vvEPA
            united states
            Environmental Protection
            Agency
            Office of Pesticides
            and Toxic Substances
            Washington, DC 2046
EPA-560/4-81-004
May 1981
            Toxic Substances
Assessment of
Testing Needs:
1,1,1 - Trichloroethane

Support Document
Proposed Health and
Environmental  Effects
Test Rule

Section 4
Toxic Substances
Control Act

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EPA 560/'2-81-004
HAY 1.981
ASSESSMENT OF TESTING NEEDS:
l,l,l-TRICHLOROETHANE
PROPOSED
SUPPORT DOCUMENT
HEALTH AND ENVIRONMENTAL EFFECTS
TOXIC SUBSTANCES CONTROL ACT
SECTION 4
TEST RULE
ASSESSMENT DIVISION
OFFICE OF TOXIC SUBSTfu~CSS
Washington, D.C. 20~OO
U.S. ENVIRONMENTAL PROTECTION AGENCY
OFFICE OF PESTICIDES AND TOXIC SUBSTANCES
Washington, D.C. 20460

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TABLE OF CONTENTS
Introduction and Summary of Proposed Testing................. 1


1. production and Uses. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 4

2. Exposure. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6

3. The ~4(a)(1)(B)(i) Finding .............................. 10
4. Health Effects: Sufficiency of Data and


~ecessity for Testing................................... 10
5 .
Environmental Effects:
Sufficiency of Data and
6.
Necessi ty for Testing. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 15

Chemical Fate: Sufficiency of Data and


Necessity for 1'esting ................................... 18
References. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 20

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Introduction and Summary of
?roposed Testing
l,l,l-Trichloroethane, (C13C2H3' methyl chlorofo:m, C~S .
number 71-55-6), is a colorless, non-flammable, volat11e 11qu1d
at standard temperature and pressure (additional physicochemical
data appear in section 6). It is an excellent solvent for
greases, oils, tars, waxes and a wide ralige of other organic
material.
The Interagency Testing Committee (ITC), organized under
Section 4(e) of the Toxic Substances Control Act, recommended
that l,l,l-trichloroethane be tested for carcinogenicity,
mutagenicity, teratogenicity and other chronic effects with
specific attention to neurological, cardiovascular and renal
systems, and that epidemiology studies be conducted (USEPA 1978b).
Because of the large production volume, extensive release to
the environment and the number of people potentially exposed to
l,l,l-trichloroethane, both occupationally and as consumers, the
EPA is proposing testing under Section 4(a)(I)(B) of the Toxic
Substances Control Act. This section of the Act provides for
testing requirements, if among other conditions, a chemical
substance is or may be produced in substantial quantities, and
(I) it enters or may reasonably be anticipated to enter the
environment in substantial quantities or (II) there is or may be
significant or substantial human exposure to such substance.
This document supports the three statutory findings required
to be made under ~4(a)(I)(B) TSCA regarding the exposure/release
potential, the sufficiency of available data and the necessity
for testing, and identifies the recommended testing.
1

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S\.X'J:Tar 1
of ~ '::.~:3 -:. ':.!Y"..J
:)e~l31..':ns
~ffects of
Concern
Cisp:;sition
Testing
Reccrnmended
byITC
c:f
'resting
Health Effects
Acute effects
oral, dennal and inhalation
dernal irri tation/ corrosion
eye irritation/corrosion
skin sensitization
Chronic effects
~utagenicity
Reproductive effects
Teratogenicity
Oncogenicity
Neurotoxicity
Environmental Effects
Aquatic vertebrates
acute
freshwater ooldwater
freshwater warrrwater
saltwater coldwater
saltwater warmwater
G.'1ronic
freshwater ooldwater
freshwater warrrwater
saltwater coldwater
saltwater warrrwater
Aquatic invertebrates
acute
freshwater
saltwater
chronic
freshwater
saltwater
lethality
Not prc:poseda
Not proposeda
Not prc:poseda
Not Proposeda
Chronic effects
neurological
cardiovascular
renal
Not proposedb
Not proposed?
Not proposedD
Mutagenicity
Not proposedC
Not Prcposeda
Teratogenicity
Proposed
Not proposedb
Oncogenici ty
Not proposedd
Epidemiology
Not proposede
Proposed
Not proposeda
a
Not proposed
Not proposedc
Proposed
Proposed
C
Not proposed
Proposed
Not proposeda
a
Not proposed
Proposed
Proposed
2

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3u;rroar.l :)f 1'eSliJ."Y.; Jecis lcr.s
(Contil"~ued )
Effects of
Concern
Testing
Recamrended
byI'IC
Dispcsiticn
of
Testing
Aquatic plants
algae
freshwater
saltwater
Not proposeda
Not proposeda
vascular
freshwater
sal twater
Not proposedC
C
Not proposed
Birds
acute
terrestrial
waterfcwl
Not proposeda
Not proposeda
chronic
terrestrial
waterfcwl
Prcposed
Proposed
MalTU't'als
acute
chronic
Not proposeda
Not propcseda
Terrestrial invertebrates
~'Tot prcposedC
Terrestrial plants
seed gennination/root
elongation
ear ly seedling grONth
full life cycle
Proposed
Proposed
\TO"'" ':)-C>'"V">S ,,,,,.:;C
'.'0 '- .....J.. ,j:-''"'" '-<.......(.
Bioconcentration
aquatic vertebrate
aquatic benthic irl'7~~2brate
terrestrial plant
7\Tot ~xcposeda.
~1ot .'?rq::csedd
?r~sed
":u teration of microorganism function
Ecosystan effects
~\fot proposedC
Not proposedC
Chemical Fate
Persistence
Transport
Not prcposedC
Not proposeda
~Adeq~ate.information already available
Tes~~ng ~n progress
CTesting will be EPA's responsibility
dNO test standards available
~o suitable cohort identified

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1 .
PRODUCTION AND USES
1.1
Production
In the U.S" l,l,l-trichloroethane is produced by three
manufacturers at three production sites. The Dow facility in
Freeport, Texas had a 1979 capacity of 450 million pounds
(204,300 kkg*), the PPG facility at Lake Charles, Louisiana had a
1979 capacity of 325 million pounds (147,550 kkg), and the Vulcan
facility at Geismar, Louisiana had a 1979 capacity of 200 million
pounds (90,800 kkg) for a total of 975 million pounds (442,650
kkg) production capacity at the three sites. This represents
approximately a 40% increase in capacity from 1977. Actual
production of l,l,l-trichloroethane rose from 266.3 million
pounds (120,900 kkg) in 1970 to 645 million pounds (292,830 kkg)
in 1978 (Price et ale 1980). The U.S. International Trade
Commission reported the production of l,l,l-trichloroethane to be
716 million pounds (325,064 kkg) in 1979 (USITC 1980). The rapid
growth was caused in part by the use of l,l,l-trichloroethane as
a replacement for trichloroethylene and perchloroethylene because
of the potential environmental and health problems associated
with those chemicals (Chemical and Engineering News 1979).
Recent estimates project a growth rate of about 2% per year
through 1983 (Chemical Marketing Reporter 1979). Imports of
l,l,l-trichloroethane are negligible. However, approximately 30
million pounds (13,620 kkg) were exported in 1979.
About 60 percent of the domestic production of 1,1,1-
trichloroethane is obtained from vinyl chloride, about 30 percent
is based on the use of vinylidene chloride as raw material and
the remainder is produced by thermal chlorination of ethane
(Midwest Research Institute 1979). The first process involves
the hydrochlorination of vinyl chloride to l,l-dich1oroethane,
which is then thermally or photolytically chlorinated. Tnermal
chlorination of l,l-dichloroethane at 400°C gives a greater than
95 percent yield of I, I, I-trichloroethane. The basic reaction
involved in the second process is the hydrochlorination of
vinylidene chloride in the presence of ferric chloride
catalyst. The yield of pure product is over 98 percent and t~e
process yields no by-products. The third process involves t}1e
noncatalytic continuous chlorination of ethane to produce 1,1,1-
trichloroethane and several other products, depending on the
reaction conditions. The yield of pure product may be as high as
93 percent.
The U.S. Federal specifications for l,l,l-trichloroethane,
technical, inhibited, calls for 94.5 percent purity by volume.
Individual halogenated grade impurities must not exceed 0.5
percent and total halogenated impurities are limited to I
percent. The acidity (as HCl) is restricted to 5 ppm and no free
halogens are allowed (Walter et ale 1976).
*
1 pound = 0.454 kg
4

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~ll commercial products of l,l,l-trl~hloroethane contain
stabi:izers. Chlorine can be removed from unstabilized 1,1,1-
trichloroethane by metals such as iron, aluminum and zinc,
producing metal chlorides which can further degrade the
chemical. Hydrogen chloride, which is extremely corrosive, is
produced as a result of these reactions and also by the
interaction of uninhibited l,l,l-trichloroethane, oxygen and
moisture. Therefore, metal stabilizers and acid acceptors are
generally added to l,l,l-trichloroethane. Several hundred have
been patented as additives, although most are not used
regularly. The concentration of specific stabilizers that have
been identified in various commercial products is shown below:
Additive
Volume, %
Nitromethane
Butylene oxide
Dioxane
Dioxolane
Methyl ethyl ketone
Toluene
see-Butyl alcohol
Isobutyl alcohol
0.4 - 1.8
0.4 - 0.8
2.5 - 3.5
1.0 - 1.4
1.0 - 1.4
1.0 - 1.4
0.2 - 0.3
1.0 - 1.4
Not all of these stabilizers are present in every product,
but often several are used in combination. The combined
concentration does not exceed 8% by volume (Price et al. 1980).
1 .2.
Uses
l,l,l-Trichloroethane is not used consumptively as an
intermediate in the synthesis of any organic chemicals.
Distribution of l,l,l-trichloroethane in its major non-
consumptive uses is shown below:
Use
Percent of total
1978 production
Million Pounds
(kkg)/year
1978
Metal cleaning
Aerosols
Adhesives
Textiles
Paints
Inks
Drain cleaners
Film cleaning
Pharmaceuticals
Leather tanning
Miscellaneous
66.1%
7.0%
7.0%
1.0%
1.8%
1.0%
0.5%
0.1%
0.1%
0.1%*
2.8%
422.3
45.0
44.6
6.6
11.3
6.4
3.4
0.7
0.5
0.2
17.5
(Katz et al. 1980)
*
Sum does not equal 100%
5
(191,724)
(20,430)
(20,248)
(2,996)
(5,130)
(2,905)
(1,543)
(317)
(227)
( 91)
(7,945)

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~he use of l,l,l-trichloroethane has grown signi=ica~~~y
over the last 15 years. It is used in the aircraf~ indust~f for
cleaning airframes, engine components, electronic instruments,
and air systems~ in the electronics industry for cleaning =elays,
resistors, and diodes~ in the printed circuit industry for
selectively removing photo resistant inks, soldering flux, and
other contaminantsj in the textile industry for cleaning yarns,
threads, and finished cloth~ and in industries where there is a
need to clean molds, castings, and processing equipment. 1,1,1-
Trichloroethane is also used as a solvent in aerosols, printing
inks, contact adhesives, shoe polish formulations, lapping
compounds, and clothing spot removers, and for cleaning of fiber
glass, business machines, and small electronic parts. It is used
in the grain industry in the flotation of weevils and in the
petroleum industry for the extraction of oil from well drilling
cores (Price et al. 1980).
Metal cleaning by the cold cleaning and vapor degreasing
processes is the primary end use and also the primary source of
~~lease of the chemical. In cold cleaning, the industrial part
~o oe cleaned is sprayed, dipped or agitated in the solvent. In
t}1e solvent vapor degreasing process the object to be cleaned is
i~~ersed in the solvent and then subjected to boiling solvent
?3pOr as the final step in cleaning. Emissions from these
c~erations are fugitive in nature and include losses due to
2vaporation from the solvent bath, convection, carryout, leaks
and waste solvent disposal (Price et al. 1980).
~
~CPOSURE
2,1.
Human Exposure
In the ~ational Occupational Hazard Survey (NOHS)
~~proximately 2.6 million workers were estimated to be exposed to
l/l,l-trichloroethane (NOHS 1980). However, there is little
information available about the levels of l,l,l-trichloroethane
~o .vhich workers have been exposed routinely.
l/l,l-Trichloroethane exposures during open-top vapor
degreasing operations were described by Skory et al. (1974) based
on studies conducted at 275 industrial degreasing operations
using the chlorinated solvents l,l,l-trichloroethane,
trichloroethylene and perchloroethylene. Solvent vapor
concentrations were monitored in the breathing zone of the
degreaser operator while parts were immersed, during cleaning and
spraying and during removal and unloading. Concentrations of
l,l,l-trichloroethane found during different phases of the work
were: idling degreaser, 76 ppm (average peak concentrations 187
ppm)~ racking and loading, 73 ppm (average peak concentration 164
ppm)~ cleaning parts, 95 ppm (average concentrations 182 ppm)~
unloading parts, 131 ppm (average peak concentration 268 ppm).
l,l,l-Trichloroethane has been identified in a substantial
number of consumer products including drain cleaners, water
6

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repellant sprays, adhesl ves I moth ?roo~ ers, spot removers, :11e:.'1.1
cleaners, furnit~re ?olishes, oven protectorants, grease ~r.d::l
removers and insecticides. There are no data available ~~
indicate levels of ambient exposures. However, during use
periods, it is expected that these levels will be momentarily
high. Furthermore, liquid 1,1, I-trichloroethane has been shm,n
to be absorbed throuah the skin (Beaver 1977). Dermal absorp ':ion
may be a significant~route of exposure to l,l,l-trichloroethane
in a number of consumer products. Apart from the known
occupational exposures, it is expected that many millions of
people are likely to be exposed to l,l,l-trichloroethane as a
consequence of consumer use.
2.2.
Environmental Exposure
Measurable amounts of l,l,l-trichloroethane have been
reported in the atmosphere, soil, rainwater, marine and fresh
surface waters and ground water (Price et al. 1980). Residues of
l,l/l-trichloroethane have been measured in the tissues of
aquatic and terrestrial plants and animals (McConnell et. al,
1975, Pearson and McConnell 1975).
Infor;nation on concentrations of l,l,l-trichloroethane found
in soil is sparse. In the study of soil in the vicinity of
producers aDd users, Bat~elle (1977) found concentrations i~ the
low parts pe~ trillion level and occasionally in the low parts
per billion range. '1'11e range of concentrations varied from "not
detected" (less than 6 picograms) to a high of 3.4 ppb of 1,1,1-
trichloroethane at ~he Dow Chemical facility in Freeport, Texas.
Ewing et al. (1977) collected and assayed approximately 200
water samples for various organic substances. These samples were
collected from 14 heavily industrialized river basins. Ninety-
one of the sites were located along major rivers such as the
Hudson, the 8elaware, ~he Mississippi, the Chio, and ~he
Tennessee. Fifty-seven samples ~ere collected in tidal areas and
estuaries, such as the gudson River estuary. the Delaware River
estua~J, Mobile Bay, Galvesto" Bay, Los ~ngeles Ha=~or, San
Francisco 3ay and Puget Sound. Twelve sites were lo~ated in ~an-
made canals and three in major lakes. Since industrial
wastewater is often treated at municipal sewage treatment plants,
four samples were taken from effluent discharge structures.
l,l,l-Trichloroethane was detected in 18 of the approximately 200
samples analyzed and the concentrations ranged from less than
1 ppb to 8 ppb in these surface waters.
A recent pilot study (Feiler 1979) conducted for EPA on the
fate of priority pollutants in publicly owned treatment works
(POTWs) sampled two POTWs with significantly different
characteristics in terms of size, percent industrial flow, age,
operation, sludge conditioning methodology, and capacity
utilized. The PO~N having a large industrial influent
contribution from serving major industries (pharmaceutical
manufacture, petrochemicals, plating operations, and automotive
foundries) had influent concentrations of 1,1,1- trichloroethane
7

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averaging about 16 ppb with levels as high as 220 ppb. The other
POTW, which was typical of a residential treatment facility,
averaged about 2 ppb with a maximum less than 10 ppb. Effluent
sampling indicated that for both POTWs 1, 1, I-trichloroethane was
well removed (60-100 percent) but not concentrated in plant
sludges.
Pearson and McConnell (1975) report l,l,l-trichloroethane
concentrations of 0.09 ppb in rainwater collected in Runcorn,
England. The highest concentrations that these researchers
measured in upland river waters was 0.3 ppb. These same authors
also reported that they have never detected organo-chlorines in
well waters. Levels of 1,l,l-trichloroethane as high as 3,700
ppb were found in the ground water near wells in Southington,
Connecticut as a result of improper industrial waste disposal.
(Hall 1980).
With a normal detection limit of 0.2 ppb, Pearson and
McConnell (1975) determined that the maximum concentration in
Liverpool Bay sea water was 3.3 ppb between April and August,
1973. In Liverpool Bay sediments, the maximum combined
concentration of l,l,l-trichloroethane and carbon tetrachloride
was 9.9 ppb.
Only the study conducted in England by McConnell et al.
(1975) reported concentration of l,l,l-trichloroethane in
foodstuffs. Olive oil (Spanish) contained the highest level of
l,l,l-trichloroethane (10 ppb), followed by tea in packets
(7 ppb).
A summary of the measured concentrations of 1,1,1-
trichloroethane in the environment in 1978 is presented below:
Source
Concentration
Jrinking water
17 ppb in Freeport, Texas
~cndrinking water at
yroducer sites
344 ppb in Geismar, Louisiana
Soil
3.4 ppb in Freeport, Texas
Sediment
6.1 ppb in Freeport, Texas
Sediment
5.5 ppb for combined 1,1,1-
trichloroethane, chloroethane
and carbon tetrachloride in
Liverpool, England
Waste water
8.5 ppb in Cincinnati, Ohio
Ambient air at manufacturing
site
155 ppb in Geismar, Louisiana
8

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Awbient air at user sites
10 P9b :~ ;~bu~n, Washington
,;'nbient air in selected
7]. S. cities
:~4 ppb in 3ayonne, New Jersey
Foods
10 ppb in Spanish olive oil
The emissions to the atmosphere as a function of source for
1978 are listed below (Katz et al. 1980). As previously
indicated, metal cleaning represents the primary end-use and also
poses the potential for widespread population exposure. The
following data tend to support that finding in that metal
cleaning alone represents at least 75% of the potential release
to the air.
  1978 Emission Losses to Air in
  Million pounds (kkg) and
Source percentage of total released to air
Production    
1. Fran Vinyl Chloride 0.21 (95) 0.04%
2. From 'linylidene Chloride 0.15 (67) 0.03%
3. Fran Ethane 0.03 (14) 0.01%
Metal Cleaning 351.70 (159,500) 75%
Aerosols  39.90 (18,100) 8%
Adhesives  38.37 (17,400) 8%
Textiles  6.44 (2,920) 1%
Paints  10.91 (4,950) 2%
Inks  6.13 (2,780) 1%
Drain Cleaners 0.61 (278) 0.1%
Pha.rmaceuticals 0.27 (124) 0.06%
Film Cleaning 0.48 (218) 0.1%
Leather Tanning 0.23 (104) 0.05%
Catalyst Preparation 0.06 (28) 0.01%
Miscellaneous 14.82 (16,730) 3%
TOTAL RELEASED 'ID 470.31 (213,300) (100%)
THE AIR*   
*An additional 63 million pounds (28,602 kkg) are released
to the environment via solid waste and water.
9

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3 .
T3E )4'a)(1)(B)(i) FINDI~G
From the information presented i~l ~~8 preceJ1ng sections, it
is evident that ~rl,l-trichlor8ethane is produced i~ substantial
quantities (an esti~a~ed 715 million pounds (325,064 ~~g) ~n
1379) that it enters t~e environment in substantial quantities
(~n estimated 533 million pounds (241,982 kkg) in 1978) and that
there may be significant or substantial exposure to humans, both
occupationally and as consumers.
4.
HEALTH EFFECTS - SUFFICIENCY OF DATA AND
NECESSITY FOR TESTING
4.1.
Acute Effects
4.1.1. Oral, dermal and inhalation lethality
The results of tests to determine oral, dermal and
inhalation lethality are summarized in Table 1. These effects
are adequately characterized and no further testing is necessary.
4.1.2.
Dermal irritation/corrosion
Adequate data are available to assess the dermal irritation
?otential of l,l,l-trichloroethane, therefore, no testing is
'0eing proposed.
A study by Torkelson et ale (1958) showed only a slight
reddeni~g and scaliness occurred on abraded and unabraded rabbit
skin. These effects increased only slightly with repeated
exposures and healed when the application ceased.
4.1.3.
Eye irritation/corrosion
Adequate data are available to assess the eye irritation
potential of l,l,l-trichloroethane, therefore, no further testing
lS being proposed.
Torkelson et al. (1958) observed rabbit eyes treated with
t~,vo drops of l,l,l-trichloroethane for three minutes, one hour,
=,,-:;.c1 c~e r +:"',';0 and seven days after administration. The test
:l.a:.erial ',vas found to produce slight conjunctival irritation with
essentially no corneal involvement.
4.1.4.
Skin
sensitization
The Agency has reviewed data on skin sensitization received
from the Dow Chemical Co. (1981) and while certain data points
make interpretation of the study difficult, there is enough
information available to reasonably predict that the data are
adequate. Chlorothene VG @ was not found to be a skin
sensitizer. The Agency is not proposing additional testing at
this time.
10

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Table 1
~cute Lethal Toxicity of l,l,l-Trichloroethane
Species    Route and   Parameter Value Ref~rence
(strain/sex)    Duration       
Rat       Oral    LDSO 12.3 mg/kg a.
(Wistar, M)           
Mouse       Oral    LDSO 11.24 mg/kg a.
(not given, F)          
Guinea pigs    Oral    LD50 9.47 mg/kg a.
(Heterogeneous, :2)         
Rabbits      Oral    LlJ5 () 5.66 mg/kg a.
(Heterogeneous, F)         
Rat       Intraperitoneal LD50 3.8 ml/kg b.
(Sprague - Dawley, M)         
~1ouse       Intraperitoneal LD50 3.5 ml/kg c.
(Swiss - ~'lebster,F)          
Dog       Intraperitoneal LD50 3.1 ml/kg d.
(lvlongre 1, M, F)           
Rat       Inhalation- 7 hrs LC50 14,250 ppm e.
(Wistar, M, F)          
Rat       Inha1ation- 4 hrs LC50 18,400 ppm e.
(Sprague - Dawley, M)         
Rabbits      Dermal   LD50 >15 g/kg a.
(unknown)            
a. Torkelson et al. (1958)
b. Gehring (1968) 
c. Klaassen and Plaa (1969)
d. Klaassen and Plaa (1967)
e. Adams et al. (19S0)
f. Siegel et al. (1971)
11

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4.2.
Chronic Effects
The ITC expressed interest in the effects of chronic
exposure to l,l,l-trichloroethane emphasizing the neurological,
cardiovascular and renal systems. There is insufficient
information available to assess any of these effects. The EPA is
not proposing to require testing for these effects because: (1)
a two year chronic oncogenicity study in rodents is currently
being conducted by the National Toxicology Program (NTP), and (2)
EPA will work with NTP to attempt to make arrangements for NTP to
focus attention on the cardiovascular, neurological and renal
systems in its histopathological analyses if appropriate sources
of funding can be found. EPA believes that dysfunctions in these
systems may be delineated by detailed pathology and will be
sufficient for the Agency's needs in the assessment of chronic
effects.
Two chronic studies were found in the literature. A gavage
study in mice and rats (NCI 1977) resulted in premature death of
a significant number of the animals from chronic murine pneumonia
and the study was terminated prematurely. An inhalation study in
rats by Quast et al. (1978) was conducted for six hours/day, five
days/week for one year at doses of 875 and 1,750 ppm. Although
the animals were held for observation for 19 months following
exposure, the duration of dosing in this study is not considered
sufficiently long to qualify it as a fully adequate chronic
study.
4.3.
Reproductive Effects
Several studies naV8 contributed information useful in
assessing the reproduc~ive effects of l,l,l-trichloroethane.
Considering the investi(::reJ.tions presented in this section, the
Agency, for the purpose of this proposal is not recommending
testing at this time.
One study detected effects of reproductive significance
(Adams et ale 1950), described by the authors as varying degrees
of testicular degeneration. Since no mating studies were
performed it is not possible to determine whether or not post
natal development or fertility was affected. The effect was
detected in guinea pigs at a dose level of 5,000 ppm and not
detected in rats, dogs or rabbits under similar dosing
conditions. However, toxic effects (liver degeneration and
decreased weight gain as compared to controls) were observed in
the guinea pigs from the 1,500 and Q50 ppm dose groups and no
testicular pathology was noted in these two exposure groups.
Neither of two other studies (NCI 1977; Quast et ale 1978) showed
any effects to the gonads in rats or mice. However, neither of
these studies was designed to fully evaluate reproductive
effects. (See Chronic Effects, Section 4.2.)
The EPA has sponsored testing designed to identify the
potential reproductive effects resulting from exposure to 1,1,1-
12

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7..:.:-:.chloroethane i:1 ,:!ri:1k:.ng wat.ar (30r~e?~.:~(:3. e:: 03.1. 1976).
9relLninary results 9r9sented as an .3.DS1:.::ac't. (~iddle et al.
1.981) I 1,1, i-trichloroethane '....as1.dministered ::0 :nale and female
mice on a daily basis at concentrations ::>r iJ, 0.58, 1. 75, and
3.83 ~g/ml. These concentrations correspond to dose levels of 0,
99.4, 2640 and 8520 mg/kg. According to the authors, there
appeared to be no dose dependent effects on fertility, gestation,
'liability or lactation indices. Furthermore, gros~ necropsy of
?Q generation mice did not show any compound or dose related
etfects.
In
It must be recognized that the results of the EPA sponsored
study have not been reviewed in great detail at this time. It is
assumed that if the experimental protocol was meticulously
followed, adequate data sufficient to ascertain possible
reproductive effects would be provided.
4.4.
Teratogenicity
There is insufficient information available to adequately
characterize the teratogenic effects of l,l,l-trichloroethane.
Because of this insufficiency of data and the lack of ongoing
testing, the EPA is proposing to require teratogenicity testing
of l,l,l-trichloroethane according to EPA standards.
Only two studies were found which appear to bear upon this
question. Schwetz et al. (1975) determined that 1,1,1-
trichloroethane was not a teratogen in mice and rats after
exposure to 875 ppm vapor for 7 hours/day from days 6-15 of
gestation. There were, however, several deficiencies in this
study that make the negative results inconclusive. The
investigators failed to distinguish if the poor fertility among
the mice was the result of infertility or early embryonic
resorption. No maternal toxicity was demonstrated for the mice
and the only indication of toxicity in the rats was slightly
enlarged livers. Only one dose level was administered whereas
three are generally used in this type of test.
The teratogenic potential of 1,1, I-trichloroethane? '.va3 also
evaluated in an 2::':; -:::.. :::~- -;~- -~-~ ~'~ ~.~ 211. (1981). Rats.v~'-:'2
exposed to 2100 p~ - ~ )'-;'~-' '7 days a week throughout
gestation. The r23~::3 ~~ iadicated that 1,1,1-
trichloroethane was not teratogenic at the single dose level
tested. As in the previous study (Schwetz et al. 1975), t~o
deficiencies were noted that also made the results of this study
inconclusive. No maternal toxicity could be demonstrated for the
rat, and only one dose level was administered whereas three dose
levels are generally required.
4.5.
Mutagenicity
Studies by Margard (1978) and Simmon et al. (1977) have
shown that l,l,l-trichloroethane is mutagenic in Salmonella
typhimurium strains TA1535, TAlOO and TA1537. There are however,
no studies which assess the ability of l,l,l-trichloroethane to
induce chromosomal aberrations.
13

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"SPA believes that mutagenic ris.\: ::::om .:x:,osu:::,,'.= to ~,1,1.-
trichloroethane can most reasonab ly ''Je .:ie::erm~ned 0'1 ,?erforming a
sequence of tests for both gene muta~io!1 and chr~rnosomal
aberration. In such a scheme, the perf~rmance of ~ert~in tests
is triggered by positive or negative results from prev~ous tests.
At this time, EPA is not proposing test requirements :.:,:->r the
mutagenicity sequence because the Agency has not yet defined the
criteria for determining whether the results of each test are
positive or negative. Therefore, EPA plans to sponsor all tests
in the lower tiers of the sequence. On the basis of its test
results, EPA will decide whether to propose that the final tests
of each sequence be performed pursuant to a subsequent test rule.
Oncogenicity

There is insufficient information available (see Chronic
Effects, Section 4.2.) to determine the oncogenic potential of
l,l,l-trichloroethane. The EPA is not proposing to require
testing for oncogenicity, however, because the National
Toxicology Program is currently conducting a two-year
oncogenicity study in rats and mice, it is anticipated that the
data from this study will be sufficient for the Agency's needs.
4.6.
4.7.
Neurotoxicity
l,l,l-Trichloroethane is an anesthetic which produces non-
specific central nervous system depression in humans after single
exposures to 500 to 2650 ppm of the vapor (Torkelson et al. 1958,
Stewart et al. 1961, Stewart et al. 1969, Dornette and Jones
1960). As previously stated, studies of acute exposure in the
range of 350 to 550 ppm have indicated that l,l,l-trichloroethane
impairs performance on cognitive and reaction time tasks (Salvini
et al. 1971, Gamberale and Hultengren 1973). It is expected that
neuropathology data may be obtained from the ongoing NTP bioassay
which would elucidate chronic neurotoxic effects (see Chronic
Effects, Section 4.2.). The EPA is also interested in
neurobehavioral functions and behavioral teratogenicity, but is
not proposing to require testing for these effects at this time
because of the lack of test standards.
4.8.
Epidemiology
The ITC recommended that an epidemiologic study be performed
for 1, 1, I-trichloroethane. The EPA has identified several such
studies but none is considered a fully adequate epidemiologic
study. In spite of this insufficiency of data, the EPA is not
proposing to require that an epidemiologic study be performed at
this time because a suitable cohort has not been identified.
Kramer et al. (1978) conducted a matched paired
investigation primarily of cardiovascular parameters and one
neurological test. The results were generally negative, but the
validity of the investigation was questioned because the study
population could not be adequately characterized, particularly
with respect to occupational exposures. The data provided to
14

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assess the completeness of pair matching also were incomplete.
:n addition, EKG data were not obtained from 20% of the matched
pairs, thus, possibly biasing comparisons. Taken as a whole, the
suitability of the cohort is left in doubt.

NIOSH conducted an industrial hygiene and medical survey of
Hill Air Force Base workers exposed to solvents (NIOSH 1977). ~o
unusual chronic effects were found, but acute responses usually
associated with exposure to solvents were observed. This study
is difficult to assess because of the multiple chemical exposures
involved.
S.
ENVIRONMENTAL EFFECTS - SUFFICIENCY OF DATA AND
NECESSITY FOR TESTING
S .1 .
Aquatic Vertebrates
S.l.l.
Acute Toxicity
Adequate data are available to assess the acute toxicity of
I,l,l-trichloroethane to warmwater freshwater fish and coldwater
saltwater fish, therefore, the EPA is not proposing to require
testing in these species. The available data on coldwater
freshwater and warmwater saltwater fish are not adequate to
assess the acute toxicity of l,l,l-trichloroethane to these
species. The EPA is proposing to require a flow-through test on
a coldwater freshwater species according to EPA standards. The
EPA will perform the testing in a warmwater saltwater species
because no TSCA Section 4 standards are available at this time.
A study by Alexander et ale (1978) has reported a flow-
through 96 hour LCSO of 52.8 mg/liter and a static 96 hour LCSO
of 105 mg/liter for the fathead minnow, a warmwater freshwater
species. Studies by McCarty (1979) and the USEPA (1978a) have
reported static 96 hour LCSO values of 51-68 mg/liter and 69.7
mg/liter for the bluegill, also a warmwater freshwater species.
Pearson and McConnell (1975) reported a flow-through 96 hour LCSO
of 33 mg/liter for the dab, a coldwater saltwater species.
The acute toxicity study by McCarty (1979) on the rainbow
trout, a coldwater freshwater species, reports a static 96 hour
LCSO of 46-59 mg/liter. This is not considered adequate because
a flow-through test is necessary for a compound as volatile as
l,l,l-trichloroethane. Similarly, the static 96 hour LCSO of
70.9 mg/liter reported by USEPA (1978a) for the sheepshead
minnow, a warmwater saltwater species, is not considered
adequate.
5.1.2.
Chronic Toxicity
There are no data on the chronic toxicity of 1,1,1-
trichloroethane to aquatic vertebrates, therefore, the EPA is
proposing to require early life stage testing in accordance with
the EPA standard on both warmwater and coldwater freshwater
lS

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species of fish and on a warmwater saltwater species. A ~est for
chronicity in a coldwater saltwater species will be performed by
E?A because no TSCA Section 4 standards are available at this
time.
5 .2.
Aquatic Invertebrates
5.2.1.
Acute Toxicity
Sufficient data are available to perform an adequate
assessment of the acute effects of l,l,l-trichloroethane on
freshwater and marine invertebrates and therefore the EPA is not
proposing to require additional testing.
Pearson and McConnell (1975) have reported a static 48 hour
LCSO of 7.5 mg/liter in barnacle larvae. The USEPA (1978a) has
reported a static 96 hour LCso of 31.2 mg/liter in mysid shrimp
and a static 48 hour LC~O of greater than 530 mg/liter in
Daphnia. McCarty (19791 reported a static 48 hour LCSO of 9.7-
12.8 mg/liter in Daphnia. Procedures to limit losses due to
vola tili ty were in these studies / t:1erefore, the results of
static testing are acceptable.
5.2.2.
Chronic Toxicity
There are no data on chronic toxicity of 1/1/1-
trichloroethane to aquatic invertebr~tes. Therefore, the EPA is
proposing to require complete life ~Y21e testing on a freshwater
and saltwater invertebrate species according to the EPA standard
to provide these data.
Aquatic Plant Toxicit~
5.3.
There are adequate data to ~SS2SS the toxicity of 1,1,1-
trichloroethane to freshwater anc saltwater species of algae.
The USEPA (1978a) has reported 24, 48 and 96 hour EC~Os greater
than 669 ppm for Selenastrum ca'?c'..comutum and Skelefonema
.:::ostatum. No da~a are available ':.~") i3.SSeS3 the toxicity of 1,1,1-
trichloroethane to aquatic vascular ylants. ~owever, because no
TSCA Section 4 standards are availi3.ble, EPA will perform the
testing.
5.4.
Birds
5.4.1.
Acute Toxicity
Adequate data are available to assess the acute toxicity of
l,l,l-trichloroethane to terrestrial birds, therefore, the EPA is
not proposing to require additional testing. A study by Wildlife
International Ltd. (1978) reported an acute oral LDSO in the
bobwhite quail was greater than 2510 mg/kg.
Although there are no data on acute toxicity to waterfowl,
EPA is not proposing to require this testing for the following
16

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reasons: 1) ~~e very low ac~te toxicity to the bobwhite quail
(see preceding paragraph), 2) the low exposure potential due to
the high volatility (Vapor pressure = 100 mm Hg at 20'C); and 3)
:.he low bioconcentration potential of l,l,l-trichloroethane as
Lldicated by its low log P t (2.49) and by the data of the USEPA
(1978a) showing a low biocggcentration factor in a fish test.
5.4.2.
Chronic Toxicity
There are no data on the chronic effects of 1,1,1-
trichloroethane exposure to avian species. Therefore, the EPA is
proposing to require chronic toxicity testing on a terrestrial
bird and a waterfowl according to the EPA standard.
5.5 .
Terrestrial Plants
5.5.1.
Root Elongation/Seed Ge~ination
No data are available on the effects of 1,1,1-
trichloroethane on seed germination or root elongation in ~igher
terrestrial plants. Therefore, the EPA is proposing to require
root elongation/seed germination testing according to the EPA
standard.
5.5.2.
Early Seedling Growth
No data are available on the effects of 1,1,1-
trichloroethane on early seedling growth in terrestrial plants.
Therefore, the EPA is proposing to require ea~ly seedling growth
testing according to the EPA standard.
5.5.3.
Full Life Cycle
No data are available on the effects of 1,1,1-
trichloroethane on the full life cycle of terrestrial plants.
EPA is not proposing testing because no TSCA Section 4 standards
are available. Testing for such effects will be the
responsibility of EPA.
5.6.
Bioconcentration - Plant Uotake/Translocoation
~ ,
Adequate data are available to assess bioconcentration in
aquatic vertebrates and aquatic benthic invertebrates, therefore,
the EPA is not proposing to require testing in these species.
There are no data on plant uptake/translocation. The Agency is
proposing to require that this test be performed according to EPA
standards.
The USEPA (1978a) reported a steady-state bioconcentration
factor of 9X (9 times higher in tissue than in ambient water) for
l,l,l-trichloroethane in the bluegill, based on a 28 day test.
This test was judged adequate to assess bioconcentration
potential in aquatic vertebrates.
17

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Although there are no data on bioconcentration in aquatic
benthic invertebrates, ~PA is not proposing to require such
testing for the following reasons: 1) the log Poet is low
(2.49); 2) the bioconcentration factor in the in v~vo fish test
is low (9); 3) there is no significant difference in acute
toxicity testing results among freshwater and saltwater
vertebrates and invertebrates; and 4) in a modeling excercise
performed by Athens Environmental Research Laboratory (USEPA
1981), partioning data indicated that in an aqueous ecosystem
0.1-25% of l,l,l-trichloroethane was associated with the sediment
whereas 99.9-75% was associated with the water column, which
suggests that exposure to organisms associated with sediments is
not likely to be high. The weight of this evidence favors a
conclusion that the data available are adequate to perform a risk
assessment on bioconcentration potential in aquatic benthic
invertebrates.
5. 7 .
Other Effects of Concern
The EPA is not proposing testing for other effects of
concern (toxicity to terrestrial invertebrates, microorganisms,
ecosystems) because no TSCA Section 4 standards are available.
Testing for such effects if needed will be the responsibility of
EPA.
6.
CHEMICAL FATE - SUFFICIENCY OF DATA h~D
NECESSITY FOR TESTING
The Agency will use physicochemical data to determine the
persistence, location, concentration and transport of 1,1,1-
trichloroethane into the environment. With the exception of
anerobic biodegration data which will be provided by EPA-
sponsored testing, the data available are believed sufficient to
characterize the environmental fate of l,l,l-trichloroethane.
Boiling Point
74.0°C
Melting Point.
-33.0°C
Density
1.3249 gm/cm3 at 20°C
Vapor Pressure
99.75 mm Hg at 20°C
log Poct
2.49
Water Solubility
0.095 g/100g (950 ppm)
Dissociation Constant
Not Relevant
Particle Size
Not Relevant
18

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Hydrolysis
Spectra
Adsorption/Desorption
Biodegradation
Data on the ~ydrolysis of 1,:,1-
t=ichloroethane are adequate. The
hydrolytic half-life appears to be in
the range of 5 to 9 months; the
estimated half-life in seawater at ph 8
and 25°C is 39 months (Pearson and
McConnell 1975).
l/l/l-Trichloroethane does not
absorb visible and near ultraviolet
radiation. (Price et al. 1980)
Data on adsorption/desorption
of l,l,l-trichloroethane are
adequate. The chemical has been found
to move readily through soils and
sediments. (Price et al. 1980)
Because of l,l,l-trichloroethane's use
as a septic tank degreaser, EPA is
concerned over groundwater
contamination by the chemical. The
Agency finds that there are no data to
assess the anaerobic biodegradation of
the chemical and that data are needed
to better characterize its fate under
such conditions. The EPA plans to
sponsor anaerobic degradation testing
because no TSCA Section 4 standards are
available at this time.
19

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REFERE~CES
Adams EM, Spencer HC, Rowe VK, Irish DO. 1950. Vapor toxicity
of l,l,l-trichloroethane (methyl-chlorofor~) determined by
experiments on laboratory animals. Arch. Ind. Hyg. Occup. Med.
1:225-236.
Alexander HC, McCarty WM, Barlett EA. 1978. Toxicity of
perchloroethylene, trichloroethylene, l,l,l-trichloroethane, and
methylene chloride to fathead minnows. Bull. Environ. Contam.
Toxicol. 20:344-352.
Battelle Columbus Laboratories. 1977. Multimedia
methyl chloroform. EPA - 560/6-77-030. Office of
Substances, U.S. Environmental Protection Agency,
\vashington, D.C.
levels:
Toxic
Beaver ER Jr.
observations.
1977. 1,1,1-Trichloroethane physiological
?rofessional Safety 22:20-21.
Borzelleca JF, Munson AE, Dewey RL. Virginia Commonwealth
University, ~edical College of Virginia, Richmond, VA. 1976.
The effects of sel~cted organic contaminants in drinking water on
the functions of the reproductive, nervous, and immune systems.
~ashington, D.C.: Office of Drinking Water, u.S. Environmental
?rotection ~gency. Grant CR 806481.
Chemical an~ Engineering News. 1379.
solvents re~ains bleak. 57(44) :10-13.
Outlook for organic
Chemical Har~(eting Reporter.
trichloroethane. 216(24):9.
1979.
Chemical profile, 1,1,1-
Dornette WHL, Jones Jp. 1960. Clinical experiences with 1,1,1-
trichloroethane. A preliminary report of 50 anesthetic
administrations. Anesthe. Analg. 30:249-253.
Dow Chemical U.S.A. 1981. Skin sensi~ization study in human
subjects. 1969. Midland, MI: Dow Chemical U.S.A.
Ewing BB, Chian ESK, Cook JC, Evans CA, Hopke PK, Perkins EG.
1977. Monitoring to detect previously unrecognized pollutants in
surface water. EPA-560/6-77-01S.
Feiler H. 1979.
treatment works.
Fate of priority pollutants in publicly owned
EPA-440/l-79-300.
Gamberale F, Hultengren M. 1973. Methylchloroform exposure
II. Psychophysiological functions. Work Environ. Health
10:82-92.
20

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Gehring ?J. 1968. Hepatotoxic potency of various ch.~0rinated
hydrocarbon vapors relative to their narcotic and let~al
potencies in ~ice. ~~xical. Appl. Pharmacol. 13:287-298.
Hall DW; Viste DR. Warzyn Engineering Inc. 1980. Hydrogeologic
investigation, EPA/JRB Associates, Town of Southington,
Connecticut. Draft Final Report. Warzyn Project No. C 8909.
McLean, VA: JRB Associates.
Katz, McCartin T, Phuoc LT, Shannon T, Wagner K. 1980.
materials balance: Methylchloroform. Final Report--JRB
Associates, Inc., McLean, Va. (Contract No. 68-01-5793).
Level II
Klaassen CD, Plaa GL. 1967. Relative effects of various
chlorinated hydrocarbons on liver and kidney function in dogs.
Toxicol. Appl. Pharm. 10:119-131.
Klaassen CD, Plaa GL. 1969. Comparison of the biochemical
alterations elicited in livers from rats treated with carbon
tetrachloride, chloroform, l,l,2-trichloroethane and 1,1,1-
trichloroethane. Biochem. Pharm. 18:2019-2027.
Kramer CG, Ott MG, Fulkerson JE, Hicks N.
workers exposed to l,l,l-trichloroethane:
study. Arch. Environ. Health 33:331-342.
1978. Health of
a matched-pair
Margard W (Battelle). 1978. Summary report on in vitro bioassay
of chlorinated hydrocarbon solvents to Detrex Chemical
Industries, Inc. July 31, 1978.
McCarty WM. 1979.
Trade Secret) 1979.
Submitted by Dow Chemical Co. (FIFRA ~10
McConnell, Ferguson DM, Pearson CR. 1975. Chlorinated
hydrocarbons and the environment. Endeavor 34(13):13-18.
Midwest Research Institute. 1979. An assessment of the need for
limitations on trichloroethylene, methy1ch1oroform, and
perchloroethylene. U.S. Environmental Protection Agency, Office
of Toxic Substances, EPA-560/11-79-009, Washington, D.C. 234 p.
National Cancer Institute (NCI). 1977. Bioassay of 1,1,1-
Trichloroethane for Possible Carcinogenicity. CAS No. 71-55-6.
NCI-CG-TR-3.
National Institute for occupational Safety and Health (NIOSH).
1977. Survey Report of Hill Air Force Base - Building 100. DHEW
Report, May 2, 1978.

National Occupational Hazard Survey (NOHS). 1980.
National Institute for Occupational Safety and Health,
Cincinnati, Ohio.
21

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Pearson CR, McConnell G. 1975. Chlorinated Cl and C2
hydrocarbons in the marine environment. Proc. R. Soc.
Ser. 3. 189:305-332.
Lcndon,
Price ML, Lutz GA, Tolle D. 1980. Risk Assessment of 1,1,1-
Trichloroethane. Final Report - Battelle Columbus Laboratories,
Columbus, Ohio. (Contract No. 60-01-0543).
Quast JF, Rampy LW, Balmer MF, Leong BKJ, Gehring PJ.
Toxicologic and Carcinogenic Evaluation of a 1,1,1-
Trichloroethane Formulation by Chronic Inhalation in
October 6, 1978. Dow Chemical Company, Midland, MI.
1978.
Rats.
Riddle BL, Carchman RA, Borzelleca JF. 1981. Effects of 1,2-
dichloromethane and l,l,l-trichloroethane in drinking water on
reproduction and development in mice. (Abstract). The
Toxicologist 1(1):26.
Salvini M, Binaschi 5, Riva M. 1971. Evaluation of the
psychophysiological functions in humans exposed to the "Threshold
Limit Value" of l,l,l-trichloroethane. Br. J. Ind. Med. 28:286-
292.
Schwetz BA, Leong BKJ, Gehring PJ. 1975. The effect of
ma'ternally inhaled trichloroethylene, perchloroethylene, methyl
chloroform, and methylene chloride on embryonal and fetal
development in mice and rats. Toxicol. Appl. Pharm. 32:34-96.
Siegel J, Jones RA, Coon RA, Lyon JP. 1971. Effects on
experimental animals of acute, repeated and continuous inhalation
exposures to dichloroacetylene mixtures. Toxicol. Appl. ?harm.
18:168-174.
Simmon VF, Kauhanen K, Tardiff RG. 1977. Mutagenic acti',Ti':.:! of
chemicals identified in drinking water. Dev. Toxicol. Environ.
Sci. 2: 249-258.
Skory LW, Fulkerson J, Ritzema D. 1974. Vapor degreasing
solvents. When safe? Prod. Finish. pp 2-9.
Stewart RD, Gay HR, Erley DS, Hake CL, Schaffer AW. 1961.
Human exposure to l,l,l-trichloroethane vapor: Relationship of
expired air and blood concentrations to exposure and toxicity.
Am. Ind. Hyg. Assoc. J. 22:252-262.
Stewart RD, Gay HH, Schaffer AW, Erley DS, Rowe VK. 1969.
Experimental human exposure to methyl chloroform vapor. Arch.
Environ. Health 19:467-472.
Torkelson TR, Oyen F, M.cCollister D, Rowe VK. 1958. Toxicity of
l,l,l-trichloroethane as determined on laboratory animals and
human subjects. Am. Ind. Hyg. Assoc. J. 19:353-362.
22

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USEPA, 1978a. Indepth studies on health and environmental
impacts of selected water pollutants. u.s. EPA Contract No. 68-
Ql-4646.
DSEPA. 1978b. Second Report of the TSCA Interagency Testing
Committee to the Administrator, Environmental Protection
Agency. Washington, D.C: Environmental Protection Agency-
USEPA. 1981. Modeling exercise (Exposure Analysis Modeling
Systems, EXAMS). Modeling of fate of l,l,l-trichloroethane in an
aquatic ecosystem. Athens Environmental Research Laboratory,
Athens, Georgia.
USITC. 1980. u.S. International Trade Commission. Synthetic
Organic Chemicals. United States ?roduction and Sales. USITC
publication 1001, p. 269, Washington, DC.
Walter P, Craigmill A, Villaume J, Sweeney S, Miller GL.
Chlorinated hydrocarbon toxicity (l,l,l-trichloroethane,
trichloroethylene and tetrachloroethylene). Prepared for
~TIS PB-257-185.
1976.
CPSC,
wildlife International Ltd. Submitted by Dow Chemical Co.
(FIFRA ~lO Trade Secret) 1979.
York RG, Sowry B, HastiDgs L, Manson J.
prenatal toxicity of methyl chloroform.
Toxicologist 1(1):28.
1981. Evaluation of the
(Abstract). The
23

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5027'2 -101
REPORT DOCUMENTATION I.L_REPORT NO.
PAGE I E PAS 6 0 / 2 - 8 J -- 0 0 4
4. rrtle and Subtitle
I~
3. Recipient's Accession No.
S. Report Oate
Assessment of Testing Needs: l,l,l-Trichloroethane
Support Document, Proposed Health and Environmental
Effects Test Rule, TSCA Section 4

7. Author(s)
6.
-
a. Performinc O,.anizatJon RePt. NO.
,. Performi.. O,..nization Ne.... and Address

Assessment Division/Office

Substances

401 M Street, S.W.
Washington, DC 20460
10. ProjectlTuk/Woric Unit No.
of Pesticides and Toxic
11. ContI'8Ct(C) or Grent(G) No.
(C)
(G)
1~ ~nc O,..nization Name and Address
U.S. Environmental Protection
401 M Street, S.W.
Washington, DC 20460
13. Type of Report & Period eo......d
Ag-en c y
14.
15. Supplementary Not..
--- --_. -. - ---
- IS. Abstract (Umit 200 -Fda)
Approxima.tely 716 million pounds (325,064 kkg) of l,l,l-trichloroethane
were produced in the United States in 1979. Because of the excellent solvent
prcperties of the chanical, its ma.jor use is in the rretal cleaning industry.
Extensi ve huma.n exposure occurs both in the work place and fran consumer use
of products containing l,l,l-trichloroethane. In 1979, 75 percent of the
total production was estima.ted to have been released into the environrrent.
Measurable arrounts have been reported in the atrrosphere, soil, rainwater,
ma.rine and fresh water surface waters and groundwater.
Because of the large production volurre, extensive release to the
environment and the number of people potentially exposed to 1,1,1-
trichloroethane, both occupationally and as consumers, the EPA is proposing to
recornrend testing under Section 4(a) (1) (B) of the Toxic Substances Control
Act. Testing is being proposed in the follewing areas Where data were found
to be insufficient: Structural Teratogenicity; Aquatic vertebrates - acute
and chronic toxicity; Aquatic invertebrates - chronic toxicity; Birds -
chronic toxicity; Terrestrial plants - root elongation/seed germination, early
seedling grCMth; Bioconcentration - plant uptake/translocation.
17. Document Analysis e. Oescriptors
II.. Identifiers/Open-Ended Terms
Co COSATI FIeld/Group
Release unlimited
19. Security Class (This Report)

unclassified
20. Security Class (This Pace)
unclassified
21. NO. of Pac..
1 a. Availability Statement
~ Price
(See AHSI-Z39.18)
See Instructions on Rave,..
OPTIONAL FORM 272 (4-17)
(Formerly NTI5-35)
Department of Commerce

1< U.S. GOVERNMENT PRINTING OFFICE, 1981 - 720-016/5995 REGION 3-1

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United States
Environmental Protection
Agency
Wathington DC 20460
pfficial Business
Penalty for Private Use $300
Po~ageand 00
Fees paid
Environ.mental ~.
ProtectIOn -
Agency ~.'
EPA 335

Third-Class
EPA 560/4-81-004

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