March 31, 1987
TRICHLOROETHYLENE
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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Trichloroethylene March 31, 1987
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This Health Advisory is based upon information presented in the Office
of Drinking Water'.s Health Effects Criteria Document (CD) for Trichloroethylene
(U.S. EPA, 1985a). 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 # 86-118106/AS. The toll free number is (800)
336-4700; in Washington, D.C. area: (703) 487-4650.
II. GENERAL INFORMATION AND PROPERTIES
CAS No. 79-01-6
Structural Formula
C1-HC=C-C12
Trichloroethylene
Synonyms
TCE, trichloroethene, acetylene trichloride, Tri, Trilene
Uses
Industrial solvent and degreaser for metal components
Properties (Torkelson and Rowe, 1981; Windholtz, 1983)
Chemical Formula C2HC13
Molecular Weight 131.40
Physical State Colorless liquid
Boiling Point 86.7°C
Vapor Pressure 77 mm (25°C)
Density at 25°C 1.4 g/mL
Water Solubility 0.1 g/1 00 mL (20-C)
Odor Threshold (water) 0.5 mg/L
Odor Threshold (air) 2.5-900 mg/m3
Organoleptic Threshold (water) 0.31 mg/L (Amoore and Hautala, 1983)
Conversion Factor 1 ppm » 5.46 mg/m3
Occurrence
0 Trichloroethylene (TCE) is a synthetic chemical with no natural
sources.
*. Production of,,TCE was 200 million ,lbs in.1982 (U.S. ITC, 1983).
' - . . „ ?" VJ
0 The major sourjce'of TCE released to the- environment is from its use
'as a metal degreaser. Since TCE is'nojb consumed during this use, the
.majority of all TCE production is.,released to the environment. Most
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Trichloroethylene March 31, 1987
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of the releases occur to the atmosphere by evaporation. However, TCE
which is not lost to evaporation becomes heavily contaminated with
grease and oil and has been disposed of by burial in landfills, dumping
on the ground or into sewers. Because metal working operations are
performed nationwide, TCE releases occur in all industrialized areas.
Releases of TCE during production and other uses are relatively minor.
0 Trichloroethylene released to the air is degraded in a matter of a few
days. Trichloroethylene released to surface waters migrates to the
atmosphere in a few days or weeks where it also degrades. Photo-
oxidation appears to be the predominant fate of this compound (U.S.
EPA, 1979). Trichloroethylene which is released to the land does not
degrade rapidly, migrates readily to ground water and remains in
ground water for months to years. Under certain conditions, TCE in
groundwater appears to degrade to dichloroethylene and vinyl chloride.
Trichloroethylene also may be formed in ground water by the degradation
of tetrachloroethylene (Parsons et al., 1984; Vogel and McCarty,
1985). Trichloroethylene, unlike other chlorinated compounds, does not
bioaccumulate in individual animals or food chains.
8 Because of the large and dispersed releases, TCE occurs widely in the
environment. Trichloroethylene is ubiquitous in the air with levels
in the ppt to ppb range. Trichloroethylene is a common contaminant
in ground and surface waters with higher levels found in ground
water. Surveys of drinking water supplies have found that 3% of all
public systems derived -from well water contain TCE at levels of 0.5
ug/L or higher. A small number of systems (0.04%) have levels higher
than 100 ug/L. Public systems derived from surface water also have
been found to contain TCE but at lower levels. Trichloroethylene has
been reported to occur in some foods in the ppm range.
0 The major sources of exposure to TCE are from contaminated water and
to a lesser extent air; food is only a minor source of TCE exposure
(U.S. EPA, 1983).
III. PHARMACOKINETICS
Absorption
0 Data on absorption of ingested TCE are limited. When a dose of 200
mgA9 of 14C-TCE in corn oil was administered to rats, 97% of the
dose was recovered during 72 hours after dosing (DeKant et al., 1984).
Distribution
° Doses of 0, 10, 100 or 1,000 mg TCE/kg/day were administered by gavage
to rats five days/week for six weeks (Zenick et al., 1984). Marginal
increases in TCE tissue levels were detected in the 10 mg/kg/day and
100 mgAg/day dose groups. Compared to controls, a marked increase
in TCE levels in most tissues was observed in the highest dose group.
Trichloroethylene was distributed in all tissues examined with the
highest concentrations in the fat, kidney, lung, adrenals, vas
deferens, epididymis, brain and liver.
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Trichloroethylene March 31, 1987
Metabolism
0 Studies indicate that TCE is metabolized to trichloroethylene oxide,
trichloracetaldehyde, trichloroacetic acid, monochloroacetic acid,
trichloroethanol and trichloroethanol glucuronide (U.S. EPA, 1985a).
Excretion
0 Trichloroethylene and its metabolites are excreted in urine, by
exhalation and, to a lesser degree, in sweat, feces and saliva
(Soucek and Vlachova, 1959).
IV. HEALTH EFFECTS
Humans
Short-term Exposure .
0 Oral exposure of humans to 15 to 25 ml (21 to 35 g) quantities of TCE
resulted in vomiting and abdominal pain, followed by transient uncon-
sciousness (Stephana, 1945).
Long-term Exposure
0 Studies of humans exposed occupationally have shown an increase in
serum transaminases, which indicates damage to the liver parenchyma
(Lachnit, 1971). Quantitative exposure levels were not available.
Animals
>—
Short-term Exposure
0 The acute oral LDso of TCE in rats is 4.92 g/kg
(NIOSH, 1980).
Long-term Exposure
0 Rats exposed to 300 mg/m3 (55 ppm) TCE five days/week for 14 weeks
had elevated liver weights (Kimmerle and Eben, 1973).
Reproductive Effects
0 No data were available on the reproductive effects of TCE.
Developmental Effects
•
0 No data were available on the developmental effects of TCE.
Mutagenicity
0 Trichloroethylene was mutagenic in Salmonella typhimurium and in the
B. coli K-12 strain, utilizing liver microsomes for activation (Greim
et al., 1975, 1977).
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Trichloroethylene March 31, 1987
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Carcinogenicity
0 Technical TCE (containing epichlorohydrin and other compounds) was
found to induce a hepatocellular carcinogenic response in B6C3F-J mice
(NCI, 1976). Under the conditions of this experiment, a carcinogenic
response was not observed in Osborne-Mendel rats. The "time-weighted"
average doses were 549 and 1,097 mg/kg for both male and female rats.
The time-weighted average daily doses were 1,169 and 2,339 mgA9 f°r
male mice and 869 and 1,739 mg/kg for female mice.
0 Epichlorohydrin-free TCE was reported to be carcinogenic in B6C3F!|
mice when administered in corn oil at 1,000 mg/kg/day, 5 days/wk, for
103 weeks (NTP, 1982). It was not found to be carcinogenic in female
Fischer 344 rats when administered in corn oil at 500 or 1,000 mg/kg/day,
5 days/wk, for 103 weeks. The experiment with male rats was considered
to be inadequate since these rats received doses of TCE that exceeded
the maximum tolerated dose.
0 TCE has been shown to be carcinogenic in mice utilizing the inhalation
as well as the oral route of exposure. The National Cancer Institute
(1976) and the National Toxicology Program (1982) each conducted an
oral gavage study with TCE, one contaminated with epichlorohydrin and
the other free of epichlorohydrin, respectively. In these studies,
as described above, B6C3Fi mice were used, and the results were
unequivocally positive, showing liver neoplasms.
0 In an inhalation study, Henschler et al. (1980) reported dose-related
malignant lymphomas in female mice exposed to 100 or 500 ppm TCE vapor
6 hrs/day, 5 days/wk, for 18 months (HANtNMRI strain). However, the
authors downplayed the significance of this observation, indicating
that this strain of mice has a high incidence of spontaneous lymphomas.
0 Fukuda et al. (1983) found pulmonary adenocarcinomas in female ICR
mice on exposure to TCE vapor*
0 Henschler et al. (1984) tested Swiss (ICR/HA) mice and reported that
when the animals were treated by gavage with TCE in corn oil, no
statistical differences were observed in the incidence of cancers.
The results of this study can be questioned because the dose schedule
was often interrupted even with half of the original dose. Therefore,
it is very difficult to assess the exposure. A slight increase in
tumors was found in all groups treated with TCE but did not approach
statistical significance.
0 The Van Duuren study (1979) with skin applications of TCE in ICR/HA
mice does not negate the positive findings with other strains of mice
and other routes of exposure.
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
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Trichloroethylene March'31, 1987a
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are available that identify a sensitive noncarcinogenic end point of toxicity.
Ihe HAs for noncarcinogenic toxicants are derived using the following formula:
HA = JNOAEL or LOAEL) x (BW) „ mg n ( ug/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 and Ten-day Health Advisory
Suitable data were not available to estimate One-day and Ten-day Health
Advisories.
Longer-term Health Advisory
No suitable data are available from which to calculate a Longer-term
Health Advisory.
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*—She Lif-etime-HA—ia 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.
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Trichloroethylene March 31, 1987a
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Trichloroethylene may be classified in Group Bi Probable Human Carcinogen,
according to EPA's weight-of-evidence scheme for the classification of carcino-
genic potential (U.S. EPA, 1986). Because of this, caution must be exercised
in making a decision on how to deal with possible lifetime exposure to this
substance. The risk manager must balance this assessment of carcinogenic
potential against the likelihood of occurrence of health effects related to
non-carcinogenic end-points of toxicity. In order to assist the risk manager
in this process, drinking water concentrations associated with estimated
excess lifetime cancer risks over the range of one in ten thousand to one
in a million for the 70 kg adult, drinking 2 liters of water per day, are
provided in the following section. In addition, in this section, a Drinking
Water Equivalent Level .(DWEL) is derived. A DWEL is defined as the medium-
specific (in this case, drinking water) exposure which is interpreted to be
protective for non-carcinogenic end-points of toxicity over a lifetime of
exposure. The DWEL is determined for the 70 kg adult, ingesting 2 liters of
water per day. Also provided is an estimate of the excess cancer risk that
would result if exposure were to occur at the DWEL over a lifetime.
Neither the risk estimates nor the DWEL take relative source contribution
into account. The risk manager should do this on a case-by-case basis,
considering the circumstances of the specific contamination incident that.has
occurred.
The study by Kimmerle and Eben (1973)is the most appropriate from which
to derive the DWEL. This.study evaluated the subacute exposure to trichloro-
ethylene via inhalation by adult rats for some 14 weeks following, exposure to
55 ppm (300 mg/m^), five days a week. Indices of toxicity include hemato-
logical investigation, liver and renal function tests, blood glucose and organ/
body weight ratios. Liver weights were shown to be elevated while other test
values were not different from controls. The elevated liver weights could be
interpreted to be the result of hydropic changes or fatty accumulation. The
no-observed-effect level was not identified since only a single concentration
was administered. From these results, a LOAEL of 55 ppm (300 mg/m3) was
identified. Ifeing the LOAEL, the DWEL is derived as follows:
Step 1: Determination of the Total Absorbed Dose (TAD)
TAD - OOP mg/m3) (8 m3/dav) (5/7) (0.3) ,7,35 mg/kg/day
(70 kg )
where:
300 mg/m3 « LQAEL for liver effects in rats
8 m3/day = Volume of air inhaled during the exposure period
5/7 » Conversion factor for adjusting from 5 days/week exposure
to a daily dose
0.3 « Ratio of the dose absorbed.
70 kg » Assumed weight of adult.
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Trichloroethylene March 31, 1987
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Step 2: Determination of the Reference Dose (RfD)
RfD « 7.35 mg/kg/day = 0.00735 mg/kg/day
(100) (10) y/ y/ *
where:
7.35 mg/kg/day » TAD.
1,000 = uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a LOAEL from an animal study.
Step 3: Determination of the Drinking Water Equivalent Level (DWEL)
DWEL = (0*00735 mg/kg/day)(70 kg) _ 0%26 mg/L (260 ug/L)
2 L/day
where:
0.00735 mg/kg/day = RfD.
70 kg = assumed body weight of an adult.
2 L/day = assumed daily water consumptiion of an adult.
The estimated excess cancer risk associated with lifetime exposure to
drinking water containing TCE at 260 ug/L is approximately 1 X 10~4. This
estimate represents the upper 95% confidence limit from extrapolations prepared
by EPA's Carcinogen Assessment Group using the linearized, multistage model.
The actual risk is unlikely to exceed this value, but there is considerable
uncertainty as to the accuracy of risks calculated by this methodology.
Evaluation of Carcinogenic Potential
0 IARC (1982) has classified TCE in Group 3.
0 Trichloroethylene has been classified in Group B2: Probable Human
Carcinogen. This classification for carcinogenicity was determined
by a technical panel of EPA's Risk Assessment Forum using the EPA
risk assessment guidelines for carcinogens (U.S. EPA, 1986). This
category is used for agents for which there is "sufficient evidence*
for human carcinogenicity from animal studies and for which there is
"inadequate evidence" or "no data" from human studies.
0 Using the improved multistage linearized model, it can be estimated
that water with TCE concentrations of 280 ug/L» 28 ug/L or 2.8 ug/L
may increase the risk of one excess cancer per 1 04, 105 or 106 people
exposed, respectively. These estimates were calculated from the 1976
NCI bioassay data, which utilized TCE contaminated with epichlorohydrin.
Since then, an NTP (1982) bioassay utilizing epichlorohydrin-free TCE
has become available; the data from this bioassay have been reviewed
and evaluated for carcinogenicity, and epichlorohydrin-free TCE has
been reported to be carcinogenic in mice.
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Trichloroethylene March 31, 1987
VI. OTHER CRITERIA, GUIDANCE AND STANDARDS
0 ACGIH (1984) has recommended a threshold limit value (TLV) of 50 ppm
270 mg/m3) and a short-term exposure limit (STEL) of 150 ppm
mg/m3.
0 The HAS (1980) recommended One- and Seven-day SNARLS of 105 and 15 mg/L,
respectively .
0 The WHO ( 1 981 ) recommended a drinking water guidance level of 30 ug/L
based on a carcinogenic end point.
0 The EPA (U.S. EPA, 1980) recommended a water quality criterion of
6.77 mg/L for effects other than cancer.
0 The EPA (U.S. EPA, 1985d) has promulgated a Recommended Maximum
Contaminant Level (RMCL) of zero based upon its classification as a
known or probable human carcinogen and has proposed a Maximum Contami-
nant Level (MCL) of 0.005 mg/L based on its RMCL and appropriate
feasibility studies.
VII. ANALYTICAL METHODS
Analysis of TCE is .by a purge-and-trap gas chromatographic procedure
used for the determination of volatile organohalides in drinking water
(U.S. EPA, 1985b). This method calls for the bubbling of an inert
gas through the sample and trapping TCE on an adsorbant material.
The adsorbant material is heated to drive off the TCE onto a gas
chromatographic column. This method is applicable to the measurement
of TCE over a concentration range of 0.01 to 1500 ug/L. Confirmatory
analysis for TCE is by mass spectrometry (U.S. EPA, 1985c). The
detection limit for confirmation by mass spectrometry is 0.2 ug/L.
VIII. TREATMENT TECHNOLOGIES
0 Treatment technologies which will remove TCE from water include
granular activated carbon (GAG) adsorption, aeration and boiling.
0 Dobbs and Cohen (1980) developed adsorption isotherms for several
organic chemicals including TCE. It was reported that Pibrasorb®
300 carbon exhibited adsorptive capacities of 7 mg, 1.6 mg and 0.4 mg
TCE/gm carbon at equilibrium concentrations of 100, 10 and 1 mg/L,
respectively. USEPA-DWRD installed pilot-scale adsorption columns
at different sites in New England and Pennsylvania. In New England,
contaminated well water with TCE concentrations ranging from 0.4 to
177 mg/L was passed through GAG columns until a breakthrough concen-
tration of 0.1 mg/L was achieved with empty bed contact time (EBCT)
of 18 and 9 minutes, respectively (Love and Eilers, 1982). In
Pennsylvania, TCE concentrations ranging from 20 to 130 mg/L were
reduced to 4.5 mg/L by GAG after 2 months of continuous operation
. (ESE, 1985).
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Trichloroethylene March 31, 1987
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TCE is amenable to aeration on the basis of its Henry's Law Constant
of 550 atm (Kavanaugh and Trussell, 1980). In a full plant-scale
(3.78 MGD) redwood slat tray aeration column, a removal efficiency of
50-60% was achieved from TCE initial concentrations of 8.3-39.5 mg/L
at an air-to-water ratio of 30:1 (Hess et al., 1981). In another
full plant-scale (6.0 MGD) multiple tray aeration column study, TCE
removal of 52% was achieved from 150 mg/L (Hess et al., 1981). A
full plant-scale packed tower aeration column removed 97-99% of TCE
from 1,500-2,000 mg/L contaminated groundwater at air-to-water ratio
of 25:1 (ESE, 1985).
Boiling also is- effective in eliminating TCE from water on a short-term,
emergency; basis. Studies have shown 5 minutes of vigorous boiling
will remove 95% of TCE originally present (Love and Eilers, 1982).
r '
Air stripping is an effective, simple and relatively inexpensive process
for removing TCE and other volatile organics from water. However, use
of this process then transfers the contaminant directly to 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 other
hazards associated with the chemical.
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Trichloroethylene March 31, 1987
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IX. REFERENCES
ACGIH. 1984. American Conference of Governmental Industrial Hygienists.
Documentation of the threshold limit values. 4th ed. 1980-1984 Supplement.
pp. 406-408.
Amoore, J.E., and E. Hautala. 1983. Odor as an aid to chemical safety:
Odor thresholds compared with threshold limit values and volatilities
for 214 industrial chemicals in air and water dilution. J. Appl. Tox.
3:272-290.
deKant, W. Metzderm and 0. Henschler. 1984. Novel metabolites of trichloro-
ethylene through dechlorination reactions in rats, mice and humans.
Biochem. Fharmacol. 33:2021-2027.
Dobbs, R.A., and J.M. Cohen. 1980. Carbon adsorption isotherms for toxic
organics. EPA 600/8-80-023, Office of Research and Development, MERL,
Wastewater Treatment Division, Cincinnati, Ohio.
ESE. 1985. Environmental Science and Engineering. Draft technologies and
costs for the removal of volatile organic chemicals from potable water
supplies. ESE No. 84-912-0300 prepared for U.S. EPA, Science and Technology
Branch, CSD, ODW, Washington, D.C.
Fukuda, K., K. Takemoto and H. Tsuruta. 1983. Inhalation carcinogenicity of
trichloroethylene in mice and rats. Ind. Health. 21:243-254.
Greim, H., D. Bimboes, G. Egert, W. Giggelmann and M. Kramer. 1977. Muta-
genicity and chromosomal aberrations as an analytical tool for in vitro
detection of mammalian enzyme-mediated formation of reactive metabolites.
Arch. Toxicol. 39:159.
Greim, H., G. Bonse, Z. Radwan, D. Reichert and D. Henschler. 1975. Muta-
genicity ^n vitro and potential carcinogenicity of chlorinated ethylenes
as a function of metabolic oxirane formation. Biochem. Pharmacol.
24:2013.
Henschler, D., W. Romen, H.M. Elsasser, D. Reichert, E.Eder and Z. Radwan.
1980. Carcinogenicity study of trichloroethylene by long-term inhalation
in the animal species. Arch. Toxicol. 43:237-248.
Henschler, D., H. Elsasser, W. Romen and E. Eder. 1984. Carcinogenicity
study of trichloroethylene, with and without epoxide stabilizers, in
mice. J. Cancer Res. Clin. Oncol. 104:149-156.
Hess, A.F., J.E. Dyksen and G.C. Cline. 1981. Case study involving removal
of organic chemical compounds from ground water. Presented at Annual
American Water Works Association Conference, St. Louis, Missouri.
IARC. 1982. IARC monographs on the evaluation of the carcinogenic risk of
' '• chemicals to humans. Supplement 4, Lyon, France..
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Trichloroethylene March 31, 1987
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Kavanaugh, M.C., and R.R. Trussell. 1980. Design of aeration towers to
strip volatile contaminants from drinking water. JAWWA. December.
Kimmerle, G., and A. Eben. 1973. Metabolism, excretion and toxicology of
trichloroethylene after inhalation* 1. Experimental exposure on rats.
Arch. Toxicol. 30:115.
Lachnit, V. 1971. Halogenated hydrocarbons and the liver. Wien. Klin.
Wochenschr. 83(41 ):734.
Love, O.T., Jr., and R.G. Eilers. 1982. Treatment of drinking water containing
trichloroethylene and related industrial solvents. JAWWA. August.
MAS. 1980. National Academy of Sciences. Drinking Water and Health. Volume 3.
National Academy Press. Washington, DC.
NCI. 1976. National Cancer Institute. Carcinogenesis bioassay of trichloro-
ethylene. U.S. Department of Health, Education and Welfare, Public
Health Service, CAS No. 79-01-6, February.
NIOSH. 1980. Registry of Toxic Effects of Chemical Substances. U.S. Depart-
ment of Health and Human Services. DHHS (NIOSH) 81-116.
NTP. 1982. National Toxicology Program. Carcinogenesis bioassay for tri-
chloroethylene. CAS # 79-01-6. No. 82-1799. (Draft).
Parsons, P., P.R. Wood and J. DeMarco. 1984. Transformation of.tetrachloro-
ethene and trichloroethene in microcosms and groundwater. JAWWA,
26(2):56f.
Soucek, B., and D. Vlachova. 1959. Metabolites of trichloroethylene excreted
in the urine by man. Pracoc. Lek. 11:457.
Stephens, C.A. 1945. Poisoning by accidental drinking of trichloroethylene.
Brit. Med. J. 2:218.
Torkelson, T.R., and V.K. Rowe. 1981. Halogenated aliphatic hydrocarbons.
Ini Industrial Hygiene and Toxicology. 3rd ed. Vol. 2B. John Wiley
and Sons, New York. p. 3553.
U.S. EPA. 1979. U.S. Environmental Protection Agency. Water Related Environ-
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Standards, EPA-440/4-79-029.
U.S. EPA. 1980. U.S. Environmental Protection Agency. Ambient water quality
criteria document for trichloroethylene. Office of Water Research and
Standards. Cincinnati, Ohio.
U.S. EPA. 1983. U.S. Environmental Protection Agency. Trichloroethylene
occurrence in drinking water, food, and air. Office of Drinking Water.
U.S. EPA. 1985a. U.S. Environmental Protection Agency. The drinking water
criteria document on trichloroethylene. Office of Drinking Water.
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Trichloroethylene March 31, 1987
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O.S. EPA. 1985b. Method 502.1. Volatile Halogenated Organic Compounds in
Water by Purge and Trap Gas Chromatography, Environmental Monitoring and
Support Laboratory, Cincinnati, Ohio 45268.
U.S. EPA. 1985c. Method 524.1. Volatile Organic Compounds in Water by Purge
and Trap Gas Chromatography/Mass Spectrometry, Environmental Monitoring
and Support Laboratory, Cincinnati, Ohio 4E26S.
U.S. EPA. I985d. U.S. Environmental Protection Agency. National primary
drinking water regulations; Volatile synthetic organic chemicals; final
rule and proposed rule. Federal Register 50(219):46880-46933.
U.S. EPA. 1986. U.S. Environmental Protection Agency. Guidelines for
carcinogenic risk assessment. Federal Register 51(185):33992-34003.
September 24. :
U.S. ITC. 1983. United States International Trade Commission. Synthetic
organic chemicals. United States production, USITC Publication 1422.
Washington, D.C. 20436. •
van Duuren, B.L., B.M. Goldschmidt, G. Lowengart, A.C. Smith, S. Melchionne,
I. Seldman and 0. Roth. 1979. Carcinogenicity of halogenated olefinic
and aliphatic hydrocarbons in mice. J. Natl. Cancer Znst. 63:1433-1439.
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