^ March 31, 1987
820K87003
TRANS-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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trans-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.
156-60-5
Structural Formula
1,2-DCE; trans-1,2-DCE; 1,2-dichloroethene
0 In a mixture with the cis-1,2- isomer, as captive intermediates in
the production of other chlorinated solvents.
Properties (Irish, 1963; Windholz et al., 1976)
Chemical Formula
Molecular Weight
Physical State
Freezing Point
Boiling Point
Melting Point
Density
Vapor Pressure
Specific Gravity
Water Solubility
Log Octanol/Water Partition
Coefficient
Taste Threshold (water)
Odor Threshold (water)
Odor Threshold (air)
1 mg/L
1 ppm
C2H2C12
96.95
clear, colorless liquid
-49.4°C
47°C
265 mm Hg (25°C)
1.27 (25°C)
6300 ug/L (25°)
Not available
Not available
1,100 ppm (Lehmann and Schmidt-Kehl, 1936)
252 ppm (25°c and 760 Torr.)
3.97 mg/m3 (25°c and 760 Torr.)
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trans-1,2-Dichloroethylene March 31, 1987
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Occurrence
0 The 1,2-dichloroethylenes are synthetic chemicals with no known natural
sources (U.S. EPA, 1983).
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 used
as captive intermediates. Releases are expected to be small. The 1,2-
dichloroethylenes, particularly the cis- isomer, have been identified
as 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-dichlo-
roethylenes in the environment. However, the behavior of these
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 degrade chemically 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, 1,2-di-
chloroethylenes are expected to migrate with ground water. 1,2-Di-
chloroethylenes have been shown to degrade biologically 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.
0 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 are greater than 0.5 ug/L in approximately 1 % of all
ground waters. 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. The 1,2-dichloroethylenes in air are in the opt range
except near production sites where they may reach the low ppb range.
Based upon their volatility and limited use, levels of 1,2-dichloro-
ethylenes in foo'd 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.
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III. PHARMACOKINETICS
Absorption
0 trans-1,2-Dichloroethylene is a neutral, low molecular weight, lipid
soluble material which should be readily absorbed by any route (oral,
inhalation, dermal) at the levels expected to be encountered in
contamination incidents (U.S. EPA, 1984a).
Distribution
0 Kinetic data to define the tissue distribution of trans-1,2-dichloro-
ethylene after oral exposure are not available. If this isomer follows
the same absorption and distribution pattern as 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. In rat liver microsomal preparations,
supplemented with NADPH, trans-1,2-dichloroethylene was transformed to
2,2-dichloroethanol and 2,2-dichloroacetic acid (Costa and Ivanetich,
1982). Presumably, these products were formed by reduction or oxidation
of 2,2-dichloroacetaldehyde.
0 The positions of the chlorine moieity on the chlorinated ethylenes
appear to play an important role in metabolism. Trans-1,2-dichloro-
ethylene (which possesses a relatively greater degree of asymmetry)
was metabolized at a slower rate than cis-1,2-dichloroethylene in an
in vitro hepatic microsomal system (Costa, 1983).
Excretion
No data concerning the excretion of trans-1,2-dichloroethylene are
available. If it is similar to 1,1-dichloroethylene, then the rate
of elimination will 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 (Irish, 1963). It appears that
the trans- isomer is about twice as potent as the cis- isomer in
depressing the central nervous system (Albrecht, 1927).
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Animals
Short-term Exposure
0 The oral LD5Q in the 200 g rat was 1,300 mgA9 (Freundt et al., 1977).
When administered intraperitoneally, the LD50 was six-fold higher
(7,800 mg/kg).
0 At high exposure (8,000 to 16,000 ppm) levels, trans-1,2-dichloroethylene
can cause narcosis and death in rats in four hours (Torkelson and Rowe,
1981).
0 No significant immunological effects were observed in male mice
exposed by gavage to 22 or 220 mg/kg for 14 consecutive days (Munson
et al., 1982). In addition, no changes in body or organ weights
(liver, kidney, thymus and lung) were observed.
Long-term Exposure
0 Freundt et al. (1977) exposed Wistar rats to air containing trans-1,2-
dichloroethylene at 0, 200, 1,000 or 2,000 ppm (0 to 7,940 mg/m3).
Brief (8-hour) or prolonged (8 hours/day, 5 days/week for 1, 2, 8 or
16 weeks) exposure at 200 ppm produced slight degeneration of the
liver lobule and lipid accumulation in the Kupffer cells. At 8 and
16 weeks of exposure, severe pneumonic infiltration was observed.
Exposure at 1000 ppm for 8 hours resulted in significant reductions
in serum albumin, urea nitrogen and alkaline phosphatase. Eight-hour
exposures at both 200 and 1,000 ppm produced a significant decrease
in the number of leucocytes.
Reproductive Effects
0 No information was found in the available literature on the potential
of trans-1,2-dichloroethylene to produce reproductive effects.
Developmental Effects
0 No information was found in the available literature on the potential
of trans-1,2-dichloroethylene to produce developmental effects.
Mutagenicity^
0 trans-1,2-Dichloroethylene at a medium concentration of 2.3 mM was
not mutagenic, with or without microsomal activation, when assayed
in £. coli K12 (Greim et al., 1975).
0 trans-1,2-Dichloroethylene did not cause point mutation, mitotic gene
conversion or mitotic recombination in a diploid strain of Saccharomyces
cerevisiae, with or without microsomal activation (Galli et al. (1982a).
They also reported that it had no genetic effects in an in vivo (intra-
venous host-mediated assay) mutagenicity study (Galli et al., 1982b).
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Carcinogenicity
0 No information was found in the available literature on the carcinogenic
potential of trans-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) . /L ( /L)
(UF) x ( L/day)
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
Freundt et al. (1977) reported the effects of trans-1,2-dichloroethylene
after inhalation by mature female Wistar rats (180 to 200g) at 200 ppm (800
mg/m3, the currently established TLV/MAC in many countries) or at 1000 or
3000 ppm (4000 or 12000 mg/rn3, respectively). A brief (8 hour) exposure at
200 ppm did not result in significant adverse effects on the liver. There
was slight pulmonary capillary hyperemia and distention of the alveolar
septum. This effect was, most likely, transitory in nature and would not
occur after oral administration.
A number of biochemical and hematological parameters also were tested.
No changes in serum cholesterol, albumin, uric acid, urea nitrogen, glucose,
alkaline phosphatase, SCOT or SGPT were observed after the single 8-hour
exposure at 200 ppm. Exposure at 1,000 ppm for 8 hours resulted in significant
reductions in serum albumin, urea nitrogen and alkaline phosphatase. Eight-
hour exposures at both 200 and 1,000 ppm caused a significant decrease in the
number of leucocytes. Since leucocyte count may be affected by external
stimuli [physical exertion, stress and food intake (Lentner, 1984)], the
number of leucocytes in this study (2.5 x 103) appears to be lower than normal
for rats [6 to 17 x 103/mm3 (Harkness and Agner, 1983)] and there is no dose
response noted in the 200 and 1,000 ppm groups, it is difficult to evaluate
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trans-1,2-Dichloroethylene March 31, 1987
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the reported decrease in leucocytes. Accordingly, this parameter will not be
used in setting the NOAEL. Clinico-chemical parameters were not studied at
the 3,000 ppm exposure level.
A NOAEL of 200 ppm over a single 8-hour exposure was identified for
trans-1,2-dichloroethylene based upon the normal biochemical parameters and
on the slight liver effects in only 1 of 6 rats.
The One-day Health Advisory for the 1 0-kg child is calculated as follows:
Step 1: Determination of the total absorbed dose (TAD)
TAD = 200 x 3.97 (mg/m3) x 0.006 (m3/hr) x 8 = 2QQ -
(0.19 kg) y/ y
where:
200 x 3.97 (mg/m3) = total absorbed dose converted from ppm to mg/m3.
0.006 = conversion factor to obtain m3/hr for 190 g rats,
i.e., 100 ml/min x 60 min/hr divided by 1,000,000
(ml to m3).
8 = duration of exposure in hours.
0.19 = average weight in kg of exposed rats.
Step 2: Determination of a One-day Health Advisory
One-day HA = (200 mg/kg/day) (10 kg) = 2Q.O mg/L (20,000 ug/L)
(100) (1 L/day)
where:
200 mgAg/day = TAD.
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.
Ten-day Health Advisory^
Appropriate studies for the calculation of the Ten-day HA are not available.
The Longer-term HA for a 10 kg child (1.43 mg/L) is recommended as a conservative
estimate for a ten-day exposure.
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Longer-term Health Advisory
Freundt et al. (1977) also studied the effects of administering trans -
1,2-dichloroethylene at 200 ppm (8 hr/day for 5 days/week) for 16 weeks.
They found slight to severe fatty infiltration in the parenchymal and Kupffer
cells of the liver (5 of 6 rats) and severe pneumonic infiltration (3 of 6
rats).
Based on the liver and lung effects, a LOAEL of 200 ppm was identified
for trans-1,2-dichloroethylene.
The Longer-term HA is calculated as follows:
Step 1: Determination of the total absorbed dose (TAD)
TAD = 200 mgAg (see One-day HA)
Step 2: Determination of a Longer-term HA for a 10-kg child
Longer-term HA = (200 mg/kg/day) (5) (10 kg) = U43 /L (1,43o Ug/L)
(1,000) (7) (1 L/day)
where:
200 mg/kg/day = LOAEL for hepatic and pulmonary effects.
5/7 = correction factor for 5 day/week dosing regimen.
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 = assunved daily water consumption of a child.
A Longer-term HA for a 70-kg adult is calculated as follows:
Longer-term HA = (200 mg/kg/day) (5) (70 kg) = 5 /L (5,000 ug/L)
(1,000) (7) (2 L/day)
where:
200 mg/kg/day = LOAEL for hepatic and pulmonary effects.
5/7 = correction factor for 5 day/week dosing regimen.
70 kg = assumed body weight of an adult.
1,000 = uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a LOAEL from an animal study.
2 L/day =-assumed daily water consumption of an adult.
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trans-1,2-Dichloroethylene March 31, 1987
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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 trans-1,2-dichloroethylene do not exist
at this time. Data from the chronic drinking water study in rats as used
for the Lifetime Health Advisory for 1,1-dichloroethylene will be used in-
stead. The same caveats and assumptions as were described above for the
Longer-term HA also apply here.
The Lifetime HA is calculated from a 2-year chronic study in rats (Quast
et al., 1983). 1,1-Dichloroethylene, at 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 change. 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 (DWEL) and Lifetime HA for the 70-kg
adult are calculated as follows:
Step 1: Determination of the Reference Dose (RfD)
RfD = (1° nig/kg/day) = 0.01 mg/kg/day
(1,000)
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trans-1, 2-Dichloroethylene March 31, 1987
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where:
10 mgAg/day = LOAEL.
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 /L (350 /L)
(2 L/day)
where:
0.01 mg/kg/day = RfD.
70 kg = assumed body weight of an adult.
2 L/day * assumed daily water consumption of an adult.
Step 3: Determination of the Lifetime Health Advisory
Lifetime HA = (0.035 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 which describe the carcinogenic potential
of trans-1,2-dichloroethylene.
0 Applying the criteria described in EPA's guidelines for assessment of
carcinogenic risk (U.S. EPA, 1986), trans-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/m^) (ACGIH, 1982)
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trans-1,2-Dichloroethylene March 31, 1987
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VII. ANALYTICAL METHODS
°- Analysis of trans-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 of
1/2-dichloroethylenes 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
measurement of 1,2dichloroethylene over a concentration range of
0.03 to 1500 ug/L. Confirmatory analysis for 1,2-dichloroethylene is
done by mass spectrometry (U.S. EPA, 1985a). The detection limit
for confirmation by mass spectometry is 0.2 ug/L.
VIII. TREATMENT TECHNOLOGIES
Very few data are available concerning the removal of trans-1,2-
dichloroethylene from drinking water. However, the available data
suggest that both granular activated carbon (GAC) adsorption and
aeration will be somewhat effective in reducing the levels of this
chemical in water.
Dobbs and Cohen (1980) developed adsorption isotherms for trans-1,2-
dichloroethylene. It was reported that Filtrasorb® 300 carbon
exhibited adsorptive capacities of 0.95 mg, 0.29 mg and 0.09 mg
trans-1,2-dichloroethylene/gm carbon at equilibrium concentrations of
100, 10 and 0.1 ug/L, respectively. No field data are available on
the adsorption of trans-1,2-dichloroethylene from contaminated water.
Theoretical considerations indicate that trans-1,2-dichloroethylene
is amenable to treatment by aeration on the basis of its Henry's Law
Constant of 225 atm (U.S. EPA 1985b,c). In a laboratory study,
distilled water containing 217 ug/L of trans-1,2-dichloroethylene
was passed through a diffused-air aeration column. A 97% reduction
of the compound was reported in a countercurrent operation at an
air-to-water ratio of 15:1 (U.S. EPA, 1985b,c).
Air stripping is an effective, simple and relatively inexpensive
process for removing trans-1,2-dichloroethylene and other volatile
organics from water. However, the use of this process then transfers
the contaminant directly into the air stream. When considering use
of air stripping 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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trans-1,2-Dichloroethylene March 31, 1987
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Costa, A.K. 1983. The chlorinated ethylenes: Their hepatic metabolism and
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Dobbs, R.A., and J.M. Cohen. 1980. Carbon absorption isotherms for toxic
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Filser, J.G., and H.M. Bolt. 1979. Pharmacokinetics of halogenated ethylenes
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Freundt, J.J., and J. Macholz. 1978. Inhibition of mixed function oxidases
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Galli, A., C. Bauer, G. Brenzetti, C. Corsi, R. Del Carratore, R. Nieri and
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Irish, D.D. 1963. Vinylidene chloride. In; F.A. Patty (ed), Industrial
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Lentner, C. 1984. Geigy Scientific Tables. Vol. 3, 8th Ed. Ciba-Geigy, Ltd.,
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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,
Toxicol. Appl. Pharmacol. 45:599-610.
Munson, A.E., V.M. Saunders, K.A. Douglas, L.E. Sain, B.M. Kauffman and
K.L. White, Jr. 1982. In vivo assessment of immunotoxicity. Environ.
Health Perspect. 43:41-52.
Parsons, P., P.R. Wood and J. DeMarco. 1984. Transformation of tetrachloro-
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76:56.
Qiast, J.F., C.G. Humiston, C.E. Wade, J. Ballard, J.E. Beyer, R.W. Schwetz
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