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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: -138.4ーC (-217 Deg F)
Boiling Point: -0.5ーC (31.1 Deg F)
Relative Density (Specific Gravity): 0.60 (Water=1)
Solubility in Water: Slight (3.15 Cm3 Gas/100 Cm3
Water At 0ーC)
Solubility in other Liquids:Soluble In Ethanol, Ether,
Chloroform.
Vapour Density: 2.11 (Air=1)
Vapour Pressure: 213.7 Kpa (2.1 Atm) At 21.1ーC
356 Kpa (3.5 Atm) At 37.8ーC
Critical Temperature: 152ーC (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 25ーC
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 -20ーC 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,
Guy徭 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)