EPA 749-F-94-014a
CHEMICAL SUMMARY FOR METHYLCHLOROFORM
prepared by
OFFICE OF POLLUTION PREVENTION AND TOXICS
U.S. ENVIRONMENTAL PROTECTION AGENCY
August 1994
This summary is based on information retrieved from a systematic search
limited to secondary sources (see Appendix A). These sources include
online databases, unpublished EPA information, government publications,
review documents, and standard reference materials. No attempt has been
made to verify information in these databases and secondary sources.
I. CHEMICAL IDENTITY AND PHYSICAL/CHEMICAL PROPERTIES
The chemical identity and physical/chemical properties of
methylchloroform are summarized in Table 1.
TABLE 1. CHEMICAL IDENTITY AND CHEMICAL/PHYSICAL
PROPERTIES OF METHYLCHLOROFORM
Characteristic/Property
Data
Reference
CAS No.
Common Synonyms
Molecular Formula
Chemical Structure
Physical State
Molecular Weight
Melting Point
Boiling Point
Water Solubility
Density
Vapor Density (air = 1)
KOC
Log KOW
Vapor Pressure
Reactivity
Flash Point
Henry's Law Constant
Fish Bioconcentration
Factor
Odor Threshold
Conversion Factors
71-55-6
1,1,1-trichloroethane,
chlorothene
C2H3C13
Cl H
Cl- C - C
H
Cl H
colorless liquid
133.42
-32.50C
74.10C
1334 mg/L
d20/4, 1.3376
4.63
152
2.49
100 mm Hg at 200C
nonflammable
2.76 x 10-2 atm m3/mol
<9 (measured)
100 ppm {in air)
1 ppm = 5.54 mg/m3
1 mg/m3 = 0.18 ppm
Budavari et al. 1989
Keith and Walters 1985
Budavari et al. 1989
Budavari et al. 1989
Budavari et al. 1989
CHEMFATE 1994
Budavari et al. 1989
Verschueren 1983
U.S. Air Force 1989
U.S. Air Force 1989
Verschueren 1983
U.S. Air Force 1989
U.S. Air Force 1989
HSDB 1994
Torkelson and Rowe 1981
Verschueren 1983
II. PRODUCTION, USE, AND TRENDS
A. Production
Methylchloroform is produced by three companies in the United
States. Table 2 lists the producers, along with plant locations
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and capacities. In 1991, US production was estimated to be 648
million pounds. During that same year, 162 million pounds of
methyl chloroform were exported, and imports were negligible
{Mannsville 1992) .
TABLE 2. United States Producers of Methylchloroform
Company Plant Location Plant Capacity
(In Millions of Pounds)
Dow Chemical Freeport, TX 495
PPG Industries Lake Charles, LA 350
Vulcan Chemicals Geismar, LA 200
Source: Mannsville 1992.
B. Use
Methylchloroform is most commonly used for metal cleaning, both
cold cleaning and vapor degreasing. It is commonly used as a
solvent in aerosol formulations, adhesives, coatings, inks, and
electronics. It is also used as a lubricant in cutting oils and
as a chemical intermediate for organic chemicals, such as
vinylidene chloride (Mannsville 1992; HSDB 1994). Table 3 shows
the estimated 1991 US end-use pattern for methyl chloroform.
C. Trends
Under current EPA regulations, production of methylchloroform will
be permitted only for transformation and other uses to be defined
by the EPA. Therefore, production is expected to decline to less
than 50 million pounds per year after 1995 (Mannsville 1992) .
TABLE 3. Estimated 1991 United States
End-Use Pattern of Methylchloroform
Use of Methyl Chloroform Percentage of US
Methylchloroform Use
(Typical Standard Industrial Classification
(SIC) Code) (see end note 1)
Metal Cleaning (used in a variety of SICs) 50%
Aerosols (production, SIC 2851;
used in a variety of SICs) 11%
Adhesives (production, SIC 2891;
used in a variety of SICs) 11%
Chemical Intermediate (production,
SIC 2869; use, SIC 2869) 10%
Coatings and Inks (production, SICs 2851, 2893;
used in a variety of SICs) 8%
Electronics (use, SIC 36) 4%
Miscellaneous (no applicable SIC(s)) 6%
Source: Mannsville 1992.
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III. ENVIRONMENTAL FATE
A. Environmental Release
Of the methylchloroform (1,1,1-trichloroethane) released to the
environment in 1992, as reported to the Toxic Chemical Release
Inventory by certain types of U.S. industries, 114.9 million
pounds were released into the atmosphere, 13.1 thousand pounds
released into surface water, 500 pounds released to underground
injection sites, and 76.4 thousand pounds released onto land
(TRI92 1994). Concentrations of methylchloroform measured in
untreated ground and surface waters samples from sites in over
100 U.S. cities range from 0.2 to 334 ppb (HSDB 1994). A range
of 950 to 5440 ppb methylchloroform has been measured in samples
of contaminated drinking water wells in New York, New Jersey,
Connecticut, and Maine (HSDB 1994). Arctic sea water near Sweden
contained 0.4 - 1.7 ng/L (parts per trillion) and concentrations
of 0.6 - 69 parts per trillion have been measured in rain or snow
at various locations around the globe {HSDB 1994). Atmospheric
concentrations of methylchloroform ranged from 0.074 - 0.587 ppb,
and 1.2 ppb has been measured in the workplace (HSDB 1994) . The
chemical has been detected in human mother's milk in urban areas
(HSDB 1994). Due to the large output and slow degradation of the
chemical, the atmospheric concentration is increasing by 4.8 -17%
a year (HSDB 1994).
B. Transport
Methylchloroform volatilizes rapidly to the atmosphere from water
and soil as predicted by its vapor pressure (100 mm Hg) and Henry's
law constant (2.76 x 10-2 atmum3/mol) (ATSDR 1993). Once in the
atmosphere, the chemical is transported long distances, being found
as distant as the South Pole (CHEMFATE 1994), but can be removed
from the atmosphere in rain or snow (HSDB 1994). The chemical
leaches into ground and surface waters from soil (U.S. Air Force
1989) due to its water solubility.
C. Transformation/Persistence
1. Air - The estimated half-life for methylchloroform in air is
2.2 to 4.8 years (U.S. EPA 1984). Little degradation of
methylchloroform occurs in the troposphere, but direct
photolysis occurs in the stratosphere (CHEMFATE 1994; HSDB
1994). Degradation in the troposphere also occurs slowly by
reaction with hydroxyl radicals (half-life, 3.7 years); however,
the half-life is "drastically reduced" (to 26 weeks) in the
presence of ozone or chlorine radicals {CHEMFATE 1994) .
2. Soil - Evaporation and leaching are the major routes of removal
of methylchloroform from soils (U.S. Air Force 1989). There
is little evidence to suggest that biodegradation occurs except
in acclimated soils, like those found in landfills {HSDB 1994;
U.S. Air Force 1989).
3. Water - Volatilization of methylchloroform into the atmosphere
is the main route of removal from water. The half-life in water
ranges from hours to weeks (HSDB 1994) . No photodegradation has
been measured in water but slow to moderate biodegradation
occurred after acclimatization (CHEMFATE 1994).
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4. Biota - Bioconcentration of methylchloroform in aquatic
organisms is not expected to be important based on the log
bioconcentration factor of 0.95 in bluegill (CHEMFATE 1994).
IV. HUMAN HEALTH EFFECTS
A. Pharmaeokinetics
1. Absorption - Methylchloroform is absorbed from both the lungs
and the gastrointestinal tract (U.S. EPA 1984). The chemical
was found in expired air (no quantities given) after accidental
ingestion of 1 ounce (U.S. EPA 1984). The rate of absorption in
human males exposed by inhalation to 72 or 213 ppm for 8 hours
ranges from 26 - 32% (HSDB 1994).
2. Distribution - After exposure by inhalation to mice, methyl-
chloroform was found in brain, kidney, and liver (IARC Monographs
1979), Following occupational exposures to humans of high
concentrations (no levels given), the chemical has been found in
blood, brain, liver, bile, skeletal muscle, and lungs (ACGIH
1991). The chemical is preferentially distributed to fatty
tissue but cleared after cessation of exposure (ATSDR 1993).
3. Metabolism - Methylchloroform is metabolized to trichloroacetic
acid and trichloroethanol (Torkelson and Rowe 1981). A "small
percentage" will be metabolized to carbon monoxide (HSDB 1994) .
4. Excretion - The majority of methylchloroform is eliminated
unchanged in expired air. After exposure of hurnans by inhalation
to 72 or 213 ppm for 8 hours, approximately 90% of the calculated
dose was eliminated in expired air by 8 days; urinary excretion of
glucuronide conjugated metabolites lasted about 12 days (HSDB
1994). Rats have been shown to eliminate greater than 98% of an
absorbed dose in expired air with about 0.5% converted to C02 and
the remainder excreted in the urine as trichloroacetic acid or the
glucuronide of trichloroethanol (IARC Monographs 1979).
B. Acute Toxicity
Inhalation exposure to high levels of methylchloroform can cause
central nervous system depression with death due to respiratory
failure and/or cardiac arrhythmia (see section IV.G for details
on neurotoxicity). Non-lethal doses may cause headache and
fatigue. The vapor is irritating to the eyes and nose.
1. Humans - Inhalation exposure to 1000 ppm causes eye and nasal
irritation within 30 minutes (Torkelson and Rowe 1981) .
Hypotension, premature ventricular contractions, and cardiac
arrest have been reported in patients exposed to 10,000 to
26,000 ppm methylchloroform as a surgical anesthetic (U.S. Air
Force 1989) . Transient liver and kidney dysfunction occurred
in adolescents exposed to "large" concentrations of the chemical
while sniffing glue; twenty-eight percent of sudden deaths in
glue sniffers have been attributed to methylchloroform (HSDB
1994). Fatigue, irritation, and headache were the only effects
reported in volunteers exposed to 500 ppm 7.5 hours/day, 5 days/
week for 3 weeks (U.S. EPA 1984). Accidental ingestion of 30 mL
resulted in gastrointestinal disturbance but only minimal hepatic
or renal damage; recovery was complete within 2 weeks (U.S. Air
Force 1989) .
4 of! 2
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2, Animals - Reported LD50 values for methylchloroform are greater
than 5 g/kg for rats, mice, rabbits, and guinea pigs (ACGIH 1991),
Methylchloroform is a skin irritant; application to guinea pigs
of 1 mL liquid or repeated contact over 3 days caused edema,
erythema, inflammation, and cellular degeneration (ACGIH 1991) .
Liquid methylchloroform caused only mild, transient irritation in
the eyes of rabbits (Torkelson and Rowe 1981). Cardiac sensitiza-
tion to epinephrine occurred in dogs exposed to 5000 or 10,000
ppm methylchloroform (no duration given) (ACGIH 1991) .
C. Subchronic/Chronic Toxicity
Long-term worker inhalation exposure to methylchloroform has
been reported to result in no observed permanent liver damage or
adverse changes in cardiovascular function. Repeated dermal
contact may cause transient dermatitis. Repeat dose laboratory
animal studies have shown adverse liver and kidney effects after
inhalation or oral exposure to high levels of methylchloroform.
EPA is currently reviewing information to determine if an
inhalation reference concentration (RfC)(see end note 2) can be
derived for methylchloroform.
1. Humans - A no-observed adverse effect level for long-term
occupational exposure is approximately 53 ppm (HSDB 1994) .
Epidemiological studies of workers exposed to methylchloroform
for up to 6 years showed no effects on liver or cardiovascular
function (Torkelson and Rowe 1981). "Prolonged or repeated
contact with skin" may cause transient dermatitis (HSDB 1994) .
2. Animals - Rats, rabbits, monkeys, and guinea pigs were exposed
to 500 ppm methylchloroform by inhalation 7 hours/day, 5 days/
week for 6 months with no evidence of organ damage (ACGIH 1991).
Continuous exposure for 14 weeks to 1000 ppm caused no adverse
effects in dogs or monkeys but resulted in increased liver weight
and fatty and necrotic changes in the livers of mice and rats
(Torkelson and Rowe 1981). No adverse effects were seen in rats
exposed to 875 or 1750 ppm 6 hours/day, 5 days/week, for 1 year
(Torkelson and Rowe 1981). Animals were exposed to 650, 1500,
3000, or 5000 ppm 7 hours/day, 5 days/week, for 1-3 months.
Slight reduction in growth rate at all doses and fatty liver
changes at 5000 ppm were observed in guinea pigs but rats, rabbits,
and monkeys were unaffected (U.S. EPA 1984); Rats and mice were
given methylchloroform at doses of 0.5, 1, 2, 4, or 8% in feed
(see end note 3) for 13 weeks (NTP 1994). Dose related systemic
effects included hyaline degeneration and inflammation in kidneys
of male rats, decreased body and heart weights in male mice, and
decreased body and liver weights in female mice.
D. Carcinogenicity
Available evidence is inadequate to assess the carcinogenic
potential of methylchloroform. There is no reported human cancer
information, and animal studies have failed to demonstrate
carcinogenicity. Based on no human and no animal cancer data,
the U.S. EPA (1994) classified methylchloroform as class D, not
classifiable as to human carcinogenicity.
1. Humans - No information was found in the secondary sources
searched regarding the carcinogenicity of methylchloroform to
Sofi;
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humans.
2. Animals - No increase of tumors of any kind occurred in rats
exposed by inhalation to 875 or 1750 ppm methylchloroform
6 hours/day, 5 days/week for 1 year, followed by a 19-month
observation period (U.S. EPA 1984). No cancers were seen in
rats or mice exposed to up to 1500 ppm 6 hours/day, 5 days/week,
for 2 years (U.S. Air Force 1989). High mortality occurred in
mice (time-weighted average doses, 2807 or 5615 mg/kg/day) and
rats (750 or 1500 mg/kg/day) given methylchloroform by gavage
5 days/week for 78 weeks, precluding adequate carcinogenicity
assessment (IARC Monographs 1979). Therefore, IARC classifies
methylchloroform as Group 3, not classifiable as to its
carcinogenicity to humans (IARC Monographs 1979).
E. Genotoxicity
Methylchloroform is positive for cell transformation with rat
embryo cells (RLV/1706) and for sister chromatid exchange in
mammalian cells; it was negative for alterations in mouse sperm
morphology (GENETOX 1992). Methylchloroform has been tested for
mutagenicity under Section 4 of the Toxic Substances Control Act
(TSCA). The testing was to consist of a mouse micronucleus test
and a dominant lethal test, the latter test being triggered by a
positive response in the micronucleus assay. Methylchloroform
was not a chromosome mutagen under conditions of the micronucleus
test (Cimino 1990).
F. Developmental/Reproductive Toxicity
Results of testing, requested by and submitted to EPA under
Section 4 of TSCA, indicate methylchloroform adversely affects the
developing fetus at high concentrations in air. No evidence of
reproductive toxicity has been seen in most species tested except
in guinea pigs which showed testicular degeneration at high
concentrations of methylchloroform in air.
1.
Humans - No information was found in the secondary sources
searched concerning the developmental or reproductive toxicity
nf mAi-Hvl r-Vi 1 n-rr^'FrsTm in VmmAna
of methylchloroform in humans.
2. Animals - Developmental toxicity studies have been completed
and submitted to EPA under the authority of Section 4 of TSCA
(Troast 1989). Rats (30/group) and rabbits (24/group) were
exposed by inhalation to 1000, 3000, and 6000 ppm methylchloroform
on days 6-15 and 6-18 of gestation, respectively. Developmental
toxicity (unossified/poorly ossified cervical centra, decreased
fetal weight, and increased non viable implantations in rats; and
an increase in bilateral extra 13th ribs in rabbits) was reported
at 6000 ppm. The no-observed-adverse- effect level for
developmental effects was 3000 ppm in both species. Maternal
toxicity (reduced body weight gain and food consumption) occurred
at each dose level in rats and at the two highest doses in
rabbits.
No maternal, fetal, or developmental toxicity was observed in rats
or mice exposed by inhalation to 875 ppm methylchloroform, 7
hours/day on days 6-15 of gestation (U.S. EPA 1984). Rats were
exposed to 2100 ppm, 6 hours/day, 7 days/week, beginning 2 weeks
prior to mating and continuing throughout gestation (ACGIH 1991).
Skeletal and soft tissue anomalies, observed in offspring
6 of 12
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sacrificed on gestation day 21, were attributed to developmental
delays, andneurobehavioral and developmental delays in surviving
offspring were no different from controls by 21 to 120 days of
age. Successive generations of mice were exposed to 100, 300, or
1000 ppm methylchlorofortn in drinking water for 24 to 25 weeks
(U.S. Air Force 1989). No effects on fertility, gestation, or
viability indices were observed; no developmental toxicity was
observed; and methylchloroform failed to produce dominant lethal
mutations. Testicular degeneration was observed in guinea pigs
exposed to 5000 ppm 7 hours/day, 5 days/week, for 1-3 months
(U.S. EPA 1984} .
G. Neurotoxicity
The nervous system is a major target for methylchloroform
toxicity. High concentrations of methylchloroform in air are
lethal in humans, occurring from its anesthetic effects and from
its adverse effect on the heart (cardiac arrhythmia).
1. Humans - Deaths due to central nervous system depression and
cardiac arrhythmia have occurred from inhalation of
methylchloroform in poorly ventilated areas (ACGIH 1991) and
from recreational glue sniffing (HSDB 1994). The anesthetic
effects of methylchloroform increase with the duration of
exposure and concentration of the chemical (Torkelson and Rowe
1981). Loss of equilibrium occurs by 60 minutes from exposure
to 1000 ppm (Torkelson and Rowe 1981). For some individuals,
the onset of anesthesia occurs at 500 ppm (Torkelson and Rowe
1981), but, 350 ppm for 2 hours is the apparent lowest-observed-
adverse effect level for mental alertness (ACGIH 1991). The
concentration of 350 ppm is roughly equivalent to 69.25 mg/kg
for the 2 hour exposure period (see end note 4). Due to the
effects on cardiac function and lack of efficacy, the chemical
was abandoned as a surgical anesthetic (Torkelson and Rowe 1981) .
Accidental ingestion of 30 mL resulted in CNS depression (U.S. Air
Force 1989) .
2. Animals - Rats were exposed by inhalation to 5000 or 10,000 ppm
methylchloroform 7 hours/day, 5 days/week for 1 month (Torkelson
and Rowe 1981; U.S. Air Force 1989). At the high dose, animals
showed a staggering gait and irregular respiration within 10
minutes progressing to semiconsciousness by 3 hours; at 5000 ppm,
a mild narcotic effect was apparent within 1 hour. Cardiac
sensitization to epinephrine occurred in dogs exposed to 5000 or
10,000 ppm (no duration given) (ACGIH 1991).
ENVIRONMENTAL EFFECTS
LC50 and EC50 values for methylchloroform in aquatic organisms range
from approximately 30 to 130 mg/L; these values exceed measured
concentration in untreated ground or surface waters by several orders
of magnitude. The concentrations required for acute toxicity in
laboratory animals are not likely to be reached in the environment.
A. Toxicity to Aquatic Organisms
Methylchloroform has moderate acute toxicity to aquatic organisms;
toxicity values range between greater than 1 mg/L and 100 mg/L.
Ninety-six hour LC50 values for Pimephales promelas (fathead minnow)
under flow through or static test conditions are 52.8 mg/L and
105 mg/L, respectively (Verschueren 1983). Other reported 96-hour
7ofl2
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toxicity values for the fathead minnow include another LC50
(42.3 mg/L; flow through) and an EC50 for loss of equilibrium of
28.8 mg/L (HSDB 1994). The 7 day LC50 for Poecilia reticulata
(guppy) is 133 mg/L (Verschueren 1983).
B. Toxicity to Terrestrial Organisms
No information was found in the secondary sources searched regarding
the toxicity of methylchloroform to terrestrial organisms. However,
due to the high volatility of the chemical (vapor pressure,
100 mm Hg), it is unlikely to accumulate to toxic concentrations
in soils or surface waters. Also, based on the oral LC50 values of
>5 g/kg for laboratory animals and the lack of developmental toxicity
at high levels, it is unlikely that the chemical will be toxic to
terrestrial animals at environmental levels.
C. Abiotic Effects
In the atmosphere, methylchloroform has a long half-life (2.2-4.8
years) and may transport through the troposphere and into the
stratosphere where it can react with and destroy ozone (U.S.EPA
1984). The depletion of ozone in the upper atmosphere has been
associated with increased levels of harmful, ultraviolet radiation
reaching the Earth's surface.
VI. EPA/OTHER FEDERAL/OTHER GROUP ACTIVITY
Voluntary reduction of methylchloroform environmental releases has
occurred since 1991, as a result of a joint industry/EPA pollution
prevention initiative known as the 33/50 program. The Clean Air Act
Amendments of 1990 list methylchloroform as a hazardous air pollutant.
EPA has classified methyl chloroform as a "Class 1 Ozone Depleting
Chemical." Production of methyl chloroform is required to cease by
the end of 1995 for all uses other than transformation and essential
uses, to be defined by the EPA (Mannsville 1992). Occupational
exposure to methyl chloroform is regulated by the Occupational Safety
and Health Administration. The permissible exposure limit (PEL) is
350 parts per million parts of air (ppm) as an 8-hour time-weighted
average (TWA) (29 CFR 1910.1000),
Federal agencies and other groups that can provide additional
information on methylchloroform are listed in Tables 4 and 5.
TABLE 4. EPA OFFICES AND CONTACT
NUMBERS FOR INFORMATION ON METHYLCHLOROFORM
EPA OFFICE
LAW
PHONE NUMBER
Pollution
& Toxics
Prevention
Air
Solid Waste &
Emergency Response
Toxic Substances Control Act
(Sec. 4/8A/8D/8E)
Emergency Planning and Community
Right-to-Know Act (EPCRA)
Regulations (Sec. 313)
Toxics Release Inventory data
Clean Air Act
Comprehensive Environmental
Response, Compensation, and
Liability Act (Superfund)/
Resource Conservation and Recovery
Act / EPCRA (Sec. 304/311/312)
(202) 554-1404
(800)
(202)
(919)
535-0202
260-1531
541-0888
(800) 535-0202
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Water
Clean Water Act
Safe Drinking Water Act (Drinking
Water Standard: 0.2 mg/L)
(202) 260-7588
(800) 426-4791
TABLE 5. OTHER FEDERAL OFFICE/OTHER GROUP
CONTACT NUMBERS FOR INFORMATION ON METHYLCHLOROFORM
Other Agency/Department/Other Group
Contact Number
Agency for Toxic Substances & Disease Registry
American Conference of Governmental Industrial
Hygienists
(Recommended Exposure Limit
(see end note 5): 350 ppm)
(Recommended Short-Term Exposure Limit: 450 ppm)
Consumer Products Safety Commission
Food & Drug Administration
National Institute for Occupational Safety & Health
(Recommended Exposure Limit
(see end note 6): 350 ppm)
Occupational Safety & Health Administration
(Permissible Exposure Limit
(see endnote 7): 350 ppm)
(404) 639-6000
(513) 742-2020
(301) 504-0994
(301) 443-3170
(800) 356-4674
Check local
phone book for
phone number
under Department
of Labor
VII. END NOTES
1.Standard Industrial Classification code is the statistical
classification standard for all Federal economic statistics. The code
provides a convenient way to reference economic data on industries of
interest to the researcher. SIC codes presented here are not intended
to be an exhaustive listing; rather, the codes listed should provide an
indication of where a chemical may be most likely to be found in
commerce.
2.An inhalation reference concentration is an estimate (with uncertainty
spanning perhaps an order of magnitude) of the exposure level for the
human population, including sensitive subpopulations, that is likely to
be without an appreciable risk of deleterious effects during the time
period of concern.
3.These doses are equivalent to 250, 500, 1000, 2000, or 4000 mg/kg/day
for rats and 650, 1300, 2600, 5200, or 10,400 mg/kg/day for mice.
Calculated using standard feed consumption estimates based on the
fraction of body weight that is consumed each day as food: 0.05 and 0.13
for rats and mice, respectively (U.S. EPA 1988).
4. Calculated using the factor 5.54 (Verschueren 1983) to convert 350
ppm to 1939 mg/m3 which is multiplied by 0.036 (breathing rate for 2
hours, 2.5 m3 [standard occupational 8-hour breathing rate, 10 m3]
divided by the assumed adult body weight, 70 kg) and assuming 100%
absorption, to obtain the dose in mg/kg (U.S. EPA 1988).
5. The ACGIH exposure limit is a time-weighted average (TWA)
90F12
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concentration for an 8-hour workday during a 40-hour workweek..
6.This is a 15-minute ceiling exposure limit value that should not be
exceeded at any time.
7. The OSHA exposure limits are time-weighted average (TWA) concentrations
that must not be exceeded during any 8-hour work shift of a 40-hour
workweek.
VIII. CITED REFERENCES
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Indices, 6th ed., pp. 958-964.
ATSDR. 1993. Agency for Toxic Substances and Disease Registry.
Toxicological Profile for 1,1,1-Trichloroethane. U.S. Department of
Health and Human Services, ATSDR, Atlanta, GA. 213 pp.
Budavari S, O'Neil MJ, Smith A, Heckelman PE (Eds.). 1989. The Merck
Index, llth ed. Merck & Co., Inc., Rahway, NJ, p. 1516.
CHEMFATE. 1994. Syracuse Research Corporation's Environmental Fate Data
Bases. Syracuse Research Corporation, Syracuse, NY, Retrieved 8/15/94.
Cimino. 1990. Review of Micronucleus Study on 1,1,1-Trichloroethane.
Memorandum from M. Cimino (Toxic Effects Branch) to G. Timm (Chemical
Screening Branch), Office of Toxic Substances, USEPA, Washington D.C.
Nov 19, 1990.
GENETOX. 1992. U.S. EPA GENETOX Program, computerized data base.
Retrieved August 1994.
HSDB. 1994. Hazardous Substances Data Bank. MEDLARS Online Information
Retrieval System, National Library of Medicine. Retrieved July 1994.
IARC Monographs. "ISIS. IARC Monographs on the Evaluation of the
Carcinogenic Risk of Chemicals to Humans: Some Halogenated Hydrocarbons,
Vol. 20. IARC, Lyon, France, pp. 515-525.
Keith LH, Walters DB (Eds.). 1985. Compendium of Safety Data Sheets for
Research and Industrial Chemicals, Part II. VCH Publishers, Deerfield
Beach, pp. 1646-1647.
Mannsville. 1992, Chemical Products Synopsis, 1,1,1-Trichloroethane.
Mannsville Chemical roducts Corporation. January 1992.
NIOSH. 1992. National Institute for Occupational Safety and Health.
NIOSH Recommendations for Occupational Safety and Health Compendium of
Policy Documents and Statements. NIOSH, Cincinnati, OH. p 128.
NTP. 1994. National Toxicology Program. 13-Week Subchronic Dosed Feed
Toxicity Study with 1,1,1-Trichloroethane (TCE) (C04626C) Administered
by Microencapsulation to F344 Rats and B6C3F1 Mice. Pathology Working
Group Review, National Institute of Environmental Health Sciences,
Research Triangle Park, NC.
OSHA. 1993. Occupational Safety and Health Administration. Air
Contaminants Rule, Table Z-l, Limits for Air Contaminants. 29 CFR Part
1910, Part V, p 35346.
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Torkelson TR, Rowe VK. 1981. Halogenated Aliphatic Hydrocarbons, In:
Patty"s Industrial Hygiene and Toxicology, 3rd ed. Vol. 2B, GD Clayton,
FE Clayton, Eds. John Wiley & Sons, New York, pp. 3502-3510.
TR192. 1994. 1992 Toxics Release Inventory. Office of Pollution
Prevention and Toxics, U.S. EPA, Washington D.C.
Troast. 1989. Final Action on Section 4 Developmental Toxicity Study of
1,1,1-Trichloroethane. Memorandum from R. Troast (Test Rules Development
Branch) to J. Merenda (Existing Chemicals Assessment Division), Office
of Toxic Substances, USEPA, Washington D.C. August 23, 1989.
U.S. Air Force. 1989. 1,1,1-Trichloroethane. In: The Installation
Restoration Program Toxicology Guide, Vol. 1. Wright-Patterson Air Force
Base, OH, pp. 10-1 through 10-37.
U.S. EPA. 1984. U.S. Environmental Protection Agency. Health Effects
Assessment for 1,1,1-Trichloroethane. Office of Research and
Development, U.S. EPA, Cincinnati, OH. ECAO-CIN-H005.
U.S. EPA. 1988. U.S. Environmental Protection Agency. Methodology for
Evaluating Potential Carcinogenicity in Support of Reportable Quantity
Adjustments Pursuant to CERCLA Section 102. Carcinogen Assessment Group,
Office of Health and Environmental Assessment, U.S. EPA, Washington,
D.C. OHEA-C-073.
U.S. EPA. 1994. U.S. Environmental Protection Agency. Integrated Risk
Information System (IRIS) Online. Coversheet for Methylchloroform.
Office of Health and Environmental Assessment, U.S. EPA, Cincinnati, OH.
Verschueren K (Ed). 1983. Handbook of Environmental Data on Organic
Chemicals, 2nd ed. Van Nostrand Reinhold Co., New York, pp. 1129-1131.
APPENDIX A: SOURCES SEARCHED FOR FACT SHEET PREPARATION
AQUIRE. 1994. Aquatic Information Retrieval online data base. Chemical
Information Systems, Inc., a subsidiary of Fein-Marquart Assoc.
ATSDR. 1989-1994. Agency for Toxic Substances and Disease Registry.
Toxicological Profiles. Chamblee, GA: ATSDR.
Budavari S, O"Neil MJ, Smith A, Heckelman PE (Eds.). 1989. The Merck
Index, llth ed. Rahway, N.J.: Merck & Co., Inc.
CHEMFATE. 1994. Syracuse Research Corporation'^ Environmental Fate
Data Bases. Syracuse Research Corporation, Syracuse, NY.
Clayton GD, Clayton FE, Eds. 1981-1982. Patty"s Industrial Hygiene and
Toxicology, 3rd ed. New York: John Wiley & Sons.
GENETOX. 1994. U.S. EPA GENETOX Program, computerized database.
HSDB. 1994. Hazardous Substances Data Bank. MEDLARS Online
Information Retrieval System, National Library of Medicine.
IARC. 1979-1994. International Agency for Research on Cancer. IARC
Monographs on the Evaluation of Carcinogenic Risk of Chemicals to Man.
Lyon: IARC.
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NIOSH (National Institute for Occupational Safety and Health). 1992.
NIOSH Recommendations for Occupational Safety and Health. Compendium of
Policy Documents and Statements. Cincinnati, OH: NIOSH.
NTP. 1994. National Toxicology Program. Toxicology and Carcinogenesis
Studies. Tech Rep Ser.
NTP. 1994. National Toxicology Program. Management Status Report.
Produced from NTP Chemtrack system. April 8, 1994. National Toxicology
Program, Research Triangle Park, NC.
OSHA. 1994. Occupational Safety and Health Administration. Table Z-2.
Limits for Air Contaminants.
RTECS. 1994. Registry of Toxic Effects of Chemical Substances.
MEDLARS Online Information Retrieval System, National Library of
Medicine.
U.S. Air Force. 1989. The Installation Restoration Toxicology Guide,
Vols. 1-5. Wright-Patterson Air Force Base, OH.
U.S. EPA (U.S. Environmental Protection Agency). 1991. Table 302.4
List of Hazardous Substances and Reportable Quantities 40 CFR, part
302.4:3-271.
U.S. EPA. Most current. Drinking Water Regulations and Health
Advisories. Office of Drinking Water, U.S. Environmental Protection
Agency, Washington, D.C.
U.S. EPA. Most Current. Health Effects Assessment Summary Tables.
Cincinnati, OH: Environmental Criteria and Assessment Office, U.S.EPA.
U.S. EPA reviews such as Health and Environmental Effects Documents,
Health and Environmental Effect Profiles, and Health and Environmental
Assessments.
U.S. EPA. 1994. Integrated Risk Information System (IRIS) Online.
Cincinnati, OH: Office of Health and Environmental Assessment.
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