820K87114
1,1,1-TRICHLOROETHANE
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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1,1,1-Trichloroethane March 31, 1987
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This Health Advisory is based on information presented in the Office of
Drinking Water's Health Effects Criteria Document (CD) for 1,1,1-Trichloro-
ethane (U.S. EPA, 1984a)« The HA and CD formats are similar for easy reference,
Individuals desiring further information on the toxicological data base or
rationale for risk characterization should consult the CD. The CD is available
for review at each EPA Regional Office of Drinking Water counterpart (e.g.,
Water Supply Branch or Drinking Water Branch), or for a fee from the National
Technical Information Service, U.S. Department of Commerce, 5285 Port Royal
Rd., Springfield, VA 22161, PB # 86-118130/AS. The toll free number is (800)
336-4700; in the Washington, D.C. area: (703) 487-4650.
II. GENERAL INFORMATION AND PROPERTIES
CAS No. 71-55-6
Chemical Structure
H Cl
I I
H-C-C-C1
I I
H Cl
Synonyms
0 1,1,1-TCA, methyl chloroform, ethane, 1,1,1-trichloro and
methyltrichloromethane.
Uses
0 In the cleaning and vapor degreasing of fabricated metal parts
0 In the synthesis of other organic chemicals
0 As a spot remover and film cleaner
0 As an additive in metal cutting oils
Properties (U.S. EPA 1984)
Chemical Formula C2H3CJ-3
Molecular Weight 133.41
Physical State colorless, nonflammable liquid
Boiling Point 74°C
Melting Point —
Density 4.6
Vapor Pressure 100 mm Hg (25°C)
Water Solubility (25°C) 44 mg/L
Log Octanol/Water Partition
Coefficient
Taste Threshold
Odor Threshold
Conversion Factor 5.4 mg/m3
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Occurrence
0 1,1,1-Trichloroethane is a synthetic chemical with no natural sources.
0 Production of 1,1,1-trichloroethane was 600 million Ibs in 1982
(U.S. ITC, 1983). About 70% of all 1,1,1-trichloroethane is used in
metal cleaning.
0 The major source of 1,1,1-trichloroethane released to the environment
is from its use as a metal degreaser. Since 1,1,1-trichloroethane is
not consumed during degreasing operations, the majority of all
1,1,1-trichloroethane production is released to the environment.
Most of the releases occur to the atmosphere by evaporation. However,
1,1,1-trichloroethane which is not lost to evaporation becomes heavily
contaminated with grease and oil and is disposed of by burial in
landfills or dumping on the ground or into sewers. Because metal
working operations are performed nationwide, 1,1,1-trichloroethane
releases occur in all industrialized areas. Releases of 1,1,1-tri-
chloroethane from other uses also may be significant.
0 1,1,1-Trichloroethane released to the air degrades slowly with an
estimated half life of from 1 *•- ° - "s. 1 ,1,1-Trichloroethane
released to surface waters migrates to the atmosphere in a few days
or weeks. 1,1,1-Trichloroethane which is released to the land does
not sorb onto soil and migrates readily to ground water. 1,1,1-Tri-
chloroethane slowly hydrolyzes in water with an estimated half-life
of greater than 6 months. 1,1,1-Trichloroethane, unlike other chlori-
nated compounds, does not bioaccumulate in individual animals or food
chains.
0 Because of the large and dispersed releases, 1,1,1-trichloroethane
occurs widely in the environment. 1,1,1-Trichloroethane is ubiquitous
in the air with levels in the low ppb range, and is a common contami-
nant 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 1,1,1-trichloroethane
at levels of 0.5 ug/L or higher. A small number of systems (0.1%)
have levels higher than 100 ug/L. Public systems derived from surface
water also have been found to contain 1,1,1-trichloroethane bat at
lower levels. 1,1,1-Trichloroethane has been reported to occur in
some foods in the ppb range.
0 The major sources of exposure to 1,1,1-trichloroethane are from con-
taminated water and, to a lesser extent, air. Food is only a minor
source.
III. PHARMACOKINETICS
Absorption
0 While inhalation of 1,1,1-TCA vapor through the lungs is the common
route of entry into the body, 1,1,1-TCA also is absorbed rapidly and
completely from the gastrointestinal tract (Stewart et al., 1969).
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0 Stewart and Andrews (1966) reported an observation of non-lethal acute
intoxication after oral ingestion of a liquid ounce of 1,1,1-TCA
(0.6 g/kg bw). The concentration of 1,1,1-TCA in the expired air was
measured serially and found to be equivalent to an inhalation exposure
of 500 ppm (2,700 mg/m^) by experimental subjects.
0 Monster et al. (1979) and Humbert and Fernandez (1977) reported
1,1,1-TCA retention in subjects exposed to 70 (378 mg/m^) or 140 ppm
(756 mg/m3) respectively, to be 30 percent of the inspired air
concentration at equilibrium after 4 hours of exposure.
Metabolism
0 1,1,1-TCA is metabolized to a very limited extent by animals and humans
(Monster et al., 1979). The metabolites include trichloroethanol,
TCA-glucuronide and trichloroacetic acid which are excreted primarily
in urine; very small amounts of trichloroethanol (1 percent), however,
are excreted unchanged by the lungs.
0 Hake and his coworkers (1960), using C^-iabeled 1,1,1-TCA, determined
that less than 3% of 1,1,1-TCA is metabolized by rats following a
single intraperitoneal injection of 1,1,1-TCA.
0 More recently, estimates of the extent of metabolism in the haman
have been made from controlled inhalation exposure with unlabeled
1,1,1-TCA (Seki et al., 1975; Humbert and Fernandez, 1977; Monster
et al., 1979). From the experimentally determined retained dose and
the amounts of 1,1,1-TCA metabolites excreted into the urine, no more
than 6% of the dose is estimated to be metabolized.
0 The metabolic fate of inhaled 1,1,1-TCA in rats and mice is not
altered upon repeated exposures (Schumann et al., 1982).
Excretion
Unchanged 1,1,1-TCA is primarily excreted via lungs.
IV. HEALTH EFFECTS
Humans
Acute pulmonary congestion and edema typically are found in fatalities
resulting from inhalation of 1,1,1-TCA (Capalan et al., 1976;
Bonventre et al., 1977). Fatty vacuolation in the livers of the
exposed subjects also has been observed (Capalan et al., 1976).
Animals
Short-term Exposure
The acute oral LDsg for 1,1,1-TCA, as determined in several species
of animals, ranges from 5.7 to 14.3 g/kg (Torkelson et al., 1958).
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0 Vainio et al. (1976) found that a single oral dose of approximately
1.4 g/kg depressed some hepatic microsomal metabolic indices in rats
(including cytochrome P-450 and epoxide hydratase).
0 Bruckner et al. (1985) observed that there was relatively little
evidence of toxicity in a short-term study by gavage in rats receiving
1,1,1-TCA at 0.5 g/kg for 9 days. Higher doses of 5 and 10 g/kg
caused transient hyperexcitability and protracted narcosis, as well
as fatalities.
Long-term Exposure
0 Bruckner et al. (1985) administered 1,1,1-TCA to rats by gavage 5
times weekly for up to 12 weeks at 0, 0.5, 2.5 or 5.0 g/kg. Rats
given 2.5 or 5.0 g/kg exhibited reduced body weight gain and CNS
effects. Approximately 35% of these rats died during the first
50 days of the experiment, but only the 5.0 g/kg group showed an
increase in serum enzyme levels indicating an alteration in index
of toxicity. Ingestion of 0.5 g/kg for 12 weeks did not result in
alterations in indices of toxicity.
0 McNutt et al. (1975) exposed mice continuously by inhalation to
1,1,1-TCA at 250 (1,365 mg/m3) or 1,000 ppm (5,400 mg/m^l for 14 weeks.
Serial sacrifice of exposed and control mice from 1 to 14 weeks demon-
strated significant changes in the centrilobular hepatocytes as well
as evidence of triglyceride accumulation in the livers of the 1,000
ppm exposure group.
0 In the NCI (1977) study, diminished body weight gain and decreased
survival time were observed in both rats and mice. Male and female
rats were given 750 or 1,500 mg/kg 1,1,1-TCA in corn oil by gavage
5 times weekly for 78 weeks. Similarly, male and female mice received
approximately 2,800 or 5,600 mg/kg for 78 weeks.
0 In the NTP bioassay (1983), rats and mice were gavaged 5 times weekly
with 1,1,1-TCA in corn oil at doses of 375 or 750 mg/kg body weight
(rats) and 1,500 or 3,000 mg/kg body weight (mice), respectively, for
103 weeks.
Reproductive Effects
0 There appeared to be no dose-dependent effects on fertility, gestation,
viability indices in mice exposed to 1,1,1-TCA at dose levels of 100,
300 or 1,000 mg/kg for 35 days (Lane et al., 1982).
Developmental Effects
0 There appeared to be no dose-dependent effects on viability indices
in mice exposed to 1,1,1-TCA at dose levels of 100, 300 or 1,000 mg/kg
for 35 days (Lane et al., 1982).
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Mutagenicity
0 Simmon et al. (1977) reported that 1,1,1-TCA was mutagenic in various
strains of S_. typhimurium, with metabolic activation.
0 Loprieno et al. (1979) stated that 1,1,1-TCA was not mutagenic in
Saccharomyces cerevisiae or Schizosaccharomyes bombe.
Carcinogenicity
0 NTP (1983) has reported a significant (P <0.05) dose response trend
and increased incidences of hepatocellular carcinomas in the low- and
high-dose male and in the high-dose female mice exposed to 1,1,1-TCA
for 103 weeks. However, it should be noted that these findings are
based on the draft report and may change pending the outcome of the
ongoing NTP audit of the study.
V. QUANTIFICATION OF TOXICOLOGICAL EFFECTS
Health Advisories (HAs) are generally determined for One-day, Ten-day,
Longer-term (approximately 7 years) and Lifetime exposures if adequate data
are available that identify a sensitive noncarcinogenic end point of toxicity.
The HAs for noncarcinogenic toxicants are derived using the following formula:
HA - (NOAEL or LOAEL) x (BW) = /L < 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 Health Advisory
The study by Vainio et al. (1976) in rats is used in calculating a
One-day HA. In this study, 1,1,1-TCA at a single oral dose of approximately
1.4 g/kg depressed hepatic microsomal metabolic indices (cytochrome P-450,
epoxide hydratase) in rats. Using this dose as a NOAEL (although its signifi-
cance is not well established), a One-day HA for the 10 kg child is calculated
as follows:
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One-day HA = (1*4 gAg/day) (10 kg) = 140 mg/L or 140000 ug/L
(100) (1 L/day)
where:
1.4 g/kg/day = NOAEL based on absence of changes in hepatic microsomal
metabolic indices in rats.
10 kg = assumed body weight of a child.
100 = uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a NOAEL from an animal study.
1 L/day = assumed daily water consumption of a child.
Ten-day Health Advisory
Insufficient toxicological data are available to derive a Ten-day HA for
1,1,1-TCA. However, in order to provide a health guidance level for 1,1,1-TCA
for this duration of exposure, it is recommended that the Longer-term HA for
the 10 kg child be used (35 mg/L or 35,000 ug/L).
Longer-term Health Advisory
A subchronic oral toxicity study in rats by Bruckner et al. (1985) is
used for the Longer-term HA. In this study, rats (200 to 250 g) were given
1,1,1-TCA 5 times weekly by gavage for 12 weeks at 0, 0.5, 2.5 or 5 g/kg.
Rats given 2.5 or 5.0 g/kg exhibited reduced body weight gain and CNS effects
including transient hyperexcitability and protracted narcosis. Approximately
35% of these rats died during the first 50 days of the experiment, but only
the 5.0 g/kg group showed an increase in serum enzyme levels. Ingestion of
0.5 g/kg for 12 weeks did not result in alteration in indices of toxicity
(serum enzyme levels, organ weights or histopathological changes in the liver
and kidney).
Using 0.5 g/kg/day as a NOAEL, a Longer-term HA for the 10 kg child is
calculated as follows:
Longer-term HA = (500 mg/kg/day) (10 kg) (5/7) = 35 /L (35 000 ug/L)
(100) (1 L/day)
where:
0.5 g/kg/day = NOAEL in a 12-week study based on absence of various
parameters of toxicity in rats.
10 kg = assumed body weight of a child.
5/7 = conversion of 5 day/week exposure to daily exposure.
100 = uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a NOAEL from an animal study.
1 L/day = assumed daily water consumption of a child.
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Longer-term HA for 70 kg adult:
Longer-term HA = <500 mg/kg/day) (70 kg) (5/7) = , 25 /L (125,000 ug/L)
(100) (2 L/day)
where:
0.5 g/kg/day = NOAEL in a 12-week study based on absence of various
parameters of toxicity in rats.
70 kg = assumed body weight of an adult.
5/7 = conversion of 5 day/week exposure to daily exposure.
100 = uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a NOAEL from an animal study.
2 L/day = assumed daily water consumption of an adult.
Lifetime Health Advisory
The Lifetime HA represents that portion of an individual's total exposure
that is attributed to drinking water and is considered protective of noncar-
cinogenic adverse health effects over a lifetime exposure. The Lifetime HA
is derived in a three step process. Step 1 determines the Reference Dose
(RfD), formerly called the Acceptable Daily Intake (ADI). The RfD is an esti-
mate of a daily exposure to the human population that is likely to be without
appreciable risk of deleterious effects over a lifetime, and is derived from
the NOAEL (or LOAEL), identified from a chronic (or subchronic) study, divided
by an uncertainty factor(s). From the RfD, a Drinking Water Equivalent Level
(DWEL) can be determined (Step 2). A DWEL is a medium-specific (i.e., drinking
water) lifetime exposure level, assuming 100% exposure from that medium, at
which adverse, noncarcinogenic health effects would not be expected to occur.
The DWEL is derived from the multiplication of the RfD by the assumed body
weight of an adult and divided by the assumed daily water consumption of an
adult. The Lifetime HA is determined in Step 3 by factoring in other sources
of exposure, the relative source contribution (RSC). The RSC from drinking
water is based on actual exposure data or, if data are not available, a
value of 20% is assumed for synthetic organic chemicals and a value of 10%
is assumed for inorganic chemicals. If the contaminant is classifed 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.
In the absence of suitable ingestion toxicological data to derive a
Lifetime HA, an inhalation study in mice is considered for a Lifetime HA.
McNutt et al. (1975) exposed male mice continuously via inhalation to
1,1,1-TCA at 250 (1,365 mg/m3) or 1,000 ppm (5,460 mg/m3) for 14 weeks. Con-
trol mice were exposed to room air. Serial sacrifice of exposed and control
mice from 1 to 14 weeks demonstrated significant changes in the centrilobular
hepatocytes of animals in the 1,000 ppm (5,460 mg/m3) group. These changes
consisted of vesiculation of the rough endoplasmic reticulum with loss of
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1,1,1-Trichloroethane March 31, 1987
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attached polyribosomes, increased smooth endoplasmic reticulum, microbodies
and triglyceride droplets. A NOAEL could not be identified but a LOAEL of
250 ppm (1,365 mg/m3) from this study can be used with appropriate uncer-
tainty factors. A Lifetime HA based upon these data is derived as follows:
Step 1: Determination of the Total Absorbed Dose (TAD)
TAD - (1'365 mg/m3) (1 m3/hr) (6 hrs) (0.3) , 35 mg/kg/day
(70 kg)
where:
1,365 mg/n\3 (250 ppm) = LOAEL based on histological changes in liver
of animals.
1 m3/hr = ventilation volume for a 70 kg adult.
6 hrs = Exposure assumed to be saturable; thus, 6 hrs
is considered equivalent to exposure for a
24-hour period.
0.30 = ratio of administered dose absorbed.
70 kg = assumed body weight of an adult.
Step 2: Determination of the Reference Dose (RfD)
RfD = (35 mg/kg/day) __ 0.035 mg/kg/day
(1,000)
where:
35 mg/kg/day = TAD and LOAEL based on histological change in liver of
animals
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 = (0.035 mg/kg/day) (70 kg) = 1>0 mg/L (1/000 ug/L)
(2 L/day)
where:
0.035 mg/kg/day = RfD.
70 kg = assumed body weight of an adult.
2 L/day = assumed daily water consumption of an adult. '
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1,1,1-Trichloroethane
March 31, 1987
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Step 4: Determination of the Lifetime Health Advisory
Lifetime HA = 1 mg/L x 0.20 = 200 ug/L
where:
1 mg/L = DWEL.
0.20 = assumed relative source contribution from water.
Evaluation of Carcinogenic Potential
0 IARC (1982) has 'classified 1,1,1-trichloroethane in Group 3:
Inadequate data to evaluate.
0 Applying the criteria described in EPA's guidelines for assessment
of carcinogenic risk (U.S. EPA, 1986), 1,1,1-trichloroethane is
classified in Group D: Not classified (inadequate aniaml evidence
of carcinogenicity).
VI. OTHER CRITERIA, GUIDANCE AND STANDARDS
0 NAS (1980) has calculated a chronic SNARL of 3.8 mg/L for an adult
consuming 2 liters of water and contribution from water being 20%.
0 An ambient water quality criterion of 18.7 mg/L was calculated for an
adult consuming 2 liters of water daily (U.S. EPA, 1980).
VII. ANALYTICAL METHODS
0 Analysis of 1,1,1-trichloroethane is by a purge-and-trap gas chromato-
graphic procedure used for the determination of volatile organohalides
in drinking water (U.S. EPA, 1985a). This method calls for the
bubbling of an inert gas through the sample and trapping 1,1,1-tri-
chloroethane on an adsorbant material. The adsorbant material is
heated to drive off the 1,1,1-trichloroethane onto a gas chromato-
graphic column. This method is applicable to the measurement of
1,1,1-trichloroethane over a. concentration range of 0.03 to 1500 ug/L.
Confirmatory analysis for 1,1,1-trichloroethane is by mass spectrometry
(U.S. EPA 1985b). The detection limit for confirmation by mass
spectrometry is 0.3 ug/L.
VIII. TREATMENT TECHNOLOGIES
0 Treatment technologies which will remove 1,1,1-trichloroethane from
water include granular activated carbon (GAC) adsorption, aeration
and boiling.
0 Dobbs and Cohen (1980) developed adsorption isotherms for several
organic chemicals including 1,1,1-TCA. It was reported that
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1,1,1-Trichloroethane March 31, 1987
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Filtrasorb® 300 carbon exhibited adsorption capacities of 1.1 mg and
0.5 mg 1,1,1-TCA/gm carbon at equilibrium concentrations of 100 and
10 ug/L, respectively. U.S. EPA installed pilot-scale adsorption
columns in Connecticut and New Jersey. In Connecticut, contaminated
well water with 1,1,1-TCA concentrations ranging from 10 to 50 ug/L
was passed through a Filtrasorb® 400 GAC column. Breakthrough occurred
after 11,360 bed volumes (BV) or approximately 12 weeks of continuous
operation. In New Jersey, contaminated groundwater with an average
of 300 ug/L of 1,1,1-TCA was passed over a Witcarb® 950 GAC column.
Breakthrough occurred after 16,800 bed volumes (BV) or approximately
30 weeks of continuous operation. A similar study assessed the
effects of differing contact time and carbon adsorption of 1,1,1-TCA
(Love and Eilers, 1982). It was reported that 1,1,1-TCE concentrations
of 100 ug/L were reduced to 0.5 ug/L when loadings of 0.26 mg, 0.51 mg
and 0.74 mg 1,1,1-TCA/gm of Filtrasorb® 400 carbon for contact times
of 7.5, 15 and 22.5 minutes, respectively, were used.
0 1,1,1-TCA is amenable to aeration on the basis of its Henry's Law
Constant of 400 atm (Kavanaugh and Trusell, 1980). In a pilot-scale
diffused aeration column, removal efficiency of 90% of 1,1,1-TCA was
achieved from an initial concentration of 237 ug/L at an air-to-water
ratio of 4:1 (Love and Eilers, 1982). In a pilot-scale packed tower
aeration study, removal efficiencies of 74-97% were achieved for
42-110 ug/L 1,1,1-TCA for a broad spectrum of operating parameters
(Love and Eilers, 1982).
0 Boiling also is effective for removing 1,1,1-TCA from water on a short-
term, emergency basis. Studies have shown that 5 minutes of vigorous
boiling will remove 96% of 1,1,1-TCA originally present (Love and
Eilers, 1982).
0 Air stripping is an effective, simple and relatively inexpensive
process for removing 1,1,1-TCA 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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1,1,1-Trichloroethane March 31, 1987
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IX. REFERENCES
Bonventre, J., 0. Brennan, D. Jason, A. Henderson and M.L. Bastos. 1977.
Two deaths following accidental inhalation of dichloromethane and 1,1,1-
trichloroethane. J. Analyt. Toxicol. 4:15S-160.
Bruckner, J.V., S. Muralidhara, W.F. Mackenzie, G.M. Kyle and R. Luthra.
1985. Acute and subacute oral toxicity studies of 1,1,1-trichloroethane
(TRI) in rats. The Toxicologist. 5(1):100.
Caplan, Y.J., R.c. Backer and J.Q. Whitaker. 1976. 1,1,1-Trichloroethane:
report of a fatal Intoxication. Clin. Toxicol. 9:69-74.
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. 1984. Environmental Science and Engineering. 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, DC.
Hake, C.L., D. Waggoner, N. Robertson and V.K. Rowe, 1960. The metabolism
of 1,1,1-trichloroethane by rat. Arch. Environ. Health. 1:101-105.
Humbert, B.E., and J.G. Fernandez. 1977. Exposure to 1,1,1-trichloroethane:
contribution to the study of absorption, excretion and metabolism in
human subjects. Arch. Mai. Prof. 38:415-425.
IARC. 1982. International Agency for Research on Cancer. IARC Monographs
on the evaluation of carcinogenic risk to men. Suppl. 4.
Kavanaugh, M.C., and R.R. Trussell. 1980. Design of aeration towers to
strip volatile contaminants from drinking water. Journal AWWA. December.
Lane, R.W., B.L. Riddle and J.F. Borzelleca. 1982. Effects of 1,2-dichloro-
ethane and 1,1,1-trichloroethane in drinking water on reproduction and
development in mice. Toxicol. Appl. Pharmacol. 63:409-421.
Loprieno, N., R.A.M. Rossi, S. Fumero, G. Meriggi, A. Mondino and S. Silvest.
1979. in vivo mutagenicity studies with trichloroethylene and other
solvents. Preliminary results. Institute di ricerche biomediche.
Ivrea, Italy.
Love, O.T., Jr., and R.G. Eilers. 1982. Treatment of drinking water contain-
ing trichloroethylene and related industrial solvents. Journal AWWA.
August.
McNutt, N., R. Amster, E. McConnell and F. Morris. 1975. Hepatic lesions in
mice after continuous inhalation exposure to 1,1,1-trichloroethane.
Lab. Invest. 32:642-654.
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Monster, A.C., G. Boerstna .and M. Steenweg. 1979. Kinetics of 1,1,1-trichloro-
ethane in volunteers; influence of exposure concentration and workload.
Int. Arch. Occup. Environ. Health. 42:293-301.
NAS. 1980. National Academy of Sciences. Drinking Water and Health. Volume 3.
National Academy Press. Washington, DC
NAS. 1983. National Academy of Sciences. Drinking Water and Health. Vol. 5.
National Academy Press. Washington, DC.
NCI. 1977. National Cancer Institute. Bioassay of 1,1,1-trichloroethane
for possible carcinogenicity. CAS No. 71-55-6. Technical Report Series
No. 3. January 1977.
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