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Vinyl chloride

1. NAME
   1.1 Substance
   1.2 Group
   1.3 Synonyms
   1.4 Identification numbers
      1.4.1 CAS number
      1.4.2 Other numbers
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 Hazardous characteristics
4. USES/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 populations
5. ROUTES OF EXPOSURE
   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
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
   7.3 Carcinogenicity
   7.4 Teratogenicity
   7.5 Mutagenicity
   7.6 Interactions
8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS
   8.1 Material sampling plan
      8.1.1 Sampling and specimen collection
         8.1.1.1 Toxicological analyses
         8.1.1.2 Biomedical analyses
         8.1.1.3 Arterial blood gas analysis
         8.1.1.4 Haematological analyses
         8.1.1.5 Other (unspecified) analyses
      8.1.2 Storage of laboratory samples and specimens
         8.1.2.1 Toxicological analyses
         8.1.2.2 Biomedical analyses
         8.1.2.3 Arterial blood gas analysis
         8.1.2.4 Haematological analyses
         8.1.2.5 Other (unspecified) analyses
      8.1.3 Transport of laboratory samples and specimens
         8.1.3.1 Toxicological analyses
         8.1.3.2 Biomedical analyses
         8.1.3.3 Arterial blood gas analysis
         8.1.3.4 Haematological analyses
         8.1.3.5 Other (unspecified) analyses
   8.2 Toxicological Analyses and Their Interpretation
      8.2.1 Tests on toxic ingredient(s) of material
         8.2.1.1 Simple Qualitative Test(s)
         8.2.1.2 Advanced Qualitative Confirmation Test(s)
         8.2.1.3 Simple Quantitative Method(s)
         8.2.1.4 Advanced Quantitative Method(s)
      8.2.2 Tests for biological specimens
         8.2.2.1 Simple Qualitative Test(s)
         8.2.2.2 Advanced Qualitative Confirmation Test(s)
         8.2.2.3 Simple Quantitative Method(s)
         8.2.2.4 Advanced Quantitative Method(s)
         8.2.2.5 Other Dedicated Method(s)
      8.2.3 Interpretation of toxicological analyses
   8.3 Biomedical investigations and their interpretation
      8.3.1 Biochemical analysis
         8.3.1.1 Blood, plasma or serum
         8.3.1.2 Urine
         8.3.1.3 Other fluids
      8.3.2 Arterial blood gas analyses
      8.3.3 Haematological analyses
      8.3.4 Interpretation of biomedical investigations
   8.4 Other biomedical (diagnostic) investigations and their interpretation
   8.5 Overall interpretation of all toxicological analyses and toxicological investigations.
   8.6 References
9. CLINICAL EFFECTS
   9.1 Acute poisoning
      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
      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 Central Nervous System (CNS)
         9.4.3.2 Peripheral nervous system
      9.4.4 Gastrointestinal
      9.4.5 Hepatic
      9.4.6 Urinary
      9.4.7 Endocrine and reproductive systems
      9.4.8 Dermatological
      9.4.9 Eyes, ears, nose, throat: local effects
      9.4.10 Haematological
      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 Other
      9.4.13 Allergic
      9.4.14 Other clinical effects
      9.4.15 Special risks
   9.5 Others
   9.6 Summary
10. MANAGEMENT
   10.1 General principles
   10.2 Life supportive procedures and symptomatic treatment
   10.3 Decontamination
   10.4 Enhanced elimination
   10.5 Antidote treatment
      10.5.1 Adults
      10.5.2 Children
   10.6 Management discussion
11. ILLUSTRATIVE CASES
   11.1 Case reports from literature
12. ADDITIONAL INFORMATION
   12.1 Specific preventive measures
   12.2 Other
13. REFERENCES
14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE ADDRESSES
    VINYL CHLORIDE

    International Programme on Chemical Safety
    Poisons Information Monograph 558
    Chemical

    1.  NAME

        1.1  Substance

             Vinyl chloride

        1.2  Group

             Halogenated aliphatic hydrocarbon.

        1.3  Synonyms

             Chlorethene; chloroethene; chloroethylene;
             chlorethylene; ethylene monochloride; monochloroethene;
             monochloroethylene; VC; VCM; vinyl c monomer;
             vinyl chloride inhibited; vinyl-chloride monomer; 
             chlorure de vinyle (French); cloruro di vinile (Italian); Vinylchlorid
             (German); winylu chlorek (Polish)

        1.4  Identification numbers

             1.4.1  CAS number

                    75-01-4

             1.4.2  Other numbers

                    RTECS NUMBER: KU9625000
                    SIC Code: 2813
                    PIN (UN NUMBER): 1086
                    (Sax, 1986; Budavari, 1989, Sax, 1989)

    2.  SUMMARY

        2.1  Main risks and target organs

             Acute exposures to vinyl chloride induce central nervous
             system depression and cardiac arrhythmias.  High
             concentrations also cause irritation of the eyes and of the
             respiratory tract.  Hepatic changes have been observed
             following massive exposure in animals.
    
             Vinyl chloride is stored under pressure; exposure to the
             escaping gas may cause frostbite.
    

             Repeated exposure to vinyl chloride may cause vinyl chloride
             disease, i.e. Raynaud's phenomenon, scleroderma-like changes,
             acro-osteolysis and hepatic fibrosis.  There is a causal
             association between vinyl chloride exposure and angiosarcomas
             of the liver.  Vinyl chloride is also responsible for an
             excess of other hepatic cancers, of brain tumours, lung
             tumours and of malignancies of the lymphatic and
             haemotopoietic system, in exposed workers.

        2.2  Summary of clinical effects

             Exposure to concentrations of 8,000 to 20,000 ppm caused
             headache, nausea, dizziness and drowsiness.  Coma was
             observed above 70,000 ppm and cardiac arrhythmias at 120,000
             ppm.  Hepatic damage was observed in animals at more than
             10,000 ppm.
    
             Repeated exposure may induce Raynaud's phenomenon which
             persists after termination of exposure to vinyl chloride. 
             Scleroderma-like lesions of the fingers and osteolysis of the
             terminal phalanges are often associated with Raynaud's
             syndrome but these usually improve after cessation of
             exposure.
    
             Repeated exposure to vinyl chloride may be responsible for
             non-cirrhotic portal fibrosis which leads to portal
             hypertension.  Vinyl chloride induced angiosarcomas of the
             liver; these generally result from prolonged exposure (>10
             years) to high concentrations (>50 ppm).  The latent period
             between the first exposure and the discovery of the tumours
             varies between 15 and 30 years.  These tumours have a very
             poor prognosis.

        2.3  Diagnosis

             There are no specific tests for the diagnosis of vinyl
             chloride poisoning and/or the monitoring of exposure.
    
             Standard liver enzyme and liver function tests are indicated
             to confirm liver involvement, but are of little value in
             detecting early stage of liver injury.

        2.4  First aid measures and management principles

             Remove from the area of exposure to fresh air.  Maintain
             clear airway.  Monitor consciousness level and ECG. 
             Artificial ventilation may be needed.  If frostbite has
             occurred, wash the contaminated area with warm water until
             circulation is restored.

    3.  PHYSICO-CHEMICAL PROPERTIES

        3.1  Origin of the substance

             Vinyl chloride is a synthetic chemical obtained either
             by hydrochlorination of acetylene or by halogenation of
             ethylene (ILO, 1983; Budavari, 1989).

        3.2  Chemical structure

             Molecular weight: 62.50
    
             Molecular formula: C2H3C1
    
             Structural formula: ClCH = CH2

        3.3  Physical properties

             3.3.1  Colour

                    Colourless

             3.3.2  State/form

                    Gas

             3.3.3  Description

                    Under normal conditions of temperature and
                    pressure, vinyl chloride is a colourless gas with mild
                    ethereal odour.  It is usually handled under pressure
                    as a colourless liquid.
    
                    -Boiling point: -14°C (7°F)
    
                    -Melting point: -154°C (-245°F)
    
                    -Autoignition temperature 472°C (882°F)
    
                    -Flash point: -78°C (-112°F) (open cup)
    
                    -Specific gravity: 0.9121 (20/4°C)
    
                    -Vapour pressure: 2530 mm Hg (20°C)
    
                    -Vapour density: 2.15 (air = 1)
    
                    -Solubility: slightly soluble in water (2.4 g/l at
                    25°C)
                    soluble in ethanol, ether, carbon tetrachloride and
                    benzene
    
                    -Conversion factor: 1 ppm = 2.56 mg/m3 = 0.391 ppm
                    (25°C; 760 mm Hg)

        3.4  Hazardous characteristics

             -Explosive limits: 3.6 to 33%
    
             Vinyl chloride (vinyl chloride) is highly flammable and forms
             explosive mixtures with air (see above).  Peroxides may form
             from long-term exposure to air; these can initiate explosive
             polymerization of vinyl chloride.
    
             Vinyl chloride reacts vigorously with oxidizers.  It may
             attach iron and steel in the presence of moisture.  It is
             also incompatible with aluminium and copper.  It can liberate
             hydrogen chloride upon treatment with strong alkalis.
    
             It undergoes exothermic polymerization in the presence of
             light, or air and heat, or a catalyst.
    
             Thermal degradation of polyvinyl chloride (PVC) releases
             hydrogen chloride (HCI) and many other compounds.  The main
             toxic products found in smoke or fumes are HCI, chlorine gas,
             phosgene, and carbon monoxide.
    
             Small fires may be extinguished with dry chemical, carbon
             dioxide or halon.
    
             Vinyl chloride should be kept out of water sources and
             sewers.  Appropriate local health and pollution control
             authorities should be notified of releases.

    4.  USES/CIRCUMSTANCES OF POISONING

        4.1  Uses

             4.1.1  Uses

             4.1.2  Description

                    Vinyl chloride is used for the production of
                    vinyl chloride homo-polymer and co-polymer resins;
                    these have many applications.  It was formerly
                    considered for use as an anaesthetic agent, but was
                    finally abandoned for this purpose because of cardiac
                    arrhythmias during anaesthesia.  It has also been used
                    as a refrigerant, an extraction solvent, a propellant,
                    and for the production of methyl chloroform (ECETOC,
                    1988).

        4.2  High risk circumstances of poisoning

             Vinyl chloride is a gas at room temperature, therefore,
             the most likely circumstance of poisoning is inhalation.  As
             all processus using vinyl chloride are generally enclosed,

             inhalation results from accidental leak of liquid or vapour. 
             This may result in systemic poisoning; escaping compressed
             gas may also cause frostbite; vinyl chloride vapours can
             cause asphyxia by displacement of oxygen from the breathing
             atmosphere in cases of massive leaks (ECETOC, 1988).

        4.3  Occupationally exposed populations

             Only workers engaged in the production of vinyl chloride
             or of vinyl chloride polymers can be exposed to the toxic
             monomer.  Today all processes using vinyl chloride are
             generally enclosed and exposure of workers is unlikely.  In
             the past, the highest  air concentrations of vinyl chloride
             were found in polymerization plants.  Those workers who
             charged, discharged and cleaned the autoclaves were so highly
             exposed that subacute poisoning was not uncommon.  In
             developed countries, vinyl chloride atmospheric concentration
             at the workplace is now generally less than 1 ppm (ECETOC,
             1988).
    
             The general public may be exposed to only very small amounts
             of vinyl chloride: from inhalation of air in the vicinity of
             plants, by ingestion on foods or drinks with PVC-based
             packaging (from which vinyl chloride can migrate), and by
             inhalation of tobacco smoke (ECETOC, 1988).  Calculation of
             daily inhalation rates indicates the amount inhaled ranges
             from 4 µg/person/day to more than 100 µg/person/day for
             populations living in the immediate vicinity of some vinyl
             chloride plants.  Exposure from food sources is less than 0.1
             µg/day (ECETOC, 1988).

    5.  ROUTES OF EXPOSURE

        5.1  Oral

             Ingestion is unlikely and has not been reported.  Vinyl
             chloride may be absorbed through the digestive system.

        5.2  Inhalation

             Vinyl chloride is a gas at room temperature, therefore,
             inhalation is the major route of entry.  It has been
             responsible for most cases of poisoning.

        5.3  Dermal

             Vinyl chloride may be absorbed through the skin. 
             Escaping compressed gas may also cause frostbite.

        5.4  Eye

             Vinyl chloride vapours are moderately irritating to the
             eyes.  Contact with escaping compressed gas may cause
             mechanical injury and frostbite.

        5.5  Parenteral

             Not described.

        5.6  Others

             Not described.

    6.  KINETICS

        6.1  Absorption by route of exposure

             Vinyl chloride is absorbed via inhalation, ingestion, or
             through the skin.  However, since this substance is a gas at
             room temperature, inhalation is the major route of entry.
    
             In studies on human volunteers exposed to 2.5 to 23 ppm,
             retention of inhaled vinyl chloride in the lung was estimated
             to be 27 to 42% (ECETOC, 1988).

        6.2  Distribution by route of exposure

             Vinyl chloride is distributed throughout the body.  The
             highest concentrations are in the liver and kidneys, followed
             by the lungs and spleen (ATSDR, 1989).

        6.3  Biological half-life by route of exposure

             Not determined.

        6.4  Metabolism

             Vinyl chloride is mainly transformed in the liver.  The
             mixed function oxidase system is the major metabolic route. 
             The cytochrome P450 isozyme implicated in the metabolism
             of FCM is inducible by ethanol, phenobarbitone and
             polychlorobiphenyls.  The alcohol dehydrogenase system and
             the catalase system may also be involved.  vinyl chloride is
             first metabolised to chloroethylene oxide.  This unstable
             epoxide is then transformed into chloroacetaldehyde which is
             further converted to chloroethanol or monochloroacetic acid. 
             Chloroethylene oxide, chloroacetaldehyde and monochloroacetic
             acid are the main toxic metabolites of vinyl chloride. 
             Conjugation with glutathione is the main detoxification
             mechanism for these three compounds.  It is responsible for

             the production of the two main urinary metabolites of vinyl
             chloride: N-acetyl-S-(hydroxy-2-ethyl)-cysteine and
             thiodiglycolic acid (ECETOC, 1988):
    
             -a fast one with a half-life of 1.5 minutes;
             -a second one with a half-life of 1000 minutes;
             -a slow one with a half-life of about 4000 minutes.
    
             In humans, the main urinary metabolite of vinyl chloride is
             thiodiglycolic acid.  Its excretion increases with exposure
             to the parent compound.  The measurement of thiodiglycolic
             acid concentration in urine should, however, not be used to
             evaluate exposure to vinyl chloride because its sensitivity
             is low, and also because at usual levels of exposure, the
             results fluctuate widely (ECETOC, 1988).

    7.  TOXICOLOGY

        7.1  Mode of action

             Like many other chlorinated hydrocarbons, vinyl chloride
             itself may cause central nervous system depression and
             cardiac arrhythmias in cases of massive poisoning.
    
             Chloroethylene oxide is a highly reactive metabolite; it is
             probably responsible for most of the mutagenic and
             carcinogenic effects of vinyl chloride (ECETOC, 1988).
    
             Chloroacetaldehyde is also a metabolite of high cytoxicity
             and some mutagenic potential (ECETOC, 1988).
    
             The epoxidation of vinyl chloride to chloroethylene oxide is
             the key step in the metabolism of vinyl chloride; it is
             readily saturable; nevertheless covalent binding to DNA
             occurs at levels well below the saturation limit (Watanabe et
             al., 1978); this may explain the induction of tumours even at
             low exposure levels (Maltoni and Lefemine, 1975).
    
             The main detoxification pathway for all three toxic
             metabolites of vinyl chloride is conjugation with
             glutathione.

        7.2  Toxicity

             7.2.1  Human data

                    7.2.1.1  Adults

                             Exposure to more than 120,000 ppm
                             may be fatal (ILO, 1983).
    

                             Early inhalational experiments on human
                             subjects found vinyl chloride to be narcotic
                             at 70,000 to 100,000 ppm and to cause
                             arrhythmias at 120,000 ppm (Oster et al.,
                             1947).
    
                             Concentrations of 8,999 to 20,000 ppm caused
                             dizziness, nausea and headache (Baselt, 1982;
                             ILO, 1983).
    
                             Acute exposures in the range of 8,000 to
                             13,000 ppm for five minutes may be tolerated
                             with no apparent symptoms (ATSDR, 1989).

                    7.2.1.2  Children

                             No data.

             7.2.2  Relevant animal data

                    LD50 (oral, rat) = 500 mg/kg (RTECS, 1994)
                    LC 50 (mice) = 130,000 ppm x 2 hours (RTECS, 1994)
    
                    When mice and rats were exposed to vinyl chloride at
                    concentrations of 10,000 to 30,000 ppm for 30 minutes,
                    the principal effect was narcosis; congestion, oedema
                    and haemorrhages of the lungs and congestion of the
                    liver and kidneys were also observed (Prodam et al.,
                    1975).
    
                    Exposure of rats to 50,000 or 10,000 ppm for 6 hours
                    (Jaeger et al., 1974; Reynolds et al., 1975) produced
                    centrilobular hepatocellular vacuolisation at both
                    levels with pretreatment with phenobarbitone, and at
                    the highest level only without pretreatment.  More
                    subtle hepatic injury has been observed at lower doses
                    (15,000 ppm × 2 - 8 hr/d × 5 d/wk × 1 to 6 weeks).

             7.2.3  Relevant in vitro data

                    The relevant in vitro data concern the
                    genotoxicity of vinyl chloride (see 7.5).

             7.2.4  Workplace standards

                    Vinyl chloride is a demonstrated carcinogen,
                    and OSHA's recommended PEL (Permissible Exposure
                    Limit) is one ppm for an eight-hour TWA (Time Weighted
                    Average concentration), with a five ppm ceiling at 15
                    minutes.  The TLV (Threshold Limit value) recommended
                    by ACGIH is 5 ppm, with a short-term limit, averaged
                    over 15 minutes of 10 ppm (ACGIH, 1992).
    

                    In France, the TWA is 1 ppm for plants built after
                    1980, and 3 ppm for those built before.
    
                    In Germany, the TWA is 3 ppm for plants producing
                    polyvinyl chloride; it is only 2 ppm for other
                    plants.

             7.2.5  Acceptable daily intake

                    Vinyl chloride is a carcinogen in experimental
                    animals and man.  As a no-effect level has not been
                    established, there is no acceptable daily intake.
    
                    The EPA emission standards for chemicals released to
                    the atmosphere set a limit of 10 ppm for vinyl
                    chloride, measured at the source.
    
                    EPA has issued a maximum contaminant level of 2 ppb
                    for vinyl chloride in drinking water.
    
                    The residual vinyl chloride content in polymers in
                    contact with food should be limited to:
    
                    -5 ppb in vinyl chloride mono- or co-polymer films and
                    coatings, and plasticised polyvinyl chloride (PVC)
                    bottles;
                    -10 ppb in rigid PVC;
                    -50 ppb in water-pipes and vinyl chloride-vinylidene
                    chloride copolymer films.

        7.3  Carcinogenicity

             According to IARC, vinyl chloride is carcinogenic to
             humans (Group 1).  It has been associated with tumours of the
             liver, brain, lung, lymphatic and haematopoietic system.  A
             large number of studies have substantiated the causal
             associations between vinyl chloride and angiosarcoma of the
             liver.  vinyl chloride also causes other forms of hepatic
             cancer and other localization of angiosarcomas as well as
             brain tumours, lung tumours, and malignancies of the
             lymphatic and haematopoietic system (IARC, 1979, IARC,
             1987).
    
             Vinyl chloride administered orally, or by inhalation, to
             hamsters, mice and rats also produced tumours in the mammary
             gland, lung, Zymbal gland and skin and angiosarcomas of the
             liver.  Pretreatment with ethanol increased the incidence of
             liver tumours induced by vinyl chloride in rats (IARC, 1979;
             IARC, 1987).

        7.4  Teratogenicity

             Vinyl chloride is not a teratogen in rodents (IARC,
             1979; IARC, 1987).  Although one pape reported increased
             rates of malformations and fetal loss in cities where vinyl
             chloride plants were located (Infante et al., 1976),
             subsequent studies did not substantiate an association
             between vinyl chloride exposure and birth defects in humans
             (IARC, 1979; IARC 1987).

        7.5  Mutagenicity

             Vinyl chloride is bound covalently to isolated DNA in
             the presence of a metabolic system.  It alkylated DNA in
             several tissues of mice and rats exposed in vivo.  It was
             mutagenic to bacteria, plants and to Schizosaccharomyces
             pombe but not to other fungi; it induced gene conversion in
             yeast.  It was responsible for sex-linked recessive lethal
             mutations in Drosophila.  It induced mutation and unscheduled
             DNA synthesis in different systems of mammalian cells in
             vitro.  In vivo, it also induced chromosomal aberrations,
             sister chromatid exchanges and micronuclei in rodents
             (ECETOC, 1988).  Vinyl chloride induced sister chromatid
             exchanges in human lymphocytes in vitro (ECETOC, 1988).  An
             excess of chromosomal aberrations was observed in peripheral
             blood lymphocytes of workers (ECETOC, 1988) exposed to vinyl
             chloride 85 to 500 ppm).

        7.6  Interactions

             As the main metabolic pathway of vinyl chloride depends
             on microsomal cytochrome P450, pretreatment with inducers
             such as phenobarbitone, ethanol or PCB will increase the
             production of toxic metabolites (mainly of chloroethylene
             oxide) and the toxic effects of vinyl chloride (ECETOC,
             1988).
    
             As the three main toxic metabolites are detoxified
             through conjugation with glutathione, administration of
             N-acetylcysteine might have a protective effect; however,
             this hypothesis has never been tested.

    8.  TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS

        8.1  Material sampling plan

             8.1.1  Sampling and specimen collection

                    8.1.1.1  Toxicological analyses

                    8.1.1.2  Biomedical analyses

                    8.1.1.3  Arterial blood gas analysis

                    8.1.1.4  Haematological analyses

                    8.1.1.5  Other (unspecified) analyses

             8.1.2  Storage of laboratory samples and specimens

                    8.1.2.1  Toxicological analyses

                    8.1.2.2  Biomedical analyses

                    8.1.2.3  Arterial blood gas analysis

                    8.1.2.4  Haematological analyses

                    8.1.2.5  Other (unspecified) analyses

             8.1.3  Transport of laboratory samples and specimens

                    8.1.3.1  Toxicological analyses

                    8.1.3.2  Biomedical analyses

                    8.1.3.3  Arterial blood gas analysis

                    8.1.3.4  Haematological analyses

                    8.1.3.5  Other (unspecified) analyses

        8.2  Toxicological Analyses and Their Interpretation

             8.2.1  Tests on toxic ingredient(s) of material

                    8.2.1.1  Simple Qualitative Test(s)

                    8.2.1.2  Advanced Qualitative Confirmation Test(s)

                    8.2.1.3  Simple Quantitative Method(s)

                    8.2.1.4  Advanced Quantitative Method(s)

             8.2.2  Tests for biological specimens

                    8.2.2.1  Simple Qualitative Test(s)

                    8.2.2.2  Advanced Qualitative Confirmation Test(s)

                    8.2.2.3  Simple Quantitative Method(s)

                    8.2.2.4  Advanced Quantitative Method(s)

                    8.2.2.5  Other Dedicated Method(s)

             8.2.3  Interpretation of toxicological analyses

        8.3  Biomedical investigations and their interpretation

             8.3.1  Biochemical analysis

                    8.3.1.1  Blood, plasma or serum

                    8.3.1.2  Urine

                    8.3.1.3  Other fluids

             8.3.2  Arterial blood gas analyses

             8.3.3  Haematological analyses

             8.3.4  Interpretation of biomedical investigations

        8.4  Other biomedical (diagnostic) investigations and their
             interpretation

        8.5  Overall interpretation of all toxicological analyses and
             toxicological investigations.

             Biomedical analysis
    
             Standard liver enzymes and liver function tests are indicated
             to confirm liver involvement, but are of little value in
             detecting early stages of liver injury.  The increase of
             coproporphyrinuria - which is a consistent finding in the
             presence of vinyl chloride-induced hepatic damage - also
             lacks specificity.
    
             Urinary thiodiglycolic acid levels are unreliable in persons
             exposed to less than 5 ppm vinyl chloride.

        8.6  References

    9.  CLINICAL EFFECTS

        9.1  Acute poisoning

             9.1.1  Ingestion

                    Not reported.

             9.1.2  Inhalation

                    Massive exposure (see 7.2.1.1) to vinyl
                    chloride may induce headache, nausea, central nervous
                    system depression (dizziness, drowsiness, then coma)
                    and cardiac arrhythmias.  High concentrations also
                    cause irritation of the eyes and of the respiratory
                    tract.  Hepatic changes increased by ethanol or
                    phenobarbitone pretreatment have been observed
                    following massive exposure in animals (ECETOC, 1988);
                    such effects have not been reported in humans.

             9.1.3  Skin exposure

                    Vinyl chloride is stored under pressure;
                    exposure to the escaping gas may cause
                    frostbite.

             9.1.4  Eye contact

                    Contact with escaping compressed gas may cause
                    mechanical injury and frostbite.
    
                    Vapours of vinyl chloride are moderately irritating to
                    the eyes.

             9.1.5  Parenteral exposure

                    Not reported.

             9.1.6  Other

                    Not reported.

        9.2  Chronic poisoning

             9.2.1  Ingestion

                    Not reported.

             9.2.2  Inhalation

                    Repeated exposure to vinyl chloride may induce
                    vinyl chloride disease which is characterized by
                    scleroderma-like changes of the fingers, Raynaud's
                    phenomenon and acro-osteolysis.  Hepatic damage is
                    initially an enlargement and a proliferation of
                    hepatocytes and sinusoïdal cells.  Hepatic fibrosis
                    and peliosis may result after several years.  Portal
                    hypertension is a usual complication of hepatic
                    fibrosis.  There is a causal association between
                    exposure to vinyl chloride and the incidence of
                    angiosarcomas of the liver.  Vinyl chloride also

                    causes other forms of hepatic cancers as well as brain
                    tumours, lung tumours and malignancies of the
                    lymphatic and haematopoietic system.

             9.2.3  Skin exposure

                    No data available.

             9.2.4  Eye contact

                    Vapours of vinyl chloride are moderately
                    irritating to the eyes.

             9.2.5  Parenteral exposure

                    No data available.

             9.2.6  Other

                    Not reported.

        9.3  Course, prognosis, cause of death

             In acute poisoning, death may result from central
             nervous system depression and/or cardiac arrhythmias.
    
             There is an increased incidence of deaths from malignant
             neoplasms in vinyl chloride exposed workers.  Angiosarcomas
             of the liver have a very poor prognosis.  They generally
             result from prolonged exposure (>10 years) to high
             concentrations (>50 ppm) of vinyl chloride; the latent
             period between first exposure and diagnosis varies from 15 to
             30 years (IARC, 1979; IARC, 1987; ECETOC, 1988).

        9.4  Systematic description of clinical effects

             9.4.1  Cardiovascular

                    Vinyl chloride sensitized the hearts of dogs to
                    epinephrine-induced arrhythmias.  Cardiac arrhythmias
                    may be a complication of massive exposure to vinyl
                    chloride (Oster et al., 1947).
    
                    Repeated exposure to vinyl chloride may induce
                    Raynaud's syndrome; all the fingers may be involved or
                    only a few of them; this phenomenon generally persists
                    when exposure is terminated (Carpentier et al., 1984).
    
                    Portal hypertension may be a result of hepatic
                    fibrosis (Smith et al., 1976).
    

                    An excess of angiosarcomas of the liver has been
                    observed in workers exposed to vinyl chloride;
                    angiosarcomas of other localizations have also been
                    reported (IARC, 1979; IARC 1987).

             9.4.2  Respiratory

                    Massive exposure to vinyl chloride may be
                    responsible for irritation of the respiratory tract;
                    congestion, oedema and haemorrhages of the lungs have
                    been observed in experimental animals (Prodan et al.,
                    1975).
    
                    Impaired pulmonary function with decreased alveolo-
                    capillary permeability, as measured by single breath
                    transfer for carbon monoxide (TLCO), was observed in
                    workers exposed both to vinyl chloride and polyvinyl
                    chloride dust (Lloyd et al., 1984).
    
                    The incidence of lung cancers is increased in workers
                    exposed to vinyl chloride (IARC, 1979; IARC 1987;
                    ECETOC, 1988).

             9.4.3  Neurologic

                    9.4.3.1  Central Nervous System (CNS)

                             Vinyl chloride may cause central
                             nervous system depression.  Concentrations of
                             8,000 to 20,000 ppm induced headache, nausea,
                             dizziness and drowsiness.  At higher
                             concentrations, vinyl chloride is narcotic. 
                             Seizures may occur in deep coma induced by
                             vinyl chloride (Oster et al., 1947; Danziger,
                             1960; ECETOC 1988).
    
                             Symptoms similar to those observed in workers
                             with solvent-induced organic psychosyndromes
                             have been reported after repeated exposure to
                             vinyl chloride (Langhauer-Lewowicka et al.,
                             1983).
    
                             An excess of brain tumours has been observed
                             in workers exposed to vinyl chloride (IARC,
                             1979; IARC, 1987; ECETOC, 1988).

                    9.4.3.2  Peripheral nervous system

                             Distal axonal peripheral neuropathy
                             has been reported in exposed workers
                             (Perticoni et al., 1986).

             9.4.4  Gastrointestinal

                    Nausea, vomiting, diarrhea and abdominal pain
                    may be observed in cases of acute vinyl chloride
                    poisoning (Oster et al., 1947; Danziger, 1960; ECETOC,
                    1988).

             9.4.5  Hepatic

                    Massive vinyl chloride poisoning may produce
                    centrilobular hepatocellular vacuolisation and
                    necrosis (Jaeger et al., 1974; Prodan et al., 1975;
                    Reynolds et al., 1975).
    
                    Repeated exposures to vinyl chloride also induce
                    hepatic damage.  This is clinically and biologically
                    asymptomatic during years or decades.  the initial
                    lesion is a hyperplasia of sinusoïdal cells and of
                    hepatocytes.  Then perisinusoïdal fibrosis, portal
                    fibrosis and subcapsular fibrosis occur.  Finally,
                    non-cirrhotic portal fibrosis leads to portal
                    hypertension with hepatomegaly, splenomegaly, and
                    oesophageal varices (Lee et al., 1977; Suciu et al.,
                    1975).
    
                    There is a causal association between exposure to
                    vinyl chloride and the incidence of angiosarcomas of
                    the liver.  The latent period between the first
                    exposure and the discovery of the tumour various
                    between 15 and 30 years.  Angiosarcomas generally
                    result from prolonged exposure (>10 years) to high
                    concentrations (>50 ppm) of the monomer.  This tumour
                    has a very poor prognosis.  vinyl chloride also causes
                    other types of hepatic cancer (IARC, 1979; IARC, 1987;
                    ECETOC, 1988).

             9.4.6  Urinary

                    Not reported.

             9.4.7  Endocrine and reproductive systems

                    Vinyl chloride has no demonstrated effects on
                    endocrine and reproductive systems.

             9.4.8  Dermatological

                    Vinyl chloride is stored under pressure;
                    exposure to the escaping gas may cause frostbite.
    

                    Repeated exposure to vinyl chloride may induce
                    scleroderma-like changes of the hands.  These skin
                    lesions are generally thought to be the consequence of
                    the Raynaud's phenomenon.  The reality might be more
                    complex as scleroderma-like lesions usually disappear
                    after termination of exposure to vinyl chloride, when
                    Raynaud's phenomenon  persists (Suciu et al., 1975). 
                    Some authors have suggested that vinyl chloride
                    disease (i.e. Raynaud's phenomenon, scleroderma-like
                    changes, acro-osteolysys, protal fibrosis) might be an
                    immune complex disorder (Ward et al., 1976).

             9.4.9  Eyes, ears, nose, throat: local effects

                    Vapours of vinyl chloride are moderately
                    irritating to the eyes and the respiratory tract.
    
                    Exposure to escaping compressed gas may cause
                    frostbite.

             9.4.10 Haematological

                    Thrombocytopenia may be seen in workers
                    exposed to vinyl chloride.  It is probably a
                    consequence of splenomegaly which results from hepatic
                    fibrosis and portal hypertension (Smith et al., 1976).
    
                    The incidence of malignancies of the lymphatic and
                    haematopoietic system is increased in workers exposed
                    to vinyl chloride (IARC, 1979; IARC 1987; ECETOC,
                    1988).

             9.4.11 Immunological

                    Some authors have suggested that vinyl
                    chloride disease (i.e. Raynaud's phenomenon,
                    scleroderma-like changes, acroosteolysis, portal
                    fibrosis) might be an immune complex disorder. 
                    Circulating immune complexes were detected in some
                    patients (Ward et al., 1976).

             9.4.12 Metabolic

                    9.4.12.1 Acid base disturbances

                             Not reported.

                    9.4.12.2 Fluid and electrolyte disturbances

                             Not reported.

                    9.4.12.3 Other

                             Pathologic porphyrinuria,
                             especially increased coproporphyrinuria
                             appears to be a consistent finding in vinyl
                             chloride hepatic disease; however, the
                             specificity of this sign is very poor, as all
                             hepatic diseases and many other intoxications
                             may increase coproporphyrinuria.

             9.4.13 Allergic

                    Not reported.

             9.4.14 Other clinical effects

                    Acroosteolysis is the lysis of terminal
                    phalanges of some fingers of the hands and, sometimes,
                    of the feet.  It is generally associated with
                    scleroderma-like lesions of the skin. 
                    Remineralisation of the bone occurs after termination
                    of exposure to vinyl chloride; this process may be
                    long and persistent deformations of the fingers are
                    not infrequent (Carpentier et al., 1984; Suciu et al.,
                    1975).

             9.4.15 Special risks

                    As the first step of vinyl chloride
                    metabolism, leading to its toxic metabolites, is
                    catalysed by cytochrome P450 isozyme(s), people with
                    increased cytochrome P450 activity may have an
                    increased risk of developing systemic toxic effects:
                    alcoholic patients, subjects treated with
                    barbiturates, or workers simultaneously exposed to
                    inducers (i.e. isopropanol, acetone, methyl ethyl
                    ketone) might be particularly sensitive to the toxic
                    effects of vinyl chloride.

        9.5  Others

             No data available.

        9.6  Summary

    10. MANAGEMENT

        10.1 General principles

             The evaluation of vital functions and life-supporting
             measures are essential.  rapid and effective decontamination
             should be performed.  In cases of massive exposure, the main
             risks are central nervous system depression and the

             occurrence of cardiac arrhythmias; therefore, close clinical
             and ECG monitoring are needed.  Hepatic damage should be
             suspected.  As the main toxic metabolites of vinyl chloride
             are detoxified through conjugation with glutathione,
             administration of N-acetylcysteine might have a protective
             effect, though this has never been demonstrated.
    
             The medical surveillance of chronically exposed workers
             cannot be strictly defined: clinical and laboratory tests for
             the monitoring of exposure to vinyl chloride and/or of its
             toxic effects are poorly sensitive and non specific.  The
             main goal should be to minimize exposure and the monitoring
             of atmospheric concentrations is certainly the most efficient
             evaluation of worker's exposure.

        10.2 Life supportive procedures and symptomatic treatment

             Make a proper assessment of airway, breathing,
             circulation and neurological status of the patient.  Maintain
             a clear airway.  Administer oxygen if cyanosis is present. 
             Aspirate secretions from airway.  Start artificial
             respiration for respiratory failure.  Open and maintain at
             least one intravenous route.
    
             If frostbite has occurred, wash frostbitten area with warm
             water until circulation is restored.  Do not rub or massage
             the frozen area.

        10.3 Decontamination

             Inhalation: Take proper precautions to ensure safety of
             rescuers before attempting rescue.  Remove source of
             contamination or move victim to fresh air.  Begin artificial
             respiration if required.  Eye exposure: irrigate with flowing
             lukewarm, gently flowing water or saline, immediately and
             continuously for 15 minutes holding the eyelids open.  All
             patients should be evaluated by an ophthalmologist.  Skin
             contact: Remove all contaminated clothing and shoes.  Flush
             contaminated area with lukewarm, gently running water for at
             least 15 minutes.

        10.4 Enhanced elimination

             A good urinary output and a good respiratory state are
             mandatory.  There are no references about other methods of
             elimination.

        10.5 Antidote treatment

             10.5.1 Adults

                    As the main toxic metabolites of vinyl
                    chloride are detoxified through conjugation with
                    glutathione, administration of N-acetylcysteine might
                    have a protective effect.  This hypothesis has, to our
                    knowledge, never been tested in humans or experimental
                    models.

             10.5.2 Children

                    See 10.5.1

        10.6 Management discussion

             An overexposure to vinyl chloride vapours can produce
             different degrees of central nervous system depression from
             dizziness and light-headedness to unconsciousness and death. 
             Vapours are irritating to mucous membranes, but the liquid
             product may cause frostbite.  The main problem is chronic
             occupational exposure due to potential effects of "vinyl
             chloride disease" and oncogenic effects.  For these special
             situations, prevention is the key-word.  A constant and
             comprehensive medical control of workers is a fundamental
             requirement, as biochemical or toxicological tests are not
             specific for early diagnosis and consequent management.

    11. ILLUSTRATIVE CASES

        11.1 Case reports from literature

             Two fatalities occurred in workers exposed to vinyl
             chloride vapours, while cleaning polymerization tanks
             (Danziger, 1960).
    
             In the first case, a 21 year old worker was found dead at the
             bottom of a tank.  Autopsy revealed congestion of the liver,
             spleen and kidneys.
    
             In the second one, the victim was a 39 year old man who was
             found dead 20 minutes after he went alone in a pit.  Autopsy
             showed cyanotic nails, kerato-conjunctivitis, and congested
             kidneys.
    
             A 51 year old man was hospitalized with a 6 week history of
             anorexia, fatigue, right sided abdominal pain, and
             progressive abdominal distension.  He had experienced a
             weight loss of approximately 7 kilograms and recently
             developed jaundice.  He reported working as an autoclave
             cleaner in a PVC production plant for 9 years until 15 years
             before his hospitalization.  Clinical examination revealed

             jaundice and a massive hepatomegaly.  Liver function test
             showed increased bilirubin and gamma-glutamyltranspeptidase
             and hypoalbuminaemia.  An abdominal computed tomographic scan
             showed diffuse enlargement of the liver with an abnormal
             texture.  The patient's condition deteriorated rapidly. 
             Ascites developed, then oliguric renal failure and
             encephalopathy.  Death occurred 21 days after
             hospitalization.  Autopsy revealed a hepatic angiosarcoma
             (Riordan et al., 1991).
    
             Two cases of vinyl chloride disease involving autoclave
             cleaners at a PVC manufacturing factory were reported by Juhe
             and Weltman (1967).  Both workers had Raynaud syndromes and
             subsequently developed acro-osteolysis.  Symptoms presented
             included diffuse swelling of the hands, thickening of the
             finger end phalanges, and ivory coloured plate-like
             infiltrations on the skin of hands and wrists.  X-rays
             revealed acro-osteolysis.

    12. ADDITIONAL INFORMATION

        12.1 Specific preventive measures

             The exposure limits are fundamental points of reference
             for correct prevention.
    
             Warning properties: odour is inadequate warning of excessive
             exposure.
    
             Ventilation: control airborne concentrations below the
             exposure guideline.  Use only with adequate ventilation. 
             Local exhaust ventilation may be necessary for some
             operations.
    
             Ingestion: do not consume or store food in the work area. 
             Wash hands before smoking or eating.
    
             Inhalation: when respiratory protection is required for
             certain operations, use an approved air-purifying respirator. 
             When airborne exposure guideline may be exceeded, use an
             approved positive-pressure self-contained breathing
             apparatus.
    
             Eyes: use safety glasses.  If vapour exposure causes eye
             discomfort, use a full-face supplied air respirator.
    
             Skin: use protective clothing materials such as nitrile
             butadiene, rubber chlorinated polyethylene (CPE) and
             Viton(R).  Selection of specific items such as gloves, boots
             or full-body suit will depend on operation.
    

             Storage: store in cool, dry, well-ventilated areas, out of
             direct sunlight.  Keep material away from sparks, flames and
             other ignition sources.
    
             Spills: in case of small spills, evacuate area and let
             evaporate.  Disposal by controlled incineration with a
             scrubber attached to remove any hydrochloric acid formed.
    
             Fires: extinguish the flame bay carbon dioxide or dry
             chemical (ILO, 1983).

        12.2 Other

    13. REFERENCES

        ACGIH - American Conference of Governmental Industrial
        Hygienists (1992(TLVs Threshold Limit Values for Chemical
        Substances and Physical Agents and Biological Exposure Indices for
        1992-1993 Cincinnati, ACGIH.
    
        ATSDR - Agency for Toxic Substances and Disease Registry (1989)
        Toxicological profile for vinyl chloride.  US Department of Health
        and Human Services, Atlanta.
    
        Barr, J.T. (1982) Risk assessment for vinyl chloride in
        perspective 75th Annual Meeting of the Air Pollution Control
        Association, New Orleans, APCA, 20 p.
    
        Baselt, R.C., Cravey R.H. (1990) Disposition of toxic drugs and
        chemicals in man.  3rd ed. Chicago, Year Book Medical Publishers.
        pp.849-851.
    
        Budavari, S. ed. (1989) The Merck Index: an encyclopaedia of
        chemicals, drugs and biologicals.  11th ed. Rahway, New Jersey,
        Merck and Co. Inc.
    
        Carpentier, P., Dimitriou, R., Puech, A.M., DeGaudemaris, R.,
        Perdrix, A., Franco, A., Mallion J.M. (1984) Mode de dépistage
        objectif des troubles vasculaires périphériques chez les sujets
        exposés à la fabrication du chlorure de vinyle avec une étude
        d'une population témoin non exposée.  Arch. Mal. Prof.,
        45:298-310.
    
        Danziger, H. (1960) Accidental poisoning bay vinyl chloride:
        report of two cases. Can. Med. Asso. J. 82:828-830.
    
        ECETOC (1988) The mutagenicity and carcinogenicity of vinyl
        chloride: a historical review and assessment.  Technical report
        no. 31, Brussels, ECETOC.
    

        Heiselman, D.E., Cannon, L.A. (1990) Benzene and the aromatic
        hydrocarbons.  In: Haddad, L.M. & Winchester, J.F. eds. Clinical
        management of poisoning and drug overdose.  Philadelphia, W.
        Saunders Co. pp. 1227-1229.

        IARC (1979) Monographs on the evaluation of the carcinogenic risk
        of chemicals to man.  Vol.19.  Some monomers, plastics and
        synthetic elastomers and acrolein.  Lyon: WHO-IARC: 377-438.
    
        IARC (1987) Monographs on the evaluation of the carcinogenic risk
        of chemicals to man.  Suppl.7.  Overall evaluations of
        carcinogenicity: an updating of IARC monographs 1 to 42 Lyon:
        WHO-IARC.
    
        ILO - International Labour Office (1983) Encyclopedia of
        Occupational Health and Safety.  3rd ed. Geneva.  pp. 2256-2259.
    
        Infante, P.F., Wagoner, J.K., Waxweiler, R.J. (1976) Carcinogenic,
        mutagenic and teratogenic risks associated with vinyl chloride. 
        Mutat. Res. 41: 131-142.
    
        Jaeger, R.J., Reynolds, E.S., Conolly, R.B., Moslem, M.T., Szabo,
        S., Murphy, S.D. (1974) Acute hepatic injury by vinyl chloride in
        rats pretreated with phenobarbital.  Nature, 252: 724-726.
    
        Juhe, S., Veltman, C.  (1967) Clinical aspects of so-called vinyl
        chloride disease. Br. Med. J. 2:712-714.
    
        Langhauer-Lewowicka, H., Kurzbauer, H., Byczkowska, Z., Wocka-
        Marek, T., (1983) vinyl chloride disease.  Neurological
        disturbances.  Int. Arch. Occup. Environ. Health 52: 151-157.
    
        Lee, F.I., Harry, D.S., Adams, W.G.F., Lichtfield, M. (1977)
        Screening for liver disease in vinyl chloride workers.  Br. J.
        Ind. Med. 34:142-147.
    
        Lloyd, M.H., Gauld, S., Copland, L., Soutar, C.A. (1984)
        Epidemiological study of the lung function of workers at a factory
        manufacturing polyvinyl chloride. Br. J. Ind. Med. 41:328-333.
    
        Maltoni, C., Lefemine, G. (1975) Carcinogenicity bioassays of
        vinyl chloride: current results Ann. N. Y. Acad. Sci. 246:195-217.
    
        Proctor, N.H., Hughes, J.P. Fichman, M.L. (1988).  Chemical
        hazards of the workplace. 2nd ed. Philadelphia, J.B. Lippincott
        Co., pp.507-509.
    
        Oster, R.H., Carr, C.J., Kranz, J.C., Sauerwald, M.J. (1947)
        Narcosis with vinyl chloride.  Anaesthesia, 8:359-361.
    
        Perticoni, G.F., Abbritti, G., Cantisani, T.A., Bondi, L., Mauro,
        L. (1986) Polyneuropathy in workers with long exposure to vinyl
        chloride. Electromyography Clin. Neurophysiol. 26:41-47.
    

        Prodan, L., Sucin, I., Pisloru, V., Ilea, E., Pascu, L. (1975)
        Experimental acute toxicity of vinyl chloride.  Ann. N.Y. Acad.
        Sci. 246:154-158.
    
        Reynolds, E.S., Jaeger, R.J., Murphy, S.D. (1975) Acute liver
        injury by vinyl chloride: involvement of endoplasmic reticulum in
        phenobarbital treated rats.  Environ. Health Perspect. 11:227-233.
    
        Riordan, S.M., Loo, C.K.C., Haber, R.W., Thomas, M.C. (1991)
        Vinyul chloride related hepatic angiosarcoma in a polyvinyl
        chloride autoclave cleaner in Australia.  Med. J. Aust.
        155:125-128.
    
        RTECS.  Registry of Toxic Effects of Chemical Substances (1994)
        NIOSH, Cincinnati.  CD Rom version CCOHS, Hamilton.
    
        Sax, N.I., Lewis, R.J. (1986) Chemical review: vinyl chloride. 
        Dangerous properties of industrial materials report.  July/August,
        6(4):13-43.
    
        Sax, N.I., Lewis, R.J. (1989) Dangerous propertied of industrial
        materials.  7th ed. New York, Van Nostrand Reinhold, vol.III, pp.
        3473-3474.
    
        Smith, P.M., Crossley, I.R., William, D.M.J. (1976) Portal
        hypertension in vinyl chloride production workers.  Lancet
        2:602-604.
    
        Suciu, I., Prodan, L., Ilea, E., Paduraru, A., Pascu, L. (1975)
        Clinical manifestations in vinyl chloride poisoning.  Ann. N.Y.
        Acad. Sci 246:53-69.
    
        Ward, A.M., Udnoon, S., Watkins, J., Walker, A.E., Darke, C.S.
        (1976) Immunological mechanisms in the pathogenesis of vinyl
        chloride disease. Br. Med. J. 1:936-938.
    
        Watanabe, P.G., Zampel, J.A., Pegg, D.G., Gehring, P.J. (1978)
        Hepatic macromolecular binding following vinyl chloride exposure. 
        Toxicol. Appl. Pharmacol. 44:571.
    
        Waxweiler, R.J. (1976) Neoplastic risk among workers exposed to
        vinyl chloride.  Ann. N.Y. Acad. Sci. 271:49-57.

    14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE
        ADDRESSES

        Author: Alberto Furtado Rahde
        Rua Riachuelo 677 Ap 201
        90010-270 Porto Alegre
        Brazil
        Telephone: 55 51 227 54 19
        Telefax: 55 51 224 65 63/229 90 67/339 15 64
        Date: December 1992
    

        Reviewer: Robert Garnier
        Centre Anti-Poisons de Paris
        Hôpital Fernand Widal
        200, rue du Faubourg Saint-Denis
        75475 Paris Cédex 10
        France
        Telephone: 33 1 40 05 43 29
        Telefax: 33 1 40 05 41 93
    
        Date: July 1993
    
        Peer review: INTOX Meeting, September 1994 (Drs McKeown,
        Garnier, Hartigan-Go, Wickstrom)
    
        Editor: Dr M. Ruse (October, 1997)
    



    See Also:
       Toxicological Abbreviations
       Vinyl Chloride (EHC 215, 1999)
       Vinyl Chloride (HSG 109, 1999)
       Vinyl chloride (ICSC)
       Vinyl chloride (WHO Food Additives Series 19)
       VINYL CHLORIDE (JECFA Evaluation)
       Vinyl chloride (SIDS)
       Vinyl Chloride  (IARC Summary & Evaluation, Supplement7, 1987)
       Vinyl Chloride (IARC Summary & Evaluation, Volume 7, 1974)