited 1n Appendix A.
4.4. .AQUATIC RISK ASSESSMENT
Pertinent data regarding the effects of exposure of freshwater fauna and
flora to ds-1,2-d1chloroethylene were not located In the available litera-
ture cited In Appendix A. Acute studies with representatives from eight
families of freshwater fauna and at least three chronic studies and one
bloconcentratlon study with freshwater fauna and flora are needed to develop
a freshwater criterion by the method of U.S. EPA/OWRS (1986).
Pertinent data regarding the effects of exposure of marine fauna and
flora to cls-1,2-d1chloroethylene were not located In the available litera-
ture cited 1n Appendix A. Acute studies with representatives from eight
families of marine fauna and at least three chronic studies and one
bloconcentratlon study with marine fauna and flora are needed to develop a
saltwater criterion by the method of U.S. EPA/OWRS (1986).
4.5. SUMMARY
Pertinent data regarding the environmental toxlclty of ds-1,2-dlchloro-
ethylene were not located In the available literature cited In Appendix A.
0267d -14- 12/19/89
-------
5. PHARMACOKINIETICS
5.1. ABSORPTION
Fllser and Bolt (1979) exposed male Wlstar rats 1n a closed Inhalation
system to >500 ppm cls-1,2-d1chloroethylene and monitored the decline of the
concentration 1n the gas phase to determine the equilibration of atmospheric
cls-1,2-d1chloroethylene with the whole body. Concentrations of cls-1,2-dl-
chloroethylene In the system declined markedly for the first 1.5 hours,
Indicating rapid absorption. Data were not sufficient to estimate the rate
or extent of respiratory absorption.
Pertinent data regarding the gastrointestinal absorption of ds-1,2-
dlchloroethylene were not located 1n the available literature dted In
Appendix A. U.S. EPA (1987a), however, noted that the compound Is neutral,
UpophlUc, and has low molecular weight. Thus, the chemical should be
readily absorbed by any natural route of exposure.
5.2. DISTRIBUTION
Pertinent data regarding tissue distribution for cls-1,2-d1chloro-
ethylene following Inhalation, oral or dermal exposure of animals or humans
were not located 1n the available literature dted 1n Appendix A. U.S. EPA
(1987a), however, predicted that the highest levels of the compound would be
located In the liver and kidney, assuming this compound behaves similarly to
the structurally related 1,l-d1chloroethylene (McKenna et al., 1978).
5.3. METABOLISM
Bonse et al. (1975) reported that perfuslon of the Isolated rat liver
with ds-1,2-dlchloroethylene resulted 1n the production of dlchloroethanol
and dlchloroacetlc acid. The Initial step 1n the metabolism of ds-l,2-d1-
chloroethylene may Involve the formation of chloroethylene epoxlde, which
undergoes rearrangement to form dlchloroacetaldehyde (Henschler, 1977;
Lelbman and Ortiz, 1977).
0267d -15- 02/07/90
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According to Costa and Ivanetlch (1982), multiple forms of hepatic
mlcrosomal cytochrome P-450 bind and metabolize cls-1,2-dlchloroethylene.
These Investigators Identified 2,2-dlchloroethanol and dlchloroacetaldehyde
in rat hepatic microsomes Incubated 1n the presence of an NADPH-generatlng
system, EDTA, and cls-1,2-d1chloroethylene. 2-Chloroethanol, chloroacet-
aldehyde or chloroacetlc acid were not produced In significant amounts In
these Incubation mixtures. The Investigators proposed the metabolic scheme
presented 1n Figure 5-1 and Indicated that the nonenzymatlc rearrangement
would be expected to favor a chloride shift rather than a hydride shift.
The metabolic elimination of Inhaled cls-1,2-d1chloroethylene was
examined In male Wlstar rats exposed In a closed Inhalation system (Fllser
and Bolt, 1979). Metabolic elimination was described as a saturable
phenomenon, changing from a first-order to a zero-order process at 20 ppm.
Fllser and Bolt (1980) detected acetone 1n the expired air from male
Wlstar rats exposed 1n a closed Inhalation system to cls-1,2-dlchloro-
ethylene. The Investigators postulated that metabolites of ds-l,2-d1-
chloroethylene may Inhibit enzymes of the citric add cycle, resulting In
acetonemla and the exhalation of acetone. Acetone was not considered a
metabolite of ds-1,2-d1chloroethylene.
5.4. EXCRETION
Pertinent data regarding the excretion of ds-1,2-dlchloroethylene
following Inhalation, oral or dermal exposure of animals or humans were not
located 1n the available literature cited In Appendix A.
5.5. SUMMARY
Pharmacoklnetlc data for c1s-l,2-dlchloroethylene are limited. Gas
uptake studies in rats Indicated that ds-1,2-dlchloroethylene Is absorbed
readily from the respiratory tract (Fllser and Bolt, 1979). Because the
0267d -16- 12/19/89
-------
C IHC-CHC
/ \
C I HC—CHC I
I«• Shift
non-*nz ymIc
r«orrong«minI
HjO
C I H2CCOCI —* C I H2CC02H
•* C h I » r I d • i h I H
CIjHCCHO —- C IjHCCOjH
I
C 12 H C C H 2 0 H
FIGURE 5-1
Proposed Metabolic Scheme for the 1,2-01chloroethylenes
Source: Costa and Ivanetlch, 1982
0267d
-17-
12/19/89
-------
compound 1s neutral, UpophlUc, and has low molecular weight, H Is
expected to be readily absorbed by any natural route of exposure (U.S. EPA,
1987a). Although tissue distribution data were not located, the highest
tissue levels would be expected 1n the liver and kidneys (U.S. EPA, 1987a),
If this compound behaves similarly to 1,l-d1chloroethylene (McKenna et al.,
1978).
ds-1,2-D1chloroethylene Is metabolized by hepatic cytochrome P-450
oxIdasBs, with the formation of dlchloroacetaldehyde and dlchloroethanol
(Costa and Ivanetlch, 1982). The Initial step 1n the metabolism probably
Involves formation of a chloroethylene epoxlde that undergoes rearrangement
to dlchloroacetaldehyde (Henschler, 1977; Lelbman and Ortiz, 1977).
Metabolic elimination of ds-1,2-d1chloroethylene was described as a satur-
able process, changing from a first-order to a zero-order process at 20 ppm
(Fllser and Bolt, 1979).
Pertinent data regarding the excretion of ds-1,2-d1chloroethylene
following oral, Inhalation or dermal exposure were not located In the
available literature cited 1n Appendix A.
0267d -18- 02/07/90
-------
6. EFFECTS
6.1. SYSTEMIC TOXICITY
6.1.1. Inhalation Exposure.
6.1.1.1. ACUTE — In an unpublished study, Smyth (1937-1955)
determined that 8000 ppm ds-1,2-dlchloroethylene was not lethal to rats
exposed for 4 hours. However, rats were anesthetized In 8 minutes and died
within 4 hours after exposure to 16,000 ppm. Narcosis 1s a primary effect
1n animals exposed to ds-1,2-d1chloroethylene by Inhalation (Smyth,
1937-1955). ds-l,2-01chloroethylene also produces narcosis 1n humans
exposed to high concentrations of this chemical (ACGIH, 1986).
Freundt and Macholz (1978) showed that a single 8-hour Inhalation expo-
sure to 200, 600 or 1000 ppm ds-1,2-dlchloroethylene resulted 1n signifi-
cant, dose-dependent Increases In hexobart>1tal sleeping time, zoxazolamlne
paralysis times and the metabolic formation of 4-am1noant1pyr1ne from amlno-
pyrlne 1n adult female Wlstar rats. These Increases Indicated an Inter-
action with the mixed-function oxldase system,
6.1.1.2. SUBCHRONIC -- Pertinent data regarding the toxkHy of
ds-1,2-d1chloroethylene following subchronlc Inhalation exposure of animals
or humans were not located 1n the available literature dted 1n Appendix A.
6.1.1.3. CHRONIC -- Pertinent data regarding the toxldty of ds-1,2-
dlchloroethylene following chronic Inhalation exposure of animals or humans
were not located 1n the available literature dted 1n Appendix A.
6.1.2. Oral Exposure.
6.1.2.1. SUBCHRONIC -- Pertinent data regarding the toxldty of
cls-1,2-dlchloroethylene following subchronlc oral exposure of animals or
humans were not located 1n the available literature dted 1n Appendix A.
0267d -19- 07/20/90
-------
6.1.2.2. CHRONIC -- Pertinent data regarding the toxldty of ds-1,2-
dlchloroethylene following chronic oral exposure of animals or humans were
not located In the available literature dted 1n Appendix A.
6.1.3. Other Relevant Information. Quast et al. (1983) administered
1,l-d1chloroethylene, an Isomer of ds-1,2-d1chloroethylene, 1n drinking
water to Sprague-Dawley rats for 2 years at concentrations of 0, 50, 100 and
200 ppm. Experimental groups were composed of 48 rats/sex, while 80
rats/sex formed the control group. Adjusted doses for continuous exposure
were estimated by the Investigators at 0, 7, 10 or 20 mg/kg/day 1n males and
0, 9, 14 or 30 mg/kg/day In females. No statistically significant
differences between treated and control groups were seen regarding survival
time, body weight, food and water consumption, hematology, clinical
chemistry, urlnalysls and gross pathology. Furthermore, the authors could
not establish a relationship between exposure to 1 ,l-d1chloroethylene and
neoplastlc changes. Females In all treated groups, however, and males 1n
the highest dose group developed hepatic lesions described as
"hepatocellular swelling with mldzonal fatty change." Acute LD5Q data for
ds-1,2-dlchloroethylene have not been reported. Jenkins et al. (1972)
evaluated the hepatotoxlclty of ds-1,2-dlchloroethylene 1n rats. Groups of
three or four adult Holtzman rats were given ds-1,2-dlchloroethylene as a
single dose of either 400 or 1500 mg/kg^ by gavage In corn oil.
ds-1,2-D1chloroethylene significantly elevated the activity of liver
alkaline phosphatase at the 400 and 1500 mg/kg doses. The activities of
liver glucose-6-phosphatase, liver tyroslne transamlnase and plasma alanlne
transamlnase decreased at the 1500 mg/kg dose. It should also be noted that
although there 1s little data to Implicate ds-1,2-dlchloroethylene as a
neurotoxlcant, 1t 1s structurally similar to trlchloroethylene which Is a
neurotoxlc agent.
0267d -20- 07/20/90
-------
6.2. CARCINOGENICITY
6.2.1. Inhalation. Pertinent data regarding the cardnogenldty of
ds-l,2-d1chloroethylene following Inhalation exposure of humans or animals
were not located 1n the available literature cited 1n Appendix A.
6.2.2. Oral. Pertinent data regarding the cardnogenldty of ds-l,2-d1-
chloroethylene following oral exposure of humans or animals were not located
In the available literature dted 1n Appendix A.
6.2.3. Other Relevant Information. Other relevant Information regarding
the cardnogenldty of ds-1,2-d1chloroethylene were not located 1n the
available literature dted 1n Appendix A.
6.3. GENOTOXICITY
Relevant genotoxldty data for ds-l,2-d1chloroethylene are presented In
Table 6-1. The pattern 1s predominantly negative 1n prokaryotes and weakly
positive 1n eukaryotes. In In vitro studies 1n prokaryotes, neither
ds-1,2-d1chloroethylene alone (Cerna and Kypenova, 1977) nor In a mixture
with the trans- Isomer (Mortelmans et al.,, 1986) Induced reverse mutations
with or without metabolic activation 1n Salmonella typhlmurlum. In the
absence of activation, neither forward nor reverse mutations were Induced In
Escherkhla coll K12 (Grelm et al., 1975); however, Cerna and Kypenova
(1977) reported positive results with S. typhlmurlum using the host-mediated
assay 1n female ICR mice. In liquid suspensions of strain 07 of Saccharo-
^ _«M.^^^^—
myces cerevlslae. ds-l,2-d1chloroethylene Induced a slight but significant
dose-related Increase In ade~ recomblnants 1n the presence of metabolic
activation but only at one concentration In the absence of activation. In
the same system, an Increase In 1lv* reverse point mutations was Induced
at one concentration 1n the absence of activation (Bronzettl et al., 1984;
Gain et al., 1982). The compound had sporadic effects on the number of
0267d -21- 07/25/90
-------
TABLE 6-1
Genotoxlclty Testing of cls-1,2-D1chloroethylene
I
rv>
l\3
i
Assay
Reverse
nutation
Forward
mutation
Nilotic
recombination
Indicator
Organism
Salmonella
typhlmurlum
TA1535. TA1537,
TA98. TA100
S. typhlmurlum
TA9B. TA100.
TA1535. TA1538.
TA1950, TA1951.
TA1952
S. typhlmurlum
TA1950. TA1951.
TA1952
Escherlchla coll
K12 (gal*, arg*.
nad*)
E. coll K12
(5-methyl
tryptophan
resistance)
Saccharomyces
cerevlslae 07
Application
liquid
suspension
spot test
host-mediated
assay In female
ICR mice
liquid
suspension
liquid
suspension
liquid
suspension
Purity
(X)
els-trans
mixture
NR
NR
analytical
grade
analytical
grade
97
Concentration
or Dose
33.3-3333.3
tig/plate
0.5. 5. 50
rag/plate
0.5. 1 time
L050
2.9 mM
2.9 mM
40. 80. 100 mM
Activating
System
+/- rat and
hamster liver
S9
NA
+/- mouse liver
mlcrosomal pro-
tein and NADH
generating
system
*/- mouse liver
mlcrosomal pro-
tein and NAOH
generating
system
»/- mouse liver
mlcrosomal pro-
Response Comment
-/- NC
Applied 0.05 ml of 1.
10. 100X per plate
« Dose-effect relation-
ship reported
NC
NC
+/(*) Dose-dependent toxlclty
with lower survival
Reference
Mortelmans
et al.. 1986
Cerna and
Kypenova. 1977
Cerna and
Kypenova. 1977
Grelm et al. ,
1975
Grelm et al..
1975
Gall et al..
1982; Bronzettl
teln and NADH
generating
with S9; dose-dependent
production of ade*
recomblnants with S9
and at 100 mM without
S9; llv* revertants
at 100 mM without S9
et al.. 1984
03
O
-------
6-1 (cont.)
Assay
Gene
conversion
Indicator Application
Organism
S. cerevlslae 07 liquid
suspension
Purity Concentration Activating
(X) or Dose System
97 40. 80. 100 nfl »/- mouse liver
mlcrosomal pro-
tein and NADH
generating
Response Comment
-/- Dose-dependent toxldty
with lower survival
with S9; dose-dependent
production of ade*
recomblnants with S9
and at 100 mH without
S9; llv* revertants
at 100 mH without S9
Reference
Gall
1982;
et al
et al..
Bronzettl
.. 1984
Point
mutation
S. cerevlslae 07 liquid
suspension
97
40. 80. 100 nfl
Gene
conversion
S. cerevlslae 07
CO
i
Point
mutation
S. cerevlslae 07
o Sister
^ chromatld
•M exchange
\
o
Chinese hamster
fIbroblasts
»/- mouse liver
mlcrosomal pro-
tein and NADH
generating
Intrasangulneous
hose-mediated
assay In male
Swiss albino mice
by gavage
97
1300 mg/kg once NA
Intrasangulneous
hose-mediated
assay In male
Swiss albino mice
by gavage
97
300 mg/kg/day.
8 days «• 600
mg/kg 9th day
NA
cell culture
97
0.25-2 mg/mt
rat liver S9.
NADP
-/(*) Dose-dependent toxldty
with lower survival
with S9; dose-dependent
production of ade*
recomblnants with S9
and at 100 mH without
S9; llv* revertants
at 100 mH without S9
(») In acute tests, trp*
convertants In liver,
not kidney or lung,
and llv* revertants In
kidney, not liver or
lung: with repeated
dosing, convertants In
lung, liver or kidney
and revertants In kidney
and lung, not liver
(») In acute tests, trp*
convertants In liver,
not kidney or lung,
and llv* revertants In
kidney, not liver or
lung; with repeated
dosing, convertants In
lung, liver or kidney
and revertants In kidney
and lung, not liver
NC
Gall et al..
1982; Bronzettl
et al.. 1984
Bronzettl
et al.. 1984
Bronzettl
et al.. 1984
Sawada et al.,
1987
-------
TABLE 6-1 (cont.)
o
rvi
cr>
Assay
Chromosomal
aberrations
Indicator
Organism
Chinese hamster
flbroblasts
female ICR mice
Application
cell culture
Intraperltoneal
Injection
Purity
(X)
97
NR
Concentration
or Dose
0.25-2 mg/mi
0.5 x LOso.
single dose
Activating
System
rat liver S9.
NADP
NA
Response
NC
Comment
No significant differ-
ence with a single dose
Reference
Sawada et al..
1987
Cerna and
Kypenova. 1977
female ICR mice
Intraperltoneal
Injection
NR
0.167 x LD5o.
5-10 times
dally
NA
but Increased cells
with aberrations with
5 dally doses; dose-
dependence seen 6 hours
after 10th dose
No significant differ-
ence with a single dose
but Increased cells
with aberrations with
5 dally doses; dose-
dependence seen 6 hours
after 10th dose
Cerna and
Kypenova. 1977
NA •= Not applicable; NC « no comment; NR • not reported; ( + ) •= weakly positive
in
^
O
-------
trpf convertants and 11vf reverse point mutations 1n yeast of the same
strain recovered from various organs In an Intrasangulneous host-mediated
assay (Bronzettl et al.. 1984). In the one mammalian In vitro assay
located, ds-1,2-dlchloroethylene did not Induce chromosomal aberrations or
sister chromatld exchanges 1n Chinese hamster cells In vivo (Sawada et al.,
.1987). Ln vivo. H Induced chromosomal aberrations 1n the bone marrow of
IntraperHoneally Injected mice (Cerna and Kypenova, 1977).
6.4. DEVELOPMENTAL TOXICITY
Pertinent data regarding the teratogenldty of ds-l,2-d1chloroethylene
were not located In the available literature cited 1n Appendix A.
6.5. OTHER REPRODUCTIVE EFFECTS
Pertinent data regarding other reproductive effects of cls-1,2-dlchloro-
ethylene were not located In the available literature cited In Appendix A.
6.6. SUMMARY
Acute Inhalation exposure of animals or humans to high concentrations of
ds-l,2-d1chloroethylene vapors can produce anesthesia and narcosis (Smyth,
1937-1955; ACGIH, 1986). In rats, exposure to 16,000 ppm ds-1,2-dlchloro-
ethylene for 4 hours resulted 1n death (Smyth, 1937-1955).
The results of an acute oral toxlclty study 1n rats provided biochemical
evidence that ds-l,2-d1chloroethylene Is hepatotoxlc (Jenkins et al.,
1972). ds-l,2-D1chloroethylene significantly elevated the activity of
liver alkaline phosphatase at the 400 and 1500 mg/kg dose levels. The
activities of liver glucose-6-phosphatase, liver tyroslne transamlnase and
plasma alanlne transamlnase decreased at the 1500 mg/kg dose level.
The systemic toxldty resulting from subchronlc or chronic exposure to
ds-1,2-d1chloroethylene, either by Inhalation or oral administration, has
0267d -25- 07/25/90
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not been examined. It should be noted that although there Is Uttle data to
Implicate ds-l,2-d1chloroethylene as a neurotoxlcant, 1t 1s structurally
similar to trlchloroethylene which 1s a neurotoxlc agent.
Pertinent data regarding the .< carclnogenlcHy or teratogenldty of
cls-1,2-d1chloroethylene to animals or humans exposed by any route to this
chemical were not located 1n the available literature cited In Appendix A.
ds-1,2-D1chloroethylene yielded a positive result In a host-mediated assay
using S. cerlvlslae D7 strains In mice (Bronzettl et al., 1984) but did not
cause chromosomal aberrations or sister chromatld exchanges In Chinese
hamster cells in vitro (Sawada et al., 1987).
0267d -26- 07/25/90
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7. EXISTING GUIDELINES AND STANDARDS
7.1. HUMAN
ACGIH (1989) has not adopted TLVs for ds-1,2-d1chloroethylene; however,
the currently recommended TWA-TLV for the commercial mixture of the ds- and
trans-lsomers Is 200 ppm (790 mg/m3), based on a no-effect level of 1000
ppm 1n animals (ACGIH, 1986). Because the no-effect level for prolonged
animal Inhalation 1s -1000 ppm, ACGIH (1986) regards the TLV as sufficiently
conservative and does not recommend a STEL for the mixture. OSHA (1989)
also does not 11st a value for cls-1,2-dlchloroethylene but lists transi-
tional and final rule limits of 200 ppm (790 mg/m3) for the commercial
mixture, which Is Identical to the ACGIH (1989) recommendation. The 1-day,
10-day, longer-term and lifetime HAs recommended for cls-1,2-dlchloro-
ethylene by U.S. EPA (1987a) were 4, 1, 1 and 0.07 mg/l (child), respec-
tively. The longer-term HA for an adult was 3.5 mg/l. Only the 1-day
advisory was computed from data generated by exposure to cls-1,2-dlchloro-
ethylene; the other values were derived from experiments with 1,1-dlchloro-
ethylene.
7.2. AQUATIC
Guidelines and standards to protect aquatic life from exposure to
ds-1,2-d1chloroethylene were not located lin the available literature cited
1n Appendix A.
0267d -27- 02/07/90
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8. RISK ASSESSMENT
8.1. CARCINOGENICITY
8.1.1. Inhalation. Pertinent data regarding the cardnogenldty of
Inhalation exposure of humans or animals to cls-1,2-dlchloroethylene were
not located 1n the available literature cited In Appendix A.
8.1.2. Oral. Pertinent data regarding the cardnogenldty of oral
exposure of humans or animals to ds-l,2-d1chloroethylene were not located
In the available literature dted 1n Appendix A.
8.1.3. Other Routes. Pertinent data regarding the cardnogenldty of
ds-1,2-d1chloroethylene to humans or animals exposed by other routes were
not located 1n the available literature cited 1n Appendix A.
8.1.4. Weight of Evidence. Because data were not located regarding the
cardnogenldty of ds-1,2-dlchloroethylene In humans or In animals, the
compound Is most appropriately placed 1n U.S. EPA we1ght-of-evldence Group
D: not classifiable as to human cardnogenldty (U.S. EPA, 1986b).
8.1.5. Quantitative Risk Estimates. The absence of cancer data by either
the Inhalation or oral routes precludes derivation of potency slope factors
for either route of exposure.
8.2. SYSTEMIC TOXICITY
8.2.1. Inhalation Exposure.
8.2.1.1. LESS THAN LIFETIME (SUBCHRONIC) ~ Pertinent data regarding
the toxlclty of subchronlc Inhalation exposure to ds-1,2-dlchloroethylene
were not located 1n the available literature cited In Appendix A. As
discussed In Section 8.2.2.2., 1n the absence of chemical-specific data, it
Is appropriate to consider deriving an RfD for ds-1,2-dlchloroethylene
based on analogy to 1,1-dlchloroethylene. Inhalation data for 1,1-dlchloro-
ethylene abound and have been reviewed by U.S. EPA (1986c), but no RfD has
0267d -28- 12/19/89
-------
been derived for Inhalation exposure. It Is beyond the scope of this
document to evaluate the data on 1,1-dkhloroethylene to derive RfD values
for Inhalation exposure to that chemical. Therefore, 1t Is not currently
possible to derive an RfD for subchronlc Inhalation exposure to ds-l,2-d1-
chloroethylene by analogy to 1,1-dlchloroethylene.
8.2.1.2. CHRONIC — Pertinent data regarding chronic Inhalation
exposures to cls-1,2-dlchloroethylene were not located 1n the available
literature dted 1n Appendix A. As discussed above, 1t Is appropriate to
consider deriving an RfD for ds-1,2-d1chloroethylene based on analogy to
1,1-dlchloroethylene. The lack of an RfD for chronic Inhalation exposures
to 1,1-dlchloroethylene, however, precludes derivation of an RfD for
c1s-l,2-d1chloroethylene by analogy to 1 ,l-d1chloroethylene.
8.2.2. Oral Exposure.
8.2.2.1. LESS THAN LIFETIME (SUBCHRONIC) — Pertinent data regarding
the toxldty of subchronlc oral exposures to ds-1,2-dlchloroethylene were
not located 1n the available literature, cited In Appendix A. Chemical-
specific data are not sufficient for derivation of an RfD for subchronlc
oral exposures to ds-1,2-dlchloroethylene. Therefore, the chronic oral RfD
of 0.009 mg/kg/day derived by 'analogy to 1,l-d1chloroethylene In Section
8.2.2.2. Is adopted as the RfD for subchronlc oral exposure to ds-l,2-dl-
chloroethylene. Confidence In the key study Is medium; confidence in the
data base and RfD are low, as explained 1n Section 8.2.2.2.
8.2.2.2. CHRONIC — Pertinent data regarding chronic oral exposures
to ds-1,2-dlchloroethylene were not located in the available literature
dted In Appendix A. Because chemical-specific data are not sufficient for
derivation of an RfD, It 1s appropriate to consider data from chemicals that
are structurally and tox1colog1cally similar. Structurally similar
0267d -29- 12/19/89
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chemicals that could be considered Include trans-1,2-d1chloroethylene and
I,l-d1chloroethylene. U.S. EPA (1989) derived an oral chronic RfD of 0.02
mg/kg/day for trans-1,2-d1chloroethylene from a subchronlc drinking water
rat study and an RfD of 0.009 mg/kg/day for 1 ,l-d1chloroethylene. In
deriving lifetime HAs for els- and trans-1,2-d1chloroethylene (see Section
7.1.). U.S. EPA (1987a,b) evaluated data for 1,1-, ds-1,2- and trans-1,2-
dlchloroethylene and concluded that the noncardnogenlc effects of these
compounds are essentially Identical. Pharmacok1net1c data for the 1,1- and
l,2-1somers (U.S. EPA, 1986c) Indicate that the metabolism of all three
Isomers Is similar and Involves the formation of an epoxlde Intermediate.
Additionally,, the proposed metabolism scheme for 1,2-d1chloroethylene by
Costa and Ivanetlch (1982) postulates that a chloride shift would be favored
to the exclusion of a hydride shift (see Section 5.3.). U.S. EPA (1987a,b)
determined that the most conservative approach was to base derivation of the
lifetime has for the c1s-l,2-1somer on analogy to 1,l-d1chloroethylene,
which seems to follow a metabolic pathway very similar to the
cls-1,2-1somer. Pursuing the precedent of U.S. EPA (1987a,b), the verified
RfD of 0.009 mg/kg/day for chronic oral exposure to 1,1-dlchloroethylene Is
adopted as the RfD for chronic oral exposure to cls-1,2-d1chloroethylene.
The RfD of 0.009 mg/kg/day was based on a LOAEL of 9 mg/kg/day for liver
effects In a 2-year drinking water study using rats (Quast et al., 1983).
As stated by U.S. EPA (1989), confidence 1n the study 1s medium. Confidence
In the data base for mixed 1,2-d1chloroethylene Is low; confidence In the
RfD Is low because of the additional uncertainty associated with basing an
RfD on analogy to a similar chemical. NTP (1989) Indicated that
ds-1,2-dlchloroethylene has been selected for toxldty testing. These
tests, when completed, may permit derivation of chemical-specific RfD values.
0267d -30- 02/07/90
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9. REPORTABLE QUANTITIES
9.1. BASED ON SYSTEMIC TOXICITY
The toxldty of cls-1,2-d1chloroethylene was reviewed and evaluated 1n
Chapter 6. Pertinent data regarding systemic toxldty consequent to
subchronlc or chronic exposure to ds-1,2-d'ichloroethylene by either oral or
Inhalation exposure of humans or animals were not located 1n the available
literature cited 1n Appendix A. Therefore, an RQ cannot be derived for this
compound from chemical-specific data. An RQ of 1000, however, has been
derived by U.S. EPA (1986c) for the other two dlchloroethylene Isomers,
trans-1,2-d1chloroethylene and 1,l-d1chloroethylene. The former represents
a CS of 13.8, based on fat accumulation 1n the liver and hlstologlcal
alterations 1n the lungs of six rats exposed to 200 ppm
trans-1,2-d1chloroethylene 8 hours/day, 5 days/week for 16 weeks (Freundt et
a!., 1977). The latter represents a CS of 19.0, based on early deaths and
terminations among 12 mice exposed to 55 ppm 1,l-d1chloroethylene 6
hours/day, 5 days/week for 10 months with 12 months observation (Hong et
al., 1981). As discussed In Chapter 8, 1t Is appropriate, when
chemical-specific data are lacking, to derive risk assessment values based
on analogy to a chemical that Is structurally and lexicologically similar.
To maintain consistency with the approach used 1n Chapter 8, the RQ for
mixed 1,2-d1chloroethylene Isomers will be based by analogy on the
1,1-lsomer. Moreover, the key study for the l,l-1somer Is of a higher
quality, since H uses more animals and Is of longer duration. Therefore,
an RQ of 1000 Is recommended for cls-1,2-d'ichloroethylene, based on analogy
to I,l-d1chloroethylene (Table 9-1).
0267d -31- 02/07/90
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TABLE 9-1
ds-1,2-D1chloroethylene
Minimum Effective Dose (MED) and Reportable Quantity (RQ)
Route: Inhalation
Species/Sex: mice/male, female
Dose*: 259 mg/day
Duration: 10 months (with 12 months observation)
Effect: postexposure mortality and morlbundlty
RVd: 1.9
RVe: 10
CS: 19.0
RQ: 1000
Reference: Hong et al., 1981
*Equ1valent human dose
0267d -32- 12/19/89
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9.2. BASED ON CARCINOGENICITY
Pertinent data regarding the cardnogenlcHy of ds-1,2-d1chloroethylene
In humans or In animals were not located In the available literature dted
In Appendix A. Therefore, cis-1,2-dkhloroethylene Is most appropriately
placed 1n U.S. EPA we1ght-of-ev1dence Group D: not classifiable as to human
cardnogenlcHy (U.S. EPA, 1986b). No hazard ranking 1s assigned to
chemicals In Group 0; therefore, an RQ based on cardnogenlcHy cannot be
assigned.
0267d -33- 12/19/89
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Wang, T.C., R. Lenahan, M. Kanlck, et al. 1985. The removal of trkhloro-
ethylene contaminated groundwater at Vero Beach, Florida. Arch. Environ.
Contam. ToxUol. 14: 719-723.
Weast, R.C., M.J. Astle and W.H. Beyer.. 1988. CRC Handbook of Chemistry
and Physics, 69th ed. CRC Press, Inc., Boca Raton, PL. p. C-272.
0267d -44- 07/25/90
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Westrlck, J.J., J.W. Hello and R.F. Thomas. 1984. The groundwater supply
survey. J. Am. Water Works Assoc. 76: 52-59.
Wilson, B.H., G.B. Smith and J.F. Rees. 1986. Blotransformatlon .of
selected aklylbenzenes and halgenated aliphatic hydrocarbons In methanogenlc
aqulfler material: A microcosm study. Environ. Scl. Technol. 20: 997-1002.
Wlndholz, M., Ed., et al. 1983. The Merck Index. Merck and Co., Rahway,
NJ. p. 13-14.
0267d -45- 07/25/90
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APPENDIX A
LITERATURE SEARCHED
This HEED 1s based on data Identified by computerized literature
searches of the following:
CHEMLINE
TSCATS
CASR online (U.S. EPA Chemical Activities Status Report)
TOXLINE
TOXLIT
TOXLIT 65
RTECS
OHM TADS
STORET
SRC Environmental Fate Data Bases
SANSS
. AQUIRE
TSCAPP
NTIS
Federal Register
CAS ONLINE (Chemistry and Aquatic)
HSDB
SCISEARCH
Federal Research in Progress
These searches were conducted in July, 1989, and the following secondary
sources were reviewed:
ACGIH (American Conference of Governmental Industrial Hygienists).
1986. Documentation of the Threshold Limit Values and Biological
Exposure Indices, 5th ed. Cincinnati, OH.
ACGIH (American Conference of Governmental Industrial Hygienists).
1987. TLVs: Threshold Limit Values for Chemical Substances in the
Work Environment adopted by ACGIH with Intended Changes for
1987-1988. Cincinnati, OH. 114 p.
Clayton, G.D. and F.E. Clayton, Ed. 1981. Patty's Industrial
Hygiene and Toxicology, 3rd rev. ed., Vol. 2A. John Wiley and
Sons, NY. 2878 p.
Clayton, G.D. and F.E. Clayton, Ed. 1981. Patty's Industrial
Hygiene and Toxicology, 3rd rev. ed., Vol. 28. John Wiley and
Sons, NY. p. 2879-3816.
0267d -46- 02/07/90
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Clayton, G.D. and F.E. Clayton, Ed. 1982. Patty's Industrial
Hygiene and Toxicology, 3rd rev. ed.,, Vol. 2C. John Wiley and
Sons, NY. p. 3817-5112.
Grayson, M. and D. Eckroth, Ed. 1978-1984. K1rk-0thmer Encyclo-
pedia of Chemical Technology, 3rd ed. John WHey and Sons, NY. 23
Volumes.
Hamilton, A. and H.L. Hardy. 1974. Industrial Toxicology, 3rd ed.
Publishing Sciences Group, Inc., Littleton, MA. 575 p.
IARC (International Agency for Research on Cancer). IARC Mono-
graphs on the Evaluation of Carcinogenic Risk of Chemicals to
Humans. IARC, WHO, Lyons, France.
Jaber, H.M., W.R. Mabey, A.T. L1u, T.W. Chou and H.L. Johnson.
1984. Data Acquisition for Environmental Transport and Fate
Screening. Prepared by the Office of Health and Environmental
Assessment, Washington, DC. for the Office of Solid Waste, and
Emergency Response, Washington, DC. EPA 600/6-84-009. NT1S
PB84-243906, PB84-243955. p. 45.
NTP (National Toxicology Program). 1987. Toxicology Research and
Testing Program. Chemicals on Standard Protocol. Management
Status.
Ouellette, R.P. and J.A. King. 1977. Chemical Week Pesticide
Register. McGraw-Hill Book Co., NY.
Sax, I.N. 1984. Dangerous Properties of Industrial Materials, 6th
ed. Van Nostrand Relnhold Co., NY.
SRI (Stanford Research Institute). 1987. Directory of Chemical
Producers. Menlo Park, CA.
/
U.S. EPA. 1986. Report on Status Report In the Special Review
Program, Registration Standards Program and the Data Call In
Programs. Registration Standards and the Data Call In Programs.
Office of Pesticide Programs, Washington, DC.
USITC (U.S. International Trade Commission). 1986. Synthetic
Organic Chemicals. U.S. Production and Sales, 1985, USITC Publ.
1892, Washington, DC.
Verschueren, K. 1983. Handbook of Environmental Data on Organic
Chemicals, 2nd ed. Van Nostrand Relnhold Co., NY.
Wlndholz, M., Ed. 1983. The Merck Index, 10th ed. Merck and Co.,
Inc., Rahway, NJ.
Worthing, C.R. and S.B. Walker, Ed. 1983. The Pesticide Manual.
British Crop Protection Council. 695 p.
0267d -47- 02/07/90
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In addition, approximately 30 compendia of aquatic toxldty data were
reviewed, Including the following:
Battelle's Columbus Laboratories. 1971. Water Quality Criteria
Data Book. Volume 3. Effects of Chemicals on Aquatic Life.
Selected Data from the Literature through 1968. Prepared for the
U.S. EPA under Contract No. 68-01-0007. Washington, DC.
Johnson, W.W. and M.T. Flnley. 1980. Handbook of Acute Toxldty
of Chemicals to F1sh and Aquatic Invertebrates. Summaries of
Toxldty Tests Conducted at Columbia National Fisheries Research
Laboratory. 1965-1978. U.S. Dept. Interior, F1sh and Wildlife
Serv. Res. Publ. 137, Washington, DC.
McKee, J.E. and H.W. Wolf. 1963. Water Quality Criteria, 2nd ed.
Prepared for the Resources Agency of California, State Water
Quality Control Board. Publ. No. 3-A.
Plmental, D. 1971. Ecological Effects of Pesticides on Non-Target
Species. Prepared for the U.S. EPA, Washington, DC. PB-269605.
Schneider, B.A. 1979. Toxicology Handbook. Mammalian and Aquatic
Data. Book 1: Toxicology Data. Office of Pesticide Programs, U.S.
EPA, Washington, DC. EPA 540/9-79-003. NTIS PB 80-196876.
0267d -48- 12/19/89
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APPENDIX B
Summary Table for c1s-1.2-01chloroethylene
Species
Inhalation Exposure
Subchronlc ID
Chronic ID
Carclnogenlclty 10
Oral Exposure
Subchronlc rat
Chronic rat
Carclnogenlclty ID
REPOBTABLE QUANTITIES
Based on chronic toxlclty:
Based on Carclnogenlclty:
Exposure
10
ID
ID
50 ppro 1.1-dlchloroethylene
In drinking water for 2 years
(9 mg 1.1-dlchloroethylene/kg/day)
50 ppm 1,1-dlchloroethylene
In drinking water for 2 years
(9 sag 1.1-dlchlorosthylene/kg/day)
J ID
1000*
10
Effect RfO or q]*
ID ID
ID ID
10 ID
LOAEL for 0.009
liver lesions mg/kg/day*
LOAEL for 0.009
liver lesions mg/kg/day*
10 ID
Reference
NA
NA
NA
Quasi
et al.. 1983
Quast
et al.. 1983
NA
Hong et al . .
1981
NA
•Values derived for 1.1-dlchloroethylene adopted for 1,2-dlchloroethylene mixed Isomers based on analogy
10 - Insufficient data; NA = not applicable
CD
10
-------
APPENDIX C
DOSE/DURATION RESPONSE GRAPHS FOR EXPOSURE TO ds-1,2-OICHLOROETHYLENE
C.I. DISCUSSION
Dose/duration-response graphs for Inhalation and oral exposure to
ds-1,2-d1chloroethylene, generated by the method of Crockett et al. (1985)
using the computer software by Durkin and Meylan (1988) developed under
contract to ECAO-Clnclnnatl are presented 1n Figures C-l through C-3. Data
used to generate these graphs are presented 1n Section C.2. In the genera-
tion of these figures, all responses are classified as adverse (FEL, AEL or
LOAEL) or nonadverse (NOEL or NOAEL) for plotting. The ordlnate expresses
Inhalation exposure In either of two ways. In Figure C-l, the experimental
concentration, expressed as mg/m3, was multiplied by the time parameters
of the exposure protocol (e.g., hours/day and days/week), and Is presented
as expanded experimental concentration [expanded exp cone (mg/m3)]. In
Figure C-2, the expanded experimental concentration was multiplied by the
animal Inhalation rate 1n mVday and divided by the animal body weight In
kg to calculate a dally dose In mg/kg/day. The dally dose was then multi-
plied by the cube root of the ratio of the anlmaV.human body weight to
adjust for species differences In metabolic rate (Mantel and Schnelderman,
1975). The result was multiplied by an absorption coefficient of 0.5 to
adjust to an equivalent absorbed dose and then multiplied by 70 kg, the
reference human body weight, to express the human equivalent dose as mg/day
for a 70 kg human [human equlv dose (mg/day)]. For oral exposure, the
ordlnate expresses dose as human equivalent dose. The animal dose In
mg/kg/day Is multiplied by the cube root of the ratio of tbe animal :human
body weight to adjust for species differences In basal metabolic rate
(Mantel and Schnelderman, 1975). The result Is then multiplied by 70 kg,
0267d -50- 12/19/89
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9
U
0
U
X
t
Q
t1
c
t
&
X
fc!
•1800"
100
I I
8.001
(Inhalation Exposure)
0.01
HUMRN EQUIU DURflTIOH (fraction lifespan)
ENVELOP METHOD
Key: F . FEL
L - LOAEL
N . NOEL
Solid line - Adverse Effects Boundary
Dashed line » No Adverse Effects Boundary
FIGURE C-l
Dose/Duration-Response Graph for Inhalation Exposure to
c1s-D1chloroethy!ene: Envelope Method (Expanded Experimental Concentration)
0267d
-51-
12/19/89
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A
>
«
\
9
V
•0
fi
0
u
I
v
1080
I I I
0.001
(Inhalation Exposure)
J I
e.ei
HUMRN EOUIU DURRIION (fraction lifespan)
ENUELOP METHOD
Key: F . FEL
L - LOAEL
N . NOEL
Solid line • Adverse Effects Boundary
Dashed line - No Adverse Effects Boundary
FIGURE C-2
Dose/Duration-Response Graph for Inhalation Exposure to
ds-l,2-D1chloroethylene: Envelope Method (Human Equivalent Dose)
0267d
-52-
12/19/89
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V
U
(!)
0
a
M
0
•i
1808
i i r
LI
8.001
(Oral Exposure)
e.ei
HUMflN EQUIU DURflTION (fraction lifespan)
Key: L - LOAEL
FIGURE C-3
Dose/Duration-Response Graph for Oral Exposure to
ds-1,2-D1chloroethylene: Envelope Method
0267d
-53-
12/19/89
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the reference human body weight, to express the human equivalent dose as
mg/day for a 70 kg human [human equlv dose (mg/day)].
The adverse effects boundary (solid line) 1s drawn by Identifying the
lowest adverse effect dose or concentration at the shortest duration of
exposure at which an adverse effect occurred. From this starting point, an
Infinite line 1s extended upward, parallel to the dose axis. The starting
point 1s then connected to the lowest adverse effect dose or concentration
at the next longer duration of exposure that has an adverse effect dose or
concentration equal to or lower than the previous one. This process Is
continued to the lowest adverse effect dose or concentration. From this
point, a line parallel to the duration axis 1s extended Infinitely to the
right. The adverse effects region lies above the adverse effects boundary.
Using the envelope method, the no adverse effects boundary (dashed line)
Is drawn starting with the point representing the highest no adverse effects
dose or concentration. From this point, a line parallel to the duration
axis Is extended to the dose or concentration axis. The starting point is
then connected to the next equal or lower no adverse effect dose or concen-
tration at a longer duration of exposure. When this process can no longer
be continued, a line parallel to the dose or concentration axis 1s dropped
to the duration axis. The no adverse effects region lies below the no
adverse effects boundary. At both ends of the graph between the adverse
effects and no adverse effects boundaries are regions of ambiguity. The
area (1f any) resulting from Intersections of the adverse effects and no
adverse effects boundaries Is defined as the region of contradiction.
In the censored data method, all no adverse effect points located In the
region of Contradiction are dropped from consideration, and the No Adverse
effects boundary Is redrawn so that It does not Intersect the Adverse
0267d -54- 02/07/90
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effects boundary and no region of contradiction 1s generated. This method
results In the most conservative definition of the no adverse effects region.
F1gue C-l represents the dose/duration response graph of Inhalation data
expressed as expanded concentration and generated by the envelope method.
The boundary for the region of adverse effects 1s defined by a PEL (Rec. #1)
for anesthesia In 8 minutes followed by death within 4 hours In rats
Inhaling 1600 ppm cls-1,2-d1chloroethylene and a LOAEL (Rec. #3) for dose-
dependent Increases 1n hexobarbHal sleeping time, zoxalamlne paralysis time
and Increased formation of 4-am1noant1pyr1ne from amlnopyrlne, Indications
of Interaction with the mixed function ox'idases In rats Inhaling 200 ppm.
The boundary for the region of no adverse effects Is defined by a single
NOEL (Rec. #2) for absence of fatalities In rats Inhaling 8000 ppm ds-1,2-
dlchloroethylene. No region of contradiction was generated by overlap of
the boundaries; hence, there 1s no need for use of the censored method.
Figure C-2 represents the same data expressed as the human equivalent dose.
Data were insufficient for the derivation of an Inhalation RfD.
Figure C-3 presents the dose/duration response graph of oral data
generated by the envelope method. Since there 1s only one datum (a LOAEL
for Increased liver alkaline phosphatase activities 1n rats dosed once with
400 mg/kg, used to construct the graph) (Rec. #1) no boundaries can be
drawn, no region of contradiction can be generated, and there Is no need for
use of the censored method. Data regarding oral exposure to ds-l,2-d1-
chloroethylene were Insufficient for derivation of an RfD. Adoption of the
verified oral RfD for the l,l-1somer of the compound was recommended Instead.
0267d -55- 07/25/90
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C.2. DATA USED TO GENERATE DOSE/DURATION-RESPONSE GRAPHS
C.2.1. Inhalation Exposure.
Chemical Name:
CAS Number:
Document Title:
Document Number
Document Date:
Document Type:
ds-1 ,2-d1chloroethylene
156-59-2
Health and Environmental
ds-1 ,2-dichloroethylene
NR
NR
HEED
Effects Document on
========================
RECORD #1: Species:
Sex:
Effect:
Route:
================
Rats
NR
PEL
Inhalation
Body Weight:
Reported Dose:
Converted Dose:
Exposure Period:
Duration Observation:
Molecular Weight:
Inhalation hours/day:
Inhalation days/week:
# Inhal. Exp. days:
0.35 kg
1600 ppm
6340 mg/m3
1 day
1 day
4.00
Comment:
Citation:
Comment:
Citation:
Number Exposed: NR
Number Responses: NR
Type of Effect: DEATH
SHe of Effect: BODY
Severity Effect: 10
Given 8000, 16,000 ppm
Death within 4 hours
continuous exposure.
Smyth, 1937-1955
4 hours. Anesthesia In 8 minutes.
after exposure. Not expanded to
RECORD #2: Species:
Sex:
Effect:
Route:
Rats
NR
NOEL
Inhalation
Body Wt:
Reported Dose:
Converted Dose:
Exposure Period:
Duration Observation:
Molecular Weight:
Inhalation hours/day:
Inhalation days/week:
# Inhal . Exp. days:
0.35 kg
8000 ppm
3170 mg/m3
1 day
1 day
4.00
Number Exposed: NR
Number Responses: 0
Type of Effect:
Site of Effect:
Severity Effect: 10
See previous record.
Smyth, 1937-1955
0267d
-56-
02/07/90
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RECORD #3:
Comment:
Citation:
Species:
Sex:
Effect:
Route:
Rats
F ema1e
LOAEL
Inhalation
Number Exposed: 10
Number Responses: NR
Type of Effect: ENZYM
SHe of Effect: BODY
Severity Effect: 1
Body Weight:
Reported Dose:
Converted Dose:
Exposure Period:
Duration Observation:
Molecular Weight:
Inhalation hours/day:
Inhalation days/week:
# Inhal. Exp. days:
8
NR
ENZYM
LIVER
1
0.35 kg
200 ppm
793 mg/m3
day
day
8.00
Given 0, 200, 600, 1000 ppm, not expanded to continuous
exposure. Dose-dependent Increase 1n hexobarbltal sleeping
time, zoxazolamlne paralalysls time (8 rats), and Increased
formation of 4-am1no-ant1pyr1ne In liver mlcrosomes (10 rats).
Freundt and Macholz, 1978
C.2.2. Oral Exposure.
Chemical Name: c1s-l,2-D1chloroethylene
CAS Number:
Document Title:
Document Number:
Document Date:
Document Type:
156-59-2
Health and Environmental Effects Document on
ds-1,2-D1chloroethylene
NR
NR
HEED
RECORD #1
Comment:
Citation:
Species:
Sex:
Effect:
Route:
Rats
Male
LOAEL
Gavage
Body Weight:
Reported Dose:
Converted Dose:
Exposure Period:
Duration Observation: 1 day
Number Exposed: 4
Number Responses: NR
Type of Effect: ENZYM
SHe of Effect: LIVER
Severity Effect: 1
Given 0, 400, 1500 mg/kg, single dose.
liver alkaline phosphatase activity.
Jenkins et al., 1972
0.35 kg
400 mg/kg/day
400 mg/kg/day
1 day
Significant Increase In
NR = Not reported
0267d
-57-
02/07/90
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