EPA 749-F-94-014a

                                     prepared by
                                     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      online databases,  unpublished EPA information,  government publications,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.


         The chemical identity and physical/chemical properties of
      methylchloroform are summarized in Table 1.

      CAS No.
      Common Synonyms

      Molecular Formula
      Chemical Structure
      Physical State
      Molecular Weight
      Melting Point
      Boiling Point
      Water Solubility
      Vapor Density (air = 1)
      Log KOW
      Vapor Pressure
      Flash Point
      Henry's Law Constant
      Fish Bioconcentration
      Odor Threshold
      Conversion Factors
     Cl  H
                                  Cl- C - C
     Cl  H
colorless liquid
1334 mg/L
d20/4, 1.3376
100  mm Hg at 200C

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
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

          A.  Production

             Methylchloroform is produced by three companies in the United
             States.   Table 2 lists the producers, along with plant locations
1 of 12

       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.


           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).
3of 12

             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).


          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

            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


            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.
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

               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

               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).


         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

            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.


          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
                                   PHONE NUMBER
       & Toxics
      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) 535-0202
8of 12

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
      Other Agency/Department/Other Group
                                  Contact Number
      Agency for Toxic Substances & Disease Registry
      American Conference of Governmental Industrial
        (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

      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

      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)

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

ACGIH. 1991. American Conference of Governmental Industrial Hygienists,
Inc. Documentation of the Threshold Limit Values and Biological Exposure
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.

      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
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