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Butane

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
   1.5 Main brand names, main trade names
   1.6 Main manufacturers, main 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 Hazardous characteristics
4. USES
   4.1 Uses
      4.1.1 Uses
      4.1.2 Description
   4.2 High risk circumstance 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 Other
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 and excretion
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)
   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 Neurological
         9.4.3.1 Central nervous system (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 Other
      9.4.7 Endocrine and reproductive systems
      9.4.8 Dermatological
      9.4.9 Eye, ear, 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 Others
      9.4.13 Allergic reactions
      9.4.14 Other clinical effects
      9.4.15 Special risks
   9.5 Other
   9.6 Summary
10. MANAGEMENT
   10.1 General principles
   10.2 Life supportive procedures and symptomatic/specific 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 ADDRESS(ES)
    Butane

    International Programme on Chemical Safety
    Poisons Information Monograph 945
    Chemical

    This monograph contain the following sections
    completed: 1, 2, 3, 4.1, 5, 7.1, 7.2, 9, 10, 11


    1.  NAME

        1.1  Substance

             Butane

        1.2  Group

             Aliphatic hydrocarbon

        1.3  Synonyms

             n-Butane; Butyl hydride;
             Methylethylmethane

        1.4  Identification numbers

             1.4.1  CAS number

                    106-97-8

             1.4.2  Other numbers

                    UN/NA NUMBER(S):   1011
                    RTECS NUMBER(S):   EJ4200000
                    EU EINECS/ELINCS NUMBER:  203-448-7

        1.5  Main brand names, main trade names

        1.6  Main manufacturers, main importers

    2.  SUMMARY

        2.1  Main risks and target organs

             Butane is a simple asphyxiant (that is, depriving victim
             of oxygen) with explosive and flammable potential. It is also
             widely used substance of abuse. The main target organs are in
             the central nervous and cardiovascular system.

        2.2  Summary of clinical effects

             Abuse:
    
             Initial effects:  Euphoria, excitation, blurred vision,
             slurred speech, nausea, vomiting, coughing, sneezing,
             increased salivation.
    

             As dose increases: disinhibition, confusion, perceptual
             distortion, hallucinations (ecstatic or terrifying),
             delusions (which may lead to aggressive or risk taking
             behaviour), tinnitus, ataxia. 
    
             Large doses: nystagmus, dysarthria, tachycardia, central
             nervous system (CNS) depression, drowsiness, coma and sudden
             death which may result from anoxia, vagal inhibition of the
             heart, respiratory depression, cardiac arrhythmias or trauma.
    
             Other exposures: (leakage from tanks)
             Headaches, drowsiness and coma.

        2.3  Diagnosis

             As there is no typical clinical finding in butane
             inhalation poisoning except possible unconsciousness, the
             diagnosis is made upon the history of exposure to butane in
             poorly ventilated spaces.
             In case of abuse the spraying of liquified gas directly into
             the throat, the presence of irritation followed by depression
             of CNS, together with cardiac dysrrhythmias and history of
             abuse make the diagnosis.

        2.4  First aid measures and management principles

             Abuse:
    
             Supportive and symptomatic care.  All patients should be
             given bed rest, monitored on an ECG, in a quiet environment
             for at least 4 hours. DO NOT GIVE STIMULANTS
             (e.g. adrenaline or noradrenaline, except for resuscitation). 
             Recovery normally occurs quickly once exposure has ceased but
             support of the cardiovascular and respiratory systems may be
             needed.
    
             Cardio-respiratory resuscitation, if necessary, with
             conventional treatment of arrhythmias and convulsions, with
             intensive support. Arrhythmias may respond well to beta
             blockers (e.g. atenolol). Respiratory arrest generally
             recovers with assisted ventilation. Vagal inhibition of the
             heart can lead to bradycardia or cardiac arrest. Treat
             accordingly.
    
             Other exposures:
    
             Remove from exposure to a place of fresh air. Treat hypoxia.
             Give symptomatic and supportive treatment. Assess
             neurological status.

    3.  PHYSICO-CHEMICAL PROPERTIES

        3.1  Origin of the substance

        3.2  Chemical structure

             Molecular formula: C4H10
             Molecular mass: 58.12
             Structural Formula: CH3-CH2-CH2-CH3

        3.3  Physical properties

             3.3.1  Colour

                    Colourless

             3.3.2  State/Form

                    Gas

             3.3.3  Description

                    Butane is an aliphatic hydrocarbon of
                    low-molecular weight.
                    Colourless gas with a natural gas or gasoline-like
                    odour.
    
                    Melting Point: -138.4C (-217 Deg F)
                    Boiling Point: -0.5C (31.1 Deg F)
                    Relative Density (Specific Gravity): 0.60 (Water=1)
                    Solubility in Water: Slight (3.15 Cm3 Gas/100 Cm3
                    Water At 0C)
                    Solubility in other Liquids:Soluble In Ethanol, Ether,
                    Chloroform.
                    Vapour Density: 2.11 (Air=1)
                    Vapour Pressure: 213.7 Kpa (2.1 Atm) At 21.1C
                                     356 Kpa (3.5 Atm) At 37.8C
                    Critical Temperature: 152C (305.6 Deg F)
                    Critical Pressure:  3,797 Kpa (37.47 Atm)
    
                    Conversion Factor:
                    1 Ppm = 2.38 Mg/M3; 1 Mg/M3 = 0.42 Ppm At 25C
    
                    Odour Threshold:
                    6,160 Mg/M3 (2,582 Ppm) (Recognition).  One source
                    indicates that the odour threshold exceeds 5,000 Ppm.

        3.4  Hazardous characteristics

             Compounds sold as 'butane' often contain mixtures of
             methane, ethane, propane, iso-butane and n-butane (Ramsey et
             al., 1989).

    4.  USES

        4.1  Uses

             4.1.1  Uses

             4.1.2  Description

                    Butane is found in aerosols, lighter fuel and
                    refills, small blow torches and camping stoves.  It is
                    used in organic synthesis. Pure grades are used in
                    calibrating instruments and as a food additive.
                    It is widely available.

        4.2  High risk circumstance of poisoning

        4.3  Occupationally exposed populations

    5.  ROUTES OF EXPOSURE

        5.1  Oral

        5.2  Inhalation

             Abuse:
             Direct spraying directly into the throat is the most common
             way of taking butane. Other methods are bagging (inhaling
             from a plastic bag and huffing (inhaling from a cloth or
             handkerchief).
    
             Other exposures:
             Accidental release in a confined area.

        5.3  Dermal

        5.4  Eye

        5.5  Parenteral

        5.6  Other

    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 and excretion

    7.  TOXICOLOGY

        7.1  Mode of action

             It is a simple asphyxiant and causes toxicity by
             displacing oxygen (Ellenhorn and Barceloux, 1988).  There are
             no direct systemic effects.

        7.2  Toxicity

             7.2.1  Human data

                    7.2.1.1  Adults

                             In the United Kingdom between 1988
                             and 1990, 398 people (mainly teenagers) died
                             due to abuse of fuel gas. Butane from lighter
                             refill canisters has accounted for three
                             times as many deaths as any other product
                             after the victim sprayed it down their
                             throats to attain euphoria (Russell, 1993). 
                             In studies, concentrations in air as low as
                             15% produce myocardial sensitisation and
                             dysrhythmias (Aviado and Beley, 1974).

                    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)

        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
                             "Basic analyses"
                             "Dedicated analyses"
                             "Optional analyses"

                    8.3.1.2  Urine
                             "Basic analyses"
                             "Dedicated analyses"
                             "Optional analyses"

                    8.3.1.3  Other fluids

             8.3.2  Arterial blood gas analyses

             8.3.3  Haematological analyses
                    "Basic analyses"
                    "Dedicated analyses"
                    "Optional 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

                    Initial effects: Euphoria, excitation, blurred
                    vision, slurred speech, nausea, vomiting, coughing,
                    sneezing, increased salivation.
    
                    As dose increases: disinhibition, confusion,
                    perceptual distortion, hallucinations (ecstatic or
                    terrifying), delusions (which may lead to aggressive
                    or risk taking behaviour), tinnitus, ataxia.
    

                    Large doses: nystagmus, dysarthria, tachycardia, CNS
                    depression, drowsiness, coma and sudden death which
                    may result from anoxia, vagal inhibition of the heart,
                    respiratory depression, cardiac arrhythmias or trauma
                    (Ashton, 1990).

             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

                    Vagal inhibition of the heart: is a reflex
                    response associated with stimulation of the vagal
                    nerve (ie. irritation of the larynx).  By spraying the
                    butane directly into the throat the jet of fluid can
                    cool rapidly to -20C by expansion (Ramsey et al.,
                    1989).   Sudden, or severe stimulation of the vagus
                    may result in profound bradycardia or even cardiac
                    arrest (Shepherd, 1989).
    
                    Cardiac arrhythmias: There is some experimental
                    evidence that butane can 'sensitise' the myocardium to
                    the action of adrenaline and other endogenous
                    catocholamines (Aviado and Beley, 1974).  This
                    'sensitisation' is thought to be more profound in the
                    presence of hypoxia (Shepherd, 1989).  'Sensitisation'
                    is erroneous as it is more likely that butane is a
                    membrane stabilising agent that actually stabilizes
                    the myocardial cell membrane to depolarisation. 
                    However, because of the variable response of

                    individual cells and the complex way in which the
                    myocardial electrical impulses are propagated this
                    'stability' blocks their transmission and leads to an
                    increased risk of arrhythmias. Butane is quickly
                    absorbed into the fatty tissues that line the nerve
                    fibres and then is slowly released back into the blood
                    stream, this is the probable cause of the acute,
                    direct 'postponed' deaths.
    
                    Adrenaline is released for a number of reasons and
                    influences, stress and fear being the most common. The
                    higher the level of adrenaline the greater the
                    cardiovascular effect and the more likely is the 
                    production of  arrhythmias.  There are several reasons
                    for raised adrenaline concentrations, for example:
                    hallucination which may be disturbing and frightening,
                    a desire to run, abusers who are being chased by the
                    authorities or increase during sexual activities
                    (Shepherd, 1989).

             9.4.2  Respiratory

                    Anoxia: either by occlusion of airways or
                    decreased oxygen content of inspired air

             9.4.3  Neurological

                    9.4.3.1  Central nervous system (CNS)

                             Respiratory depression:  euphoria
                             and other 'positive' effects are associated
                             with other effects, e.g. CNS depression which
                             may involve the respiratory centre of the
                             brain and therefore, theoretically, high
                             concentrations inhaled continuously could
                             lead to respiratory arrest (Shepherd, 1989).

                    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  Other

             9.4.7  Endocrine and reproductive systems

             9.4.8  Dermatological

             9.4.9  Eye, ear, 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  Others

             9.4.13 Allergic reactions

             9.4.14 Other clinical effects

             9.4.15 Special risks

        9.5  Other

        9.6  Summary

    10. MANAGEMENT

        10.1 General principles

             Supportive and symptomatic care. All patients should be
             on bed rest, monitored on an ECG, in a quiet environment for
             at least 4 hours. DO NOT GIVE STIMULANTS
             (e g adrenaline or noradrenaline, except for resuscitation). 
             Recovery normally occurs quickly once exposure has ceased but
             support of the cardiovascular and respiratory systems may be
             needed.
    
             Cardio-respiratory resuscitation, if necessary, with
             conventional treatment of arrhythmias and convulsions, with
             intensive support. Arrhythmias may respond well to beta
             blockers (e.g. atenolol). Respiratory arrest generally
             recovers with assisted ventilation. Vagal inhibition of the
             heart can lead to bradycardia or cardiac arrest. Treat
             conventionally.

        10.2 Life supportive procedures and symptomatic/specific
             treatment

             See section 10.1

        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

              Ventricular fibrillation
             A 15 year old boy habitually inhaled butane by spraying it on
             to a towel and inhaling to gain a euphoric state.  The
             effects normally took 20 minutes to wear off.  A few moments
             after one such sniffing episode he suffered severe anterior
             chest pain, screamed, ran downstairs and collapsed.  When the
             ambulance arrived he was pulseless and apnoeic.  CPR was
             started and on arrival to hospital he was in VF and had DC
             cardioversion 3 times in 30 minutes.  He was given
             intravenous (IV) lignocaine, atropine and calcium.  ECG
             showed sinus tachycardia with left-bundle-branch block. 
             Within 2 hours the QRS complex reverted to normal and there
             was widespread ST segment elevation.  He was ventilated for
             36 hours due to cerebral oedema and made a complete recovery
             in 4 weeks (Gunn et al., 1989).
    
              Myocardial infarction
             A 15 year old boy was found unresponsive and cyanosed after
             inhaling butane from a plastic bag.  CPR was given, he was
             intubated and ventilated.  He was in VT and VF which was
             treated with lignocaine, CPR and cardioversion.  On arrival
             at hospital he was in asystole; sodium bicarbonate,
             adrenaline, atropine, naloxone and lignocaine were given, he
             converted to sinus tachycardia.  He had generalised tonic
             clonic seizures, treated with diazepam, phenytoin and
             phenobarbitone. It was determined by ECG that he had suffered
             an anterolateral MI and was treated with dobutamine and
             captopril.  CT scan showed bilateral hemispheric infarcts. 
             He was ventilated for 13 days.  During his hospital admission
             his cardiac status improved but he suffered memory and
             personality problems at the time of discharge (Bauman et al.,
             1991)).
    

              Hemiparesis
             A 15 year old boy inhaled half a can of butane then fell to
             the ground with his right leg 'dead'.  On examination he was
             alert and orientated with a marked right sided hemiparesis,
             power was reduced to grade 1/5 in both arm and leg.  Within
             24 hours the power in the right hand and forearm was grade
             3/5 and he was able to stand with assistance. On discharge 5
             days later he had pronounced upper limb proximal muscle
             weakness and hemiplegic gait.  CT scan was normal (Gray and
             Lazarus, 1993).

    12. Additional information

        12.1 Specific preventive measures

        12.2 Other

    13. REFERENCES

        Ashton CH. (1990) Solvent Abuse: Little Progress after 20
        years.  BMJ  300:135-36
    
        Aviado DM & Beley MA. (1974) Toxicity of Aerosol Propellants on
        the Respiratory and Circulatory System 1. Cardiac Arrhythmias in
        the Mouse.  Toxicology 2: 31-42
    
        Bauman JE, Dean BS & Krenzelok EP. (1991) Myocardial Infarction
        and Neurodevastation following Butane Inhalation.  Vet. Hum
        Toxicol. 4: 150
    
        Ellenhorn MJ & Barceloux DG (1988) Medical Toxicology - Diagnosis
        and Treatment of Human Poisoning.  New York: Elsevier. pp
        946-968.
    
        Gray MY & Lazarus JH. (1993) Butane Inhalation and Hemiparesis.
        Clinical Toxicology 31(3): 483-485
    
        Gunn J, Wilson J & Mackintosh AF (1989) Butane Sniffing Causing
        Ventricular Fibrillation.  Lancet i: 617
    
        Ramsey J, Anderson HR, Bloor K & Flanagan RJ (1989) Mechanism of
        Sudden Death Associated with Volatile Substance Abuse.  Human
        Toxicol.  8: 261-69
    
        Russell J. (1993) Fuel of the Forgotten Deaths.  New Scientist
        1859 (137): 21-23
    
        Shepherd RT. (1989) Mechanism of Sudden Death Associated with
        Volatile Substance Abuse.  Human Toxicol  8: 287-92

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

        Author:     Medical Toxicology Unit,
                    Guys and St Thomas Trust
                    Avonley Road, London SE14 5ER, UK
    
        Date:       October, 1997
    
        Review:     As for author. 1997
    
        Peer review:         INTOX meeting, March 1998, London, UK 
                             (Members of group: Drs G. Allridge, L.
                             Lubomovir, R. Turk, C. Alonso, S. de Ben, K.
                             Hartigan-Go, N. Bates)
    
        Editor:     Dr M.Ruse (September, 1998)

    



    See Also:
       Toxicological Abbreviations
       Butane (ICSC)
       BUTANE (JECFA Evaluation)