United States
       Environmental Protection
Drinking Water Health Advisory
  for 1,1,2,2-Tetrachloroethane

This page has been intentionally left blank

  Drinking Water Health Advisory
     for 1,1,2,2-Trichloroethane
            Prepared by:

Health and Ecological Criteria Division
   Office of Science and Technology
           Office of Water
U.S. Environmental Protection Agency
       Washington, DC 20460

  Document Number: 822-R-08-012
          Date: April, 2008

This page has been intentionally left blank


                               TABLE OF CONTENTS





  2.2     USES	4


  3.1     AIR	5
  3.2     FOOD	5
  3.3     WATER	5
  3.4     SOIL	6
  3.5     OTHER SOURCES	6


  4.1     HUMAN STUDIES	7
    4.1.1  Short-term Exposure	7
    4.1.2  Long-term Exposure	7
    4.1.3  Reproductive and Developmental Effects	7
    4.1.4  Carcinogenicity	7
  4.2     ANIMAL STUDIES	8
    4.2.1  Short-term Exposure	8
    4.2.2  Long-term Exposure	10
    4.2.3  Reproductive and Developmental Effects	10
    4.2.4  Genotoxicity	11
    4.2.5  Carcinogenicity	12
    4.3.1  Noncancer Effects	13
    4.3.2  Cancer Effects	13





9.0    REFERENCES	29
                                            iii                                April 2008

iv                                April 2008



TABLE 1. Physical and Chemical Properties	3
                                                                        April 2008

vi                                April 2008



This document was prepared by Oak Ridge National Laboratory, Oak Ridge, Tennessee, work
assignment 2006-002-2, under the U.S. EPA IAG Number DW-89-92209701. The Lead EPA
Scientist is Joyce Morrissey Donohue, Ph.D., Health and Ecological Criteria Division, Office of
Science and Technology, Office of Water, U. S. Environmental Protection Agency.
                                         vii                              April 2008

This page has been intentionally left blank
                  viii                                April 2008

                             LIST OF ABBREVIATIONS

ALT         alanine aminotransferase
AST         aspartate aminotransferase
atm          atmosphere
ATSDR      Agency for Toxic Substances and Disease Registry
BMD        benchmark dose
BMDL       benchmark dose lower confidence limit
BV          bed volumes
bw          body weight
CAS         Chemical Abstracts Registry
CHO         Chinese hamster ovary (cells)
CSF         cancer slope factor
DCA         dichloroacetic acid
DNA         deoxyribonucleic acid
DW         drinking water
DWI         drinking water intake
DWEL       drinking water equivalent level
FDA         Food and Drug Administration
GAC         granular activated carbon
gd           gestation day
GGT+       y-glutamyl transpeptidase-positive
HA          Health Advisory
HSDB       Hazardous Substance Data Bank
IARC        International Agency for Research on Cancer
IRIS         Integrated Risk Information System
kg           kilogram
Kow         octanol-water partition coefficient
L            liter
LD50         lethal dose for 50% of tested animals
LOAEL      lowest observed adverse effect level
m3           cubic meters
mg          milligram
min          minute
mL          milliliter
NCI         National Cancer Institute
NOAEL      no observed adverse effect level
NIOSH      National Institute for Occupational Safety and Health
NPL         National Priorities List
NTP         National Toxicology Program
OW         Office of Water
ppb          parts per billion
ppm         parts per million
ppt          parts per trillion
April 2008

RCRA       Resources Conservation and Recovery Act
RfD         reference dose
RR          relative risk
RSC         relative source contribution
SDH         sorbitol dehydrogenase
TRI         Toxics Release Inventory
UF          uncertainty factor
USGS        U.S. Geological Survey
U.S. EPA    U.S. Environmental Protection Agency
VOC         volatile organic compound
                                                                          April 2008

                                                                 1 , 1 ,2,2-Tetrachloroethane


The Health Advisory (HA) Program, sponsored by the Office of Water (OW), provides
information on the, environmental properties, health effects, analytical methodologies, and
treatment technologies for regulated and unregulated drinking water contaminants. HAs establish
nonregulatory concentrations of drinking water contaminants at which adverse health effects are
not anticipated to occur over specific exposure durations (one-day, ten-days, several years, and a
lifetime). HAs serve as informal technical guidance to assist Federal, State and local officials,
and managers of public or community water systems in 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.

The Health Effects Support Document for 1,1,2,2-Tetrachloroethane (U.S. EPA, 2006) is the
peer-reviewed, risk assessment that supports this HA. It can be accessed at
http://www.epa. gov/ogwdw/ccl/pdfs/reg_determine2/healtheffects_ccl2-
                                 will provide a more comprehensive summary of the
available data. The less than lifetime HA values were independently peer reviewed by the Office
of Water.
                                                                            April 2008

           April 2008


2.1 Physical and Chemical Properties

1,1,2,2-tetrachloroethane is a chlorinated hydrocarbon that is occasionally found as a
contaminant in treated drinking water.  At room temperature the pure compound is a

Synonyms: Acetylene tetrachloride; sym-Tetrachloroethane; s-Tetrachloroethane

Registered Trade Names: Bonoform; Cellon; Westron
TABLE 1. Physical and Chemical Properties
CAS Number
Chemical Formula
Molecular Weight
Physical State
Boiling Point
Melting Point
Density (at 20C)
Vapor Pressure
Log Kow
Water Solubility at 20C
Water Solubility at 25C
Odor Threshold (water)
145.1 - 146.5C
4.62 mm Hg (25C)
9 mm Hg (30C)
2.87 g/L
2.86 g/L
0.50 ppm
                                                                          April 2008

2.2 Uses
TABLE 1. Physical and Chemical Properties
Odor Threshold (air)
Taste Threshold
Conversion Factors
(at 25C, 1 atm)
1.5 ppm; 3-5 ppm;
2.9 ppm for 10 min
1 ppm= 6.98 mg/m3
1 mg/m3= 0.14 ppm
                  NA = Not available
                  Refs: ATSDR, 1996, 2006; HSDB, 2004; Lobo-Mendonca, 1963
Prior to the 1980' s, 1,1,2,2-tetrachloroethane was a starting material for the production of other
chlorinated hydrocarbons (Archer, 1979). It was used commercially as a metal degreaser;
extractant for oils and fats; a component of paint removers, varnishes and lacquers; and in
photographic films (Hawley, 1981). 1,1,2,2-Tetrachloroethane can still occur as a chemical
intermediate in or as a byproduct from the production of a variety of other chlorinated organic
compounds (ATSDR, 1996)
                                                                           April 2008



1,1,2,2-Tetrachloroethane is no longer produced as a commercial product  in the United States,
and importation is thought to be minimal (ATSDR, 2006). Toxics Release Inventory (TRI) data
show that total releases to the environment have declined from about 50,000 pounds per year to
about 5,000 pounds per year over the past ten years (U.S. EPA, 2004b).

3.1 Air

Much of the data on the concentrations of 1,1,2,2-tetrachloroethane in ambient and indoor air
have come from sampling programs conducted in the 1980s or earlier.  They may not be relevant
now that production of 1,1,2,2-tetrachloroethane in the U.S. has ended (ATSDR, 1996). In the
most recent studies, the median ambient air concentration was less than the detection limit, with
most of the samples showing concentrations less than or equal to 10 ppt (Pratt et al., 2000; Shah
and Heyerdahl, 1988). However, between 1996 and 2001, releases to air declined (14 to 3
thousand pounds per year) and accounted for the largest fraction (>50%) of the total releases
reported to the TRI (U.S. EPA,  2004b).

1,1,2,2-Tetrachloroethane released to air gradually accumulates in the troposphere and degrades
by photolysis with a half life  of about 50 to 60 days.  The remainder diffuses slowly into the
stratosphere where it degrades by photolysis (ATSDR, 2006).

3.2 Food

1,1,2,2-Tetrachloroethane was not detected in any of the foods sampled during the recent FDA
Total Diet Study monitoring of volatile organic chemicals in foods (Fleming-Jones and Smith,
2003; FDA, 2003). Bioaccumulation data were not identified for fish from waters contaminated
with 1,1,2,2-tetrachlorethane, however, based on measured bioconcentration values in bluegill
sunfish and fat head minnows, bioaccumulation in aquatic organisms is likely to be low
(ATSDR, 2006).

3.3 Water

The U.S. EPA monitored for  1,1,2,2-tetrachloroethane  in finished drinking water from 1988 to
1992 and again from 1993-1997. The decrease in detections of 1,1,2,2-tetrachlorethane over this
timeframe coincides with the cessation of production in the US and the decline in use and
discharge to the environment observed in the TRI data. The percent of samples with detections
decreased from 0.16% to 0.02% and the 99th percentile concentration of detections decreased
from 112 |ig/L to 3.9 |ig/L (U.S. EPA, 2006). During the 1993-1997 monitoring, 22 of 28,000
systems reported a detection of 1,1,2,2-tetrachloroethane at least once during the 5 year period.
States with detections were evenly distributed across the United States.

The Unites States Geological Service Surveys did not detect 1,1,2,2-tetrachloroethane in ambient
surface waters studied or in 204 urban or 1,267 rural wells at a detection level of 0.2 jig/L
                                                                           April 2008


(Delzer and Ivahnenko, 2003; Squillace et al., 1999). Data on TRI releases to surface water
indicate that the levels dropped precipitously in 1995 from about 2,000 pounds per year to about
a tenth or less of that amount in subsequent years (U.S. EPA, 2004b).

Levels of 1,1,2,2-tetrachloroethane in surface waters may be reduced through volatilization to
the atmosphere and hydrolysis. The volatilization half-life was estimated to be 6.3 hr for a
modeled  flowing river and 6.1 days from a modeled lake (Thomas, 1982).  The hydrolysis half-
life in water is shorter at neutral to alkaline pHs ( ~ 600 days) than at neutral or acid pHs (30-40
days) (Haag and Mill, 1988)

3.4 Soil

Releases  to soil can occur as a result of disposal in landfills or accidental spills of products or
wastes containing the compound. Information on the Toxics Release Inventory (TRI) indicate
that between 1994 and 2004 releases to landfills occurred in only three years, and the amounts
were only 1,1, and 66 pounds (U.S. EPA, 2004b).  An analysis of test wells around RCRA
disposal sites, determined that 25 of 479 sites had levels above the detection limit (Plumb, 1991).
Based on ATSDR's HazDat database  (HazDat, 1996), 1,1,2,2-tetrachloroethane was found in
soil or sediment samples at 47 of 273  current or pastNPL sites.

Chlorinated hydrocarbons such as 1,1,2,2-tetrachloroethane may be degraded in soil through
biotic and abiotic  processes that, in time, can reduce the concentration to below detection levels
(O'Loughlin et al., 1999; 2003;Lorah  et al., 2003).

3.5 Other Sources

In a survey of 1,159 common household products, 216 contained 1,1,2,2-tetrachloroethane (Sack
et al., 1992). Trace amounts were commonly found in adhesives,  oils, greases, and lubricants.
Concentrations in these products were uniformly near the method detection limits (detection
limits not reported).   The presence of  1,1,2,2-tetrachloroethane in commercial products has most
likely paralleled the decline in use and production over the past 15 years. A study by Bi et al.
(2005) detected 1,1,2,2-tetrachloroethne in environmental tobacco smoke at levels of 3  to 6
                                                                            April 2008



4.1 Human Studies

4.1.1  Short-term Exposure

Lethal doses for humans range between 357 mg/kg (Lilliman, 1949) and > 1,000 mg/kg (Hepple,
1927; Mant, 1953).  Death occurs between 3 to 20 hours after exposure. In a case report of a
medical accident, doses of 70 to 117 mg/kg of undiluted 1,1,2,2-tetrachloroethane caused loss of
consciousness, shallow breathing, and pronounced lowering of blood pressure in the orally
exposed patients (Sherman, 1953; Ward, 1955). There were no fatalities and the reported effects
disappeared about an hour after the exposure.

There are a number of occupational case reports where workers were exposed to 1,1,2,2-
tetrachloroethane either alone  or in combination with other chemicals by way of respiration
and/or dermal contact. The majority of these reports lack information on exposure levels.
Symptoms reported include tremors, dizziness, numbness, and drowsiness, fatigue, irritability,
headache, and in severe cases, coma (Hamilton, 1917; Jeney et al., 1957; Lobo-Mendonca, 1963;
Minot and Smith, 1921; Parmenter, 1921). Autopsy records from one fatal incident reported
inflammation and cirrhosis of the liver, enlargement of the heart and spleen, and bleeding in the
gastrointestinal tract (Coyer, 1944); the victim died 20 days after exposure.

4.1.2  Long-term Exposure

There are no well documented reports of adverse health effects from longer-term exposure to
1,1,2,2-tetrachloroethane.  Existing records come from occupational situations and utilization of
the data in the health assessment of 1,1,2,2-tetrachloroethane is  confounded by co-exposures to
other chemicals and a lack of quantitative exposure information. Effects that have been reported
include loss of body weight, jaundice, hepatitis, an enlarged liver, slight anemia, increased
mononuclear cells, white blood cells, and platelets (Horiguchi et al., 1964; Koelsch, 1915;
Willcox et al., 1915; Jeney et al., 1957; Minot and Smith, 1921).

4.1.3  Reproductive and Developmental Effects

No data were identified that apply to developmental or reproductive effects in humans exposed
to 1,1,2,2-tetrachloroethane.

4.1.4  Carcinogenicity

There is one study that reports an increased relative risk of death due to genital cancers (relative
risk [RR] =4.56), leukemia (RR=1.77), and other lymphatic cancers (RR=5.19) among a group
of military personnel who were exposed to tetrachloroethane in  field processing units where
clothing was impregnated with N,N-dichlorohexachlorodiphenylurea in a tetrachloroethane
solvent (Norman et al., 1981).  None of these relative risk values were statistically significant
                                                                            April 2008


within 90% confidence bounds.  The period between exposure and the epidemiology study was
31 years (1946-1976). Quantitative data on exposures to 1,1,2,2-tetrachloroethane and to other
chemicals during military service and subsequent employment were lacking. Given the lack of
statistical significance, poor exposure information, and co-exposure to other chemicals,
confidence in the results of this study is low.

4.2 Animal Studies

4.2.1  Short-term Exposure

The oral LDso values for 1,1,2,2-tetrachloroethane in rats fall between 250 mg/kg and 330
mg/kg (Gohlke, et al., 1977; Schmidt et al., 1980; Smyth et al., 1969).  The only available LD50
value for mice is 1,476 mg/kg (Paolini, et al. 1992).

The available short term studies of 1,1,2,2-tetrachloroethane toxicity cover durations of 1 to 21
days.  The liver appears to be the primary target organ in all studies. The single dose and 4 day
studies are limited in that they evaluated only clinical signs and measures of hepatic toxicity.

A single oral dose of 100 mg/kg given to ten male Wister rats was associated with hepatic
necrosis and fatty degeneration of the liver. No changes in relative liver weight or body weight
were observed when the animals were sacrificed about 20 hours after exposure (Schmidt et al.,

In another study, single doses of 143.5, 287, 574, or 1148 mg/kg were administered by gavage in
corn oil to groups of 4-6 male Sprague-Dawley rats (Cottalasso et al. 1998). The animals were
sacrificed 24 hours later and the liver excised for analysis.  Levels of aspartate aminotransferase
(AST) and alanine aminotransferase (ALT) activity were significantly elevated at doses of >287
mg/kg. A significant increase in liver triglycerides was  observed at >574 mg/kg.  This study did
not examine a full array of standard toxicological endpoints, and there was no control group.
Based on the limited endpoints observed, the  143.5 mg/kg dose is a NOAEL and the 287 mg/kg
dose a LOAEL.

Groups of 5-6 male Osborne-Mendel rats were exposed  to doses of 0, 25, 75, 150, or 300
mg/kg/day by gavage in corn oil for 4 days in a study by Dow Chemical Company (1988). The
animals in the highest dose group exhibited central nervous system depression, and frank signs
of toxicity that lead to elimination of the fourth dose for this group.  After sacrifice, enlargement
of hepatic cells in the centrilobular region, increased glycogen deposits, hepatic mitosis and
hyperplasia were seen at doses of 75  mg/kg/day and above.  Body weight was significantly
depressed at the highest dose.  When groups of six male B6C3F1 mice were exposed under the
same  conditions, centrilobular swelling and a centrilobular hepatocyte swelling was noted at a
dose of 75 mg/kg/day and hepatic mitosis was increased at the highest dose. The no observed
adverse effect level (NOAEL) in this study was 25 mg/kg/day for both mice and rats and the
lowest observed adverse effect level (LOAEL) was 75 mg/kg/day based on effects in the liver.
                                                                            April 2008


The NTP (2004) conducted a 15-day range finding study of 1,1,2,2-tetrachloroethane in groups
of five/sex F344/N rats and B6C3F1 mice.  The chemical was administered through
microcapsules incorporated in the feed at levels of 0, 3325, 6650, 13300, 26600, or 53200 ppm
(0, 300, 400, 500 mg/kg/day for the first 4 rat dose groups; doses were not provided by NTP for
the highest two  dose groups because they were sacrificed early). Due to excessive scattering of
feed NTP  did not determine doses for mice; however they were approximately 0, 600, 1200,
2400 mg/kg/day for the lowest 4 dose groups based on the conventions of EPA,  1988). As with
the rats the highest two dose groups were sacrificed early. The animals were examined for
clinical signs, body weights, and food intake. At termination, the animals were sacrificed;
selected organs  were weighed and the tissues were examined histologically. All rats except
those in the lowest dose group lost weight during the study. At the lowest dose, relative liver and
kidney weight were increased.  Some of the liver lesions were observed in both the controls and
treated animals. The LOAEL for the rats was identified by the authors as 300 mg/kg/day (3325
ppm); there was no NOAEL. The results in mice were similar to those in rats except that the
liver damage in the exposed mice was more prominent and increased in severity with dose.
Effects were seen in all dose groups of mice; however, the authors did not identify a dose for
mice in association with the lowest feed concentration of 3325 ppm because excessive spilling of
the feed prevented  an accurate assessment of intake.

NTP (1996) examined 1,1,2,2-tetrachloroethane in a study of the renal toxicity of halogenated
ethanes. Groups of five male F344/N rats received 0, 104 or 208 mg/kg/day tetrachloroethane by
gavage for 21 days. All animals were examined for body weight, clinical signs,  urinalysis,  organ
weights, and gross  pathology. Histology was conducted on the liver and right kidney.  The
animals in the high dose group showed clinical signs of frank toxicity (i.e. death, respiratory
difficulty,  emaciation, diarrhea). In the low-dose group, absolute and relative liver weights were
greater than those of the controls and mild to moderate hepatic cytoplasmic vacuolization was
observed.  The authors did not consider the cytoplasmic vacuolization to be an adverse effect.
No effects on survival, body weight gain, urinalysis, absolute and relative kidney weight, or
kidney histopathology were observed. The 104 mg/kg dose can be considered a marginal
LOAEL based on the observed hepatic effects.
                                                                            April 2008


4.2.2  Long-term Exposure

A 2004 subchronic study by the National Toxicology Program (NTP) using  groups of F-344 rats
and B6C3F1 mice (10/dose/sex) provides the most comprehensive dose-response data on the
noncancer effects of 1,1,2,2-tetrachloroethane.  The study revealed that rats were more sensitive
to the noncancer effects of 1,1,2,2-tetrachlorethane than mice. In the rat study, the animals were
maintained for 14 weeks on diets containing 0, 268, 589, 1180, 2300, or 4600 ppm (0, 20, 40, 80
170 or 320 mg/kg/day) microencapsulated  1,1,2,2-tetrachloroethane. They were examined for
clinical signs daily; body weight and food consumption were recorded weekly. Blood samples
were analyzed for hematological and serum biochemistry measurements. Complete
histopathological examinations were conducted on animals in the high dose group and on the
liver,  spleen, bone, and bone marrow of animals in the lower dose groups; reproductive organs
were analyzed for all animals.

Adverse effects indicative of frank toxicity were observed at the two highest doses. They
included weight loss, hematological changes, increased biomarkers of liver damage, and hepatic
necrosis.  Less severe but statistically significant, dose-related effects on the liver (increased
serum ALT and SDH activity,  increased liver weight, hepatocyte vacuolization), decreased red
blood cell measures indicative of possible anemia, and testicular effects were observed across the
lowest three dose groups, especially for the males. There were no significant indications of
neurotoxic effects in the three lowest dose groups (the only ones tested) as measured using a
battery of tests specific for neurotoxicity. According to the study authors, 40 mg/kg/day was the
LOAEL for systemic effects, however, hepatocyte cytoplasmic vacuolization of minimal severity
occurring in the males in the lowest dose group might justify treating the 20 mg/kg/day  dose
level as a minimal LOAEL.  The cytoplasmic vacuolization was present in all treated groups, but
not in the controls, and increased in severity with increasing dose.

In the NTP (2004) study, similar changes in body weight, liver enzyme activity, and liver and
kidney weights were observed in B6C3F1 mice given doses of 589, 1120, 2300, 4550 or 9100
ppm (These corresponded to doses of 0,  100, 200, 370,  700, and 1360 mg/kg/day for the males
and 0, 80, 160, 300, 600, and 1400 mg/kg/day for the females based on data supplied by NTP .
Dose levels of 160 mg/kg/day for females and 200 mg/kg/day for males (1120 ppm) were
identified as the LOAELs. Dose levels of 80 mg/kg/day for females and 100 mg/kg/day for
males (589 ppm) were the NOAELs. These levels are higher than the NOAEL and LOAEL in
the rat studies.

4.2.3  Reproductive and Developmental Effects

Reproductive Effects. As part of the NTP (2004) subchronic study on rats, sperm motility,
testicular weight, vaginal condition, and estrus cycle were evaluated.  There was a dose-related
decrease in sperm motility at concentrations of 40 mg/kg/day and greater.  The left epididymis
weight was decreased at dose of >80 mg/kg/day and the right epididymis at >170 mg/kg/day.
Estrus cycles were altered in females only at frankly toxic dose levels.
                                           10                               April 2008


No oral one- or two-generation studies of reproductive toxicity were identified. A limited one-
generation inhalation study using a control and single dose (13.3 mg/m3) did not result in any
effects on body weight, visual malformations, or survival at birth or over an 84 day postnatal
observation period (Schmidt et al., 1972).

Developmental Effects. NTP (1991 a,b) conducted screening studies of developmental toxicity
in Sprague-Dawley rats and Swiss CD-I mice). The dams were evaluated for Food
consumption, body weights and clinical signs during treatment. At termination live and dead
pups, implantation sites, resorption sites, and fetal body weights were recorded. Neither study
evaluated external, visceral or skeletal abnormalities. Accordingly, the data base for
developmental and reproductive toxicity is limited.

In groups of 8-9 pregnant Sprague-Dawley rats receiving dietary doses of 0, 34, 98, 180, 278, or
330 mg/kg/day from gd 0 to gd 20, weight gain in the dams was significantly decreased in all but
the lowest dose group as were the average fetal body weights (NTP,  199la). Total pup resorption
was seen in one animal from the 98 mg/kg/day dose group and 4 of 9 animals in the 330
mg/kg/day dose group. The NOAEL for the dams and pups was 34 mg/kg/day based on the
parameters evaluated (live and dead pups, implantation sites, resorption sites, clinical signs,
maternal  and fetal body weights); the LOAEL was 98 mg/kg/day based on the decreased weight
gain by the dams and the significantly lower body weight for the pups.
In a second developmental toxicity study, Swiss CD-I mice, received target dietary doses of 0,
987, 2120, 2216, or 4575 mg/kg/day (NTP,  1991b).  The 987 mg/kg  dose was the LOAEL for
the dams based on clinical signs of toxicity, effects on body weight, and liver histopathology.
Total resorptions occurred in  2 of 8 dams in the 2120 mg/kg/day dose group, but not in any
animals from the lowest dose group (987 mg/kg/day). All but one dam died in the 2216
mg/kg/day dose group as did  all of the animals in the high dose group.

4.2.4 Genotoxicity

Predominantly negative results have been reported for the induction of bacterial gene mutations,
with and  without metabolic activation (Haworth et al., 1983; Milman et al., 1988; Nestmann et
al., 1980; Warner et al., 1988) with a few exceptions (Brem et al.,  1974; Mersch-Sundermann et
al., 1989a). However, 1,1,2,2-Tetrachloroethane induced sister chromatid exchanges in CHO
cells (Galloway et al., 1987) and in BALB/c3T3 mouse cells (Colacci et al., 1992) but did not
cause chromosomal aberrations in the CHO cells. It did not induce DNA growth, repair and
synthesis in mouse and rat hepatocytes (Williams, 1983; Milman  et al.,  1988) or cause
unscheduled DNA synthesis in human embryonic intestinal cells (McGregor,  1980).

Results for in vivo cell transformation in mammalian cells have been mixed, with positive results
(Colacci  et al., 1992,  1993) and negative results (Little, 1983; Tu et al.,  1985; Milman et al.,
1988) reported. A dose-related increase in the number of micronucleated monochromatic
erythrocytes per thousand cells was recorded in an in vivo mouse micronucleus test using doses
of about  100 to 1400  mg/kg/day (NTP, 2004). The mouse micronucleus results, in conjunction
                                           11                               April 2008


with the in vitro tests for sister chromatid exchange, indicate that 1,1,2,2-tetrachloroethane can
have clastogenic effects.

4.2.5 Carcinogenicity

The key study for the evaluation of the carcinogenicity of 1,1,2,2-tetrachloroethane is an NCI
(1978) bioassay in which groups of Osborne- Mendel rats and B6C3F1 mice (50 per sex per dose
group) were given 1,1,2,2-tetrachloroethane in corn oil by gavage 5 days/ week for 78 weeks.
The doses normalized for 7 days/week were 44 and 78 mg/kg/day for male rats, 31 and 55
mg/kg/day for female rats, and 101 and 202 mg/kg/day for both male and female mice.  After
cessation of dosing the rats were observed for 32 additional weeks and the mice for 12 weeks.
Dosing occurred 5 days/week and the dose levels were adjusted (up then down) during the study
and required normalization for the assessment. Vehicle controls (20/sex) received corn oil at the
same rate as the high-dose animals; untreated controls were not intubated.

No statistically significant increase in the incidence of neoplasms was observed in rats but there
were two males with hepatocellular carcinomas and one with a hepatic preneoplastic nodule in
the high dose group leading NCI to classify the results in males as equivocal because these
tumors are rare in Osborne Mendel rats.  There was a highly significant dose-related increase in
the incidence of hepatocellular carcinomas in both male (3/36, 13/50, 44/49) and female (1/40,
30/48, 43/47) mice.  The reported values for the control group are the combination of the
untreated and vehicle treated controls).
4.3 Proposed Mode of Action

1,1,2,2-Tetrachloroethane is almost completely absorbed from the gastrointestinal tract (Dow,
1988; Mitoma et al., 1985). Data on tissue distribution are limited, but autoradiography after iv
dosing and adverse effects in the liver, kidney and testes after oral dosing demonstrate
distribution to these organs (Eriksson and Brittebo, 1991; NTP,  1996, 2004).  Dichloroacetic
acid (DCA) appears to be the major metabolite of 1,1,2,2-tetrachloroethane after single
intraperitoneal doses ranging from 160 to 320 mg/kg 14C labeled compound (Yllner, 1971).
Other metabolites identified in the urine of treated rats by Yllner (1971) were trichloroethanol,
trichloroacetic acid, oxalate and glycolate; the latter two are metabolites of DCA. Excretion of
the chlorine from 1,1,2,2-trichloroethane occurs primarily through metabolites in the urine; a
substantial portion of the carbon is completely metabolized to carbon dioxide and excreted in
exhaled air based on single dose studies.  Some unmetabolized 1,1,2,2-tetrachloroethane is also
removed from the body with exhaled air. Lack of multiple dose  studies is a weakness of the
1,1,2,2-tetrachloroethane database because DCA, the principle metabolite inhibits its own
metabolism. Therefore, in multiple dose studies the distribution of metabolites might well have
differed from that observed in the single dose studies.
                                            12                                April 2008


4.3.1  Noncancer Effects

The hepatic toxicity of 1,1,2,2-tetrachloroethane is thought to be due to the formation of free
radical intermediates and/or toxic metabolites such as DC A, trichloroethanol or trichloroacetic
acid (ATSDR, 1996, Paolini et al.,1992; Tomasi et al., 1984. Yllner, 1971) DCA is an
important metabolite of 1,1,2,2-tetrachloroethane and shares some common manifestations of
toxicity such as hepatic necrosis, increased liver weight, glycogen accumulation, testicular
toxicity, and neurotoxicity in rats and mice (U.S. EPA, 2003).  1,1,2,2-Tetrachloroethane has
also been implicated in the impairment of heme synthesis in the liver of treated animals, an effect
which may account for the decrease in hemoglobin or hematocrit levels seen in several short
term toxicity studies (NTP, 2004; Minot and Smith, 1921).

4.3.2  Cancer Effects

Haseman (1984) has reported that an increased incidence of hepatocellular carcinomas in
B6C3F1 mice after exposure to 1,1,2,2-tetrachloroethane is not unusual because many chemicals
increase the spontaneous rate of such tumors in this strain, however, DCA, the main metabolite
of 1,1,2,2-tetrachloroethane, also causes liver tumors in both B6C3F1 mice and F-344 rats (U.S.
EPA,  2003).

There have been numerous studies of the possible mechanisms through which DCA may cause
the development of liver tumors.  Like, 1,1,2,2-tetrachloroethane, DCA is a weak mutagen,
inducing mutations and chromosome damage in in vitro and in vivo assays predominantly at high
concentrations (U.S. EPA, 2003). Peroxisome proliferation, reparative hyperplasia, DNA
hypomethylation, tumor promotion, impaired intracellular communication, and abnormal cell
signaling have all been investigated as possible mechanisms leading to liver tumors after DCA
exposure (U.S. EPA, 2003). A clear mode of action for DCA tumorigenicity has yet to be
defined. A study of liver tissues from DCA treated rats concluded that based on observed
patterns of lesion frequency and their progression across the time- and dose-range evaluated
there might be three distinct routes to the development of malignant tumors (Carter et al., 2003).
Tumors in the liver appeared to develop from eosinophilic, dysplastic and basophilic/clear cells.
The majority of the tumors seemed to develop from the basophilic/clear cells.

Few studies of possible mechanisms for 1,1,2,2-tetrachloroethane carcinogenicity, have been
conducted. Studies  of initiation and promotion using the production of GGT + foci in the livers
of male Osborne-Mendel rats and an in vitro two-stage BALB/c3T3 cell transformation assay in
athymic CD1/BR mice indicate that 1,1,2,2-tetrachloroethane is a weak initiator that also can
function as a tumor promoter (Story et al., 1986; Colacci et al.,1992, 1993).
                                           13                               April 2008

14                               April 2008



HAs describe nonregulatory concentrations of drinking water contaminants at which adverse
health effects are not anticipated to occur over specific exposure durations. HAs are developed
for both short-term and long-term (Longer-term and Lifetime) exposure periods based on data
describing noncarcinogenic endpoints of toxicity.

Short Term exposures can include One-day and Ten-day exposure periods. One-day and Ten-
day HAs use parameters that reflect exposures and effects for a 10 kg child consuming 1 liter of
water per day.

A Longer-term HA covers an exposure period of approximately 7 years, or 10 percent of an
individual's lifetime. Longer-term HAs can incorporate parameters for either a child (10 kg body
weight consuming 1  liter per day water) or an adult (70 kg body weight consuming 2 liters per
day water) parameters.

A Lifetime HA covers an individual's lifetime, approximately 70 years. A lifetime HA considers
a 70 kg adult consuming  2 Liters of water per day. The lifetime HA is considered protective of
non-carcinogenic adverse health effects over  a lifetime exposure. A relative source contribution
from water is also factored into the lifetime HA calculation to account for contaminant exposures
from other sources (air, food, soil, etc) of the  contaminant. For those substances that are
Carcinogenic to Humans, Likely To be Carcinogenic to Humans (U.S. EPA,  2005), known
(Group A), or probable (Groups BI and B2) human carcinogens (U.S. EPA, 1986a), the
development of a Lifetime Health Advisory is not usually recommended. A Lifetime HA can be
calculated for substances that are possible carcinogens (U.S. EPA, 1986) or provide "Suggestive
Evidence of Carcinogenicity, but Not Sufficient to Assess Human carcinogenic Potential" (U.S.
EPA 2005).

The One-day, Ten-day, or Longer-term HA is derived using the following formula:

                             HA = NOAEL or LOAEL x BW

NOAEL or LOAEL    =    No- or Lowest-Observed-Adverse-Effect Level (in mg/kg bw/day)
                           from a study of an appropriate duration
BW                 =    Assumed body  weight of a child (10 kg) or an  adult (70 kg).
UF                  =    Uncertainty factor in accordance with EPA guidelines
DWI                =    Assumed human daily consumption for a child (1 L/day) or an
                           adult (2 L/day)

The Lifetime HA is calculated in a three-step process:
                                          15                               April 2008


Step 1:  Adopt a pre-existing Reference Dose (RfD or calculate an RfD using the following

                           RfD = NOAEL. LOAEL or BMDL
NOAEL or LOAEL    =   No- or Lowest-Observed-Adverse-Effect Level (in mg/kg bw/day).
BMDL                =   Lower confidence bound on the Bench Mark Dose (BMD).  The
                          BMD and BMDL are obtained through modeling of the dose-
                          response relationship.
UF                   =   Uncertainty factor established in accordance with EPA guidelines.

The RfD is an estimate (with uncertainty spanning perhaps and order of magnitude) of a daily
human exposure to the human population (including sensitive subgroups) that is likely to be
without  an appreciable risk of deleterious effects during a lifetime. It can be derived from a
NOAEL, LOAEL, or benchmark dose with uncertainty factors generally applied to reflect
limitations in the data used.

Step 2:  Calculate a Drinking Water Equivalent Level (DWEL) from the RfD . The DWEL
assumes that 100% of the exposure comes from drinking water.

                                   DWEL = RfDxBW
  RfD                =   Reference Dose (in mg/kg bw/day).
  BW                =   Assumed body weight of an adult (70 kg).
  DWI                =   Assumed human daily consumption for an adult (2 L/day)

Step 3:  The Lifetime HA is calculated by factoring in other sources of exposure (such as air,
food, soil) in addition to drinking water using the relative source contribution (RSC) for the
drinking water.

                              Lifetime HA = DWEL x RSC
 DWEL             =    Drinking Water Equivalent Level (calculated from step 2)
 RSC                =    Relative source contribution

Note. The procedure for establishing the RSC is described in U.S. EPA (2000) Human Health
Methodology (pages 4-5 to 4-17). The methodology can be  accessed at:
                                          16                              April 2008


5.1 One-day Health Advisory

The study by Dow (1988) was selected for use in the derivation of the One-day HA because it
provided the lowest LOAEL among the short term-studies with an appropriate duration.  Several
endpoints related to liver toxicity were evaluated.  The single dose studies of Schmidt et al.
(1980) and Cottalasso et al. (1998) and the 14 day and 21 day studies of NTP (1996, 2004) also
identify the liver as a major target organ for short-term 1,1,2,2-tetrachloroethane exposures. The
animal data are supported by the limited clinical information identifying the liver as a target
organ in humans.

In the Dow (1988) study, enlargement of hepatic cells in the centrilobular region, glycogen
deposits, hepatic mitosis and hyperplasia were seen in Osborne Mendel rats at  a dose of 75
mg/kg/day (LOAEL) and centrilobular hepatic swelling was observed in B6C3F1 mice at the
same dose.  The NOAEL was 25 mg/kg/day.  The LOAEL in the Schmidt et al. (1980) single
dose study using male Wistar rats was 100 mg/kg/day based on hepatic necrosis and fatty
degeneration of the liver. There was no NOAEL.  Cottalasso et al. (1998) observed increased
serum ALT and AST activity (biomarkers for liver damage) in groups of Sprague-Dawley rats at
a LOAEL of 287 mg/kg/day and a NOAEL of 143.5 mg/kg/day.

Each of these studies has its limitations because of the small number of animals evaluated (4 to
10/dose group), the use of a single sex, and the less-than-complete evaluation of toxicological
endpoints. However, the three studies provide data on two species, three strains of rats, and
show a common impact on the liver which is supported by the longer-term, more-
comprehensive studies. These factors justify the use of the NOAEL from the Dow (1988) study
as the basis of the One-day HA.

The One-day HA for a 10-kg child is calculated as follows:

           One Day HA = 25 mg/kg/day x 10 kg =2.5 mg/L (rounded to 3 mg/L)
                            lOOx IL/day
25 mg/kg/day         =    NOAEL for hepatotoxicity in rats (Dow, 1988).
10 kg                =    Assumed body weight of a child
100                  =    Uncertainty factor, chosen for interspecies (10) and intraspecies
                           (10) differences
1 L                  =    Assumed daily water consumption of a child.

5.2 Ten-day Health Advisory

The studies by Dow Chemical corporation (1988), NTP (1996) and NTP (2004) were selected to
serve as the basis for the Ten-day HA for 1,1,2,2-tetrachloroethane.  The NTP  (1996) study in
rats used a 3-week (21-day) exposure duration and identified a lower LOAEL (104 mg/kg/day)
than did the 2-week NTP (2004) study in rats (300 mg/kg/day). There was no NOAEL in either
study. The DOW Chemical Corporation study (1988) provided a NOAEL (25  mg/kg/day) as
                                          17                              April 2008


well as a LOAEL. All three studies identified the liver as the target organ for 1,1,2,2-
tetrachloroethane and the observed impacts on the liver were consistent across the studies. The
histological changes effects seen at the LOAEL in the NTP (1996) study were classified as mild
to moderate centrilobular vacuolization and were not considered as adverse by the authors. The
LOAEL (104 mg/kg/day) in the NTP (1996) study is roughly comparable to the LOAEL in the
4-day Dow Chemical Corporation study (75 mg/kg/day).

The advantage of using the Dow (19880 study for quantification of the ten day HA is the fact
that it identified a NOAEL of 25 mg/kg/day for liver effects and the LOAEL is lower than the
LOAELS from the other two studies. Accordingly the ten-day HA calculation is based in the
NOAEL from the Dow (1988) study and the same as that for one-day HA. Accordingly the ten-
day Ha is 3 mg/L.

5.3 Longer-term Health Advisory

The study by NTP (2004) was selected to serve as the basis for the Longer-term HA for 1,1,2,2-
tetrachloroethane.  In this study, the LOAEL for changes in hepatocyte vacuolization, relative
liver weight, and increased activity of serum liver enzymes (ALT, SDH) in F-344 male rats
following dietary exposure for 14 weeks was 40 mg/kg/day. Male rats were more sensitive to
the effects of 1,1,2,2-tetrachloroethane than the females and F-344 rats were more sensitive than
B6C3F1 mice (NTP, 2004). This study was selected because it was of high quality, used an
appropriate duration, and was conducted in an appropriate species for the evaluation of
noncancer effects.

From the NTP (2004) data set, U.S. EPA (2006) derived a Benchmark Dose (HMD) of 13.08
mg/kg/day and a lower bound limit on the Benchmark Dose (BMDL) of 10.71 mg/kg/day for a
one standard deviation increase in the relative liver weight compared to controls.  In addition to
relative liver weights, the changes in  serum ALT and SDH, hemoglobin concentrations, and
sperm motility were also modeled.  Adequate fit was achieved for all but the sperm motility data
and the lowest BMD/BMDL values were those for relative liver weight. The BMD analysis in
the Health Effects Support Document is located on pages 8-3 to 8-6.

For a 10 kg child, the Longer-term HA is calculated as follows:

       Longer-term HA = 10.71 mg/kg/day x 10 Kg =0.36 mg/L (rounded to 0.4 mg/L)
                             300 x 1 L/day
10.71 mg/kg/day       =    BMDL, Benchmark Dose, lower-bound confidence bound for a
                           one standard deviation increase in relative liver weight compared
                           to controls (NTP, 2004)
10 kg                 =    Assumed body weight of a child
300                  =    Uncertainty factor, chosen for interspecies (10) and intraspecies
                           (10) differences and  an incomplete database (3)
1 L                   =    Assumed daily water consumption of a child.
                                          18                               April 2008


For an adult, the Longer-term HA is calculated as follows:

        Longer-term HA = 10.71 mg/kg/day x 70 Kg = 1.25 mg/L (rounded to 1 mg/L)
                              300 x 2 L/day
10.71 mg/kg/day       =    BMDL, Benchmark Dose, lower-bound confidence bound for a
                           one standard deviation increase in relative liver weight compared
                           to controls (NTP, 2004)
70 kg                 =    Assumed body weight of an adult
300                   =    Uncertainty factor, chosen for interspecies (10) and intraspecies
                           (10) differences and an incomplete database (3)
2L                    =    Assumed daily water consumption of an adult.

Note: The 3-fold database UF is based on the need for a multigenerational study of reproductive
toxicity and additional studies of developmental toxicity that examine the fetus for visceral and
skeletal abnormalities. The available NTP developmental screening assays do not examine these

5.4 Lifetime Health Advisory

The subchronic study by NTP was selected as the basis of the oral RfD of 0.02 mg/kg/day (U.S.
EPA, 2006). As described above, the LOAEL for male F-344 rats in this study was 40 mg/kg/day
based on hepatocyte vacuolization, increased relative liver weights, and increased activity liver
enzymes (ALT, SDH) in serum following dietary exposure for 14 weeks was 40 mg/kg/day.
Male rats were more sensitive to the effects of 1,1,2,2-tetrachloroethane than the females and F-
344 rats were more sensitive than B6C3F1 mice (NTP, 2004). This study was selected because it
was of high quality, provided a thorough evaluation of noncancer endpoints and included more
doses than the NCI chronic cancer study.

The RfD was derived from the lower-bound limit based on the dose associated with a one
standard deviation increase in relative liver weight (10.71 mg/kg/day) in animals exposed to
1,1,2,2-tetrachloroethane in their diet for 14 weeks.  The change in relative liver weight was
accompanied by hepatocyte vacuolization and increased activity levels of liver enzymes (ALT
and SDH) in the serum. The activities of the liver enzymes were also modeled. The BMDLio for
a one standard  deviation change in ALT was 29.13 mg/kg/day and  that for SDH was 31.69
mg/kg/day. The BMDL for the increases in liver weight was chosen  as the point of departure for
the RfD because 7 of 10 male mice showed histological evidence of hepatocyte cytoplasmic
vacuolization at the lowest dose tested (20 mg/kg/day), a factor which justified choosing the
lowest BMDL  from the modeled responses. The BMD analysis in the Health Effects Support
Document is found on pages 8-3 to 8-6. The RfD is calculated from the BMDL as follows:

         RfD = 10.71  mg/kg/dav = 0.0107  mg/kg/day (rounded to 0.01 mg/kg/day)
                                          19                               April 2008

10.71 mg/kg/day       =    BMDL, Benchmark Dose, lower-bound confidence bound for a
                           one standard deviation  increase in relative liver weight compared
                           to controls (NTP, 2004)
1000                  =    Uncertainty  factor, chosen for interspecies (10) and intraspecies
                           (10) differences, the less than chronic duration of the study (3),
                           and an incomplete database (3)

Note: The application of a 3-fold uncertainty factor for extrapolation from a subchronic to a
chronic duration was justified based on the fact that the NCI (1978) study in Osborn Mendel rats,
using higher dose levels than the BMDL did not identify cirrhosis or other major histological
liver problems. However, the NCI (1978) study did not monitor for serum biochemistry or
hematological effects. Accordingly, a UF of 3 was selected because of the differences in the rat
strains used in the subchronic and chronic  studies and the  limited monitoring of effects other
than tumors in the chronic  study. The justification for the 3-fold database deficiency adjustment
is provided under the Longer-term HA discussion above.

A Drinking Water Equivalent Level (DWEL) can be derived from the oral  RfD as follows:

            DWEL = 0.01 mg/kg/dav x 70 Kg = 0.35 mg/L (rounded to 0.4 mg/L)
                             2 L/day
0.01 mg/kg/day        =    Oral Reference Dose
70 Kg                =    Assumed body weight of an adult
2L/day                =    Assumed daily water consumption of an adult.

1,1,2,2-tetrachloroethane has been classified as likely to be carcinogenic to humans (U.S. EPA,
2006). Therefore, the development of a Lifetime Health Advisory is not recommended. The
cancer risk at the DWEL is 1  x 10"3 (See section 5.5).

5.5 Evaluation of Carcinogenic Potential

The HA evaluation of carcinogenic potential includes the U.S. EPA descriptors for the weight of
evidence of the likelihood that the agent is a human carcinogen and the conditions under which
the carcinogenic effects may be expressed, as well as  a quantitative estimate of cancer potency
(slope factor), where available. The Cancer  Slope Factor (CSF) is the result of the application of
a low-dose extrapolation procedure and is  presented as the risk per mg/kg/day of the
contaminant.  In cases where a CSF has been derived, HAs include the drinking water
concentrations equivalent to an upper-bound excess lifetime cancer risk of one-in-ten-thousand
(1 x 10"4), one-in-one-hundred-thousand (1 x 10"5),  to one-in-one-million (1 x 10"6).

Cancer assessments conducted before 1996 used the five-category, alpha-numeric system for
classifying carcinogens established by the  Guidelines for Carcinogen Risk Assessment (U.S.
                                           20                               April 2008


EPA, 1986a). The EPA currently requires that all new cancer risk assessments comply with the
Guidelines for Carcinogen Risk Assessment (U.S. EPA, 2005) or, if conducted between 1996
and 2005, comply with the draft versions of the 2005 Cancer guidelines.

The OW has classified 1,1,2,2-tetrachloroethane as likely to be carcinogenic to humans (U.S.
EPA. 2006) following the 2005 Cancer Guidelines,  The current IRIS cancer classification for
1,1,2,2-tetrachloroethane is Group C: a possible human carcinogen (U.S. EPA, 1986b). The
International Agency for Research on Cancer (IARC,  1999) classifies 1,1,2,2-tetrachloroethane
in Group 3; data in humans inadequate and limited evidence in experimental animals. The
principal 1,1,2,2-tetrachloroethane metabolite, DCA, is classified as likely to be carcinogenic to
humans (U.S. EPA, 2003).

Using the Benchmark Dose approach and the linear multistage model, the OW determined a CSF
of 8.5 x 10"2 (mg/kg/day)"1 using the data for female mice from the NCI (1978) study following
the procedures of the 2005 Cancer Guidelines. The data for the male mice did not provide and
adequate fit with the multistage model.  The quantitative cancer assessment in the Health Effects
Support Document is on pages 8-10 to 8-13". The concentration in drinking water corresponding
to a 10"6 risk is 4 x 10"4mg/L, that for a 10"5 risk is 4 x 10"3 mg/L and that for a 10"4 risk is 4 x 10"
                                           21                               April 2008

22                               April 2008



The OW Human Health Ambient Water Quality Criterion (AWQC) for 1,1,2,2-tetrachloroethane
is 0.17 |ig/L.  The AWQC is used by states in establishing regulatory limits for ambient water
and in developing fish advisories.

Six states have established regulatory or guidance values for 1,1,2,2-tetrachloroethane in
drinking water (HSDB, 2004). California and New Jersey have Standards of l|ig/L. Arizona has
a guideline value of 0.17 ng/L; Wisconsin and Minnesota a value of 0.2 jig/L and Florida a value
of 1 ng/L. Three States (Connecticut, Delaware, and Oregon) have standards of 0.17 jig/L
1,1,2,2-tetrachloroethane for ambient water and fish ingestion (ATSDR, 1996).

ATSDR (2006) has established an intermediate-duration oral Minimal Risk Level (MRL) for
1,1,2,2-tetrachloroetane of 0.5 mg/kg/day based on a BMDLio of 53.88 mg/kg/day for hepatic
necrosis for the rats in the NTP (2004) 14-week study using a total UF of 100. An intermediate
duration value applies to exposures ranging from 15 to 364 days.
                                           23                               April 2008

24                               April 2008



Two analytical methods are available for detecting 1,1,2,2-tetrachloroethane in drinking water.
EPA Methods 502.2 and 524.2 rely on purge and trap gas chromatography (GC) followed by
either electrolytic conductivity detection (ELCD) or mass spectrometry (MS). The method
detection limit (MDL) for Method 502.2 is reported to range from 0.01 to 0.02 //g/L, and the
average recovery is reported to range from 99 to 100 percent (U.S. EPA, 1995a). The MDL for
Method 524.2 is reported to range from  0.04 to 0.2 //g/L, and the average recovery is reported to
range from 91 to 100 percent (U.S. EPA, 1995b).
                                          25                              April 2008

26                               April 2008



Potential treatment technologies for removing 1,1,2,2-tetrachloroethane from water include air
stripping and activated carbon. Air stripping involves the continuous contact of air with the
water being treated, allowing dissolved volatile contaminants to transfer from the source water to
the air.  Compounds that have a Henry's Law Constant above that for dibromochloropropane
(0.003 mol/mol) or that for ethylene dibromide (0.013 mol/mol) are considered to be amenable
to air stripping (Speth et al., 2001).  The Henry's Law Constants for 1,1,2,2-tetrachloroethane
have been reported to be 0.012 mol/mol and 0.016 mol/mol (Speth et al., 2001). Granular
activated carbon (GAC) treatment removes contaminants via the physical and chemical process
of sorption: the contaminants attach to the carbon surface as water passes through the carbon
bed.  Contaminants with an adsorption capacity, expressed as the Freundlich isotherm constant
(K), above 200  jig/g (L/|ig)1/n are considered to be amenable to GAC treatment (Speth et al.,
2001). Speth and Adams (1993 as cited in Speth et al., 2001) report that the Freundlich (K) value
for 1,1,2,2-tetrachloroethane is 823 |ig/g (L/|ig)1/n.

Home drinking water treatment units have varying abilities to remove contaminants from tap
water. The following site allows the user to identify treatment units according to the
contaminants they can remove: htt^/w^wjisf^r^/Certifigd^WTTJ/. At this time there are no
units identified  that have been evaluated for removal of 1,1,2,2-tetrachloroethane (see reduction
claim type) but units that are certified as effective for removal of other chlorinated ethanes are
                                           27                               April 2008

28                               April 2008



Archer, W.L. 1979. In: Grayson H. and D. Eckroth (Eds.). Kirk-Othmer Encyclopedia of
Chemical Technology. 3rd ed. Vol. 5:722-742. As cited in: ATSDR, 1996.

ATSDR. 1996. Agency for Toxic Substances and Disease Registry. Toxicological Profile for
1,1,2,2-Tetrachloroethane. U.S. Department of Health and Human Services, Public Health
Service, Atlanta, GA.

ATSDR. 2006 Agency for Toxic Substances and Disease Registry. Toxicological Profile for
1,1,2,2-Tetrachloroethane. U.S. Department of Health and Human Services, Public Health
Service, Atlanta, GA.

Bi, X, G Sheng, Y Feng, et al. 2005. Gas and particulate-phase specific tracer and toxic organic
compounds in environmental tobacco smoke. Chemosphere 61(10):1512-1522.  As cited in
ATSDR, 2006.

Brem, H., A.B. Stein, H.S. Rosenkranz .1974. The mutagenicity and DNA-modifying effect of
haloalkanes. Cancer Res. 34:2576-2579. As cited in: WHO, 1998.

Cal EPA (California Environmental Protection Agency). 2003. Public health goal for 1,1,2,2-
tetrachloroethane in drinking water. Office of Environmental Health Hazard Assessment.
Available from: .

Callen, D.F., C.R. Wolf,  R.M. Philpot. 1980. Cytochrome P-450 mediated genetic activity and
cytotoxicity of seven halogenated aliphatic hydrocarbons in Saccharomyces cerevisiae. Mutat.
Res.77:55-63. As cited in: WHO, 1998.

Carter, JH;  Carter, HW; Deddens, JA; et al. (2003) A 2-year dose-response study of lesion
sequences during hepatocellular carcinogenesis in the male B6C3Fimouse given the drinking
water chemical dichloroacetic acid. Environ Health Perspect 111:53-64.

Colacci, A., A. Albini, A. Melchiori, et al. 1993. Induction of malignant phenotype in BALB/c
3T3 cells by 1,1,2,2-tetrachloroethane. Int. J. Oncol. 2:937-945.

Colacci, A., S. Grilli, G.  Lattanzi, et al. 1987. The covalent binding of 1,1,2,2-tetrachloro-ethane
to macromolecules  of rat and mouse organs. Teratogenesis, Carcinogenesis, andMutagenesis
7:465-474. As cited in: WHO, 1998.

Colacci, A., P. Perocco, S. Bartoli, et al. 1992. Initiating activity of 1,1,2,2-tetrachloroethane in
two-stage BALB/c  3T3 cell transformation. Cancer Lett. 64:145-153.
                                           29                               April 2008


Cottalasso, D., A. Bellocchio, C. Domenicotti, et al. 1998. 1,1,2,2-Tetrachloroethane-induced
early decrease of dolichol levels in rat liver microsomes and Golgi apparatus. J. Tox. Env. Health

Coyer, H.A. 1944. Tetrachloroethane poisoning. Ind. Med. 13:230-233. As cited in: ATSDR,
1996 and Cal EPA, 2003.

Crebelli, R., R. Benigni, J. Franekic, et al. 1988. Induction of chromosome malsegregation by
halogenated organic solvents m Aspergillus nidulans: unspecific or specific mechanism? Mutat.
Res. 201:401-411. As cited in: WHO, 1998.

DeAngelo, A.B., S. Herren-Freund, M.A. Perreira, et al.  1986.  Species sensitivity of the
induction of peroxisome proliferation by trichloroethylene and its metabolites. The Toxicologist
6:113.  As cited in: ATSDR, 1996.

Delzer, G.C.,T. Ivahnenko. 2003. Occurrence and temporal variability of methyl tert-butyl ether
(MTBE) and other volatile organic compounds in select sources of drinking water: Results of the
focused survey. U.S. Geological Survey Water-Resources Investigations Report WRIR 02-4084,
p. 65. Available on-line at: http://sd.water.usgs.gov/nawqa/pubs/wrir/wrir02_4084.html. Link to
document from: http://sd.water.usgs.gov/nawqa/vocns/nat_survey.html.

Dow Chemical Company. 1988. The metabolism and hepatic macromolecular interactions of
1,1,2,2-tetrachloroethane (TCE) in mice and rats. D002628.

Eriksson, C., E.B. Brittebo. 1991. Epithelial binding of 1,1,2,2-tetrachloroethane in the
respiratory and upper alimentary tract. Arch.  Toxicol. 65:10-14.

Fleming-Jones, M.E., R.E Smith. 2003. Volatile organic compounds in foods: A five year study.
J. Agric. FoodChem. 51:8120-8127.

FDA. 2003. Food and Drug Administration. Food and Drug Administration Total  Diet Study:
Summary of residues found, ordered by pesticide. 91-3 -01-4. Center for Food Safety and
Nutrition. Washington, DC. http://www.cfsan.fda.gov/~acrobat/tdslbyps.pdf.

Galloway, S.M.,  MJ. Armstrong, C. Reuben,  et al. 1987. Chromosome aberrations and sister
chromatid exchange in Chinese hamster ovary cells: evaluations of 108 chemicals. Environ. Mol.
Mutagen. 10 (Suppl. 10): 1-175. As cited in: NTP, 2004.

Gohlke R., P. Schmidt, H. Bahmann. 1977. 1,1,2,2-Tetrachloroethane and heat stress in animal
experiment. Morphological results [article in German]. Z. Gesamte. Hyg. IHRE Grenzgeb.
                                                                           April 2008


Gupta, K.C., A.G. Ulsamer, R. Gammage. 1984. Volatile organic compounds in residential air:
Levels, sources and toxicity. Proc. APCA Annual Meeting 77:84-1.3, 9. As cited in: ATSDR,

Haag, W.R., T. Mill. 1988. Effect of a subsurface sediment on hydrolysis of haloalkanes and
epoxides. Environ. Sci. Technol. 22:658-663. As cited in: ATSDR, 1996.

Hallen, R.T., J.W. Pyne Jr., P.M. Molton. 1986. Transformation of chlorinated ethenes and
ethanes by anaerobic microorganisms. In: 192nd National Meeting ACS Division Environmental
Chemistry, pp. 344-346. As cited in: ATSDR, 1996.

Hamillton, A. 1917. Military medicine and surgery. J. Am. Med. Assoc. 69:2037-2039. As cited
in: ATSDR,  1996.

Haseman, J.K. 1984. Results from 86 two-year carcinogenicity studies conducted by the
National Toxicology Program. J. Toxicol. Environ. Health 14:621-637. As cited in: ATSDR,

Hawley, G.G. 1981. Condensed Chemical Dictionary. 10th ed. New York, NY: Van Nostrand
Reinhold Co. As cited in: ATSDR,  1996.

Haworth, S., T. Lawlor, K. Mortelmans, et al.. 1983. Salmonella mutagenicity test results for 250
chemicals. Environ. Mutagen. Suppl. 1:3-142. As cited in: NTP, 2004.

HAZDAT. 1996. Database. Agency for Toxic Substances and Disease Registry (ATSDR),
Atlanta, GA. As cited in ATSDR, 1996.

Hepple, R.A. 1927. An unusual case of poisoning. J. Army Medical Corps 49:442-445.  As cited
in: ATSDR,  1996.

Horiguchi, S., S. Morioka, T. Utsunomiya, et al. 1964. A survey of the actual conditions of
artificial pearl factories with special reference to the work using tetrachloroethane. Jpn. J. Ind.
Health 6:251-256. As cited in: ATSDR, 1996.

HSDB. 2004. Hazardous Substance Data Bank.  1,1,2,2-Tetrachloroethane. Hazardous
Substances Data Bank query of 1,1,2,2-tetrachloroethane. Retrieved October. 10, 2004.
Bethesda, MD: National Library of Medicine, Specialized Information Services Division,
Toxicology and Environmental Health Information Program,  TOXNET. Last updated March 05,

IARC 1999.  1,1,2,2-Tetrachloroethane.  In: IARC Monographs on the Evaluation of
Carcinogenic Risks to Humans, volume 71. Re-evaluation of Some Organic Chemicals.
International Agency for Research on Cancer. World Health Organization. Geneva. Switzerland.
                                                                          April 2008

Jeney, E., F. Bartha, L. Kondor, et al. 1957. Prevention of industrial tetrachloroethane
intoxication-Part III. Egeszsegtudomany 1: 155-164. As cited in: ATSDR, 1996 and U.S. EPA,

Kanada, M., M. Miyagawa, M. Sato, et al.  1994. Neurochemical profile of effects of 28
neurotoxic chemicals on the central nervous system in rats. (1) Effects of oral administration on
brain contents of biogenic amines and metabolites. Ind. Health 32:145-164. As cited in: WHO,

Kincannon, D.F., A. Weinert, R. Padorr, et al. 1983. Predicting treatability of multiple organic
priority pollutant wastewater from single-pollutant treatability studies. In: Bell, M.R. (ed.).
Proceedings 37th Industrial Waste Conference. Ann Arbor, MI: Ann Arbor Science, pp. 641-
650.  As cited in: ATSDR, 1996.

Koelsch, F. 1915. Industrial  poisonings by  celluloid varnishes in the airplane industry. Muench
Medizin Wochensch. 62:1567-1569. As cited in:  ATSDR, 1996.

Koizumi, A., M. Kumai, M.  Ikeda. 1982. Enzymatic formation of an olefin in the metabolism of
1,1,2,2-tetrachloroethane: an in vitro study. Bull. Environ. Contam.  Toxicol. 29:562-565. As
cited in: ATSDR, 1996.

LaRegina, J., J.W. Bozzelli,  R. Harkov, et al. 1986. Volatile organic compounds at hazardous
waste sites and a sanitary landfill in New Jersey. An up-to-date review of the present situation.
Environ. Prog. 5:18-27. As cited in: ATSDR, 1996.

Lehman, K.B, L. Schmidt-Kehl. 1936. Study of the 13 most important chlorohydrocarbons from
the standpoint of industrial hygienics. Arch. Hyg. 116:132-268. As cited in: ATSDR, 1996 and
U.S. EPA, 1989).

Lilliman, B. 1949. Suggested mechanism of poisoning by liquid tetrachloroethane. Analyst
74:510-511. As cited in: ATSDR, 1996.

Little, A.D. 1983. Cell Transformation Assays of 11 Chlorinated Hydrocarbon Analogs (Final
Report). US Environmental Protection Agency, Office of Toxic Substances (ICAIR Work
Assignment No. 10; Document No. 40+8324457). As cited in WHO, 1998.

Lobo-Mendonca, R. 1963. Tetrachloroethane - A survey. Brit. J. Ind. Med. 20:51-56. As cited in:
ATSDR, 1996 and U.S. EPA, 1989.

Lorah, M.M., M.A. Voytek,  J.D. Kirshtein, et al. 2003. Anaerobic Degradation of 1,1,2,2-
Tetrachloroethane and Association with Microbial Communities in a Freshwater Tidal Wetland,
Aberdeen Proving Ground, Maryland: Laboratory Experiments and Comparisons to Field Data.
USGS Water-Resources Investigations Report 02-4157.
                                                                           April 2008

Mant, A.K. 1953. Acute tetrachl or ethane poisoning. A report on two fatal cases. Br. Med. J. 655-
656. As cited in: ATSDR, 1996.

McGregor, D.B. 1980. Tier II Mutagenic Screening of 13 NIOSH Priority Compounds,
Individual Compound Report, 1,1,2,2-Tetrachloroethane, Report No. 26. Inveresk Research
International Limited, Musselburgh EH21 7UB Scotland. NIOSH, Cincinnati, OH. As cited in:
ATSDR,  1996 and WHO, 1998.

Mersch-Sundermann, V.  1989. The mutagenicity of organic microcontamination in the
environment. II. The mutagenicity of volatile organic halogens in the Salmonella microsome test
(Ames test) with regard to the contamination of groundwater and drinking-water [Article in
German]. Zentralblatt. fur Bakteriologie undMikrobiologie, Hygiene B 187:230-243.

Milman, H.A., D.L. Story, E.S. Riccio, A. Sivak, A.S. Tu, G.M. Williams, C. Tong, C.A. Tyson.
1988. Rat liver foci and in vitro assays to detect initiating and promoting effects of chlorinated
ethanes and ethylenes. Annals of the New York Academy of Sciences 534:521-530. As cited in:
WHO, 1998.

Minot, G.R., L.W. Smith. 1921. The blood in tetrachlorethane poisoning. Arch. Intern. Med.
28:687-702. As cited in: ATSDR,  1996.

Mirsalis, J.C., C.K. Tyson, K.L. Steinmetz, et al. 1989. Measurement of unscheduled DNA
synthesis and S-phase synthesis in rodent hepatocytes following in vivo treatment; testing of 24
compounds. Environ. Mol. Mutagen. 14:155-164.

Mitoma, C., T. Steeger, S.E. Jackson, et al. 1985. Metabolic disposition study of chlorinated
hydrocarbons in rats and mice. Drug Chem.  Toxicol. 8(3): 183-194.

Mudder, T.I., J.L. Musterman. 1982. Development of empirical structure biodegradability
relationships and biodegradability testing protocol for volatile and  slightly soluble priority
pollutants. Presentation Amer. Chem. Sot. Division Environmental Chemistry, Kansas City MO,
September 1982, pp. 52-53. As cited in: ATSDR, 1996.

NCI. 1978. National Cancer Institute. Bioassay of 1,1,2,2-Tetrachloroethane for Possible
Carcinogenicity. NTIS PB277 4537GA, DHEW/PUB/Nffl-78-827, 90.

Nestmann, E.R., EG-H. Lee, T.I. Matula, et  al. 1980. Mutagenicity of constituents identified  in
pulp and paper mill effluents using the Salmonella mammalian-microsome assay. Mutat. Res.
79:203-212. As cited in:  WHO, 1998.

Nestmann, E.R., EG-H Lee.  1983. Mutagenicity of constituents of pulp and paper mill effluent in
growing cells of Saccharomyces cerevisiae.  Mutat. Res.  119:273-280. As cited in: WHO, 1998.
                                                                           April 2008


Norman, I.E., Jr, C.D. Robinette, J.F. Fraumeni, Jr. 1981. The mortality experience of Army
World War II chemical processing companies. J. Occup. Med. 23:818-822.

NTP. 1991a. National Toxicology Program. Range Finding Studies: Developmental Toxicity 
1,1,2,2-Tetrachloroethane When Administered via Feed in CD Sprague-Dawley Rats. Research
Triangle Park, NC, US Department of Health and Human Services, National Institutes of Health,
National Toxicology Program (NTP-91-RF/DT-017).

NTP. 1991b. National Toxicology Program. Range Finding Studies: Developmental Toxicity 
1,1,2,2-Tetrachloroethane (Repeat) When Administered via Feed in Swiss CD-I Mice. Research
Triangle Park, NC, US Department of Health and Human Services, National Institutes of Health,
National Toxicology Program (NTP-91-RF/DT-020).

NTP. 1996. National Toxicology Program. NTP Technical Report on Renal Toxicity Studies of
Selected Halogenated Ethanes Administered by Gavage to F344/N Rats. U.S. DHHS, Public
Health Service, National Institute of Health. NIH Publication 96-3935, Tox-45.

NTP. 2004. National Toxicology Program.  Toxicity  Studies of 1,1,2,2-tetrachloroethane
Administered in Microcapsules  in Feed to F344/N rats and B6C3F1 mice. National Institutes of
Health, National  Toxicology Program (NIH Publication 04-4414).

O'Loughlin, E., D. Burris, C. Delcomyn. 1999. Reductive dechlorination of trichloroethene
mediated by humic-metal complexes. Environ. Sci. Technol. 33: 1145-1147.

O'Loughlin, E., H. Ma, D. Burris. 2003. Catalytic effects of Ni-humic complexes on the
reductive dehalogenation of Cl  and C2 chlorinated hydrocarbons. In E.A. Ghabbour and G.
Davies (eds.). Humic Substances: Nature's Most Versatile Materials. New York: Taylor and
Francis, Inc. pp. 297-324.

Paolini, M., E. Sapigni, R. Mesirca, et al. 1992. On the hepatotoxicity of 1,1,2,2-
tetrachloroethane. Toxicol. 73:101-115.

Parmenter, D.C.  1921. Tetrachloroethane poisoning  and its prevention. J. Ind. Hyg. 2:456-465
As cited in: AT SDR, 1996.

Pellizzari, E.D. 1982. Analysis for organic vapor emissions near industrial and chemical waste
disposal sites. Environ. Sci. Technol.  16:88 1-785. As cited in: ATSDR,  1996.

Plumb, R.H. 1991. The occurrence  of Appendix IX organic constituents in disposal site ground
water. Ground WaterMonit. Rev.\\(2}: 157-164. As cited in: ATSDR, 1996.

Pratt, CG, K Palmer, Cy wu, et al.,  2000. An assessment of air toxics in Minnesota. Environ.
Health Perspect.  108(9):815-825. As cited in ATSDR (2006).
                                                                          April 2008


Price, N.H., S.D. Allen, A., U. Daniels, et al. 1978. Toxicity data for establishing "immediately
dangerous to life or health" (IDLH) values. NTIS PB87-163531. As cited in: ATSDR, 1996.

Sable, G.V., T.P. Clark. 1984. Volatile organic compounds as indicators of municipal solid waste
leachate contamination. Waste Manage. Res. 2: 119-130. As cited in: ATSDR, 1996.

Sack, T.M., D.H. Steele, K. Hammerstrom, et al. 1992. A survey of household products for
volatile organic compounds. Atmos. Environ. 26A:1063- 1070. As cited in: ATSDR, 1996.

Schmidt, R. 1976. The embryotoxic and teratogenic effect of tetrachloroethane experimental
studies. Biol. Rundsch. 14:4220-223.

Schmidt, P., S. Binnevies, R. Gohlke, R. Roth.  1972. Subacute action of low concentration of
chlorinated ethanes on rats with and without additional ethanol treatment. I. Biochemical and
toxicometrical aspects, especially results in subacute and chronic toxicity studies with 1,1,2,2-
tetrachloroethane. Int. Arch. Arbeitsmed. 30:283-298.

Schmidt, P., R. Gohlke, A. Just, et al. 1980.  Combined action of hepatotoxic substances and
increased environmental temperature on the liver of rats. J. Hyg. Epidemiol. Microbial. Immunol.
(Prague) 24:271-277.

Schmidt, P., IP. Ulanova, G.G. Avilova, S.M. Binnevis. 1975. Comparison of the processes of
adaptation of the organism to monotonic and intermittent action of 1,1,2,2-tetrachloroethane.
Gigiena Truda i Professional'nye Zabolevaniya 2:30-34. As cited in: WHO, 1998.

Shah, J.J., E.K. Heyerdahl. 1988. National ambient volatile organic compounds (VOCs) database
update.  Research Triangle Park, NC. U.S. Environmental Protection Agency, Atmospheric
Sciences Research Laboratory. As cited in ATSDR, 1996.

Sherman, J.B. 1953. Eight cases of acute tetrachloroethane poisoning. J. Trop. Med. Hyg.
56:139-140. As cited in: ATSDR, 1996.

Smyth, H.F., Jr, C.P. Carpenter, C.S. Weil, et al. 1969. Range-finding toxicity data-List VII. Am.
Ind. Hyg. Assoc. J. 30:470-476. As cited in:  ATSDR, 1996.

Speth, T.F., M.L. Magnuson, C.A. Kelty, C.J. Parrett. 2001. Treatment studies of CCL
contaminants.  In: Proceedings, AWWA Water Quality Technology Conference.  Nashville, TN.
November 11-15, 2001.

Speth, T.F., J.Q. Adams. 1993. GAC and air stripping design support for the Safe Drinking
Water Act. In: Clark, R. and S. Summers (eds.), Strategies and Technologies for Meeting
SDWA Requirements. Lewis Publishers, Ann Arbor, MI, pp. 47-89. As cited in: Speth et al.,
                                                                           April 2008


Squillace, P.J., MJ. Moran, W.W. Lapham, et al. 1999. Volatile organic compounds in untreated
ambient groundwater of the United States,  1985-1995. Environ. Sci. Technol. 33(23):4176-4187.
Available on-line at: http://sd.water.usgs.gov/nawqa/pubs/journal/EST.voc.squillace.pdf. Link to
document (and appendices) from http://sd.water.usgs.gov/nawqa/pubs/.

Staples, C.A., A.F. Werner, TJ. Hoogheem. 1985. Assessment of priority pollutant
concentrations in the United States using STORET database. Environ. Toxicol. Chem. 4: 13 1-
142. As cited in: AT SDR, 1996.

Story, D.L., E.F. Meierhenry, C.A. Tyson,  et al.  1986. Difference in rat liver enzyme-altered foci
produced by chlorinated aliphatics and phenobarbital. Toxicol. Ind.Health 2:351-362.

Tabak, H.H., S.A. Quave, C.I. Mashni, et al. 1981. Biodegradability studies with organic priority
pollutant compounds. J. Water Pollut. Control Fed.  53:1503-1518. As cited in: ATSDR, 1996.

Thomas, R.G. 1982. Volatilization from water. In: Lyman W.J., W.F. Reehl, D.H. Rosenblatt
(eds.). Handbook of Chemical Property Estimation Methods. Chapter 15. New York, NY:
McGraw-Hill Book Co. pp. 15-1 tol5-34. As cited in: ATSDR, 1996.

Tomasi, A., E. Albano, A. Bini, et al. 1984. Free radical intermediates under hypoxic conditions
in the metabolism of halogenated carcinogens. Toxicol. Pathol. 12(3):240-6. As cited in:
Paolini, 1992.

Tu, A.S., T.A. Murray, K.M. Hatch, et al. 1985. In vitro transformation of BALB/c3T3 cells by
chlorinated ethanes and ethylenes. Cancer Lett. 28:85-92. As cited in: WHO, 1998.

U.S. EPA. 1986a. United States Environmental Protection Agency. Guidelines for carcinogen
risk assessment. Fed.  Reg.  51(185):33992-34003.

U.S. EPA. 1986b. United States Environmental Protection Agency. Integrated Risk Information
System (IRIS): 1,1,2,2-Tetrachloroethane (Cancer Assessment 1986). Available on-line at:
http://www.epa. gov/iri s/subst/0193 .htm.

U.S. EPA. 1988 Recommendations for and documentation of biological values for use in risk
assessment. EPA 600/6-87/008.

U.S. EPA (United States Environmental Protection Agency). 1989. 1,1,2,2-Tetrachloroethane
Drinking Water Health Advisory. Office of Water.

U.S. EPA. 1995a. United States Environmental Protection Agency. Volatile organic compounds
in water by purge and trap capillary column gas chromatography with photoionization and
electrolytic conductivity detectors in series. Revision 2.1. In: Methods for the Determination of
Organic Compounds in Drinking Water, Supplement III.  EPA Report 600-R-95-131. August,
                                                                           April 2008


U.S. EPA. 1995b. United States Environmental Protection Agency. Measurement of purgeable
organic compounds in water by capillary column gas chromatography/mass spectrometry.
Revision 4.1. In: Methods for the Determination of Organic Compounds in Drinking Water,
Supplement III. EPA Report 600-R-95-131.

U.S. EPA. 2000. United States Environmental Protection Agency. Methodology for Deriving
Ambient Water Quality Criteria for the Protection of Human Health.  EPA-822-B-00-004. Office
of Science and Technology, Office of Water, Washington, DC.

U.S. EPA. 2003. United States Environmental Protection Agency. Toxicological review of
dichloroacetic acid in support of summary information on Integrated Risk Information System
(IRIS). National Center for Environmental Assessment, Washington,  D.C. EPA/635/R-03/007.

U.S. EPA. 2004a. United States Environmental Protection Agency. OPPTS Chemical Ingredient
Database (updated weekly). Available on-line at:
http://www.cdpr.ca.gov/docs/epa/epachem.htm (accessed October 10, 2004).

U.S. EPA. 2004b. United States Environmental Protection Agency. TRI Explorer: Trends.
Search for 1,1,2,2-tetrachloroethane. Available on-line at:
http://www.epa.gov/triexplorer/trends.htm (last modified November 18, 2005, accessed April 20,

U.S. EPA. 2005. United States Environmental Protection Agency. Guidelines for Carcinogen
Risk Assessment.  EPA/630/P-03/001B. Risk Assessment Forum, Washington, DC.

U.S. EPA. 2006. United States Environmental Protection Agency. Health Effects Support
Document for 1,1,2,2-Tetrachloroethane. Draft Report. Office of Water, Health and Ecological
Criteria Division, Washington, DC.

Vogel, E.W., M.J.M. Nivard. 1993. Performance of 181 chemicals in aDrosophila assay
predominantly monitoring interchromosomal  mitotic recombination. Mutagen. 8(1):57-81. As
cited in: WHO, 1998.

Ward, J.M. 1955. Accidental poisoning with tetrachloroethane. Br. Med. J. 1:1136. As cited in:
ATSDR, 1996.

Warner, J.R., TJ. Hughes, L.D. Claxton. 1988. Mutagenicity of 16 volatile organic chemicals in
a vaporization technique with Salmonella typhimurium TA100. Environ. Mol. Mutagen. 11
(Suppl. 11):111.  As cited in: WHO, 1998.

WHO (World Health Organization). 1998. Concise international chemical assessment document;
1,1,2,2-tetrachloroethane. Geneva.
                                                                          April 2008


Willcox, W.H., B.H. Spilsbury, T.M. Legge. 1915. An outbreak of toxic jaundice of a new type
amongst aeroplane workers-Its clinical and toxicological aspect. Trans. Med. Soc. London 38:
129-156. As cited in ATSDR, 1996.

Williams, G. 1983. DNA Repair Tests of 11 Chlorinated Hydrocarbon Analogs.  Final Report.
EPA Contract. US Environmental Protection Agency, Office of Toxic Substances (Document
No. 40+8324292). As cited in: WHO, 1998.

Wolff, L. 1978. The effect of 1,1,2,2-tetrachloroethane on passive avoidance learning and
spontaneous locomotor activity. Activ. Nerv. Sup. (Praha) 20:14-16. As cited in: ATSDR, 1996.

Woodruff, R.C., J.M. Mason, R. Valencia, S. Zimmering. 1985. Chemical mutagenesis testing in
Drosophila. 5. Results of 53 coded compounds tested for the National Toxicology Program.
Environ. Mutagen. 7:677-702. As cited in: WHO, 1998.

Yllner, S. 1971. Metabolism of l,l,2,2-tetrachloroethane-14C in the mouse. ActaPharmacol.
Toxicol. 29:499-5 12. As cited in: ATSDR, 1996.
                                                                          April 2008