March  31,  1987

                                  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.

    1,2-Dichloroethane                                      March 31,  1987

         This Health Advisory is based on information presented in the Health
    Assessment Document for 1,2-Dichloroethane (Ethylene Dichloride) (U.S. EPA,
    1985a).  Individuals desiring further information on the toxicological data
    should use this document.  Information on the Quantification of Toxicological
    Effects (QTE) section is contained in the QTE Document (PB#86-118080).  Both
    documents are 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 Road, Springfield, VA 22161.  The toll-free number
    is (800) 336-4700; in the Washington, D.C. area: (703) 487-4650.

    CAS No.  107-06-2

    Structural Formula
                                        H    H
                                        I     I
                                   Cl - C -  C - Cl
                                        I     I
                                        H    H

                                  1 , 2-Dichloroethane


         0  Ethylene dichloride, EDO, 1,2-DCE

    Uses (U.S. EPA, 1985a)

         0  The major use for EDC is in the production of vinyl chloride.  In
            addition, it is used as a starting material for the production of
            other solvents, as an additive (lead scavenger) in gasolines and is
            widely exported.  Some of its minor uses include its use as a solvent
            in metal degreasing and textile and PVC cleaning, in paints, coatings
            and adhesives, as a grain fumigant, a varnish and finish remover,
            in soaps and scouring compound, as a wetting and penetrating agent,
            in ore flotation and as a chemical intermediate.

    Properties  (EPA, 1985a; Amoore and Hautala, 1983)
            Chemical Formula
            Molecular Weight                  98.96
            Physical State                    Clear, colorless, volatile, oily liquid
            Boiling Point                     83.7°C
            Melting Point                     -35.3°C
            Density (20°C)                    1.2529 g/mL
            Vapor Pressure                    64 torr (20°C)
            Water Solubility (208C)           8820 mg/L
            Log Octanol/Watar Partition       1.48
            Organoleptic Threshold (water)    29 mg/L
            Odor Threshold (air)              3 ppm
            Conversion Factor                 1 ppm • 4.05 mg/rn^

     1,2-Dichloroethane                                      March 31, 1987



          0  Dichloroethane is a synthetic chemical with no natural sources.

          0  Production of dichloroethane was approximately 12 billion pounds in
             1983 (U.S. ITC,  1984).  However, the vast bulk of dichloroethane is
             used as a feed stock for the production of other chlorinated compounds
             and it is not readily released to the environment.  Releases of
             dichloroethane largely result from the approximately 3 million pounds
             used as solvents and metal cleaners.

          •  Releases of dichloroethane are largely to air, with smaller amounts
             released to surface and ground waters.  Because metal working opera-
             tions are performed nationwide, dichloroethane releases occur in all
             industrialized areas.

          *  Dichloroethane released to the air slowly degrades over a few months.
             Photooxidation is thought to be the predominant environmental process
             determining the fate of 1,2-dichloroethane (U.S. EPA, 1979).  Dichloro-
             ethane released to surface waters migrates to the atmosphere in a few
             days or weeks where it also degrades.  Dichloroethane released to the
             land does not sorb onto soil but migrates readily to ground water
             where it is expected to remain for months to years.

          0  Due to dichloroethane1s limited releases, it is a relatively rare
             environmental contaminant.  Dichloroethane has been detected in both
             ground and surface waters but, unlike other volatile organic compounds,
             higher levels were reported in surface waters than in ground waters.
             The Agency estimates that 0.3% of all ground water supplies contain
             concentrations of dichloroethane ranging from 0.5 to 5 ug/I«—-Surface
             waters contain higher levels, with 3% of all wells estimated to have
             from 0.5 to 20 ug/L.  Dichloroethane commonly occurs in air in urban
             and suburban areas at concentrations of less than 0.2 ppb.  No infor-
             mation on the levels of dichloroethane in food have been reported.

          0  For the majority of the U.S. population, the greatest source of
             dichloroethane exposure is from air.  Drinking water is the greatest
             source only for populations with drinking water levels greater than
             6 ug/L.



          0  1,2-Dichloroethane is absorbed by humans and laboratory animals
             through the lungs (Spencer et al., 1951; Urusova, 1953) gastro-
             intestinal tract (Alumot et al., 1976) and skin (Urusova, 1953).

          0  The proportions of a dose of 1,2-dichloroethane absorbed through the
             skin and gastrointestinal tract are unknown.  The nature of its other
             chemical and physical properties would suggest that this substance
             would be absorbed completely when ingested.

1,2-Dichloroethane                                      March 31, 1987



     0  Forty-eight hours after the administration of a single oral dose of
        150 mg/kg of 1,2-dichloroethane to rats, the liver and kidneys were
        reported to have the highest concentration of the chemical.  Success-
        ively lower concentrations occurred in the forestomach, stomach and
        spleen (Reitz et al.r 1980).

     0  1,2-Dichloroethane readily passes the blood/brain barrier.  Distribu-
        tion is also known to occur into milk (Urosova, 1953).


     0  Following intraperitoneal administration to mice, 1,2-dichloroethane
        is metabolized to 2-chloroethanol, converted to alcohol and aldehyde
        dehydrogenases, to monochloroacetic acid, and further dehalogenated by
        enzyme interaction of monochloroacetate with glutathione or cysteine
        to yield 5-carboxymethylcysteine and thiodiacetic acid (Yllner,

     0  Urinary metabolites of 1,2-dichloroethane intraperitoneally administered
        to mice include chloroacetic acid, 2-chloroethanol, 5-carboxymethyl
        cysteine, conjugated 5-carboxymethyl cysteine, thiodiacetic acid and
        5,5-ethylene-bis-cysteine (Yllner, 1971a,b).
     0  Following oral administration of 1,2-dichloroethane (750 mg/kg) or
        2-chloroethanol (80 mg/kg) to rats, the blood level of 2-chloroethanol
        at four hours was 67.8 or 15.8 ug/mL, respectively (Kokarovtseva and
        Kiseleva, 1978).  These levels declined in accordance with first-order
        kinetics with a half-life of about nine hours.  The relatively low
        blood concentrations found were postulated to be due to initial
        sequestration of 1,2-dichloroethane in adipose and other tissues
        with gradual diffusion redistribution as liver metabolism of 1,2-
        dichloroethane to chloroethanol and chloroethanol to chloroacetic
        acid proceeded..
        Mice intraperitoneally injected with a dose of 0.05 to 0.17 gAg of
        1,2-dichloroethane excreted 11 to 46% of the dose, unchanged, via the
        lungs; 5 to 13% of the dose was metabolized to carbon dioxide and
        water; 50 to 73% of the dose was excreted as urinary metabolites
        (Yllner, 1971a).

        Within 48 hours after dosing, 96% of the radioactivity of a single
        oral dose of 150 mg/kg was eliminated from the body by rats (Reitz
        et al., 1980).

    1,2-Dichloroethane                                      March 31,  1987




         0  Clinical symptoms of acute 1,2-dichloroethane poisoning by ingestion
            usually appear within two hours after exposure and typically include
            headache, dizziness, general weakness, nausea, vomiting of blood and
            bile, dilated pupils, heart pains and constriction, pain in the
            epigastric region, diarrhea and unconsciousness.  Pulmonary edema
            and increasing cyanosis also may occur.  These symptoms may disappear
            if exposure is sufficiently brief (Wirtschafter and Schwartz, 193$;
            McNally and Fostvedt, 1941).

         0  A 14-year-old male who drank 15 ml (340 mg/kg) of 1,2-dichloroethane
            died six days later despite supportive treatment (Yodaiken and Babcock,
            1973).  During treatment, serum enzyme and calcium levels  increased,
            blood glucose decreased and blood clotting time increased.  Autopsy
            findings revealed extensive liver necrosis and epithelial  cell damage
            in the entire cortico-tubular structure of the kidneys accompanied by
            degeneration in the proximal tubules.

         0  While not all instances of 1,2-dichloroethane ingestion are fatal,
            death has resulted in the majority of reported cases.  Death is most
            often attributed to circulatory and respiratory failure (Budanova,
            1965; Yodaiken and Babcock, 1973; Luzhnikov et a.l., 1974,  1976; and
            Zhizhonkov, 1976).

         0  A number of neurological effects following ingestion of 20 to 200 ml
            of 1,2-dichloroethane have been reported (Akimov et al.,  1976, 1978).
            The most common of these involved disturbances in consciousness,
            mental disorders and cerebellar and extrapyramidal disorders.


    Short-term Exposure

         •  Information on the acute oral toxicity of 1,2-dichloroethane indicates
            the following:  rat LD5n - 680 mgAg; rabbit LDso - 860 mg/kg; (NIOSH,

         0  The principal acute effect of 1,2-dichloroethane in mammals is central
            nervous system depression with unconsciousness and coma resulting
            from exposure to high concentrations (Spencer et al., 1951; Irish,
            1963).  Visible signs of 1,2-dichloroethane  poisoning include rest-
            lessness, intolerance to handling, extreme weakness, intoxication,
            dizziness, muscle incoordination, irregular  respiration and loss of
            consciousness.  Deaths occurring within a few hours after  recovery
            from narcosis are usually the result of shock or cardiovascular
            collapse; deaths delayed by several days most often result from
            renal damage.

 1,2-Dichloroethane                                      March 31,  1987


 Reproductive Effects

      0  No reproductive  effects, as measured by  fertility, gestation,  viability
         or lactation  indices,  pup  survival and weight gain,  were indicated in
         a multigeneration  reproduction study using  male and  female ICR Swiss
         mice receiving 0,  5,  15 or 50 mg/kg/day  in  drinking  water.  No effect
         on the  adult  generations was  evident after  25 weeks  of  dosing  as
         measured  by body weight, fluid intake  or gross paiiioiogy  (Lane et al.,

 Developmental Effects

      0  In a study in which male and  female mice were exposed to  1,2-dichloro-
         ethane  in drinking water at doses  of 0,  5,  15 or  50  mg/kg/day,  no
         statistically significant  dose-related developmental effects were
         observed, as  indicated by  incidence of fetal  visceral or skeletal
         anomalies (Lane  et al., 1982).


      0  1,2-Dichloroethane has been shown  to be  weakly mutagenic in Salmonella
         typhimurium strains TA 1530,  1535  and  1538  and in DNA polymerase-defi-
         cient Escherichia  coli (Brem  et al., 1974).

      0  1,2-Dichloroethane has been found  to be  highly mutagenic in Salmonella
         typhimurium strains TA 1530 and 1535 with S-9 activation  (Rannug  and
        • Beije,  1979).

      0  1,2-Dichloroethane has been shown  to induce sex-linked  recessive
         lethals in Drosophila melanogaster (Rapport,  1960; Shakarnis,  1969).

      0  1,2-Dichloroethane was not mutagenic in  Salmonella microsome assay
         system  (McCann et  al., 1975).


      0  In an NCI (1978) bioassay, 1,2-dichloroethane was administered by
         gavage  at levels of 47 or  95  mg/kg body  weight to Osborne-Mendel  rats
         five times per week for 78 weeks.   Statistically  significant increases
         in the  incidence of squamous  cell  carcinomas  of the  forestomach and
         hemangiosarcomas of the circulatory system  were observed in male
         rats(p  <0.04).   Female rats had a  statistically significant increased
         incidence of  adenocarcinoma of the mammary  glands (p <0.002).

      •  In the  same NCI  (1978) bioassay, B6C3Fi  mice  received 1,2-dichloroethane
         by gavage five times  per week for  78 weeks; males were  dosed at levels
         of 97 or  195  mg/Tug body weight and females  at 149 or 299 mg/kg body
	weight.  Statistically significant increases  in the  incidence  of
         mammary adenocarcinoma (p  <0.04) and endometrial  stromal polyps or
         sarcomas  (p <0.016)  were seen in female  mice. Ihe incidence of
         alveolar/bronchiolar  adenomas was  increased in both  sexes  (p <0.028).

       March 31, 1987

        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)
                        (UF) x (    L/day)
mg/L (	ug/L)
           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 and Ten-day Health Advisories

        Appropriate data for the derivation of One-day and Ten-day HAs were not
   located.  It is recommended that the Longer-term HA of 0.74 mg/L for the
   10 kg child be used as a conservative estimate for One-day and Ten-day

   Longer-term Health Advisory

        A combination of three inhalational studies in which various animal
   species were exposed to 1,2-dichloroethane for up to eight months are consid-
   ered appropriate to use in calculating a Longer-term HA.  In these studies,
   exposures of rats and guinea pigs to air containing 100 ppm 1,2-dichloroethane
   for 6 to 7 hours/day, 5 days/week resulted in no mortality and no adverse
   effects as determined by general appearance, behavior, growth, organ function
   or blood chemistry.  However, similar exposures of rats, guinea pigs, rabbits,
   and monkeys to air containing 400 or 500 ppm 1,2-dichloroethane resulted in
   high mortality and varying pathological findings including pulmonary conges-
   tion, diffused myocarditis, slight to moderate fatty degeneration of the
   liver, kidney, adrenal, and heart, and increased plasma prothrombin time
   (Heppel et al., 1946; Spencer et al., 1951; Hofmann et al., 1971).

        The Longer-term HA is calculated as follows:

   Step 1:  Determination of Total Absorbed Dose (TAD)

    TAD - (405 mq/m3) (1 m3/hr) (6 hr)  (0.3) (S/7) „ 521 mg/day , 7 4 ma/kq/dav
                             70 kg                       70 kg     *   9      y

1,2-Dichloroethane                                      March 31,  1987



        405 mg/m3 « NOAEL of 100 ppm (1  ppm * 4.05 mg/m3) for adverse effects
                    in rats and guinea pigs.

          1 m3/hr * respiratory rate of adult human (pulmonary rate/body
                    weight ratio assumed to be the same for humans and
                    test animals).

             6 hr - exposure duration per day.

              0.3 * fraction of test substance assumed to be absorbed.

              5/7 « conversion of 5-day dosing regimen to full 7-day week.

            70 kg » assumed body weight of an adult.

Step 2:  Determination of the Longer-term HA

     For a 10-kg child:

       Longer-term HA -  (7.4 mg/kg/day) (10 kg) = 0>74 mg/L (740 ug/L)
                            (100) (1 L/day)

     For a 70-kg adult:

       Longer-term HA -  (7.4 mgAg/dav) (70 kg) = 2.6 mg/L (2600 ug/L)
                             (100) (2 L/day)

        7.4 mg/kg/day - total absorbed dose (TAD).

                10 kg - assumed body weight of a child.

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

                70 kg - assumed body weight of an adult.

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

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

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

1,2-Dichloroethane                                      March 31, 1987

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 DMEL 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 classified 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.

     No appropriate data are available for determining a reference dose and
drinking water equivalent level (DWEL) for 1,2-dichloroethane.  A Lifetime
Health Advisory is not estimated for this chemical.

Evaluation of Carcinogenic Potential

     0  1,2-Dichloroethane was shown to be carcinogenic in rats and mice
        following gavage exposure in the NCI bioassay (NCI, 1978).

     0  IARC has not classified 1,2-dichloroethane (IARC, 1982).

     0  Applying the criteria described in EPA's guidelines for assessment
        of carcinogenic risk (U.S. EPA, 1986), 1,2-dichloroethane may be
        classified in Group B2: Probable Human Carcinogen.  This category is
        for agents for which there is inadequate evidence from human studies
        and sufficient evidence from animal studies.

     •  The most recent calculations by EPA's Carcinogen Assessment Group
        (CAG) indicates the cancer risk estimate for 1,2-dichloroethane
        corresponding to a 10-5 risk level is 3.8 ug/L,  using the multistage
        model (95% confidence limit) (U.S. EPA,  1985d).

     0  The linear multistage model is only one method of estimating carcino-
        genic risk.  Using the 95% upper-bound estimate of risk at 1 mg/kg/day
        for hemangiosarcomas in male rats, the following comparisons can be
        made:  Multistage, 6.0 x 10-2; Probit, 2.81 x 10-1; Weibull, 2.7 x 10~1
        (U.S. EPA, 1985a).  Each model is based on differing assumptions.  No
        current understanding of the biological mechanisms of carcinogenesis
        is able to predict which of these models is more accurate than another.

     0  While recognized as statistically alternative approaches, the range of
        risks described by using any of these modelling approaches has little
        biological significance unless data can be used to support the selection
        of one model over another.  In the interest of consistency of approach
        and in providing an upper bound on the potential cancer risk, the Agency
        has recommended use of the linearized multistage approach.

      1,2-Dichloroethane                                      March 31, 1987



           0  U.S. EPA (19S5d) has promulgated a final Recommended Maximum Contami-
              nant Level (RMCL) of zero for 1,2-dichloroethane in drinking water
              based upon its carcinogenic potential and has proposed a Maximum
              Contaminant Level (MCL) of 0.005 mg/L.

           0  Due to the lack of appropriate data, the National Academy of Sciences
              did not calculate a chronic Suggested-No-Adverse-Response-Level
              (SNARL) for 1,2-dichloroethane (NAS, 1980).

           0  ACGIH (1984)  has recommended a threshold limit value (TLV) of 10 ppm
              ( ^ 40 mg/m3) and a short-term exposure level (STEL) of 15 ppm (•«•• 60
              mg/m3) due to its hepatotoxic effects.


           0  Analysis of 1,2-dichloroethane is by a purge-and-trap gas chromato-
              graphic procedure used for the determination of volatile organohalides
              in drinking water (U.S. EPA, 1985b).  This method calls for the
              bubbling of an inert gas through the sample and trapping 1,2-dichloro-
              ethane on the adsorbant material.  The adsorbant material is heated
              to drive off the 1,2-dichloroethane onto a gas chromatographic column.
              The gas chromatograph is temperature programmed to separate the
              method analytes which are then detected by a halogen specific detector.
              This method is applicable to the measurement of 1,2-dichloroethane
              over a concentration range of 0.2 to 1,500 ug/L.  Confirmatory analysis
              for 1,2-dichloroethane is by mass spectrometry (U.S. EPA, 1985c).  The
              detection limit for confirmation by mass spectrometry is 0.3 ug/L.

           0  Treatment technologies which will remove 1,2-dichloroethane from
              water include granular activated carbon (GAC) adsorption, aeration
              and boiling.

           •  Dobbs and Cohen (1980) developed adsorption isotherms for several
              organic chemicals including 1,2-dichloroethane.  It was reported
              that Fibrasorb® 300 carbon exhibited adsorptive capacities of 3.5 mg
              and 0.5 mg 1,2-dichloroethane/gm carbon at equilibrium concentrations
              of 1,000 and 100 mg/L, respectively.  Also,  Love (1983) reported
              that Witcarb® 950 carbon exhibited adsorptive capacities of 1.9 mg
              and 0.6 mg 1,2-dichloroethane/gm carbon at equilibrium concentrations
              of 100 and 10 mg/L,  respectively.  USEPA-DWRD installed pilot-scale
              adsorption columns in New Jersey to treat contaminated groundwater
              (Love and Eilers, 1982).  A Witcarfc® 950 carbon column removed 1,2-
              dichloroethane from a concentration as high as 8 mg/L to 0.1 mg/L.
              Breakthrough occurred at 1,700 bed volumes (BV) with an empty bed
              contact time (EBCT)  of 18 minutes.  Similar studies in Louisiana
              showed removal of 1,2-dichloroethane from a concentration of 8 mg/L

1,2-Dichloroethane                                      March 31, 1987

        to less than 0.1 mg/L after 39 days of continuous operation by a
        full-scale GAC column containing Nuchar* WP-G activated carbon (Love,

        1,2-Dichloroethane is amenable to aeration on the basis of its Henry's
        Law Constant of 61 atm (Kavanaugh and Trussell, 1980).  In a pilot-
        scale diffused air aeration column, removal efficiency of 42% of
        1,2-dichloroethane was achieved at an air-to-water ratio of 4:1
        (Love and Eilers, 1982).  In a pilot-scale packed tower aeration
        study removal efficiencies of 85 to 98.5% for 1,2-dichloroethane were
        achieved on air-to-water ratios of 5-45,  respectively (ESE, 1985).

        Boiling also is. effective in eliminating 1,2-dichloroethane from water
        on a short-term, emergency basis.  Studies have shown that 5 to 10
        minutes of vigorous boiling will remove 88 to 98% of 1,2-dichloroethane
        originally present (Love, 1983).

        Air stripping is an effective, simple and relatively inexpensive
        process for removing 1,2-dichloroethane 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.

    1,2-Dichloroethane                                      March 31,  1987



    ACGIH.  1984.  American Conference of Governmental Industrial Hygienists.
         Documentation of threshold limit values.  4th ed.  1980-1984 supplement.
         pp. 181-182.

    Akimov, G.A. et al., 1976.  Changes in the nervous system in acute dichloro-
         ethane poisoning.  Voenno-meditisinskiy Zhurnal.  5:35-37.

    Akimov, G.A. et al., 1978.  Neurological disorders in acute dichloroethane
         poisoning.  Zh. Nevropatol. Psikhiatr.  78(5):687-692.

    Araoore, J.E., and E. Kautala.  1983.  Odor as an aid to chemical safety:
         Odor thresholds compared with threshold limit values and volatilities
         for 214 industrial chemicals in air and water dilution.  J. T. Appl. Tox.

    Brem, H., A. Stein and H. Rosenkrantz.  1974.  The mutagenicity and DNA-
         modifying effect of haloalkanes.  Cancer Res.  34:2576-2579.

    Budanova, L.F.  1965.  On the clinical picture specific to acute peroral
         dichloroethane poisoning.  Ter Arkh.  37(3):11 0-112.

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

    ESE.  1985.  Environmental Science and Engineering.  Draft technologies and
         costs for the removal of volatile organic chemicals from potable water
         supplies.  No. 84-912-0300.  Prepared for U.S. EPA, Science and
         Technology Branch, CSD, ODW, Washington, D.C.

    Heppel, L.A., P.A. Neal, T.L. Perrin, K.M. Endicott and V.T. Porterfield.
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