Health Advisory
                              Office  of Drinking Water
                        U.S.  Environmental Protection Agency
        The  Health Advisory  (HA) Program, sponsored by the Office of Drinking
   Water (ODW),  provides  information on  the  health  effects,  analytical  method-
   ology and treatment  technology  that would be useful in dealing with  the
   contamination of  drinking water.   Health  Advisories describe  nonregulatory
   concentrations of drinking water  contaminants at which adverse health effects
   would not be  anticipated  to  occur over specific  exposure  durations.  Health
   Advisories contain a margin  of  safety to protect sensitive members of the

        Health Advisories serve as informal technical guidance to assist Federal,
   State and local officials responsible for protecting public health when
   emergency spills  or  contamination situations occur.  They are not to be
   construed as  legally enforceable  Federal  standards.  The  HAs  are subject to
   change as new information becomes available.

        Health Advisories are developed  for One-day, Ten-day, Longer-term
   (approximately 7  years, or 10%  of an individual's lifetime) and Lifetime
   exposures based on data describing noncarcinogenic end points of toxicity.
   Health Advisories do not  quantitatively incorporate any potential carcinogenic
   risk from such exposure.   For those substances that are known or probable
   human carcinogens, according to the Agency classification scheme (Group A or
   B),  Lifetime  HAs  are not  recommended.  The chemical concentration values for
   Group A or B  carcinogens  are correlated with carcinogenic risk estimates by
   employing a cancer potency (unit  risk) value together with assumptions for
   lifetime  exposure and the consumption of drinking water.  The cancer unit
   risk is usually derived from the  linear multistage model with 95% upper
   confidence limits.   This  provides a low-dose estimate of cancer risk to
   humans that is considered unlikely to pose a carcinogenic risk in excess
   of the stated values.  Excess cancer risk estimates may also be calculated
   using the One-hit, Weibull,  Logit or Probit models.  There is no current
   understanding of  the biological mechanisms involved in cancer to suggest that
   any  one of these  models is able to predict risk more accurately than another.
   Because each  model is based  on  differing assumptions,  the estimates that are
   derived can differ by several orders of magnitude.

    1,1,1-Trichloroethane                                         March 31,  1987

         This Health Advisory is  based on information presented in the Office of
    Drinking Water's Health Effects Criteria Document (CD) for 1,1,1-Trichloro-
    ethane (U.S.  EPA,  1984a)«  The HA and CD formats are similar for  easy reference,
    Individuals desiring further  information on the toxicological data base or
    rationale for risk characterization should consult the CD.   The CD is available
    for review at each EPA Regional Office of Drinking Water counterpart (e.g.,
    Water Supply  Branch or Drinking Water Branch),  or for a fee from  the National
    Technical Information Service, U.S. Department of Commerce, 5285  Port Royal
    Rd.,  Springfield,  VA 22161, PB # 86-118130/AS.   The toll free  number is (800)
    336-4700; in the Washington,  D.C. area:  (703) 487-4650.

    CAS No.   71-55-6

    Chemical Structure
                                      H Cl
                                      I  I
                                      I  I
                                      H Cl


         0  1,1,1-TCA, methyl chloroform,  ethane,  1,1,1-trichloro and


         0  In the cleaning  and vapor degreasing of  fabricated metal parts

         0  In the synthesis of other organic chemicals

         0  As a spot remover and film cleaner

         0  As an additive in metal  cutting oils

    Properties (U.S. EPA 1984)

            Chemical Formula               C2H3CJ-3
            Molecular Weight               133.41
            Physical State                 colorless,  nonflammable liquid
            Boiling Point                  74°C
            Melting Point                  —
            Density                        4.6
            Vapor Pressure                 100 mm Hg (25°C)
            Water Solubility (25°C)         44 mg/L
            Log Octanol/Water Partition
            Taste Threshold
            Odor Threshold
            Conversion Factor              5.4 mg/m3

     1,1,1-Trichloroethane                                        March 31, 1987



          0  1,1,1-Trichloroethane is a synthetic chemical with no natural sources.

          0  Production of 1,1,1-trichloroethane was 600 million Ibs in 1982
             (U.S.  ITC,  1983).   About 70% of all 1,1,1-trichloroethane is used in
             metal  cleaning.

          0  The major source of 1,1,1-trichloroethane  released to the environment
             is from its use  as  a metal degreaser.  Since 1,1,1-trichloroethane is
             not consumed during degreasing operations, the majority of all
             1,1,1-trichloroethane production is released to the environment.
             Most of the releases occur to the atmosphere by evaporation.  However,
             1,1,1-trichloroethane which is not lost to evaporation becomes heavily
             contaminated with grease and oil and is disposed of by burial in
             landfills or dumping on the ground or into sewers.  Because metal
             working operations  are performed nationwide,  1,1,1-trichloroethane
             releases occur in  all industrialized areas.  Releases of 1,1,1-tri-
             chloroethane from other uses also may be  significant.

          0  1,1,1-Trichloroethane released to the air degrades slowly with an
             estimated half life of from 1  *•- ° -  "s.   1 ,1,1-Trichloroethane
             released to surface waters migrates to the atmosphere in a few days
             or weeks.  1,1,1-Trichloroethane which is  released to the land does
             not sorb onto soil  and migrates readily to ground water.  1,1,1-Tri-
             chloroethane slowly hydrolyzes in water with an estimated half-life
             of greater than  6  months.  1,1,1-Trichloroethane,  unlike other chlori-
             nated  compounds, does not bioaccumulate  in individual animals or  food

          0  Because of the large and dispersed releases,  1,1,1-trichloroethane
             occurs widely in the environment.  1,1,1-Trichloroethane is ubiquitous
             in the air with  levels in the low ppb range,  and is a common contami-
             nant in ground and  surface waters with higher levels found in ground
             water.  Surveys  of  drinking water supplies have found that 3% of  all
             public systems derived from well water contain 1,1,1-trichloroethane
             at levels of 0.5 ug/L or higher.  A small  number of systems (0.1%)
             have levels higher  than 100 ug/L.  Public  systems  derived from surface
             water  also have  been found to contain 1,1,1-trichloroethane bat at
             lower  levels. 1,1,1-Trichloroethane has been reported to occur in
             some foods in the ppb range.

          0  The major sources of exposure to 1,1,1-trichloroethane are from con-
             taminated water  and, to a lesser extent,  air.  Food is only a minor


          0  While inhalation of  1,1,1-TCA vapor through the lungs  is  the  common
             route of entry into  the body,  1,1,1-TCA also is absorbed  rapidly  and
             completely from the  gastrointestinal tract (Stewart et al.,  1969).

    1,1,1-Trichloroethane                                        March  31,  1987

         0  Stewart and Andrews  (1966) reported an observation of non-lethal  acute
           intoxication  after oral  ingestion  of  a liquid  ounce  of  1,1,1-TCA
           (0.6 g/kg bw).  The  concentration  of  1,1,1-TCA in the expired  air was
           measured serially and  found  to  be  equivalent  to  an inhalation  exposure
           of  500 ppm  (2,700 mg/m^) by  experimental subjects.

         0  Monster et al.  (1979)  and Humbert  and Fernandez  (1977)  reported
           1,1,1-TCA retention  in subjects exposed to 70  (378 mg/m^) or 140  ppm
           (756 mg/m3) respectively, to be 30 percent of  the inspired  air
           concentration at equilibrium after 4 hours of  exposure.


         0  1,1,1-TCA is  metabolized to  a very limited extent by animals and  humans
           (Monster et al., 1979).  The metabolites include trichloroethanol,
           TCA-glucuronide and  trichloroacetic acid which are excreted primarily
           in  urine; very  small amounts of trichloroethanol (1  percent),  however,
           are excreted  unchanged by the lungs.

         0  Hake and his  coworkers (1960),  using  C^-iabeled 1,1,1-TCA,  determined
           that less than  3% of 1,1,1-TCA  is  metabolized  by rats following a
           single intraperitoneal injection of 1,1,1-TCA.

         0  More recently,  estimates of  the extent of metabolism in the haman
           have been made  from  controlled  inhalation exposure with unlabeled
           1,1,1-TCA  (Seki et al.,  1975; Humbert and Fernandez, 1977;  Monster
           et  al., 1979).  From the experimentally determined retained dose  and
           the amounts of  1,1,1-TCA metabolites  excreted  into the  urine,  no  more
           than 6% of  the dose  is estimated to be metabolized.

         0  The metabolic fate of  inhaled  1,1,1-TCA in rats  and  mice is not
           altered upon  repeated  exposures (Schumann et al., 1982).
            Unchanged  1,1,1-TCA  is  primarily  excreted  via  lungs.
            Acute  pulmonary  congestion  and  edema  typically  are  found  in  fatalities
            resulting from inhalation of 1,1,1-TCA (Capalan et  al.,  1976;
            Bonventre et al.,  1977).   Fatty vacuolation  in  the  livers  of  the
            exposed subjects also has been  observed (Capalan et al.,  1976).
    Short-term Exposure
            The acute oral  LDsg for 1,1,1-TCA,  as  determined  in  several  species
            of animals,  ranges from 5.7  to 14.3 g/kg  (Torkelson  et al.,  1958).

1 ,1,1-Trichloroethane                                        March 31, 1987

     0  Vainio et al.  (1976) found that a single oral dose of approximately
        1.4 g/kg depressed some hepatic microsomal metabolic indices in rats
        (including cytochrome P-450 and epoxide hydratase).

     0  Bruckner et al. (1985) observed that there was relatively little
        evidence of toxicity in a short-term study by gavage in rats receiving
        1,1,1-TCA at 0.5 g/kg for 9 days.  Higher doses of 5 and 10 g/kg
        caused transient hyperexcitability and protracted narcosis, as well
        as fatalities.

Long-term Exposure

     0  Bruckner et al. (1985) administered 1,1,1-TCA to rats by gavage 5
        times weekly for up to 12 weeks at 0,  0.5, 2.5 or 5.0 g/kg.  Rats
        given 2.5 or 5.0 g/kg exhibited reduced body weight gain and CNS
        effects.  Approximately 35% of these rats died during the first
        50 days of the experiment, but only the 5.0 g/kg group showed an
        increase in serum enzyme levels indicating an alteration in index
        of toxicity.  Ingestion of 0.5 g/kg for 12 weeks did not result in
        alterations in indices of toxicity.

     0  McNutt et al.  (1975) exposed mice continuously by inhalation to
        1,1,1-TCA at 250 (1,365 mg/m3) or 1,000 ppm (5,400 mg/m^l  for 14 weeks.
        Serial sacrifice of exposed and control mice from 1 to 14 weeks demon-
        strated significant changes in the centrilobular hepatocytes as well
        as evidence of triglyceride accumulation in the livers of  the 1,000
        ppm exposure group.

     0  In the NCI (1977) study,  diminished body weight gain and decreased
        survival time were observed in both rats and mice.  Male and female
        rats were given 750 or 1,500 mg/kg 1,1,1-TCA in corn oil by gavage
        5 times weekly for 78 weeks.  Similarly, male and female mice received
        approximately  2,800 or 5,600 mg/kg for 78 weeks.

     0  In the NTP bioassay (1983), rats and mice were gavaged 5 times weekly
        with 1,1,1-TCA in corn oil at doses of 375 or 750 mg/kg body weight
        (rats) and 1,500 or 3,000 mg/kg body weight (mice), respectively,  for
        103 weeks.

Reproductive Effects

     0  There appeared to be no dose-dependent effects on fertility,  gestation,
        viability indices in mice exposed to 1,1,1-TCA at dose levels of 100,
        300 or 1,000 mg/kg for 35 days (Lane et al.,  1982).

Developmental Effects

     0  There appeared to be no dose-dependent effects on viability indices
        in mice exposed to 1,1,1-TCA at dose levels of 100, 300 or 1,000 mg/kg
        for 35 days (Lane et al., 1982).

   1,1,1-Trichloroethane                                        March 31,  1987



        0  Simmon et al. (1977)  reported  that 1,1,1-TCA was  mutagenic in various
           strains of S_. typhimurium,  with metabolic activation.

        0  Loprieno et al.  (1979)  stated  that 1,1,1-TCA was  not mutagenic in
           Saccharomyces cerevisiae or Schizosaccharomyes bombe.


        0  NTP (1983) has reported a significant (P <0.05) dose response trend
           and increased incidences of hepatocellular carcinomas in the low- and
           high-dose male and in the high-dose female mice exposed to 1,1,1-TCA
           for 103 weeks.  However, it should be noted that  these findings are
           based on the draft report and  may change pending  the outcome of the
           ongoing NTP audit of  the study.


        Health Advisories (HAs)  are generally determined for One-day, Ten-day,
   Longer-term (approximately 7  years) and Lifetime exposures if adequate data
   are available that identify a sensitive noncarcinogenic end point of toxicity.
   The HAs for noncarcinogenic toxicants  are derived using the following formula:

                 HA - (NOAEL or  LOAEL) x  (BW) = 	   /L <	 ug/L)
                        (UF) x (    L/day)
           NOAEL or LOAEL = No- or Lowest-Observed-Adverse-Effect-Level
                            in mg/kg bw/day.

                       BW = assumed body weight of a child (10 kg)  or
                            an adult (70 kg).

                       UF = uncertainty factor (10,  100 or 1,000),  in
                            accordance with NAS/ODW guidelines.

                	 L/day = assumed daily water consumption of a child
                            (1 L/day) or an adult (2 L/day).
   One-day Health Advisory

        The study by Vainio et al. (1976) in rats is used in calculating a
   One-day HA.  In this study, 1,1,1-TCA at a single oral dose of approximately
   1.4 g/kg depressed hepatic microsomal metabolic indices (cytochrome P-450,
   epoxide hydratase) in rats.  Using this dose as a NOAEL (although its signifi-
   cance is not well established), a One-day HA for the 10 kg child is calculated
   as follows:

1,1,1-Trichloroethane                                        March 31, 1987

       One-day HA = (1*4 gAg/day) (10 kg) = 140 mg/L  or  140000 ug/L
                       (100) (1 L/day)


        1.4 g/kg/day = NOAEL based on absence of changes in hepatic microsomal
                       metabolic indices in rats.

               10 kg = assumed body weight of a child.

                 100 = uncertainty factor, chosen in accordance with NAS/ODW
                       guidelines for use with a NOAEL from an animal study.

             1 L/day = assumed daily water consumption of a child.

Ten-day Health Advisory

     Insufficient toxicological data are available to derive a Ten-day HA for
1,1,1-TCA.  However, in order to provide a health guidance level for 1,1,1-TCA
for this duration of exposure,  it is recommended that the Longer-term HA  for
the 10 kg child be used (35 mg/L or 35,000 ug/L).

Longer-term Health Advisory

     A subchronic oral toxicity study in rats by Bruckner et al.  (1985) is
used for the Longer-term HA.  In this study, rats (200 to 250 g)  were given
1,1,1-TCA 5 times weekly by gavage for 12 weeks at 0, 0.5,  2.5 or 5 g/kg.
Rats given 2.5 or 5.0 g/kg exhibited reduced body weight gain and CNS effects
including transient hyperexcitability and protracted narcosis.  Approximately
35% of these rats died during the first 50 days of the experiment, but only
the 5.0 g/kg group showed an increase in serum enzyme levels.   Ingestion  of
0.5 g/kg for 12 weeks did not result in alteration in indices of  toxicity
(serum enzyme levels, organ weights or histopathological changes  in the  liver
and kidney).

     Using 0.5 g/kg/day as a NOAEL,  a Longer-term HA for the 10 kg child  is
calculated as follows:

    Longer-term HA = (500 mg/kg/day) (10 kg) (5/7) = 35   /L (35  000 ug/L)
                            (100) (1 L/day)
        0.5 g/kg/day = NOAEL in a 12-week study based on absence of various
                       parameters of toxicity in rats.

               10 kg = assumed body weight of a child.

                 5/7 = conversion of 5 day/week exposure to daily exposure.

                 100 = uncertainty factor, chosen in accordance with NAS/ODW
                       guidelines for use with a NOAEL from an animal study.

        1  L/day      = assumed daily water consumption of a child.

1,1,1-Trichloroethane                                        March 31, 1987


      Longer-term HA for 70 kg adult:

   Longer-term HA = <500 mg/kg/day) (70 kg) (5/7) = , 25   /L (125,000 ug/L)
                           (100) (2 L/day)


        0.5 g/kg/day = NOAEL in a 12-week study based  on absence of various
                       parameters of toxicity in rats.

               70 kg = assumed body weight of an adult.

                 5/7 = conversion of 5 day/week exposure to daily exposure.

                 100 = uncertainty factor, chosen in accordance with NAS/ODW
                       guidelines for use with a NOAEL from an animal study.

             2 L/day = assumed daily water consumption of an adult.

Lifetime Health Advisory

     The Lifetime HA represents that portion of an individual's total exposure
that is attributed to drinking water and is considered protective of noncar-
cinogenic adverse health effects over a lifetime exposure.  The Lifetime HA
is derived in a three step process.  Step 1 determines the Reference Dose
(RfD), formerly called the Acceptable Daily Intake (ADI).  The RfD is an esti-
mate of a daily exposure to the human population that is likely to be without
appreciable risk of deleterious effects over a lifetime, and is derived from
the NOAEL  (or LOAEL), identified from a chronic  (or subchronic) study, divided
by an uncertainty factor(s).  From the RfD, a Drinking Water Equivalent Level
(DWEL) can be determined (Step 2).  A DWEL is a medium-specific (i.e., drinking
water) lifetime exposure level, assuming 100% exposure from that medium, at
which adverse, noncarcinogenic health effects would not be expected to occur.
The DWEL is derived from the multiplication of the RfD by the assumed body
weight of an adult and divided by the assumed daily water consumption of an
adult.  The Lifetime HA is determined in Step 3 by factoring in other sources
of exposure, the relative source contribution  (RSC).  The RSC from drinking
water is based on actual exposure data or, if data are not available, a
value of 20% is assumed for synthetic organic chemicals and a value of 10%
is assumed for inorganic chemicals.  If the contaminant is classifed as a
Group A or B carcinogen, according to the Agency's classification scheme of
carcinogenic potential (U.S. EPA, 1986), then caution should be exercised in
assessing the risks associated with lifetime exposure to this chemical.

      In the absence of suitable ingestion toxicological data to derive a
Lifetime HA, an inhalation study in mice is considered for a Lifetime HA.

      McNutt et al. (1975) exposed male mice continuously via inhalation to
1,1,1-TCA at 250 (1,365 mg/m3) or 1,000 ppm (5,460 mg/m3) for 14 weeks.  Con-
trol mice were exposed to room air.  Serial sacrifice of exposed and control
mice  from  1 to  14 weeks demonstrated significant changes in the centrilobular
hepatocytes of animals in the 1,000 ppm (5,460 mg/m3)  group.  These changes
consisted  of vesiculation of the rough endoplasmic reticulum with loss of

1,1,1-Trichloroethane                                        March 31, 1987

attached polyribosomes,  increased smooth endoplasmic reticulum, microbodies
and triglyceride droplets.  A NOAEL could not be identified but a LOAEL of
250 ppm (1,365 mg/m3)  from this study can be used with appropriate uncer-
tainty factors.  A Lifetime HA based upon these data is derived as follows:

Step 1: Determination of the Total Absorbed Dose (TAD)

          TAD - (1'365 mg/m3) (1 m3/hr) (6 hrs) (0.3) , 35 mg/kg/day
                                (70 kg)
        1,365 mg/n\3 (250 ppm) = LOAEL based on histological changes in liver
                                of animals.

                      1  m3/hr = ventilation volume for a 70 kg adult.

                        6 hrs = Exposure assumed to be saturable; thus, 6 hrs
                                is considered equivalent to exposure for a
                                24-hour period.

                         0.30 = ratio of administered dose absorbed.

                        70 kg = assumed body weight of an adult.
Step 2:  Determination of the Reference Dose (RfD)

                    RfD = (35 mg/kg/day) __ 0.035 mg/kg/day
        35 mg/kg/day = TAD and LOAEL based on histological change in liver of

                1,000 = uncertainty factor, chosen in accordance with NAS/ODW
                       guidelines for use with a LOAEL from an animal study.
Step 3: Determination of the Drinking Water Equivalent Level (DWEL)

           DWEL = (0.035 mg/kg/day) (70 kg) = 1>0 mg/L (1/000 ug/L)
                          (2 L/day)


        0.035 mg/kg/day = RfD.

                  70 kg = assumed body weight of an adult.

                2 L/day = assumed daily water consumption of an adult. '

March 31, 1987
      Step 4:  Determination of the Lifetime Health Advisory

                          Lifetime HA = 1  mg/L x 0.20 = 200 ug/L


              1  mg/L = DWEL.

                0.20 = assumed relative source contribution from water.

      Evaluation of Carcinogenic Potential

           0   IARC (1982)  has 'classified 1,1,1-trichloroethane in Group  3:
              Inadequate data to evaluate.

           0   Applying the criteria described in EPA's  guidelines for assessment
              of carcinogenic risk (U.S. EPA, 1986),  1,1,1-trichloroethane is
              classified in Group D:   Not  classified  (inadequate aniaml  evidence
              of carcinogenicity).


           0   NAS (1980) has calculated a  chronic SNARL of  3.8 mg/L for  an adult
              consuming 2 liters of water and contribution  from water being 20%.

           0   An ambient water quality criterion of 18.7 mg/L was calculated for an
              adult consuming 2 liters of  water daily (U.S. EPA, 1980).


           0   Analysis of 1,1,1-trichloroethane is by a purge-and-trap gas chromato-
              graphic procedure used for the determination  of volatile organohalides
              in drinking water (U.S. EPA,  1985a).  This method calls for the
              bubbling of an inert gas through the sample and trapping 1,1,1-tri-
              chloroethane on an adsorbant material.   The adsorbant material is
              heated to drive off the 1,1,1-trichloroethane onto a gas chromato-
              graphic column.  This method is applicable to the measurement of
              1,1,1-trichloroethane over a. concentration range of 0.03 to 1500 ug/L.
              Confirmatory analysis for 1,1,1-trichloroethane is by mass spectrometry
              (U.S.  EPA 1985b).   The detection limit  for confirmation by mass
              spectrometry is 0.3 ug/L.
           0  Treatment technologies which will remove 1,1,1-trichloroethane from
              water include granular activated carbon (GAC)  adsorption,  aeration
              and boiling.

           0  Dobbs and Cohen (1980) developed adsorption isotherms  for  several
              organic chemicals  including 1,1,1-TCA.   It was  reported that

1,1,1-Trichloroethane                                        March 31,  1987


        Filtrasorb® 300 carbon exhibited  adsorption capacities  of 1.1  mg and
        0.5  mg 1,1,1-TCA/gm carbon at equilibrium concentrations  of  100 and
        10 ug/L,  respectively.  U.S.  EPA  installed pilot-scale  adsorption
        columns in Connecticut and New Jersey.   In Connecticut, contaminated
        well water with 1,1,1-TCA concentrations  ranging from 10  to  50  ug/L
        was  passed through a Filtrasorb®  400 GAC  column.  Breakthrough occurred
        after 11,360 bed volumes (BV) or  approximately  12 weeks of continuous
        operation.  In New Jersey, contaminated groundwater with an average
        of 300 ug/L of 1,1,1-TCA was  passed over  a Witcarb® 950 GAC  column.
        Breakthrough occurred after 16,800 bed volumes  (BV) or approximately
        30 weeks  of continuous operation.   A similar study assessed  the
        effects of differing contact time and carbon adsorption of 1,1,1-TCA
        (Love and Eilers,  1982).  It  was  reported that  1,1,1-TCE  concentrations
        of 100 ug/L were reduced to 0.5 ug/L when loadings of 0.26 mg,  0.51 mg
        and  0.74  mg 1,1,1-TCA/gm of Filtrasorb® 400 carbon for  contact  times
        of 7.5, 15 and 22.5 minutes,  respectively, were used.

     0  1,1,1-TCA is  amenable  to aeration on the  basis  of  its Henry's Law
        Constant of 400 atm (Kavanaugh and Trusell, 1980).  In a pilot-scale
        diffused  aeration column,  removal  efficiency of 90% of  1,1,1-TCA was
        achieved  from an initial concentration  of 237 ug/L at an  air-to-water
        ratio of  4:1  (Love and Eilers, 1982).  In a pilot-scale packed  tower
        aeration  study,  removal efficiencies of 74-97%  were achieved for
        42-110 ug/L 1,1,1-TCA for a broad  spectrum of operating parameters
        (Love and Eilers,  1982).

     0  Boiling also  is effective for removing  1,1,1-TCA from water  on  a short-
        term, emergency basis.  Studies have shown that 5 minutes of vigorous
        boiling will  remove 96% of 1,1,1-TCA originally present (Love  and
        Eilers, 1982).

     0  Air  stripping is an effective, simple and relatively  inexpensive
        process for removing 1,1,1-TCA and other  volatile organics from
        water.  However,  use  of this  process then transfers  the contaminant
        directly  to the air stream.  When considering use of air  stripping  as
        a treatment process,  it is suggested that careful  consideration be
        given to  the  overall  environmental occurrence,  fate,  route of  exposure
        and  various other  hazards  associated with the chemical.

    1,1,1-Trichloroethane                                        March 31, 1987



    Bonventre,  J.,  0.  Brennan,  D.  Jason,  A.  Henderson and M.L.  Bastos.  1977.
         Two deaths following accidental inhalation of dichloromethane and 1,1,1-
         trichloroethane.  J.  Analyt.  Toxicol.   4:15S-160.

    Bruckner, J.V., S. Muralidhara,  W.F. Mackenzie, G.M. Kyle and R. Luthra.
         1985.   Acute  and subacute oral  toxicity studies of 1,1,1-trichloroethane
         (TRI)  in rats.  The Toxicologist.   5(1):100.

    Caplan,  Y.J., R.c. Backer  and  J.Q. Whitaker.  1976.   1,1,1-Trichloroethane:
         report of a fatal Intoxication.  Clin. Toxicol.  9:69-74.

    Dobbs,  R.A.,  and J.M. Cohen.   1980.   Carbon adsorption isotherms for toxic
         organics,  EPA 600/8-80-023,  Office  of  Research  and Development,  MERL,
         Wastewater Treatment Division,  Cincinnati, Ohio.

    ESE.   1984.  Environmental Science and  Engineering.   Technologies and costs for
         the removal of volatile organic chemicals from potable water supplies.  ESE
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