EPA 749-F-94-018a

        CHEMICAL SUMMARY FOR METHYLENE CHLORIDE (DICHLOROMETHANE)
                               prepared by
                OFFICE OF POLLUTION PREVENTION AND TOXICS
                  U.S. ENVIRONMENTAL PROTECTION AGENCY
                               August 1994


     This summary is based on information retrieved from a systematic 
search limited to secondary sources (see Appendix A).  These sources
include online databases, unpublished EPA information, government
publications, review documents, and standard reference materials.  No
attempt has been made to verify information in these databases and
secondary sources.

I. CHEMICAL IDENTITY AND PHYSICAL/CHEMICAL PROPERTIES

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

           TABLE 1.  CHEMICAL IDENTITY AND CHEMICAL/PHYSICAL 
                PROPERTIES OF METHYLENE CHLORIDE
__________________________________________________________________________
                                                                          
Characteristic/Property            Data                  Reference
__________________________________________________________________________

CAS No.                       75-09-2 
Common Synonyms               MC, dichloromethane, 
                              DCM, methylene bichloride, 
                              methylene dichloride   
Molecular Formula             CH2Cl2                
Chemical Structure                Cl
                                  |     
                              H - C - H
                                  |  
                                  Cl             
Physical State                colorless liquid         Budavari et al. 1989
Molecular Weight              84.94                    Budavari et al. 1989
Melting Point                 -95C                    Budavari et al. 1989
Boiling Point                 39.75C at 760 mm Hg     Budavari et al. 1989
Water Solubility              1.32 x 104 mg/L at 20C  U.S. Air Force 1989
Density                       d20/4, 1.3255 g/mL       Budavari et al. 1989
Vapor Density (air = 1)       2.93                     NIOSH 1986
KOC                           25                       ATSDR 1993
Log KOW                       1.25                     U.S. Air Force 1989
Vapor Pressure                400 mm Hg at 24.1C      HSDB 1994
Reactivity                                     
Flash Point                   Nonflammable             U.S. Air Force 1989
Henry's Law Constant          2.57 x 10-3 atm m3/mol   U.S. Air Force 1989
Fish Bioconcentration Factor  2 (estimated)            U.S. EPA 1984
Odor Threshold                214 ppm (in air)         U.S. Air Force 1989
Conversion Factors            1 ppm = 3.48 mg/m3;
                              1 mg/m3 = 0.288 ppm      U.S. Air Force 1989
___________________________________________________________________________


II. PRODUCTION, USE, AND TRENDS

    A. Production

       There are 3 manufacturers with 5 plants producing methylene chloride 
       in the United States: Dow Chemical, Occidental Chemical, and Vulcan 
       Chemicals.  Annual capacity is about 527 million pounds.  In 1992, 
       approximately 350 million pounds of methylene chloride were produced 
       in the US.  Since 1988, production of methylene chloride has fallen 
       at an average rate of 8.6 percent per year.  Imports do not account 
       for much of U.S. methylene chloride consumption.  In 1992, it was
       estimated that 13 million pounds of methylene chloride were imported 
       into the US (Mannsville, 1993).

   B. Use

      Methylene chloride is used in many applications.  Its largest use is 
      as the principal active ingredient in organic-based paint strippers, 
      accounting for approximately 125 million pounds (35 percent of all 
      U.S. methylene chloride production in 1992).  It is used in both 
      consumer and industrial paint removers, where it is commonly present
      in 60-80% concentration.  The second largest application (88 million 
      pounds) of methylene chloride is in chemical processing.  Table 2 
      presents the estimated 1992 end use pattern for methylene chloride.

  C. Trends

     Methylene chloride demand is expected to continue to decline by over 
     30% by 1995 because of environmental and occupational concerns.  Users 
     of methylene chloride have been under strong pressure to limit usage, 
     restrict emissions, maximize recycling, and reduce worker exposure 
     (Mannsville, 1993).
      
III. ENVIRONMENTAL FATE

     A. Environmental Release

        Of the total methylene chloride released to the environment, about 
        86% is released to the atmosphere, 12% to land, and 2% to water 
        (ATSDR 1993).  The highly volatile methylene chloride [vapor 
        pressure, 400 mm Hg at 24.1C (HSDB 1994)] is released into the 
        atmosphere from industrial and consumer uses (ATSDR 1993). The 
        principal releases of methylene chloride to land are from the 
        disposal of methylene chloride products and containers in landfills 
        (ATSDR 1993).  The principal releases to surface water and 
        potentially to groundwater are via industrial effluents and 
        underground injections, respectively (ATSDR 1993).  In 1992, 
        releases of methylene chloride to environmental media, as reported 
        to the Toxic Chemical Release Inventory by certain types of U.S. 
        industries, totaled about 74 million pounds to the atmosphere, 
        221 thousand pounds to surface water, 1 million pounds to under-
        ground injection, and 79 thousand pounds to land (TRI88 1990).  
        In addition, an estimated 243 million pounds of methylene chloride 
        were released to the atmosphere in 1988 from consumer products and 
        other sources, such as hazardous waste sites (ATSDR 1993).  
        Maximum levels of methylene chloride measured in environmental 
        media are 6.7 micrograms/m3 (urban U.S. air), 39 micrograms/m3 
        (air around hazardous waste sites), 743 g/L (New Jersey surface 
        water), 3600 micrograms/L (groundwater), and 13 micrograms/L 
        (sediment) (ATSDR 1993).


    TABLE 2.  ESTIMATED 1992 U.S. END USE PATTERN OF METHYLENE CHLORIDE 
 _________________________________________________________________________
 
Use of Methylene Chloride      1992 US Consumption      Percentage of  US
[typical Standard Industrial   (in millions of pounds)  Methylene Chloride 
[Classification (SIC) code]                             Use
(see end note 1)                                 
__________________________________________________________________________
Paint Removers
  (production, SIC 2851; 
  use, various industries)              125                     35
Chemical Processing
  (SIC 2821, 2823)                       88                     25
Foam Blowing
  (various industries)                   49                     14
Metal Cleaning & Finishing
  (various industries)                   28                      8
Aerosols
  (various industries)                   25                      7
Adhesives and Coatings
  (production, SIC 2851; use, 
  various industries)                    14                      4
Electronics
  (SIC 3672)                             11                      3
Miscellaneous (see end note 2)           14                      4

TOTAL                                   354                    100
__________________________________________________________________________
Source:  Mannsville 1993


   B. Transport

      Methylene chloride tends to volatilize to the atmosphere from the 
      water and soil (ATSDR 1993; U.S. Air Force 1989).  With an organic 
      carbon partitioning coefficient (KOC) of 25, methylene chloride is 
      expected to be highly mobile in soils, and leaching of the chemical
      into groundwater is likely (ATSDR 1993).  In deep, saturated soils 
      that contain no soil air and negligible soil organic carbon, as much 
      as 96% of environmental methylene chloride may be present in the 
      soil-water phase and transported with flowing groundwater (U.S. Air
      Force 1989).

   C. Transformation/Persistence

      1. Air - The main degradation pathway for methylene chloride in the 
         atmosphere is reaction with photochemically produced hydroxyl 
         radicals (ATSDR 1993).  The estimated lifetime for the chemical 
         in the atmosphere is 130 days.  The small amount of methylene 
         chloride reaching the stratosphere (about 1%) would probably
         undergo direct photolysis (ATSDR 1993).

      2. Soil - In surface soil, volatilization to air is an important 
         fate process for methylene chloride (U.S. Air Force 1989; 
         ATSDR 1993).  The biodegradation of methylene chloride has been 
         demonstrated in the laboratory and may occur in subsurface
         soils (ATSDR 1993); however, biodegradation (except, perhaps 
         in landfills with active microbial populations) is probably not 
         a significant degradation pathway in the soil-groundwater system 
         (U.S. Air Force 1989).  It has been suggested that microorganisms 
         used in biological sewage treatment can degrade the chemical
         with suitable acclimatization (U.S. Air Force 1989).

      3. Water - An important fate process for methylene chloride is 
         volatilization; in the laboratory, the volatility half-life was 
         estimated to be 21 minutes (ATSDR 1993).  Methylene chloride has 
         been shown to hydrolyze slowly (experimental half-life in
         water at 25C, ~18 months) (ATSDR 1993).

      4. Biota - The estimated fish bioconcentration factor (BCF) for 
         methylene chloride of 2 (U.S. EPA 1984) suggests that 
         biomagnification of the chemical in the aquatic and terrestrial 
         food chains is not likely. 
         
 IV. HEALTH EFFECTS

     A. Pharmacokinetics

        1. Absorption - Studies in humans and animals have demonstrated 
           that methylene chloride is readily absorbed via the lungs and 
           the gastrointestinal tract (U.S. EPA 1984; ATSDR 1993).  Limited 
           animal data indicate some skin absorption (ATSDR 1993).

       2. Distribution - In studies with animals exposed to radiolabeled 
          methylene chloride, radioactivity was detected in the liver, 
          kidneys, lungs, brain, muscle, adipose tissues, and adrenals 
          about 1 hour after inhalation exposure; and in the liver,
          kidneys, lungs, brain, epididymal fat and testes 48 hours after 
          single oral doses (ATSDR 1993).

      3. Metabolism - The major metabolites of inhaled and ingested 
         methylene chloride are carbon dioxide probably via glutathione 
         transferase and carbon monoxide probably via mixed function 
         oxidases (ATSDR 1993).  Elevated levels of carboxyhemoglobin 
         (COHb) have been observed in exposed human subjects and
         animals (ATSDR 1993).

      4. Excretion - Methylene chloride and its metabolites are excreted 
         primarily in expired air.  Small amounts are also eliminated in 
         the urine and feces.  Following inhalation exposure, exhaled air 
         contained 58 to 79% of a dose of radiolabeled methylene chloride.

   B. Acute Effects

      Humans acutely exposed to methylene chloride experience adverse 
      effects of the central nervous system and the heart.  Animal studies 
      indicate acute exposures to high levels of methylene chloride can 
      adversely affect the liver and the kidney.

      1. Humans - Direct contact with methylene chloride causes corneal 
         burns and erythema and burning of the skin (ATSDR 1993).  The 
         lowest lethal ingested dose of methylene chloride reported for 
         humans is 357 mg/kg (RTECS 1993).  Occupational overexposure to 
         methylene chloride (concentrations were not reported) has resulted 
         in worker deaths (ATSDR 1993).  Exposure to 500 ppm methylene 
         chloride for 8 hours produced euphoria in humans (RTECS 1994).  
         The concentration of 500 ppm is roughly equivalent to a total of 
         248 mg/kg over an 8-hour period (see end note 3).  Methylene 
         chloride is metabolized to carbon monoxide in humans, resulting 
         in the formation of carboxyhemoglobin (COHb) and subsequent oxygen 
         deprivation (U.S. Air Force 1989).  The formation of COHb is 
         concentration-dependent and saturable.  Human subjects exposed to 
         100 ppm for 7.5 hours developed COHb levels of >5%, subjects
exposed 
         to 500 ppm for 1 hour had COHb levels of 1-4%, and subjects
exposed 
         to 1000 ppm for 2 hours had COHb levels of 10% (saturation) (ATSDR 
         1993).  A concentration of 2.5% COHb is associated with impairment 
         of time-interval discrimination, whereas levels of 5% COHb are 
         associated with other psychomotor effects and cardiovascular 
         changes (Amdur et al. 1991).  The cardiovascular changes include 
         increased cardiac output,  A-V  oxygen difference, and coronary 
         blood flow in patients without coronary disease.  Patients with 
         coronary heart disease and elevated COHb levels may experience 
         decreased coronary sinus blood PO2 and impaired oxidative 
         metabolism of the myocardium, producing an added burden on the 
         patient (Amdur et al. 1991).

     2. Animals - LD50/LC50 values for rats, reported in the literature 
        searched, are as follows for the various routes of exposure:  
        2100 mg/kg (oral) (ATSDR 1993), 25,287 ppm for 30 min
(respiratory), 
        and 916 mg/kg [intraperitoneal (i.p.) injection] (RTECS 1994).  
        LD50/LC50 values for mice are slightly lower.  Signs and symptoms
        of the acute toxicity of methylene chloride include (a) liver 
        damage in mice exposed orally to 133 to 665 mg/kg (IARC 1986), 
        in rats exposed by inhalation to 552 ppm, 6 hours/day for 5 days, 
        and in guinea pigs exposed by inhalation to 5200 ppm for 6 hours; 
        and (b) kidney damage in dogs and mice injected i.p. with 
        "near-lethal doses" and in rats injected i.p. with 1330 mg/kg 
        (IARC 1986).  In animals, as in humans, methylene chloride is 
        metabolized to carbon monoxide, resulting in the formation of 
        carboxyhemoglobin (COHb) and subsequent oxygen deprivation (U.S.
        Air Force 1989).  The formation of COHb is concentration-dependent 
        and saturable.  COHb levels reached 13% in rats exposed to 
        500 ppm methylene chloride for 6 hours, but no further increase 
        in COHb occurred after 6 hours' exposure to higher concentrations 
        up to 1500 ppm (U.S. Air Force 1989).

   C. Subchronic/Chronic Effects

      Humans chronically exposed to methylene chloride experience adverse 
      effects of the central nervous system and the heart.  Animal studies 
      indicate chronic exposures to high levels of methylene chloride 
      adversely affects the liver and the kidney.  EPA has derived an
      oral RfD (reference dose) (see end note 4) of 0.06 mg/kg/day for 
      methylene chloride.  

      1. Humans - Available information suggests that the central nervous 
         system and the cardiovascular system are affected by subchronic 
         or chronic exposure to methylene chloride.  Two workers were 
         exposed intermittently for 13 to 20 years; one reported leg and 
         arm pain, dizziness, fatigue, loss of appetite, and poor night
         vision; and the other reported drowsiness, headache, and tingling 
         of hands and feet (U.S. Air Force 1989).  Deaths occurring 
         following chronic inhalation exposure have been attributed to 
         cardiac injury and heart failure (U.S. EPA 1984).  No other 
         target organs were identified.

      2. Animals - The major target organs for the subchronic/chronic 
         toxicity of methylene chloride are the liver and kidney.  
         Methylene chloride, administered to F344 male and female rats 
         in their drinking water for 2 years, induced histological 
         alterations of the liver at doses 50 mg/kg/day; the no-observed-
         adverse effect level (NOAEL) for the study was 5 mg/kg/day 
         (U.S. EPA 1994).  Based on these data, the U.S. EPA (1994) 
         calculated an oral RfD of 0.06 mg/kg/day for methylene chloride.  
         In inhalation studies with methylene chloride, cytoplasmic 
         vacuolization and fatty infiltration of the liver and tubular 
         degeneration and regenerative changes of the kidneys were observed 
         in rats exposed continuously to 25 or 100 ppm of the chemical 
         for 100 days (ATSDR 1993).  Rats exposed to 500 ppm methylene
         chloride, 6 hours/day, 5 days/week for 2 years developed 
         multinucleated hepatocytes (the liver was not affected at 200 
         ppm), and increased hemosiderosis, cytomegaly, and cytoplasmic 
         vacuolization of the liver after exposure to 1000 ppm, 6 hours/
         day, 5 days/week for 2 years (ATSDR 1993).  IARC (1986) reported 
         that Sprague-Dawley rats exposed to 500 ppm methylene chloride 
         for 2 years exhibited pathological changes in the liver and kidney 
         more frequently than did control animals.

  D. Carcinogenicity

     There is inadequate evidence of carcinogenicity of methylene chloride 
     in humans.  There is sufficient evidence of its carcinogenicity in 
     animals.  EPA has classified methylene chloride as a probable human 
     carcinogen.

     1. Humans - Epidemiology studies revealed no increased risk for cancer 
        among workers who were exposed to methylene chloride for up to 22 
        years (IARC 1986; HSDB 1994).  Exposure levels of the chemical 
        ranged (for several studies) from 26 to 475 ppm.

     2. Animals - Various inhalation bioassays conducted in rodents, 
        exposed to methylene chloride concentrations up to 3500 or 4000 
        ppm 6 hours/day, 5 days/week for approximately 2 years, showed 
        statistically significant increases in the following types of 
        tumors:  benign mammary tumors and sarcomas in rats; alveolar/
        bronchiolar adenomas, alveolar/bronchiolar carcinomas, and
        hepatocellular adenomas in mice; and lymphosarcomas in hamsters 
        (IARC 1986).  Hepatocellular carcinoma and neoplastic nodules were 
        observed in female rats and male mice in the 2-year drinking water 
        study described in the Suchronic/Chronic Section.  Based on 
        inadequate human data and sufficient evidence for carcinogenicity 
        in animals, the U.S. EPA classification for methylene chloride 
        is B2, probable human carcinogen (U.S. EPA 1994).  The oral slope 
        factor (see end note 5) for methylene chloride is 0.0075 per 
        (mg/kg)/day (U.S. EPA 1994).  The inhalation unit risk (see end 
        note 6) for methylene chloride is 4.7 x 10-7 per (micrograms/m3) 
        (U.S. EPA 1994).  IARC (1987) classifies the chemical as 2B, 
        possibly carcinogenic to humans, and the National Toxicology 
        Program (NTP 1994) concluded that methylene chloride shows some 
        evidence of carcinogenicity in male rats and clear evidence of 
        carcinogenicity in female rats and in male and female mice.

   E. Genotoxicity

      In the EPA GENETOX Program, methylene chloride was positive for cell 
      transformation in rat embryo cells, mitotic recombination or gene 
      conversion in Saccharomyces cerevisiae, reverse gene mutation in 
      S. cerevisiae, and histidine reversion in the Ames assay; the
      chemical was negative in the micronucleus test and the sex-linked 
      recessive lethality assay in D. melanogaster (GENETOX 1994).  
      USEPA (1994) reports methylene chloride as mutagenic in Salmonella 
      and negative in gene mutation and chromosome aberration tests
      in mammalian cells.

  F. Developmental/Reproductive Toxicity

     There is no information on the developmental toxicity or reproductive 
     system effects of methylene chloride in humans.  Information on these 
     effects in animals is limited; no conclusions on the can be made on 
     the developmental toxicity or reproductive system effects of methylene 
     chloride from this information.    

     1. Humans - No information was found in the secondary sources 
        searched to indicate that methylene chloride is a developmental/
        reproductive toxicant in humans.

     2. Animals - No compound-related effects were observed in Charles 
        River CD male and female rats or their offspring, given oral 
        doses of up to 225 mg methylene chloride/kg/day in a two-
        generation reproductive toxicity study (HSDB 1994).  In inhalation 
        studies, the offspring of pregnant mice and rats exposed to 
        1250 ppm (7 hours/day) or 4500 ppm (exposure details not given) 
        of methylene chloride during gestation exhibited treatment-related 
        reductions in fetal weight, skeletal anomalies and/or alterations 
        in spontaneous locomotor activities (IARC 1986; ATSDR 1993). 
        There was no indication of fetal malformations in these studies, 
        even at maternally toxic concentrations.  No compound-related 
        effects were observed in Fischer 344 male and female rats or their 
        offspring exposed to methylene chloride concentrations of up to 
        1500 ppm (exposure details not given) in a two-generation
        reproductive toxicity study (HSDB 1994).

  G. Neurotoxicity

     Human and animal studies indicate that methylene chloride adversely 
     affects the central nervous system. 

     1. Humans - Inhalation of 300 to 800 ppm for 4 hours has caused 
        impairment of visual, auditory, and psychomotor functions; the 
        effects were reversible at lower concentrations (ATSDR 1993).  
        Inhalation of 515 ppm for 1 to 2 hours and 1000 ppm for 1 to 
        2 hours resulted in decreased visual evoked response; exposure to
        <500 ppm for 1-2 hours had no effect on visual evoked response 
        (ATSDR 1993).  In an additional case study of longer-term 
        exposure, a chemist who breathed 660 to 3600 ppm (mean, 900 ppm 
        in the breathing zone) for 5 years experienced forgetfulness, 
        insomnia, and auditory and visual hallucinations (U.S. EPA 1984).

     2. Animals - Various inhalation studies with methylene chloride in 
        cats have demonstrated various effects ranging from slight 
        narcosis (6000 ppm for 3 to 4 hours) to deep CNS depression 
        (10,000 ppm for 293 min) (HSDB 1994).  Gerbils exposed to 210 ppm 
        for 7 to 16 weeks (exposure details not given) exhibited decreased 
        hippocampal DNA concentration and alterations in brain amino acids
        (ATSDR 1993).
        
V. ENVIRONMENTAL EFFECTS
     
   A. Toxicity to Aquatic Organisms

      Methylene chloride has low acute toxicity to aquatic organisms; 
      lethal concentrations are generally greater than 100 mg/L.  Ninety-
      six-hour LC50 values for fish are 193 mg/L for Pimephales promelas 
      (fathead minnow; flowthrough conditions) and 220 mg/L for Lepomis 
      macrochirus (bluegill; static conditions) (AQUIRE 1993).  The 14-day 
      LC50 for Poecilia reticulata (guppy) is 294 mg/L  (AQUIRE 1993).  
      In Scenedesmus quadricauda (green algae), the toxicity threshold 
      for cell multiplication inhibition test (TT) and for mortality 
      (static conditions) is 1,450 mg/L (AQUIRE 1993).

  B. Toxicity to Terrestrial Organisms

     No information was found in the secondary sources searched for 
     terrestrial organism toxicity.  The oral LD50 in the rat, 2100 mg/kg 
     (ATSDR 1993), suggests that the chemical would not be acutely toxic 
     to terrestrial animals unless present in very high concentrations. 
     Studies in laboratory animals also suggest that methylene chloride 
     would not cause developmental/reproductive effects in terrestrial
     species at expected environmental levels (see section IV.F).

 C. Abiotic Effects

    The reaction of methylene chloride with ozone in the upper atmosphere 
    is not expected to be significant.  Most methylene chloride in the 
    lower atmosphere is removed by reaction with hydroxyl radicals 
    (ATSDR 1993).
     
VI. EPA/OTHER FEDERAL/OTHER GROUP ACTIVITY

    Voluntary reduction of methylene chloride environmental releases has 
    occurred since 1991, as a result of a joint industry/EPA pollution 
    prevention initiative known as the 33/50 program.  The 1990 Clean 
    Air Act Amendments list methylene chloride as a hazardous air 
    pollutants.

    Workplace exposure to methylene chloride is primarily regulated by the 
    Occupational Safety and Health Administration (OSHA); it has proposed 
    a reduction of the permissible exposure limit (PEL) to 25 ppm.  Other 
    federal agencies and groups (listed in Table 4) have developed 
    recommendations to assist in controlling workplace exposure. 

    Regarding consumer exposure, the Consumer Product Safety Commision 
    (CPSC) requires that all consumer products containing more than 
    1% methylene chloride carry a label warning that the contents may 
    cause cancer.  Also, the Food and Drug Administration (FDA) in 1989 
    banned the use of the chemical in hairspray and other cosmetic 
    products.

    Federal agencies and other groups that can provide additional 
    information on methylene chloride are listed in Tables 3 and 4.


                 TABLE 3.  EPA OFFICES AND CONTACT NUMBERS 
                  FOR INFORMATION ON METHYLENE CHLORIDE
________________________________________________________________________

EPA OFFICE            LAW                                PHONE NUMBER
________________________________________________________________________
Pollution Prevention  Toxic Substances Control Act
 & Toxics               (Sec. 8A/8D/8E)                  (202) 554-1404
                      Emergency Planning and Community
                       Right-to-Know Act (EPCRA)
                        Regulations (Sec. 313)           (800) 424-9346
                        Toxics Release Inventory data    (202) 260-1531
Air                   Clean Air Act                      (919) 541-0888
Solid Waste &         Comprehensive Environmental
 Emergency Response    Response, Compensation, and
                       Liability Act (Superfund)/
                      Resource Conservation and Recovery
                       Act / EPCRA (Sec. 304/311/312)    (800) 424-9346
Water                 Clean Water Act                    (202) 260-7588
                      Safe Drinking Water Act (Drinking
                        Water Standard: 0.005 mg/L)      (800) 426-4791


  Agency for Toxic Substances and Disease Registry         (404) 639-6000
  American Conference of Governmental Industrial
    Hygienists                                             (513) 742-2020
  Consumer Product Safety Commission                       (301) 504-0994
  Food and Drug Administration                             (301) 443-3170
  National Institute for Occupational Safety
   and Health (NIOSH)                                      (800) 356-4674
  Occupational Safety and Health Administration
    (Check your local phone book under U.S. Department of Labor)

__________________________________________________________________________




               TABLE 4.  OTHER FEDERAL OFFICE/OTHER GROUP CONTACT 
                 NUMBERS FOR INFORMATION ON METHYLENE CHLORIDE
________________________________________________________________________

Other Agency/Department/Group                            Contact Number
________________________________________________________________________

Agency of Toxic Substances & Disease Registry            (404) 639-6000
American Conference of Governmental Industrial Hygienists
  (Recommended Exposure Limit (see end note 7):  50 ppm) (513) 742-2020
Consumer Product Safety Commission                       (301) 504-0994
Food & Drug Administration                               (301) 443-3170
National Institute for Occupational Safety & Health
  (Recommended Exposure Limit (see end note 8):  
  Lowest Feasible Concentration)                         (800) 356-4674
Occupational Safety & Health Administration              Check local phone
  (Proposed Permissible Exposure Limit                   book for phone
  (see end note 9): 25 ppm)                              number under
                                                         Department of
                                                         Labor
__________________________________________________________________________


VII. END NOTES

1. The Standard Industrial Classification (SIC) code is the statistical
classification standard for all Federal economic statistics.  The code
provides a convenient way to reference economic data on industries of 
interest to the researcher.  SIC codes presented here are not intended to 
be an  exhaustive listing; rather, the codes listed should provide an 
indication of where a chemical may be most likely to be found in commerce.

2.Miscellaneous uses of methylene chloride include use as an extraction
solvent (including the extraction of heat-sensitive substances such as
caffeine, cocoa, and edible fats); and processing of cellulose triacetate
fiber.

3. Calculated using the factor, 3.48 (U.S. Air Force 1989), to convert 
500 ppm to 1740 mg/m3 which is multiplied by 0.143 (the standard 
occupational 8-hour breathing rate, 10 m3, divided by the assumed adult 
body weight, 70 kg) to obtain the dose in mg/kg (U.S. EPA 1988).

4. The RfD is an estimate (with uncertainty spanning perhaps an order of
magnitude) of the daily exposure level for the human population, including
sensitive subpopulations, that is likely to be without an appreciable 
risk of deleterious effects during the time period of concern.

5. The slope factor is a plausible upper-bound estimate of the probability 
of a response per unit intake of a chemical over a lifetime.  The slope 
factor is used in risk assessments to estimate an upper-bound lifetime 
probability of an individual developing cancer as a result of exposure 
to a particular level of a potential carcinogen.

6. The unit risk is a quantitative estimate in terms of risk per unit 
intake of a chemical.  The unit risk for methylene chloride incorporates 
information on pharmacokinetics and metabolism.

7. The ACGIH exposure limit is a time-weighted average (TWA) concentration 
for an 8-hour workday during a 40-hour workweek. 

8. Exposure should be reduced to the lowest feasible limit; use of only the
most reliable and protective respirators is recommended.

9. The OSHA exposure limit is a time-weighted average (TWA) concentration 
that must not be exceeded during any 8-hour workshift during a 40-hour 
workweek.
 
VIII.  CITED REFERENCES

Amdur MO, Doull J, Klaassen CD, Eds..  1991.  Casarett and Doull's 
Toxicology, 4th ed. Pergamon  Press, New York, p. 868.

AQUIRE. 1993. Aquatic Information Retrieval online data base. Chemical 
Information Systems, Inc., a subsidiary of Fein-Marquart Assoc. Retrieved 
June, 1993.

ATSDR.  1993.  Agency for Toxic Substances and Disease Registry.  
Toxicological Profile for Methylene Chloride.  Update.  ATSDR, Chamblee, 
GA, 111 pp.

Budavari S, O'Neil MJ, Smith A, Heckelman PE (Eds.).  1989.  The Merck 
Index, 11th ed.  Merck &  Co., Inc., Rahway, NJ, p. 954.

GENETOX. 1994. U.S. EPA GENETOX Program, computerized database. Retrieved 
September,  1993.

HSDB.  1994.  Hazardous Substances Data Bank.  MEDLARS Online Information 
Retrieval System, National Library of Medicine.  Retrieved June, 1994.

IARC. 1986. International Agency for Research on Cancer. Dichloromethane.  
In: IARC Monographs on the Evaluation of Carcinogenic Risk of Chemicals to 
Man, Vol. 41. IARC, Lyon, pp. 43-85.

IARC. 1987. International Agency for Research on Cancer. IARC Monographs 
on the Evaluation of Carcinogenic Risk of Chemicals to Man.  Overall 
evaluations of carcinogenicity.  An updating of Vols. 1 to 42.  IARC, Lyon, 
p. 62.

Mannsville.  1993.  Chemical Products Synopsis, Methylene Chloride.  
Mannsville Chemical Products Corporation, January, 1993.

NIOSH.  1986.  National Institute for Occupational Safety and Health.  
Current Intelligence Bulletin 46, April 18, 1986.  NIOSH, U.S. Department 
of Health and Human Services, Cincinnati, OH, 18 pp.

NTP.  1994.  National Toxicology Program.  Management Status Report.  
Produced from NTP Chemtrack system.  April 8, 1994.  National Toxicology 
Program, Research Triangle Park, NC.

RTECS.  1994.  Registry of Toxic Effects of Chemical Substances.  MEDLARS 
Online Information Retrieval System, National Library of Medicine.  
Retrieved July, 1994.

TRI92.  1994.  Toxic Chemical Release Inventory.  National Library of 
Medicine, National Toxicology Program, Bethesda, MD.  (Cited in ATSDR 1993)

U.S. Air Force.  1989.  Methylene Chloride:  In: The Installation 
Restoration Toxicology Guide, Vol. 1. Wright-Patterson Air Force Base, 
OH, pp. 1-1 through 1-37.

U.S. EPA.  1984.  U.S. Environmental Protection Agency.  Health Effects 
Assessment for Methylene Chloride.  Office of Research and Development, 
U.S. EPA, Washington, D.C., 48 pp. EPA/540/1-86-028.

U.S. EPA.  1988.  U.S. Environmental Protection Agency.  Methodology for 
Evaluating Potential Carcinogenicity in Support of Reportable Quantity 
Adjustments Pursuant to CERCLA Section 102. Carcinogen Assessment Group, 
Office of Health and Environmental Assessment, U.S. EPA, Washington, D.C., 
pp. 21, 22.  OHEA-C-073.

U.S. EPA.  1994.  U.S. Environmental Protection Agency.  Integrated Risk 
Information System (IRIS) Online.  Coversheet for Dichloromethane.  
Office of Health and Environmental Assessment, U.S. EPA, Cincinnati, OH,  
Retrieved 7/94.


APPENDIX A.  SOURCES SEARCHED FOR FACT SHEET PREPARATION

AQUIRE. 1994. Aquatic Information Retrieval online data base. Chemical 
Information Systems, Inc., a subsidiary of Fein-Marquart Assoc.

ATSDR.  1989-1994.  Agency for Toxic Substances and Disease Registry.  
Toxicological Profiles. Chamblee, GA: ATSDR.

Budavari S, O'Neil MJ, Smith A, Heckelman PE (Eds.).  1989.  The Merck 
Index, 11th ed.  Rahway, N.J.:  Merck & Co., Inc.

Clayton GD, Clayton FE.  1981-1982.  Patty's Industrial Hygiene and 
Toxicology, 3rd ed., Vol. 2C. New York:  John Wiley & Sons.

GENETOX. 1994. U.S. EPA GENETOX Program, computerized database. 

HSDB.  1994.  Hazardous Substances Data Bank.  MEDLARS Online Information 
Retrieval System, National Library of Medicine.

IARC. 1979-1994. International Agency for Research on Cancer.  IARC 
Monographs on the Evaluation of Carcinogenic Risk of Chemicals to Man. 
Lyon: IARC.

NIOSH (National Institute for Occupational Safety and Health).  1992.  
NIOSH Recommendations for Occupational Safety and Health.  Compendium of 
Policy Documents and Statements. Cincinnati, OH:  NIOSH.

NTP.  1994.  National Toxicology Program.  Toxicology and Carcinogenesis 
Studies.  Tech Rep Ser.

NTP.  1994.  National Toxicology Program.  Management Status Report.  
Produced from NTP Chemtrack system.  April 8, 1994.  National Toxicology 
Program, Research Triangle Park, NC.

OSHA.  1994.  Occupational Safety and Health Administration.  Table Z-2.  
Limits for Air Contaminants.

RTECS.  1994.  Registry of Toxic Effects of Chemical Substances.  MEDLARS 
Online Information Retrieval System, National Library of Medicine.

U.S. Air Force.  1989.  The Installation Restoration Toxicology Guide,
Vols. 
1-5.  Wright-Patterson Air Force Base, OH.

U.S. EPA (U.S. Environmental Protection Agency).  1991.  Table 302.4 List 
of Hazardous Substances and Reportable Quantities 40 CFR, part 302.4:3-271.

U.S. EPA.  Most current.  Drinking Water Regulations and Health Advisories. 

Office of Drinking Water, U.S. Environmental Protection Agency, Washington, 
D.C. 

U.S. EPA.  Most Current.  Health Effects Assessment Summary Tables.  
Cincinnati, OH: Environmental Criteria and Assessment Office, U.S.EPA.

U.S. EPA reviews such as Health and Environmental Effects Documents, 
Health and Enviornmental  Effect Profiles, and Health and Environmental 
Assessments.

U.S. EPA.  1994.  Integrated Risk Information System (IRIS) Online.  
Cincinnati, OH:  Office of Health and Environmental Assessment.