820K87007
                                                           March  31, 1987
                                  DICHLOROMETHANE

                                  Health Advisory
                              Office of Drinking Water
                        U.S.  Environmental Protection Agency
I. INTRODUCTION
        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
   population.

        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-terra
   (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.

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    Dichloromethane                                          March  31,  1987

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         This Health Advisory  is  based  upon  information presented  in  the  Office
    of Health and Environment  Assessment Criteria Document (CD)  for Dichloromethane
    (U.S. EPA,  1985a).   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 a fee from the  National Technical Information Service,  U.S. Department  of
    Commerce, 5285 Port Royal  Rd.,  Springfield,  VA 22161,  PB85  191559.  The  toll-
    free number is (800) 336-4700;  in the Washington, D.C. area:   (703) 487-4650.
II.  GENERAL INFORMATION AND  PROPERTIES

    CAS No.  75-09-2

    Structural  Formula
                                      Cl
                                       I
                                     H-C-C1
                                       I
                                      H

    Synonyms^

         0  Methylene chloride,  methylene  dichloride,  methylene  bichloride,  DCM

    Uses

         0  Solvent for insecticides, paints,  varnish  and  paint  removers  and in
            food processing;  degreasing and  cleaning fluids.

    Properties   (Verschueren,  1977;  Windholtz,  1983)

            Chemical Formula                CH2C12
            Molecular Weight                84.94
            Physical  State                  Colorless  liquid
            Boiling Point                   40°C (760  mm Hg)
            Melting Point                   -95 to -97°C
            Density                         1.3255 (20/4°C)
            Vapor Pressure                  349 mm Hg  (20°C)
            Water Solubility                20 g/L (20°C)
            Log Octanol/Water Partition      —•
              Coefficient
            Odor Threshold                  —
            Taste Threshold                  —
            Conversion Factor               —

    Occurrence

         0  Dichloromethane  (DCM)  is a synthetic chemical  with no  known natural
            sources.

         0  Production of DCM was  approximately 600 million  Ibs  in 1983  (U.S.
            ITC, 1984).

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     Dichloromethane                                               March 31, 1987

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             The major sources of DCM released to the environment are from its
             industrial uses where the majority of all DCM produced is released.
             Most of the releases occur to the atmosphere by evaporation.  However,
             large amounts of DCM are disposed of by burial in landfills or dumping
             on the ground or into sewers.  Because DCM is involved in industrial
             operations performed nationwide, releases occur in all urban areas.
             Releases of DCM during its production are relatively minor in comparison
             to releases during its use.

             Dichloromethane released to the air is degraded in a matter of a few
             days.  Dichloromethane released to surface waters migrates to the
             atmosphere in a few days or weeks where it also degrades.  Volatiliza-
             tion is the major transport process for its removal from aquatic
             systems (U.S. EPA,  1979).  Dichloromethane which is released to the
             land does not sorb onto soil and migrates readily to ground water
             where it is expected to remain for months to years.  Dichloromethane,
             unlike some other chlorinated compounds, does not bioaccumulate in
             individual animals  or food chains.

             Because of the large and dispersed releases, DCM occurs widely in the
             environment.  It is ubiquitous in the air with levels in the ppt
             range and is a common contaminant in ground and surface waters with
             higher levels found in ground water.

             Very limited information is available on the occurrence of dichloro-
             methane in food.  Dichloromethane has been reported to occur in fish.
             It is used as an extraction solvent for the -decaffination of coffee
             and other food processing operations.  Low levels of DCM have been
             reported to occur in some foods from these operations.

             The major sources of exposure to DCM are from contaminated water.
             Air and food are only a minor sources (U.S. EPA, 1980c).
III. PHARMACOKINETICS
     Absorption
             Dichloromethane  is  expected  to  be  absorbed  completely  when ingested.
             A single  oral  dose  of  1  or  50 mgAg  14C-DCM administered to male  rats
             (3/dose)  was exhaled  as  unchanged  DCM (12.3 or 72.1%,  respectively)
             within 48 hours  (McKenna and Zempel,  1981).
     Distribution
             Tissue distribution after  administration of  1  or 50 mgAg of  14c-DCM
             in water  by  gavage  to male rats  (3/dose) was  measured by McKenna and
             Zempel (1981).   The highest concentration of  radioactivity was  present
             in liver  and the lowest  in fat,  48  hours after either dose.

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    Dichloromethane                                               March  31,  1987

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    Metabolism

         0  The major metabolites  of  DCM are carbon  monoxide  and  carbon  dioxide.
            McKenna and Zempel (1981) studied the metabolism  of 14c-DCM  after
            gavage administration  to  groups  of three male Sprague-Dawley rats
            dosed at 1  or 50 mgAg«   They metabolized about 88 or 28% of the
            dose, respectively.  The  major metabolites exhaled after 48  hours
            were carbon monoxide (30.9 and 11.9% of  the 1  or  50 rag/kg doses,
            respectively) and carbon  dioxide (35.0 and 6.3% of the 1  or  50 mgAg
            doses, respectively).
    Excretion
            Metabolites  of  DCM are  excreted  in urine.   McKenna  and  Zempel  (1981)
            reported that,  in  rats  given  1 or 50 mgAg  14C-DCM,  4.52  ±0.05% or
            1.96 ±0.05%  of  the dose,  respectively,  was  excreted in  the urine
            within 48 hours.   The fecal elimination of  DCM after oral or intra-
            peritoneal administration of  DCM is low (<1.0%)  (DiVincenzo and
            Hamilton,  1975; McKenna and Zempel, 1981).
IV. HEALTH EFFECTS
    Humans
            Bonventre et al.  (1977)  described a fatal intoxication with DCM
            which was being used as  a paint remover.   Postmortem examination
            revealed the presence of DCM in the liver (14.4 mg/100 g tissue),
            blood (51 mg/dL or 510 mg/L) and brain (24.8  mg/100 g tissue).
            The carboxyhemoglobin content was 3% saturated.
    Animals
    Short-term Exposure

         0  Oral LD^gs for DCM were reported as  1,987 mgAg for mice  and 2,121
            mgAg for rats (Kimura et al.  1971;  Aviado et al.  1977).
            Kimura et al. (1971)  administered single oral doses  of DCM to young
            adult Sprague-Dawley  rats and determined that an approximate dose
            of 1 .3 gAg body weight was  the lowest dose  to induce  the  first
            observable signs of toxicity (dyspnea,  ataxia,  cyanosis and/or coma)..
    Long-term Exposure
            Bornmann and Loeser (1967)  administered DCM in drinking  water at
            2.25 g/18L (or 125 mg/L)  to 30 male and 30 female  Wistar rats for 13
            weeks.  This is equivalent  to a dose of about 15 mgAg/day assuming
            that 1 0 mL of water is consumed daily.   The animals  were examined
            for changes in behavior,  body weight, blood and urine chemistries,
            reproductive function, organ to body weight ratios and histology.
            No treatment-related effects were observed, even though  some rats
            may have consumed as much as 250 mg DCM (36.6 mgAg/day ) during this

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Dichloromethane                                               March 31, 1987

                                     -5-
        experiment.  The urine albumin test was frequently positive; however,
        the authors did not attach any biological significance to this obser-
        vation.  From this study, a NOAEL of 125 mg/kg/day was identified.

      0  Hazelton Labs (1982) reported on the toxicity and carcinogenicity of
        DCM in a chronic two-year drinking water study in Fischer 344 rats.
        Two control groups (85 and 50 rats/sex/group) received deionized
        drinking water.  Four groups of animals (85 rats/sex/group} were
        given DCM in drinking water at target doses of 5, 50, 125 and 250
        mg/kg/day.  A high-dose recovery group (25 rats/sex) was given DCM
        in drinking water at a target dose of 250 mg/kg/day for the initial
        78 weeks and deionized drinking water subsequently for the remainder
        of the study.  At 26, 52 and 78 weeks of treatment, there were incre-
        mental sacrifices of 5, 10 or 20 rats/sex/group,  respectively.  At
        104 weeks of exposure, all survivors were sacrificed.  Survival,
        body weight gains, total food consumption,  water consumption, clinical
        observations, ophthalmoscopic findings, clinical pathology, absolute
        and relative organ weights and gross and microscopic pathology were
        examined to evaluate any compound-related effects.  The dose of
        5 mgAg was identified as the no-effect level based on the absence of
        effects on body weight, hematological parameters and histopathological
        changes in the liver (incidence of foci/areas of cellular alteration
        and/or fatty changes).

Developmental Effects

      Q  No positive conclusion can be drawn regarding the potential for
        developmental effects of DCM.

      0  Maternal exposure of rats and mice to DCM (4337 mg/m3) on days 6
        through 15 of gestation was associated with soft tissue abnormalities
        in the offspring of rats and skeletal changes in the offspring of
        both rats and mice (Schwetz et al., 1975).

      0  Other workers have found no increased incidence of gross external,
        skeletal or soft tissue anomalies in offspring after maternal exposure
        of rats to DCM at 15,615 mg/m3 (6 hours/day,  7 days/wk)  before and
        during gestation.  (Hardin and Manson,  1980).

Mutagenicity

      0  DCM has been reported to be mutagenic in several bacterial and yeast
        test systems, as well as in mammalian test systems.  DCM was also
        reported to be positive in a mammalian transformation test (U.S. EPA,
        1985a).

Carcinogenic!ty

      0  In a pulmonary tumor response assay,  DCM administered intraperitoneally
        did not produce an increased incidence of lung tumors in mice (Theiss
        et al. 1977).

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   Dichloromethane                                               March 31,  1987

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        0  An inhalation bioassay conducted in male and female F344/N rats  and
           B6C3F-]  mice indicated clear evidence of carcinogenicity in male  and
           female  mice as shown by increased incidences of lung (alveolar/
           bronchiolar adenoma and/or carcinoma)  and liver (hepatocellular
           adenoma and carcinoma combined) tumors (NTP, 1985, as cited in U.S.
           EPA,  1985c).  Some evidence of carcinogenicity in male rats and
           sufficient or clear evidence of carcinogenicity in female rats was
           indicated by an increased incidence of benign neoplasms of the mammary
           gland.   These animals were exposed at concentrations of 0, 1,000,
           2,000 and 4,000 ppm for rats and 0, 2,000 and 4,000 ppm for mice,
           6 hours/day, 5 days/week for 102 weeks.

        0  Hazelton Laboratories (1982) studied the carcinogenicity of DCM  in a
           chronic two-year drinking water study  in Fischer 344 rats, using the
           protocol as described under longer-term exposure.  Hepatic histologicaJ
           alteration detected in the 50 to 250 mgAg/day dose groups (both
           sexes)  included an increased incidence of foci/areas of cellular
           alteration.  Fatty liver changes were detected in the 125 and 250
           mgAg/day groups after 78 and 104 weeks of treatment.  The authors
           stated  that DCM did not induce carcinogenicity under the conditions
           of the  study.

        0  The U.S. EPA (1985b) performed an independent assessment of the  data
           from the Hazelton Laboratories (1982)  study and determined that
           incidences of hepatic neoplastic nodules and carcinomas (combined
           in females exposed to 50 mgA9/<3ay (4.8%), 250 mgAg/day (7.1%)  and
           250 mgAg/day,  recovery group (8.0%) were significantly (P<0.05)
           higher  than that in matched controls (0%).  No significant increase
           in liver tumors was evident in any of  the male dose groups.  The U.S.
           EPA (1985b) considered data on historical cbntrol values and concluded
           that the 250 mgAg/day dose was borderline for carcinogenicity in
           Fischer 344 rats.
V. QUANTIFICATION OF TOXICOLOGICAL EFFECTS

        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 (	   /L}
                        (UF) x (	 L/day)
   where:
           NOAEL or LOAEL = No- or Lowest-Observed-Adverse-Effeet-Level
                            in mgAg bw/day.

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

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Dichloromethane                                               March 31, 1987

                                     -7-
                    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 Kimura et al. (1971) has been selected to serve as the
basis for the One-day HA for the 10 kg child because no other acute oral
studies of appropriate duration or design were located in the literature.
This study identified a LOAEL in young adult Sprague-Dawley rats on the basis
of the first observable gross signs of toxicity (i.e., dyspnea, ataxia,
cyanosis and/or coma) following administration of a single oral dose of DCM
by gavage.  The authors implied that multiple dose levels were administered
to define dose-response,  although details were not reported.  The calculations
for a One-day HA for a 10-kg child are given below:

       One-day HA » 1,326 mg/kg/day) (10 kg) = 13.3   /L (13,300 ug/L)
                       (1,000) (1 L/day)

where:

        1,326 mgAg/day = LOAEL,  based on the first observable gross signs of
                          toxicity in rats.

                  10 kg = assumed body weight of a child.  ~

                  1,000 = uncertainty factor,  chosen in accordance with ODW/NAS
                          guidelines for use with a LOAEL from an animal study.

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

Ten-day Health Advisory

     The study by Bornmann and Loeser (1967) in which DCM was administered
in drinking water at 125 mg/L to Wistar rats for 13 weeks,  has been selected
to serve as the basis for the Ten-day HA for the 10-kg child because it was
the most comprehensive short-term oral toxicity study located.

     The Ten-day HA for a 10 kg child is calculated as follows:

          Ten-day HA = <1S mg/kg/day)(10 kg) = , 5   /L (1 500 ug/L)
                          (100) (1  L/day)
where:
        15 mg/kg/day = NOAEL,  based on absence of effects on body weight gain,
                       blood and urine chemistries,  reproductive function,
                       organ/body weight ratios,  or  histopathological changes
                       in Wistar rats.

               10 kg = assumed body weight of a child.

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Dichloromethane                                               March 31, 1987

                                     -8-
                 100 = uncertainty factor, chosen in accordance with ODW/NAS
                       guidelines for use with a NOAEL from an animal study.

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

Longer-term Exposure

     There were no suitable data available from which to calculate Longer-Term
Health Advisories.

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 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.

     Dichloromethane may be classified in Group B2:  Probable Human Carcinogen,
according to EPA's guidelines for assessment of carcinogenic risk (U.S. EPA,
1986).  Because of this, caution must be exercised in making a decision on
how to deal with possible lifetime exposure to this substance.  The risk
manager must balance this assessment of carcinogenic potential against the
likelihood of occurrence of health effects related to non-carcinogenic end-
points of toxicity.  In order to assist the risk manager in this process,
drinking water concentrations associated with estimated excess lifetime cancer
risks over the range of one in ten thousand to one in a million for the 70-kg
adult, drinking 2 liters of water per day, are provided in the following
section.  In addition, in this section, a Drinking Water Equivalent Level
(DWEL) is derived.  A DWEL is defined as the medium-specific  (in this case,
drinking water) exposure which is interpreted to be protective for non-
carcinogenic end-points of toxicity over a lifetime of exposure.  The DWEL
is determined for the 70-kg adult, ingesting 2 liters of water per day.  Also
provided is an estimate of the excess cancer risk that would result if exposure
were to occur at the DWEL over a lifetime.

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Dichloromethane                                               March 31, 1987

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     Neither the risk estimates nor the DWEL take relative source contribution
into account.  The risk manager should do this on a case-by-case basis,
considering the circumstances of the specific contamination incident that has
occurred.

     The study by Hazelton Laboratories (1982) is most appropriate from which
to derive the DWEL because it is an oral chronic (two year) study that admini-
stered DCM in drinking water in multiple dose levels to rats.  This is the
most comprehensive chronic oral study available.  There were sufficient
numbers of animals in the dose groups and a dose-response was demonstrated.
A NOAEL of 5 mg/kg/day was identified in this study.

     The DWEL for a 70-kg adult is calculated as follows:

Step 1:  Determination of the Reference Dose (RfD)

                     RfD = 15 mg/kg/day) - 0.05 mgAg/day


where:

        5 mg/kg/day = NOAEL based on the absence of liver and blood effects
                      in rats.

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

Step 2:  Determination of the Drinking Water Equivalent Level (DWEL)

           DWEL = (0.05 mg/kg/dav)(70 kg)  = , >75 mg/L (1f750 ug/L)
                         (2 L/day)

where:

        0.05 mgAg/day = RfD.

                 70 kg = assumed body weight of an adult.

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

Step 3:  Determination of the Lifetime Health Advisory

     Dichloromethane is classified in Group B2:   Probable Human Carcinogen.
A Lifetime HA has not been calculated for DCM.

     The estimated excess cancer risk associated with lifetime exposure to
drinking water containing DCM at 1,750 ug/L is approximately 3.7 x 10~4.
This estimate represents the upper 95% confidence limit from extrapolations
prepared by EPA's Carcinogen Assessment Group using the linearized,  multistage
model.  The actual risk is unlikely to exceed this  value, but there is consid-
erable uncertainty as to the accuracy of risks calculated by this methodology.

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    Dichloromethane                                               March 31, 1987

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    Evaluation of Carcinogenic Potential

         0  IARC (1982) has classified DCM in group 3: Limited evidence of
            carcinogenicity in animals.

         0  Applying the criteria described in EPA's guidelines for assessment of
            carcinogenic risk (U.S. EPA, 1986), DCM 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.

         0  More recently, EPA's CAG (U.S. EPA, 1985c) estimated that the upper-
            bound incremental unit carcinogenic risk for drinking water containing
            1 ug/L DCM for a lifetime was 2.1 x 10-7 (ug/L)-1.  This risk estimate
            was the mean of the derived carcinogenic risk estimates based on the
            finding of liver tumors (not based on lung tumors) in the NTP (1985)
            draft inhalation study in female mice and the suggestively positive
            finding of liver tumors in the Hazelton (1982) unpublished ingestion
            study in male mice.  Since the extrapolation model is linear at low
            doses,  additional lifetime cancer risk is directly proportional to
            the water concentration of DCM.  Thus, levels of 10~4,  10"5 and 10-6
            are 0.48, 0.048 and 0.005 mg/L, respectively.

         0  The linear multistage model is only one method of estimating carcino-
            genic risk.  Using the 10~6 risk level, the following comparisons in
            micrograms/L may be made:   Multistage, 4.8; Probit, 74,000; Logit,
            4,000;  Weibull, 10.  Each model is based on differing assumptions.
            No current understanding of the biological mechanism of carcinogenesis
            is able to predict which of these models is more accurate than another.
            While recognized as statistically alternative approaches, the range of
            risks described by using any of these modeling 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.


VI. OTHER CRITERIA,  GUIDANCE AND STANDARDS

         0  ACGIH (1984)  has recommended a time-weighted average threshold limit
            value (TWA-TLV) of 100 ppm (   360 mg/m3) in the absence of occupa-
            tional  exposure to carbon monoxide and is based upon experimental
            data obtained from nonsmoking males at rest.  A short-term exposure
            level (STEL)  of 500 ppm is also recommended.

         0  The Occupational Health and Safety Administration (OSHA,  1979)  has
            established occupational exposure standards as follows:   an eight-hour
            time-weighted-average (TWA) of 1,737 mg/m3; an acceptable ceiling
            concentration of 3,474 mg/m3;  and an acceptable maximum peak above
            the ceiling of 6,948 mg/m3 (five minutes in any two hours).

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     Dichloromethane
March 31, 1987
                                          -11-
          0  Due to the metabolic formation of carboxyhemoglobin and the additive
             toxicity with carbon monoxide, the National Institute of Occupational
             Safety and Health (NIOSH, 1976) has recommended a ten-hour TWA exposure
             limit of 261 mg/m3 and a 1737 mg/m3 peak (15 minute sampling), in the
             presence of carbon monoxide concentrations less than or equal to 9.9
             mg/m3 (TWA).  Proportionately lower levels of DCM are required in the
             workplace when carbon monoxide concentrations greater than 9.9 mg/m3
             are present.

          0  Based on noncarcinogenic risks, a water quality criterion of 12.4 mg/L
             is the acceptable concentration of DCM in drinking water (U.S. EPA,
             1980a).  This calculation was performed by the U.S. EPA as part of the
             overall process for developing a U.S. EPA Water Quality Criteria for
             halomethanes as a group and uses a limit of 200 ppm (694 mg/m3) for
             protection against excessive carboxy-hemaglobin formation.  In that
             calculation, the EPA assumed that the average person consumes approxi-
             mately two liters of water and eats 6.5 g of contaminants in fish and
             seafood per day, and that the estimated coefficient of absorption via
             inhalation versus ingestion is 0.5.

          0  The original U.S. EPA Suggested-No-Adverse-Response-Levels (SNARLs,
             now referred to as Health Advisories) for DCM were set at 13, 1.5
             and 0.150 mg/L in drinking water for One-day,  Ten-day and Longer-term
             exposures, respectively (U.S. EPA, 1980b).  The U.S. EPA-SNARLs were
             established for a 10 kg body weight child and did not consider the
             possible carcinogenic risk that may result from exposure to a chemical.

          0  The MAS (1980) calculated one-day and seven-day NAS-SNARLs for DCM
             in drinking water based on the minimal-effect acute oral dose in rats
             reported by Kimura et al. (1971).  The NAS concluded that data on the
             no-effect dose do not exist.  Using the 1 ml/kg (1.3 gAg) minimal-
             effect acute oral dose in the rat,  assuming two liters/day of drinking
             water as the only source (consumed by a 70 kg adult) and employing a
             safety factor of 1,000, the NAS (1980) calculated the one-day SNARL.
             Since no appropriate data were available for the seven-day SNARL, the
             one-day SNARL was divided by a factor of seven (days).  However,  the
             NAS (1980) erroneously reported a value of 35 mg/L for the one-day
             and 5 mg/L for the seven-day calculation.  Re-examination of calcula-
             tions indicated that the one-day and seven-day adult NAS-SNARLs
             should be 45.5 mg/L and 6.5 mg/L,  respectively.
VII. ANALYTICAL METHODS
             Analysis of DCM is by a purge-and-trap gas chromatographic procedure
             used for the determination of volatile organohalides in drinking water
             (U.S. EPA,  1985d).  This method calls for the bubbling of an inert
             gas through the sample and trapping DCM on an adsorbant material.
             The adsorbant material is heated to drive off the DCM onto a gas
             chromatographic column.  This method is applicable to the measurement
             of DCM over a concentration range of less than 1  to 1500 ug/L;  however,
             measurement of DCM at low concentrations is difficult due to problems
             with contamination.  Dichloromethane vapors readily penetrate tubing

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      Dichloromethane                                               March 31,  1987

                                           -12-

              during the purge/trap procedure.   Confirmatory analysis  for DCM  is
              by mass spectrometry.  (U.S.  EPA 1985e).   The detection  limit for
              confirmation by mass spectrometry is  0.3  ug/L.


VIII. TREATMENT TECHNOLOGIES

           8  Limited information is available  concerning the removal  of dichloro-
              methane from drinking water.   However,  evaluation of physical and
              chemical properties and some  experimental data suggest that adsorp-
              tion by granular activated carbon (GAG) and aeration are feasible
              technologies to remove this contaminant in drinking water supplies.

           0  Dobbs and Cohen (1980) developed  adsorption isotherms for several
              organic chemicals,  including  DCM.  This study reported that Filtrasorb*
              300 exhibited adsorptive capacities of  1.3 mg and 0.09 mg DCM per gm
              carbon at equilibrium concentrations  of 1,000 mg/L and 100 mg/L,
              respectively.

           0  Another study reported activated  carbon usage of 3.9 lb/1,000 gal of
              treated water to maintain an  effluent DCM concentration  below 1  ug/L
              from a raw water influent concentration above 20 mg/L (ESE,  1982).
              This particular treatment scheme  employed two activated  carbon columns
              operating in series with extremely long empty bed contact time (262
              minutes).

           0  The calculated Henry's Law constant for DCM is 2.5 x 10-3 atm-m3/mole
              (ESE, 1982).  In a  bench-scale study, distilled water which was
              spiked with 225 ug/L of DCM was passed  through a diffused air aerator.
              The results showed  82 percent reduction in DCM at an air-to-water
              ratio of 15:1 (Love, 1983).  Dichloronethane will, therefore, be
              amenable to air stripping treatment.  Actual field performance data,
              however,  have not been reported for this  compound.

           0  Air stripping is an effective, simple and relatively inexpensive
              process for removing DCM 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
              hazards associated  with the chemical.

           0  Treatment technologies for the removal  of DCM from water have not
              been extensively evaluated except on  an experimental level.  Selection
              of individual or combinations of  technologies to attempt DCM reduction
              must be based on a  case-by-case technical evaluation, and an assessment
              of the economics involved.

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                                         -13-


IX. REFERENCES

    ACGIH.   1984.  American Conference  of Governmental  Industrial Hygienists.
         Documentation  of  the  threshold limit  values.   4th  ed.   1980-1984  supplement.
         pp.  275-276.

    Aviado,  D.M.,  S. Zakhari and T. Watanabe.   1977.  Methylene  chloride.   In;
         Non-fluorinated propellants and solvents  for aerosols,  L.  Goldberg, ed.,
         CRC Press, Inc.,  Cleveland, Ohio, pp.  19-45.

    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.  Anal. Toxicol.   1:158-160.

    Bornmann, G.,  and A. Loeser.   1967.  Zur Frage einer chronisch-toxischen
         Wirkung von Dichloromethan.  Z. Lebensm.-Unters. Forsch.   136:14-18.

    DiVincenzo, G.D., and  M.L.  Hamilton.  1975.  Fate and disposition of carbon-14
         labelled  methylene chloride in the  rat.   Toxicol.  Appl. Pharmacol.
         32:385-393.

    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.  1982.  Environmental  Science and Engineering.  Review of organic  con-
         taminants in ODW  data  base for summary of all  available treatment  tech-
         niques, compound  dichloromethane.   Prepared for U.S. EPA,  Office  of
         Drinking Water, EPA-68-01-6494.

    Hardin,  B.D.,  and J.M. Manson.  1980.  Absence of dichloromethane teratogenicity
         with inhalation exposure  in rats.   Toxicol. Appl.  Pharmacol.  52:22-28.

    Hazelton Laboratories  America, Inc.  1982.  National Coffee Association
         (prepared for  the twenty-four  month chronic toxicity and oncogenicity study
         of  methylene chloride  in  rats).  Final Report, Vols. I-IV.  Vienna, Va.:
         2112-101.  August 11,  1982.

    IARC.   1982.   IARC  monographs  on the evaluation of  the  carcinogenic risk of
         chemicals to humans.   Supplement 4, Lyon, France.

    Kimura,  E.T., D.M.  Ebert and P.W. Dodge.   1971.  Acute  toxicity and limits of
         solvent residue for sixteen organic solvents.  Toxicol. Appl. Pharmacol.
         19:699-704.

    Love, O.T., Jr.  1983.  Treatment of volatile organic compounds in drinking
         water.  NTIS,  U.S. Department  of Commerce.

    McKenna,  M.J., and  J.A. Zempel.  1981.  The dose-dependent metabolism  of
         M^C]methylene chloride following oral administration to rats.  Fd.
         Cosmet. Toxicol.  19:73-78.

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                                     -14-
NAS.  1980.  National Academy of Sciences.  Drinking Water and Health.
     Vol. 3.  National Academy Press,  Washington,  D.C.

NTP.  1985.  National Toxicology Program.  NTP technical report on the toxicology
     and carcinogenesis studies of dichloromethane (methylene chloride)
     in F344/N rats and B6C3F1 mice (inhalation studies) NTP TR 306.   Draft.
     Research Triangle Park,  N.C.  94 pp.  As cited in U.S. EPA, 1985c.

NIOSH.  1976.  National Institute for Occupational Safety and Health.  Criteria
     for a recommended standard...occupational exposure to methylene chloride.
     U.S. Department of Health, Education and Welfare (NIOSH).  Washington,
     D.C., pp. 1-3, 76-138, 142.

OSHA.  1979.  Occupational Safety and Health Administration.  General  industry
     standards.  (OSHA) 2206, Revised January, 1978.  U.S. Dept. of Labor,
     Washington,  D.C.

Schwetz,  B.A., B.J. Leong and P.J. Gehring.   1975.  The effect of maternally
     inhaled trichloroethylene, perchloroethylene, methyl chloroform,  and
     methylene chloride on embryonal and  fetal development in mice and rats.
     Toxicol. Appl. Pharmacol.  32:84-96.

Theiss,  J.C., G.D.  Stoner,  M.B. Shimkin and  E.K.  Weisberger.  1977. Test for
     carcinogenicity of organic contaminants of United States drinking waters
     by pulmonary tumor response in Strain A mice.  Cancer Res.  37:2717-2720.

U.S. EPA.  1979.   U.S. Environmental Protection Agency.  Water Related Environ-
     mental Fate  of 129 Priority Pollutants.  Office of Water Planning and
     Standards.  EPA-440/4-79-029.

U.S. EPA.  1980a.  U.S. Environmental Protection  Agency.  Ambient water
     quality criteria for halomethanes.  Office of Water Regulations and
     Standards.  Criteria and Standards Division.   Washington,  D.C.
     EPA 440/5-80-051.

U.S. EPA.  1980b.  U.S. Environmental Protection  Agency.  Advisory opinion
     for dichloromethane (methylene chloride) (Draft).  Office of Drinking
     Water.  Washington,  D.C.

U.S. EPA.  1980c.  U.S. Environmental Protection  Agency.  Dichloromethane
     occurrence in drinking water, food,  and air.  Office of Drinking  Water.

U.S. EPA.  1985a.  U.S. Environmental Protection Agency.  Health assessment
     document for dichloromethane (methylene chloride).  Office of Health and
     Environmental Assessment.  EPA-600/8-82/004F.

U.S. EPA.  1985b.  U.S. Environmental Protection Agency.  Health assessment
     document for dichloromethane (methylene chloride) (Final report). Office
     of Health and Environmental Assessment.  Washington, D.C.

U.S. EPA.  1985c.  U.S. Environmental Protection Agency.  Addendum to  health
     assessment document for dichloromethane (methylene chloride) (Final
     report). Office of Health and Environmental Assessment.  Washington, D.C,
     EPA 600/8-82-004FA.

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                                     -15-
U.S. EPA.  1985d.  U.S. Environmental Protection Agency.  Method 502.1.
     Volatile Halogenated Organic Compounds in Water by Purge and Trap Gas
     Chromatography.  Environmental Monitoring and Support Laboratory,
     Cincinnati, Ohio 45268.

U.S. EPA.  1985e.  U.S. Environmental Protection Agency.  Method 524.1.
     Volatile Organic Compounds in Water by Purge and Trap Gas Chromatography/
     Mass Spectrometry.  Environmental Monitoring and Support Laboratory,
     Cincinnati, Ohio 45268.

U.S. EPA.  1986.  U.S. Environmental Protection Agency.  Guidelines for
     carcinogen risk assessment.  Federal Register.  51(185):33992-34003.
     September 24.

U.S. ITC.  1984.  United States International Trade Commission.   Synthetic
     Organic Chemicals United States Production.  USITC Publication 1422,
     Washington, D.C. 20436.

Verschueren,  K.  1977.  Handbook of Environmental Data on  Organic Chemicals.
     2nd ed.  Van Nostrand Reinhold Company,  NY.  pp. 451-452.

Windholz, M.  1983.  The Merck Index.  10th Edition.  Merck and  Co.,  Inc.,
     Rahway,  NJ.  p. 869.

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