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Methylene chloride

1. NAME
   1.1 Substance
   1.2 Group
   1.3 Synonyms
   1.4 Identification numbers
      1.4.1 CAS
      1.4.2 Other numbers
   1.5 Main brand names/Trade names
   1.6 Main manufacturers, importers
2. SUMMARY
   2.1 Main risks and target organs
   2.2 Summary of clinical effects
   2.3 Diagnosis
   2.4 First-aid measures and management principles
3. PHYSICO-CHEMICAL PROPERTIES
   3.1 Origin of the substance
   3.2 Chemical structure
   3.3 Physical properties
      3.3.1 Colour
      3.3.2 State/form
      3.3.3 Description
   3.4 Other characteristics
4. USES/HIGH RISK CIRCUMSTANCES OF POISONING
   4.1 Uses
      4.1.1 Uses
      4.1.2 Description
   4.2 High risk circumstances of poisoning
   4.3 Occupationally exposed population
5. ROUTES OF ENTRY
   5.1 Oral
   5.2 Inhalation
   5.3 Dermal
   5.4 Eye
   5.5 Parenteral
   5.6 Others
6. KINETICS
   6.1 Absorption by route of exposure
   6.2 Distribution by route of exposure
   6.3 Biological half-life by route of exposure
   6.4 Metabolism
   6.5 Elimination by route of exposure
7. TOXICOLOGY
   7.1 Mode of action
   7.2 Toxicity
      7.2.1 Human data
         7.2.1.1 Adults
         7.2.1.2 Children
      7.2.2 Relevant animal data
      7.2.3 Relevant in vitro data
      7.2.4 Workplace standards
      7.2.5 Acceptable daily intake (ADI) and other guideline levels
   7.3 Carcinogenicity
   7.4 Teratogenicity
   7.5 Mutagenicity
   7.6 Interactions
8. TOXICOLOGICAL AND BIOMEDICAL INVESTIGATIONS
   8.1 Material
      8.1.1 Sampling
         8.1.1.1 Toxicological analyses
         8.1.1.2 Biomedical analyses
         8.1.1.3 Arterial blood gases
         8.1.1.4 Haematological investigations
      8.1.2 Storage
      8.1.3 Transport
   8.2 Toxicological analyses and their interpretation
      8.2.1 Tests for toxic ingredient
         8.2.1.1 Simple qualitative test
         8.2.1.2 Advanced qualitative test
         8.2.1.3 Simple quantitative method
         8.2.1.4 Advanced quantitative method
      8.2.2 Tests for biological samples
         8.2.2.1 Simple qualitative test
         8.2.2.2 Advanced qualitative test
         8.2.2.3 Simple quantitative method
         8.2.2.4 Advanced quantitative method
         8.2.2.5 Other dedicated methods
      8.2.3 Interpretation
   8.3 Biomedical investigations and their interpretation
      8.3.1 Biochemical analysis
         8.3.1.1 Blood
         8.3.1.2 Urine
         8.3.1.3 Other
      8.3.2 Arterial blood gas analyses
      8.3.3 Haematological analyses
   8.4 Other relevant biomedical investigations and their interpretation
   8.5 Overall interpretation
9. CLINICAL EFFECTS
   9.1 Acute poisoning by:
      9.1.1 Ingestion
      9.1.2 Inhalation
      9.1.3 Skin exposure
      9.1.4 Eye contact
      9.1.5 Parenteral exposure
      9.1.6 Other
   9.2 Chronic poisoning by:
      9.2.1 Ingestion
      9.2.2 Inhalation
      9.2.3 Skin exposure
      9.2.4 Eye contact
      9.2.5 Parenteral exposure
      9.2.6 Other
   9.3 Course, prognosis, cause of death
   9.4 Systematic description of clinical effects:
      9.4.1 Cardiovascular
      9.4.2 Respiratory
      9.4.3 Neurologic
         9.4.3.1 CNS
         9.4.3.2 Peripheral nervous system
         9.4.3.3 Autonomic nervous system
         9.4.3.4 Skeletal and smooth muscle
      9.4.4 Gastrointestinal
      9.4.5 Hepatic
      9.4.6 Urinary
         9.4.6.1 Renal
         9.4.6.2 Others
      9.4.7 Endocrine and reproductive systems
      9.4.8 Dermatologic
      9.4.9 Eye, ears, nose, throat; local effects
      9.4.10 Hematologic
      9.4.11 Immunological
      9.4.12 Metabolic
         9.4.12.1 Acid base disturbances
         9.4.12.2 Fluid and electrolyte disturbances
         9.4.12.3 Others
      9.4.13 Allergic reactions
      9.4.14 Other clinical effects
      9.4.15 Special risk
   9.5 Others
10. MANAGEMENT
   10.1 General principles
   10.2 Relevant laboratory analyses and other investigations
      10.2.1 Sample collection
      10.2.2 Biomedical analysis
      10.2.3 Toxicological analysis
      10.2.4 Other investigations
   10.3 Life supportive procedures and symptomatic treatment
   10.4 Decontamination
   10.5 Elimination
   10.6 Antidote treatment
      10.6.1 Adults
      10.6.2 Children
   10.7 Management discussion: alternatives, controversies and research needs
11. ILLUSTRATIVE CASES
   11.1 Case reports from literature
   11.2 Internally extracted data on cases
   11.3 Internal cases (added by the PC using monograph)
12. ADDITIONAL INFORMATION
   12.1 Availability of antidotes and antisera
   12.2 Specific preventive measures
   12.3 Other
13. REFERENCES
14. AUTHOR(S), REVIEWER(S) DATE (INCLUDING EACH UP-DATE), COMPLETE AUTHOR(S), ADDRESSES
    1.  NAME

        1.1  Substance

             Methylene chloride

        1.2  Group

             Halo-alkane
             alkyl halide
             alkyl chloride

        1.3  Synonyms

             dichloromethane
             methane dichloride
             methylene bichloride
             methylene chloride
             methylene dichloride
             dichlorethane (German)
             chlorure de methane (French)
             dichloromethane (French)
             dichlorometano (Italian)
             methyleenchloride (Dutch)
             metylenu chlorek (Polish)

        1.4  Identification numbers

             1.4.1  CAS

                    75-09-2

             1.4.2  Other numbers

                    UN       1593
                    RTECS    PA8050000
                    NCI      c50102
                    NIOSH    PA8050000

        1.5  Main brand names/Trade names

             Aerothene MM
             Freon  30
             Narkotill
             Solaesthin
             Solmethine

        1.6  Main manufacturers, importers

             To be added by the PCC using the monograph.

    2.  SUMMARY

        2.1  Main risks and target organs

             Methylene chloride is a highly volatile liquid. 
             Toxicity levels are time- and concentration-dependent.  Most
             poisonings are due to accidental inhalations causing headache
             and nausea; high concentrations depress the central nervous
             system, and fatalities have occurred.
             
             Methylene chloride is also an hepatotoxic agent.  Blood
             carboxyhaemoglobin levels become clinically significant at
             exposures around 500 ppm and may cause ischaemia and induce
             dysrhythmias in heart patients.  An additive effect occurs
             with other forms of carbon monoxide exposure  (e.g., from
             tobacco smoking, and exhaust systems in industry).
             
             Serious poisonings form methylene chloride exposure may occur
             without significant elevation of carboxyhaemoglobin
             levels.
             Absorption also occurs through the skin, but probably not in
             quantities sufficient to cause systemic toxicity.
             
             High vapour concentrations cause ocular pain.  Direct
             application to the eye can cause burning and temporary ocular
             damage.
             
             Ingestion is unusual.  A case study has indicated that rapid
             gut absorption occurs. A corrosive action has been observed
             on mucous membranes.
             
             Chronic inhalation exposure may result in neurological
             symptoms, including paraesthesiae, respiratory irritation and
             gastrointestinal disturbances.

        2.2  Summary of clinical effects

             Inhalation of the vapour may give rise to dizziness,
             nausea, tingling or numbness of the extremities; a sense of
             fullness in the head; a sense of heat; stupor or dullness;
             lethargy and drunkenness.  Very high concentrations may lead
             rapidly to unconsciousness, coma and death.
             
             High concentrations of vapour are irritant to the eyes. 
             Splash contacts cause an immediate burning sensation.
             
             The liquid is irritant to the skin and pain is associated
             with direct dermal application.  Second and third degree
             burns were experienced by a victim who lay comatose in
             methylene chloride for 30 minutes.

        2.3  Diagnosis

             Following serious methylene chloride exposures the
             following analyses are recommended:
             
             complete blood count
             hepatic aminotransferase levels
             creatinine levels
             urinanalysis including urine myoglobin
             blood carboxyhaemoglobin levels
             
             Serious poisonings from methylene chloride exposure may occur
             without significant elevation of carboxyhaemoglobin
             levels.
             
             Follow-up measurements of hepatic aminotransferase levels
             should be undertaken within one week of exposure.

        2.4  First-aid measures and management principles

             Inhalation:  Take proper precautions to ensure personal
             safety before attempting rescue (see Section 12.2). 
             Immediately remove the victim to fresh air.  If the victim is
             conscious, inquire immediately upon the circumstances of the
             poisoning, noting that the patient may become unconscious at
             any time.  Keep the victim at rest.  Physical activity will
             enhance total body distribution from increased blood flow. 
             Place in the recovery position and keep war.  Monitor
             respiration.  Obtain medical attention immediately.
             
             Ingestion:  Dilute with water.  (Milk is not indicated for
             dilution and may increase gut absorption of methylene
             chloride).  Induce emesis using syrup of ipecac but consider
             the risk of unconsciousness.  Obtain medical advice
             immediately.
             
             Eye contact:  Remove any contact lenses then flush the
             contaminated eyes gently with water for 10 to 15 minutes
             holding the eyelids open.  Obtain medical advice
             immediately.
             
             Skin contact:  Avoid direct contact with the chemical; wear
             impervious gloves if necessary.  Remove any contaminated
             clothing and other tight articles against the body.  Flush
             the contaminated area gently with water for 10 to 15 minutes. 
             Obtain medical attention immediately.

    3.  PHYSICO-CHEMICAL PROPERTIES

        3.1  Origin of the substance

             Methylene chloride is a synthetic halogenated
             hydrocarbon, commercially produced mainly by two methods:
             
             1.  Direct chlorination of methane (where the major product
                 methyl chloride is further chlorinated).
             
             2.  Catalytical hydrochlorination of methanol, in vapour or
                 liquid phase.
             
             (CEFIC, 1983)

        3.2  Chemical structure

             Structural formula  CH2Cl2
             
             Molecular weight  84.93  daltons.

        3.3  Physical properties

             3.3.1  Colour

                    Clear, colourless.

             3.3.2  State/form

                    Volatile liquid.

             3.3.3  Description

                    boiling point                   39.5 to 40.5 C
                    melting point                   -96.7 C
                    autoignition temperature        624 C
                    specific gravity                1.318 to 1.322
                    vapour density                  2.93 (air = 1.02)
                    vapour pressure                 46.5 kPa
                    refractive index                1.4327 (20 C)
                    percentage in "saturated" air   55% (25 C)
                    water solubility                2 g/100 mL
                    
                    Soluble in ethanol, ether and dimethylformamide.
                    
                    It has a sweetish chloroform-like odour above 300 ppm
                    which becomes unpleasant to most people at about 1000
                    ppm. At 2300 ppm it is strong and intensely irritating
                    (Clayton & Clayton 1981).
                    

                    Flammable regions may exist above -9 C.  Methylene
                    chloride is flammable at concentrations of 12 to 15%
                    in ambient air, but only with elevated temperature and
                    pressure, or in oxygen-enriched air
                    (Bretherick, 1981).
                    
                    conversion factors:  1 ppm in air  (3.5 mg/1000 L)
                                         [1 mg/1000 L = 0.29 ppm in air]

        3.4  Other characteristics

             Commercial grades of methylene chloride may contain
             0.0001 to 1% of added stabilisers, such as phenol,
             hydroquinone, p-cresol, resorcinol, thymol, 1-naphthol or
             amines (RSC/CEC, 1986).
             
             Although non-flammable, methylene chloride may, in the
             presence of heat and moisture, form hydrochloric acid, carbon
             dioxide, carbon monoxide, and phosgene.  Phosgene formed by
             thermal decomposition caused death when paint remover was
             used in a poorly ventilated area heated by a kerosene strove
             (CEFIC, 1983).
             
             Fire management:  Wear full protection clothing including
             self-contained breathing apparatus.  Use water spray to keep
             fire-exposed containers cool.
             
             Spill management:  For large spills, evacuate area.  Wear
             full protective clothing and self contained breathing
             apparatus.  Absorb spilled material onto sand and remove to
             lined drums for disposal.
             
             To dispose, send to licensed reclaimers or permitted
             incinerators.  Do not dump into sewers.  Compliance with
             local regulations must be ensured.

    4.  USES/HIGH RISK CIRCUMSTANCES OF POISONING

        4.1  Uses

             4.1.1  Uses

             4.1.2  Description

                    Methylene chloride has a variety of
                    applications based mainly on its high solvency power
                    and low boiling point.  Uses include:
                    
                    -   paint and varnish stripper formulations (retail
                        and trade)
                    -   extraction in food and pharmaceutical industries
                    -   as a solvent in aerosol formulations

                    -   process solvent in cellulose ester production, and
                        fibre and film forming
                    -   adhesive formulations
                    -   process solvent in polycarbonate production
                    -   plastic processing
                    -   extraction of fats and paraffins
                    -   metal and textile treatment
                    -   secondary blowing agent in flexible polyurethane
                        foams
                    -   registered insecticide (USA) for commodity
                        fumigation of various grains
                    -   fruit-ripening agent
                    -   refrigerant

        4.2  High risk circumstances of poisoning

             Small or enclosed areas which are poorly ventilated
             enable a build up of vapour concentration.
             
             In industry, impairment of "senses" in workers following
             inhalation of methylene chloride may cause "careless"
             accidents and injury.

        4.3  Occupationally exposed population

             Paint and varnish stripping operations (greater than 30%
             of total methylene chloride production is used in paint
             stripper formulations).
             
             Solvent workers and degreasers.

    5.  ROUTES OF ENTRY

        5.1  Oral

             Unlikely unless intentional harm or accidental splashing.

        5.2  Inhalation

             Most significant and frequent route of exposure and the
             primary concern with respect to toxicity.

        5.3  Dermal

             Limited absorption through intact skin occurs, but
             probably not in quantities sufficient to cause systemic
             toxicity.

        5.4  Eye

             Significant absorption unlikely - data unavailable.

        5.5  Parenteral

             No data available at time of preparation of monograph.

        5.6  Others

             No data available at time of preparation of monograph.

    6.  KINETICS

        6.1  Absorption by route of exposure

             Inhalation:  Most occupational exposures occur via the
             respiratory tract.  Of the inhaled amount, 55% is absorbed at
             rest, 40% with light work, and 25% with heavy physical work. 
             However, total net absorption is greater with work, due to an
             increased respiratory ventilation rate.
             
             Blood: air partition coefficient at 37 C  approx. 8 to 10
             Fat: air partition coefficient at 37 C    approx. 150 to 160
             
             Studies in man show that steady state is achieved rapidly
             after inhalation. This usually occurs in less than one hour,
             with no substantial increase after 7.5 hours.  In the 50 to
             500 ppm range, net values of 52 to 75% are absorbed at steady
             state (lower values at higher concentrations) (Illing &
             Shillaker, 1985).
             
             No differences have been noted between the sexes but net
             absorption is greater in obese individuals (Illing &
             Shillaker, 1985).
             
             An 8-hour exposure to 250 ppm increases the
             carboxyhaemoglobin level to greater than 8% (Ellenhorn &
             Barceloux, 1988).
             
             Dermal:  The degree of absorption is dependent on the type of
             skin, (thickness, vascularity, age), surface area, and
             duration of exposure.
             
             Immersion of only one thumb in methylene chloride for 30
             minutes produced a mean peak breath concentration of 3.1 ppm;
             by 2 hours post-exposure the mean value was 0.699 (Stewart &
             Dodd, 1964).
             

             Topical application of 99% pure methylene chloride on the
             mouse skin gave a rapid absorption rate compared to other
             halogenated hydrocarbons (Tsurata, 1975).  However, it is
             unlikely that toxic levels are attainable through dermal
             absorption of the hands and forearms in industry.  Dermal
             confinement may accentuate toxicity, e.g. by occlusion under
             "skin" formed by paint remover applications, or splashed
             articles of clothing.

        6.2  Distribution by route of exposure

             Although initial studies in humans suggested that
             methylene chloride may be stored in fat tissue, recent
             investigations have failed to detect significant retention in
             fat or other tissue stores (Ellenhorn & Barceloux,
             1988).

        6.3  Biological half-life by route of exposure

             The half-life of methylene chloride is dependent on the
             length of exposure and the time of sampling and so is
             variable.  However, the concentration in the expired breath
             approximately follows the blood concentration (Hearne et al.,
             1987).

        6.4  Metabolism

             The liver is the primary site of metabolism.
             
             Metabolic conversion to carbon monoxide occurs.  The half-
             life of carboxyhaemoglobin is almost twice that following an
             equivalent inhalation of carbon monoxide.  This is because
             hepatic biotransformation to carbon monoxide is dependent on
             the enzymatic metabolic rate (see Section 6.4), and the rate
             at which methylene chloride is released from tissue stores. 
             Consequently, carboxyhaemoglobin production may continue for
             several hours following cessation of exposure to methylene
             chloride (Hayes & Laws, 1991).  In one specific case, a 5-
             hour treatment with 100% oxygen was required to reduce blood
             carboxyhaemoglobin levels from 13% to 7.5%.
             
             Hepatic conversion occurs via two pathways (Hayes & Laws,
             1991):
             
             1.  Mixed functions oxidase system of cytochrome P450.  A
                 high affinity low capacity pathway, forming carbon
                 monoxide, carbon dioxide and chloride, via a
                 formylchloride intermediate.  This pathway is associated
                 with detoxification and is saturable at a few hundred
                 ppm.
             

             2.  Cytosolic transformation (glutathione transferase
                 dependent) where formaldehyde and formic acid
                 intermediates are produced.  This is a low affinity high
                 capacity system associated with intoxication which shows
                 no indication of saturation up to vapour concentrations
                 of 10,000 ppm.
             
             The extent to which each pathway contributes to total hepatic
             metabolism varies in humans, especially with exposure levels. 
             Thus, toxicity extrapolation between high and low doses is
             complex.

        6.5  Elimination by route of exposure

             Inhalation:  Methylene chloride and its metabolites are
             chiefly excreted via the lungs with small amounts appearing
             in the urine and bile (Illing & Shillaker, 1985).  Low doses
             of 14C-labelled methylene chloride were excreted mainly as
             14C-carbon monoxide (with 14C-carbon dioxide) whereas high
             concentrations were excreted in the expirate largely
             unchanged as 14C-methylene chloride.
             
             Dermal:  A thumb immersion experiment into 80 mL of methylene
             chloride for 30 minutes resulted in an expiratory
             concentration peaking at 2 to 3 ppm in less than 30 minutes. 
             This value decreased to 0.7 ppm after 2 hours (Stewart &
             Dodd, 1964).

    7.  TOXICOLOGY

        7.1  Mode of action

             Methylene chloride acts primarily as a CNS depressant,
             as do other halogenated hydrocarbons.  Its metabolites,
             chloride ion and carbon monoxide, respectively cause acidity
             and reduces the oxygen-carrying capacity in the blood
             (Dreisbach & Robertson, 1987).
             
             However, methylene chloride is the least toxic of the
             chloromethanes (Clayton & Clayton, 1981) and complete
             recovery has been attained in a significant number of cases. 
             Methylene chloride had been used as a general anaesthetic
             until fatalities occurred (Hayes & Laws, 1991).
             
             The metabolite, carbon monoxide, may increase the risk of
             death in people with compromised myocardial function (e.g.,
             angina), enhancing ischaemia and increasing the risk of
             arrhythmias.
             
             In fatal exposure in dogs, it was concluded that the fall in
             arterial blood pressure, rise in venous pressure, and the
             slowing of the heart were probably due to depression of the
             medullary centres and later depression of the cardiac muscle.

             Respiratory depression involved the medullary centres at
             first, but later there was a temporary hypoxic stimulation
             when circulatory failure was well advanced.  The heart
             usually stopped before respiration (Hayes & Laws,
             1991).

        7.2  Toxicity

             7.2.1  Human data

                    7.2.1.1  Adults

                             Exposure to approximately 1000 ppm
                             for several hours resulted in blood
                             carboxyhaemoglobin levels as high as 15%
                             (Hayes & Laws, 1991).
                             
                             In one case, exposure to 20,000 ppm for more
                             than 30 minutes resulted in coma (Ellenhorn &
                             Barceloux, 1988).
                             
                             The adult fatal dose by ingestion or
                             inhalation has been estimated to be 25 mL
                             (Dreisbach & Robertson, 1987).
    
                                                                         
    Vapour Conc.      Effect                     Exposure time
                                                                         
    300 ppm           odour threshold            no acute effects up
                      100 to 280 ppm             to 7.5 hours
    
    300 to 800 ppm    psychomotor/sensory
                      impaired                   40 min
    
    500 to 1000 ppm   light-headedness           1 to 2 hrs
    
    2300 ppm          irritation, dizziness      5 min
    
    2300 ppm          nausea                     30 min
    
    up to 5000 ppm    headache, fatigue,
                      irritation
    
    7200 ppm          paraesthesia, irritation   8 min
    
    8000 to
    20000 ppm         narcosis                   0.5 to 4 hrs
    
    50,000 ppm
    plus              immediate danger to
                      life or health
                                                                         
    

                    7.2.1.2  Children

                             No data available.

             7.2.2  Relevant animal data

                    Inhaled
                    
                    Rat      LCLO = 88000/m3/30 minutes
                    Dog      LCLO = 14108 ppm/7 hours
                    Rabbit   LCLO = 10000 ppm/7 hours
                    Mouse    LCLO = 14400 ppm/7 hours
                    
                    Subcutaneous
                    
                    Dog      LDLO = 2700 mg/kg
                    Rabbit   LD50 = 2700 mg/kg
                    Mouse    LDLO = 6460 mg/kg
                    
                    Oral
                    
                    Rat      LD50 = 2136 mg/kg
                    Dog      LDLO = 3000 mg/kg
                    Rabbit   LDLO = 1900 mg/kg
                    
                    (RTECS, 1987)

             7.2.3  Relevant in vitro data

                    No data available.

             7.2.4  Workplace standards

                    Currently, the limit in Britain is 100 ppm for
                    long term exposures and 250 ppm for short term
                    exposure (Reynolds, 1989).
                    
                    The Occupational Safety and Health Administration
                    (OSHA) established an 8-hour TWA of 500 ppm to prevent
                    acute narcosis and liver injury.  In 1976 the National
                    Institute for Occupational Safety and Health (NIOSH)
                    recommended a TLV of 75 ppm due to the unacceptable
                    carboxyhaemoglobin level of 5% following exposure
                    during an 8 hour work shift.
                    
                    Exposure at the ACGIH level (100 ppm) would permit
                    occupational exposure at the rate of 50 mg/kg/day. 
                    The ACGIH has proposed lowering the current threshold
                    limit to 50 ppm because of possible tumorigenicity in
                    animals (Hayes & Laws, 1991).

             7.2.5  Acceptable daily intake (ADI) and other guideline
                    levels

                    No value has been established.
                    
                    The Food and Drug Administration (USA) has permitted:
                    
                    10 ppm residual in decaffeinated coffee;
                    no greater than 2.2% in hops extract;
                    no greater than 30 mg/kg spice oleoresins as a residue
                    after spice extraction; but it has banned its use as
                    an ingredient in cosmetics (RSC/CEC, 1986).

        7.3  Carcinogenicity

             Methylene chloride has been reported to produce benign
             mammary tumours and malignant liver and lung neoplasms in
             several animal species.  From this evidence the US
             Environmental Protection Agency considers methylene chloride
             a possible human carcinogen, although significant variation
             in metabolic pathways may exist between the species.
             
             Methylene chloride does not appear to be directly genotoxic
              in vivo, but it does produce altered homeoestasis in the
             lung and liver of mice (tissues susceptible to tumour
             development) and it is therefore probable that methylene
             chloride does affect a later stage of the tumorigenic
             process.  However, a review of the mechanistic and
             pharmacokinetics data for methylene chloride indicate a very
             low likelihood that this material is a carcinogen in humans
             (Hayes & Laws, 1991).
             
             A long term epidemiologic study (1964 to 1984) of chronic
             methylene chloride exposure to workers in a Kodak
             photographic plant, reported no statistically significant
             increase in deaths from lung and liver cancer.  An increase
             in pancreatic deaths was noted (8 compared to an expected
             value of 3.1).  However, this has been disputed by the
             National Toxicological Program (USA) (Hearne et al.,,
             1990).
             
             Excess liver and biliary tract cancer deaths were reported in
             an epidemiological study of workers exposed to methylene
             chloride in a fibre production plant.  However, the data were
             inadequate to draw firm conclusions (RSC/CEC, 1986).

        7.4  Teratogenicity

             No teratogenic effects were found in pregnant rats
             exposed to 4500 ppm vapour during gestation (Hayes & Laws,
             1991).
             
             Schwetz et al., (1975)  exposed to pregnant mice and rats to
             methylene chloride vapour in concentrations which were twice
             the maximum allowable limit for human industrial exposure
             (1225 ppm).  Both species were exposed for 7 hour periods
             daily, on days 6 through 15 of gestation.  No foetal toxicity
             or teratogenicity was found.
             
             Poisoning from a metabolite of methylene chloride, carbon
             monoxide, in pregnancy can result in foetal and infant death
             or severe neurological impairment in the off-spring (Koren,
             1990).

        7.5  Mutagenicity

             There is no significant evidence that methylene chloride
             is a mutagen.  No unscheduled DNA synthesis occurred in V79
             cells or primary human fibroblasts.  A higher percentage of
             mutations in the Drosophila did not occur (CEFIC, 1983).  No
             increase in cytogenic aberrations of rat bone marrow cells
             were noted following 6 months repeated exposure to 500, 1500
             or 3500 ppm (Clayton & Clayton, 1981).

        7.6  Interactions

             Methylene chloride is often formulated with other
             contaminants.  These other substances may enhance or reduce
             its toxic effects (see Section 3.4).
             
             Since methylene chloride elevates carboxyhaemoglobin levels,
             symptoms of carbon monoxide poisoning may occur, especially
             in patients with cardiopulmonary disease or workers who are
             exposed to other sources of carbon monoxide (Ellenhorn &
             Barceloux, 1988).

    8.  TOXICOLOGICAL AND BIOMEDICAL INVESTIGATIONS

        Exposure measurements include blood methylene chloride and
        carboxyhaemoglobin levels in addition to air sampling.  For
        average sedentary, non-smoking workers, maximum allowable
        exposures (200 ppm) produce methylene chloride levels of 80 ppm in
        expired air and 0.18 mg/100 ml in blood, and carboxyhaemoglobin
        levels of 6.8% (Ellenhorn & Barceloux, 1988).

        8.1  Material

             8.1.1  Sampling

                    No data available.

                    8.1.1.1  Toxicological analyses

                    8.1.1.2  Biomedical analyses

                    8.1.1.3  Arterial blood gases

                    8.1.1.4  Haematological investigations

             8.1.2  Storage

                    No data available.

             8.1.3  Transport

                    No data available.

        8.2  Toxicological analyses and their interpretation

             8.2.1  Tests for toxic ingredient

                    No data available.

                    8.2.1.1  Simple qualitative test

                    8.2.1.2  Advanced qualitative test

                    8.2.1.3  Simple quantitative method

                    8.2.1.4  Advanced quantitative method

             8.2.2  Tests for biological samples

                    8.2.2.1  Simple qualitative test

                    8.2.2.2  Advanced qualitative test

                    8.2.2.3  Simple quantitative method

                    8.2.2.4  Advanced quantitative method

                    8.2.2.5  Other dedicated methods

                             No data available.

             8.2.3  Interpretation

        8.3  Biomedical investigations and their interpretation

             8.3.1   Biochemical analysis

                    8.3.1.1  Blood

                             After serious methylene chloride
                             exposures the following analyses are
                             recommended:
                             
                             1.  complete blood count
                             2.  hepatic amino transferase levels
                             3.  creatinine levels
                             4.  blood carboxyhaemoglobin levels
                             
                             Serious poisonings from methylene chloride
                             exposure may occur without significant
                             elevation of carboxyhaemoglobin levels.
                             
                             Follow-up measurements of hepatic amino-
                             transferase levels should be undertaken
                             within one week of exposure.
                             
                             (Ellenhorn & Barceloux, 1988)

                    8.3.1.2  Urine

                             After serious methylene chloride
                             exposures urinanalysis including urine
                             myoglobin should be undertaken (Ellenhorn &
                             Barceloux, 1988).  Haemoglobin products in
                             urine indicate intravascular haemolysis
                             (Dreisbach & Robertson, 1987).

                    8.3.1.3  Other

                             Blood in the stools will indicate
                             gastrointestinal injury (Dreisbach &
                             Robertson, 1987).
                             
                             Radiographic examination will reveal the
                             extent of ulceration of the duodenum and
                             jejunum after ingestion (Dreisbach &
                             Robertson, 1987).

             8.3.2  Arterial blood gas analyses

                    No data available.

             8.3.3  Haematological analyses

                    No data available.

        8.4  Other relevant biomedical investigations and their
             interpretation

             No data available.

        8.5  Overall interpretation

             No data available.

    9.  CLINICAL EFFECTS

        9.1  Acute poisoning by:

             9.1.1  Ingestion

                    Methylene chloride is a potent irritant of
                    mucous membranes.  Rapid gut absorption has been
                    indicated, with resulting anaesthetic deaths in
                    laboratory animals (Clayton & Clayton, 1981).
                    
                    An ingestion of 0.5 to 1 L of paint remover, mostly
                    consisting of methylene chloride, resulted in coma,
                    intravascular haemolysis and, later jejunal ulceration
                    and diverticular formation (Reynolds, 1989).
                    
                    Narrowing of the intestinal lumen may occur as a
                    result of erosions.  Pharyngeal erosions may disturb
                    the swallowing mechanism, resulting in aspiration
                    pneumonia (Dreisbach & Robertson, 1987).

             9.1.2  Inhalation

                    Concentrations of 1,000 ppm produce
                    lightheadedness and alterations in visual reflexes. 
                    Exposures greater than 2,000 ppm have resulted in
                    nausea and lassitude after 30 min.  At levels between
                    7,000 and 10,000 ppm, paraesthesiae and eye irritation
                    occur.  In one case, a concentration greater than
                    20,000 ppm led to coma.  Methylene chloride may
                    produce pulmonary oedema by a direct toxic effect
                    (Ellenhorn & Barceloux, 1988).
                    
                    Paraesthesia occurred in the extremities within 8
                    minutes at 7,200 ppm; pulse acceleration to 100/min
                    occurred after 16 minutes.  Within the first 20
                    minutes, congestion of the head, slight eye
                    irritation, and a sense of heat was experienced.  At
                    2,300 ppm, nausea occurred within 30 minutes, however
                    there was no feeling of dizziness after one hour of
                    exposure.  Experiments have shown that exposure to
                    25,000 ppm  for two hours is not lethal (Sax,
                    1984).
                    

                    CEFIC (1983) notes that narcotic effects occur at
                    1,000 ppm and higher, and pre-narcotic actions,
                    anaesthetic-like effects, headache and irritation to
                    the eyes occur at vapour concentrations greater than
                    500 ppm.  Significant CNS effects occur at exposures
                    of 300, 500 and 800 ppm (Illing & Shillaker,
                    1985).
                    
                    Most symptoms subside with discontinued exposure,
                    although respiration and circulation should still be
                    monitored in severe poisonings (Von Oettingen,
                    1955).
                    
                    CEFIC (1983) records that phosgene formed by thermal
                    decomposition caused death when paint remover was used
                    in a poorly ventilated area heated by a kerosene
                    stove.

             9.1.3  Skin exposure

                    CEFIC (1983) reports skin absorption, but not
                    in  amounts sufficient to cause adverse systemic
                    effects.  Methylene chloride also has a defatting
                    action on the skin.
                    
                    NBOSH (1981), however, state that under certain
                    conditions skin uptake may significantly contribute to
                    toxicity.
                    
                    Methylene chloride, both as a liquid and a vapour, is
                    a potent cutaneous and mucous membrane irritant
                    (Ellenhorn & Barceloux, 1988).  Significant pain, then
                    pain and numbness followed by burns were experienced
                    after immersion. Second and third degree burns were
                    experienced by a victim who lay comatose in methylene
                    chloride for 30 minutes (Ellenhorn & Barceloux,
                    1988).

             9.1.4  Eye contact

                    High vapour concentrations can cause ocular
                    pain (CEFIC, 1983), and psychological tests of visual-
                    motor performance and critical flicker frequency
                    showed some impairment of performance (Grant,
                    1986).
                    
                    Splash contacts cause an immediate burning sensation
                    which subsides in 15 to 20 minutes after flushing the
                    eye with water  Generally there is not persistent
                    damage (Grant, 1986).

             9.1.5  Parenteral exposure

                    No data available.

             9.1.6  Other

                    No data available.

        9.2  Chronic poisoning by:

             Long-term exposure to methylene chloride causes damage
             to the CNS and the liver (IARC, 1979).

             9.2.1  Ingestion

                    Not applicable.

             9.2.2  Inhalation

                    IARC (1979) state that long term occupational
                    exposure damages the CNS and liver.  However, there is
                    no evidence that this increases mortality.
                    
                    ACGIH (1980) reports that a 1 year exposure to
                    methylene chloride caused the development of
                    encephalosis, acoustic and optical delusions, and
                    hallucinations in a chemist.  Concentrations
                    frequently exceeded 500 ppm, and were measured at 660,
                    800 and 3,600 ppm near the floor.  Liver disease has
                    been noted in workers exposed to methylene
                    chloride.
                    
                    A case of dementia was attributed to 20-year
                    occupational exposure to 500 to 1,000 ppm methylene
                    chloride (Ellenhorn & Barceloux, 1988).

             9.2.3  Skin exposure

                    Skin may become rough and dry with prolonged
                    and repeated contact, and therefore susceptible to
                    infection and irritation.  Erythema and scaling may
                    occur.
                    
                    Methylene chloride can be absorbed by intact skin, but
                    probably not in quantities sufficient to cause
                    systemic toxicity (Stewart & Dodd, 1964).

             9.2.4  Eye contact

                    Chronic exposure is unlikely due to its acute
                    irritant properties (see Section 9.1.4).

             9.2.5  Parenteral exposure

                    No data available.

             9.2.6  Other

                    No data available.

        9.3  Course, prognosis, cause of death

             The predominant effects of methylene chloride are due to
             its narcotic properties.  Depending on exposure and
             concentration, symptoms vary from light headedness to stupor,
             irritability, drunkenness and gait disturbances.  Eventually,
             unconsciousness and lack of response to painful stimuli
             result, then coma and death.
             
             Respiration initially increases, but is then slowed. 
             Pulmonary oedema may occur.

        9.4  Systematic description of clinical effects:

             9.4.1  Cardiovascular

                    Cardiac function of 24 healthy workers
                    chronically exposed to methylene chloride at
                    concentrations of 60 to 475 ppm was monitored by ECG. 
                    No increase in ventricular and supraventricular
                    ectopic activity, or episodic depression of the ST
                    segment occurred.  Furthermore, no evidence of ECG
                    abnormalities or cardiac sensitization to adrenaline
                    have been noted in healthy subjects rendered
                    unconscious by acute exposure.
                    
                    Increased carboxyhaemoglobin levels from methylene
                    chloride metabolism will reduce the oxygen content of
                    blood perfusing the myocardium.  Arrhythmias may occur
                    in patients already suffering from cardiovascular
                    stress (angina/coronary artery disease) where
                    carboxyhaemoglobin levels of 2 to 3% saturation can
                    adversely affect such individuals.
                    
                    Carboxyhaemoglobin levels reach up to 5% in normal
                    smokers and 12% in heavy smokers.  Following 500 ppm
                    exposures of methylene chloride, smokers can reach
                    carboxyhaemoglobin levels of 15% and more.  These
                    levels, however, are non-hazardous in healthy
                    individuals (Rosenberg & Hathaway, 1990).

             9.4.2  Respiratory

                    Pulmonary oedema may occur from acute
                    exposures.  Phosgene produced from the combustion of
                    methylene chloride may cause a delayed toxicity to the
                    lung (Ellenhorn & Barceloux, 1988).

             9.4.3  Neurologic

                    The predominant effects are due to CNS
                    depression. Depending on exposure and concentration,
                    symptoms vary from light headedness, nausea, headache,
                    concentration and co-ordination impairment to stupor,
                    irritability, drunkenness and gait disturbances. 
                    Eventually, unconsciousness and lack of response to
                    painful stimuli result, then coma and death (Ellenhorn
                    & Barceloux, 1988).
                    
                    No evidence of long-term damage could be attributed to
                    methylene chloride inhaled at levels of < 100 ppm and
                    evaluation of motor conduction velocities of ulnar and
                    median nerves, ECG, or psychological tests designed to
                    detect minimal brain damage (Hayes & Laws,
                    1991).

                    9.4.3.1  CNS

                             Encephalopathy has occurred after
                             repeated exposure to 500 ppm levels
                             (Dreisbach & Robertson, 1987).

                    9.4.3.2  Peripheral nervous system

                             Generalized neural depression occurs.

                    9.4.3.3  Autonomic nervous system

                             Generalized neural depression occurs.

                    9.4.3.4  Skeletal and smooth muscle

                             No data available.

             9.4.4  Gastrointestinal

                    Ingestion has resulted in jejunal ulceration
                    and diverticular formation from which strictures may
                    develop.  Methylene chloride is a potent irritant of
                    mucous membranes (Roberts & Marshall, 1976).

             9.4.5  Hepatic

                    Although methylene chloride is a weak
                    hepatotoxin in animals there is no firm link to
                    chronic liver disease in industrial workers.  Raised
                    serum concentrations of alanine aminotransferase
                    levels (not aspartate) developed 1 week after exposure
                    and resolved the following week (Ellenhorn &
                    Barceloux, 1988).

             9.4.6  Urinary

                    9.4.6.1  Renal

                             A previously healthy man exposed to
                             methylene chloride vapour developed
                             myoglobinuria and acute tubular necrosis
                             leading to renal failure (Ellenhorn &
                             Barceloux, 1988).
                             
                             Intravascular haemolysis has lead to gross
                             haematuria.  Haemoglobinuria and increase in
                             carboxyhaemoglobin levels in rats have been
                             noted (Illing & Shillaker, 1985).

                    9.4.6.2  Others

                             No data available.

             9.4.7  Endocrine and reproductive systems

                    Methylene chloride has been reported to produce
                    benign mammary tumours in experimental animals, but
                    has not been reported in humans.  However, methylene
                    chloride can enter breast milk and the foetus through
                    the placenta, like many other organic solvents
                    (Rosenberg & Hathaway, 1990).
                    
                    Exposure of rats to inhaled concentrations of
                    methylene chloride as high as 1500 ppm for 6 hours/day
                    did not affect any reproductive parameters over two
                    generations (Hayes & Laws, 1991).

             9.4.8  Dermatologic

                    Methylene chloride can cause burns, and elicit
                    a defatting action on the skin.  Erythema and scaling
                    have been noted.

             9.4.9  Eye, ears, nose, throat; local effects

                    High vapour concentrations can cause ocular
                    pain (CEFIC 1983), and psychological tests of visual-
                    motor performance and critical flicker frequency
                    showed some impairment of performance (Grant,
                    1986).
                    
                    Splash contacts cause an immediate burning sensation
                    which subsides in 15-20 minutes after flushing the eye
                    with water.  Generally there is no persistent damage
                    (Grant, 1986).

             9.4.10 Hematologic

                    Victims of an industrial accident involving
                    excessive inhalation of methylene chloride had
                    moderate leukocytosis and moderate depression of red
                    cell count and haemoglobin level (Hayes & Laws,
                    1991).

             9.4.11 Immunological

                    No data available.

             9.4.12 Metabolic

                    9.4.12.1 Acid base disturbances

                             Hepatic biotransformation forms
                             chloride ions, which in turn induce
                             acidosis.

                    9.4.12.2 Fluid and electrolyte disturbances

                             Lung oedema may result from a
                             direct toxic effect on the lungs (Ellenhorn &
                             Barceloux, 1988).

                    9.4.12.3 Others

                             No data available.

             9.4.13 Allergic reactions

                    No data available.

             9.4.14 Other clinical effects

                    No data available.

             9.4.15 Special risk

                    In glueing operatives, methylene chloride was
                    found to cross the placenta and occur in breast milk
                    (Barlow & Sullivan, 1982).  Chlorinated hydrocarbons
                    were found in breast milk up to 17 hours post
                    exposure.
                    
                    Maternal carbon monoxide levels in the blood from
                    methylene chloride metabolism may lead to foetal and
                    infant death or severe neurological impairment in the
                    off-spring (Koren, 1990).
                    
                    Since methylene chloride elevates carboxyhaemoglobin
                    levels, symptoms of carbon monoxide poisoning may
                    occur, especially in patients with cardiopulmonary
                    disease or workers who are exposed to other carbon
                    monoxide sources (Ellenhorn & Barceloux,
                    1988).

        9.5  Others

             No data available.

    10. MANAGEMENT

        10.1 General principles

             Initial attention should be directed toward removal
             from exposure, supportive respiration and monitoring for
             dysrhythmias.
             
             Oxygen is the primary therapy for reduction of
             carboxyhaemoglobin levels. Levels may continue to rise 5 to 6
             hours following acute exposure, in which peak values of
             approximately 25% have generally been reported. The
             carboxyhaemoglobin half-life in room air is approximately 5.3
             hours.  This may be reduced to 60 to 90 minutes with 100%
             oxygen, and in more severe cases 20 to 40 minutes following
             hyperbaric oxygen treatment.  Monitoring heart function for
             dysrhythmias is indicated.
             
             Hyperbaric oxygen has been used successfully to treat carbon
             monoxide poisoning following inhalation of methylene chloride
             (Rudge, 1990).
             
             Baseline liver function tests with periodic monitoring will
             detect possible hepatic toxicity (Ellenhorn & Barceloux,
             1988).
             
             Steroids have been recommended (Dreisbach & Robertson, 1987).

        10.2 Relevant laboratory analyses and other investigations

             10.2.1 Sample collection

                    Methylene chloride can be detected in exhaled
                    air several hours post exposure.  Inhalation of 200
                    ppm in ambient air will result in expiratory
                    concentrations of around 80 ppm, and exhaled air will
                    generally reflect ambient levels up to about 500 ppm. 
                    Methylene chloride can be directly measured in the
                    blood shortly after exposure.  25-90% of the absorbed
                    methylene chloride is eliminated within 2 hours post-
                    exposure.  After 16 hours, none will be detected in
                    the blood.
                    
                    Metabolic production of carbon monoxide will only be
                    detected in the blood about 30 minutes after exposure
                    in non-smokers.

             10.2.2 Biomedical analysis

                    A variety of tests may be employed to monitor
                    chronically exposed individuals for methylene chloride
                    poisoning, e.g.
                    
                    carboxyhaemoglobin level:
                    arterial blood gas
                    hepatic enzyme levels
                    urinalysis
                    serial ECGs.

             10.2.3 Toxicological analysis

                    Exposure measurements include blood methylene
                    chloride and carboxyhaemoglobin levels as well as air
                    sampling.  For average sedentary, non-smoking workers,
                    maximum allowable exposures (200 ppm) produce
                    methylene chloride levels of 80 ppm in expired air and
                    0.18 mg/100 mL in blood, and carboxyhaemoglobin levels
                    of 6.8% (Ellenhorn & Barceloux, 1988).
                    
                    Methylene chloride concentrations following fatal
                    inhalation after home use of a paint remover were:
                    
                             510 mg/L in blood
                             248 mg/kg in brain
                             144 mg/kg in liver
                    
                    The blood carboxyhaemoglobin concentration was 3%
                    (Baselt, 1982).

             10.2.4 Other investigations

                    No data available.

        10.3 Life supportive procedures and symptomatic treatment

             Immediately remove the victim to fresh air.  If the
             victim is conscious, inquire immediately upon the
             circumstances of the poisoning, noting that the patient may
             become unconscious at any time.  Keep the victim at rest.
             Physical activity will enhance total body distribution from
             increased blood flow.  Place in the recovery position and
             keep warm.  Monitor respiration.  Positive pressure 100%
             oxygen will help reduce blood carboxyhaemoglobin levels. 
             This may take several hours.  This is an important factor if
             cardiac function is already compromised (e.g., patients with
             angina pectoris).  Monitor for dysrhythmias.
             
             Further treatment is symptomatic.  Monitor for possible
             haemolytic reaction.  Administer hydrocortisone
             intravenously, 200 mg every hour.  Treat aspiration pneumonia
             with antibiotics.  Blood transfusions may be necessary if
             gastric bleeding is excessive.  Treat acidosis and pulmonary
             oedema (Dreisbach & Robertson, 1987).

        10.4 Decontamination

             Ingestion:  Milk is not indicated for dilution and may
             increase gut absorption of methylene chloride.
             
             Eye contact:  Remove any contact lenses then flush the
             contaminated eyes gently with water for 10 to 15 minutes
             holding the eyelids open.  Corneal application of fluorescein
             will display evidence of abrasion.
             
             Skin contact:  Avoid direct contact with the chemical; wear
             impervious gloves if necessary.  Remove any contaminated
             clothing and other tight articles against the body.  Flush
             the contaminated area gently with water for 10 to 15
             minutes.
             
             Ingested methylene chloride may be removed by emesis
             (consider whether there is a risk of impending
             unconsciousness) and/or gastric lavage, and activated
             charcoal.  However, the efficacy of such treatment is not
             known (Ellenhorn & Barceloux, 1988).

        10.5 Elimination

             No methods are available to enhance elimination from
             inhalations.

        10.6 Antidote treatment

             10.6.1 Adults

                    No specific antidote.

             10.6.2 Children

                    No specific antidote.

        10.7 Management discussion:  alternatives, controversies and
             research needs

             In Case 3 (see Section 11.1) where a victim ingested
             0.5  to 1 L of paint remover, recovery was fast and induction
             of diuresis was believed to play an important role in the
             prevention of acute renal damage (Roberts & Marshall,
             1976).
             
             Ingested methylene chloride may be removed by emesis and/or
             gastric lavage, and activated charcoal.  However, the
             efficacy of such treatment is not known and therefore should
             be investigated (Ellenhorn & Barceloux, 1988).

    11. ILLUSTRATIVE CASES

        11.1 Case reports from literature

             Case 1    Industrial inhalation, adults (Hayes & Laws, 1991)
             
             Four night-shift workers extracting plant oleoresin using
             methylene chloride in a room were found unconscious at
             7:15 am.  One worker died when the ambulance arrived.  The
             others had been unconscious for up to 3 hours, and were semi-
             conscious or drowsy on arrival at the hospital at 7:30 am. 
             They were fully conscious by 10:00 am, and had no memory of
             smelling methylene chloride.  All survivors were coughing
             when they reached the hospital, but rales and respiratory
             irritation were detected in only two.  Some had a slight
             fever for a day or two, and one complained of eye irritation. 
             All had moderate leukocytosis, and moderate depression of red
             cell counts and haemoglobin level.  They were discharged
             after 4 to 8 days.
             
             Analysis of the lungs of the man found dead revealed a
             concentration of 265 ppm.
             
             Case 2    Occupational inhalation, adults (Hayes & Laws,
             1991)
             
             Two painters experienced headache, faintness, giddiness,
             irritability, numbness and tingling of the extremities, loss
             of appetite, and apathy when they used methylene chloride to
             remove paint from the walls of a large closed room.
             
             Case 3    Deliberate ingestion, adult (Roberts & Marshal,
             1976)
             
             A 38-year-old man drank 0.5 to 1 L of a paint remover
             containing methylene chloride as the active ingredient, and
             was deeply unconscious and unresponsive to painful stimuli 90
             minutes later.  Areas of skin where liquid had spilled from
             his mouth were erythematous and blistered.
             
             He was tachypnoeic but his pulse and blood pressure were
             well-maintained.  Gross haemoglobinuria and metabolic
             acidosis were present.  Diuresis was promoted with 80 mg
             frusemide with 0.9% sodium chloride and 5% dextrose
             alternately.  During the first 24 hours the patient passed 18
             L of urine and the haemoglobinuria ceased.
             
             The patient regained consciousness 15 hours after the
             incident, with no detectable cerebral damage.  A later effect
             was the development of jejunal ulceration requiring blood
             transfusions and, 6 months after the incident, diverticula. 
             There was no hepatic damage and no evidence of cardiac
             toxicity.  Acute renal damage was apparently averted by the
             early induction of diuresis.
             
             Case 4    Eye contact, adult (Grant, 1986)
             
             A man splashed his eye with a paint-remover containing
             methanol and propylene dichloride in addition to methylene
             chloride.  He flushed his eye with water immediately, but
             lost about 20% of his corneal epithelium.  The eye healed
             completely in two days.
             
             Case 5    Eye contact, child (Grant, 1986)
             
             A boy had methylene chloride splashed in his eyes from an
             exploding bubbling-type christmas-tree ornament.  There were
             cells in the anterior chambers which, following treatment
             with corticosteroid eye drops, cleared in six weeks.

        11.2 Internally extracted data on cases

             No case histories available.

        11.3 Internal cases (added by the PC using monograph)

    12. ADDITIONAL INFORMATION

        12.1 Availability of antidotes and antisera

             Not applicable.

        12.2 Specific preventive measures

             An approved air purifying respirator will provide
             protection at excess atmospheric levels.  Use should only be
             of single short term exposures, as their effectiveness is
             limited.
             
             If TLV guidelines are greatly exceeded, approved positive
             pressure self-contained breathing apparatus should be
             used.
             
             For prolonged or frequent contact, impervious protective
             clothing should be used.  Chemical goggles are recommended,
             but full face respirators must be used if vapours cause
             ocular pain.

        12.3 Other

             No data available.

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        rat skin. Industrial Medicine 15(3-4):131-139.
        
        Von Oettingen WF (1955)  The halogenated aliphatic, olefinic,
        cyclic, aromativ, & aliphatic-aromatic hydrocarbons including the
        halogenated insecticides.  Their toxicity and potential dangers. 
        Public Health Service Bulletin, No. 414 USA Department of Health,
        Education and Welfare.

    14.  AUTHOR(S), REVIEWER(S) DATE (INCLUDING EACH UP-DATE), COMPLETE
         AUTHOR(S), ADDRESSES

        Author:     Dr A.W Temple
                    National Toxicology Group
                    University of Otago Medical School
                    P.O. Box 913
                    Dunedin
                    New Zealand
        
                    Tel:     64-3-4797244
                    Fax:     64-3-4770509
        
        Date:                January 1992
        

        Peer Review:         Newcastle-upon-Tyne, United Kingdom, February
                             1992
        
        Editor:              M.Ruse
        
        Finalised:  IPCS, April 1997

    



    See Also:
       Toxicological Abbreviations
       Methylene chloride (EHC 164, 1996, 2nd edition)
       Methylene chloride (EHC 32, 1984, 1st edition)
       Methylene chloride (HSG 6, 1987)