Eucalyptus oil
| 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 substance |
| 3.2 Chemical structure |
| 3.3 Physical properties |
| 3.3.1 Colour |
| 3.3.2 State/Form |
| 3.3.3 Description |
| 3.4 Other characteristics |
| 3.4.1 Shelf-life of the substance |
| 3.4.2 Storage conditions |
| 4. USES |
| 4.1 Indications |
| 4.1.1 Indications |
| 4.1.2 Description |
| 4.2 Therapeutic dosage |
| 4.2.1 Adults |
| 4.2.2 Children |
| 4.3 Contraindications |
| 5. ROUTES OF ENTRY |
| 5.1 Oral |
| 5.2 Inhalation |
| 5.3 Dermal |
| 5.4 Eye |
| 5.5 Parenteral |
| 5.6 Others |
| 6. KINETICS |
| 6.1 Absorption by route of exposure |
| 6.2 Distribution by route of exposure |
| 6.3 Biological half-life by route of exposure |
| 6.4 Metabolism |
| 6.5 Elimination and excretion |
| 7. PHARMACOLOGY AND TOXICOLOGY |
| 7.1 Mode of action |
| 7.1.1 Toxicodynamics |
| 7.1.2 Pharmacodynamics |
| 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 |
| 7.3 Carcinogenicity |
| 7.4 Teratogenicity |
| 7.5 Mutagenicity |
| 7.6 Interactions |
| 8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS |
| 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 contact |
| 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 |
| 9.4.3.2 Peripheral nervous system |
| 9.4.3.3 Autonomic |
| 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 the 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) |
Eucalyptus oil
International Programme on Chemical Safety
Poisons Information Monograph 031
Pharmaceutical
1. NAME
1.1 Substance
Eucalyptus oil
1.2 Group
Essential oils
1.3 Synonyms
Oleum Eucalypti
Essencia de Eucalipto
Essence of Eucalyptus Rectifiee
Eucalypti Aetheroleum
Cineole
1.4 Identification numbers
1.4.1 CAS number
8000-48-4
1.4.2 Other numbers
UN 2319
1.5 Main brand names, main trade names
1.6 Main manufacturers, main importers
2. SUMMARY
2.1 Main risks and target organs
The main risk is aspiration secondary to vomiting and
loss of consciousness.
Target organs are the central nervous system, the lungs and
the gastointestinal system.
2.2 Summary of clinical effects
Poisoning affects the nervous system (loss of
consciousness, hypoventilation, depression of reflexes and
convulsions), the gastrointestinal system (abdominal pain,
vomiting and diarrhoea) and the respiratory system
(respiratory depression,dyspnoea, pneumonitis and
bronchospasm). Gastrointestinal effects are frequently the
initial effects although drowsiness may occur in a few
minutes and coma within 10 minutes. The patient may vomit
while drowsy or unconscious and aspiration is a major risk.
Tachycardia and weak irregular pulse has been noted. Muscle
weakness and ataxia may occur. Nephritis is rare but has been
recorded. Both miosis and mydriasis can occur (miosis being
more common). Central nervous system (CNS) depression or
vomiting have been delayed up to four hours. Recovery is
often within 24 hours.
It is a mild skin irritant.
Chronic effects have not been reported.
2.3 Diagnosis
In the absence of a relevant history the odour of
eucalyptus should help make the diagnosis succinct. The
breath, vomit and urine may all smell of eucalyptus.
2.4 First-aid measures and management principles
First-aid measures. Avoid milk. All ingestions require
medical assessment.
Stabilise patient by providing basic life support (ie.
airway, breathing and circulation).
Management is mainly symptomatic and supportive. The main
risk is aspiration because the principle toxic effects are
vomiting and depression of conscious state. Therefore
aggressive gastrointestinal decontamination without airway
protection may in itself be harmful. Attempts to induce
vomiting must be avoided. The best option for treating minor
or moderate poisoning is close observation.
Asymptomatic patients should be observed for six hours . If
respiratory manifestations develop after ingestion,
aspiration may have occured. An initial chest examination
(including chest x-ray) is indicated. If no abnormalities are
detected on initial chest examination, repeat six hours after
ingestion.
Careful gastric lavage and instillation of activated charcoal
or colonic washout solution should only be attempted under
general anaesthesia with endotracheal intubation.
3. PHYSICO-CHEMICAL PROPERTIES
3.1 Origin of substance
Eucalyptus oil is obtained by tesifying the oil
distilled from leaves of various species of Eucalyptus. The
major active ingredient is cineole (eucalyptol). Medicinal
eucalyptus oil contains not less than 70 % W/W of cineole; it
also contains pinene and other terpenes and may contain small
quantities of phellandrene (Reynolds, 1982). Depending on the
source -and purity- up to forty one compounds have been
detected in eucalyptus oil the main component being cineole
(Brophy et al., 1985).
3.2 Chemical structure
Chemical name:
1,3,3-Trimethyl-2-oxabicyclo[2.2.2.]-octane
Other chemical names:
1,8-epoxy-p-menthane
Molecular formula of cineole (eucalyptol): C10H18O
(Budavari, 1996)
Molecular weight: 154.25 (Budavari, 1996)
3.3 Physical properties
3.3.1 Colour
Colorless to pale yellow liquid (Budavari, 1996)
3.3.2 State/Form
Liquid-oil
3.3.3 Description
Odour: Camphoraceous odour (Reynolds, 1996,
Merck, 1996).
Taste: Pungent, spicy, cooling taste (Merck, 1996).
Solubility: Insoluble in water (Merck, 1996)
Soluble 1 in 5 of alcohol 70%,
Miscible with alcohol (90%), dehydrated
alcohol, oils, fats and paraffins
(Reynolds, 1982).
Miscible with ether, chloroform, glacial
acetic acid.
Boiling point of cineole (eucalyptol): 176°C to 177°C.
Density of cineole (eucalyptol) 0.921 to 0.923
(Budavari, 1996).
3.4 Other characteristics
3.4.1 Shelf-life of the substance
No data available.
3.4.2 Storage conditions
Products containing eucalyptus oil should be
stored at a temperature not exceeding 25°C in well
filled containers. Protect from light (Reynolds,
1982). Liquid products containing eucalyptus oil are
best stored in child resistant containers.
4. USES
4.1 Indications
4.1.1 Indications
4.1.2 Description
Eucalyptus oil has been used for inhalation as
a decongestant often in combination with other
volatile substances.
It has been used orally for catarrh and coughs.
It has been applied as a rubefacient.
It has been used as a flavouring (Reynolds, 1996).
It is used extensively as a cleaning solvent.
It is used extensively as a fragrance.
It is used as an antiseptic, febrifuge and expectorant
in herbal medicine (Newell, 1996).
4.2 Therapeutic dosage
4.2.1 Adults
Recommended adult oral dose is 0.05 mL to 0.2
mL (Reynolds, 1982).
Has been used as a topical rubefacient at 0.5% to 3%.
4.2.2 Children
There is no recommended oral paediatric dose.
4.3 Contraindications
Not relevant.
5. ROUTES OF ENTRY
5.1 Oral
Well absorped orally. Absorption expected to increase in
the presence of lipid substances such as milk.
5.2 Inhalation
Inhalation of the liquid or aerosol can be directly
toxic to the lungs. No data available on systemic absorption
via the lungs in humans.
5.3 Dermal
No data available
5.4 Eye
No data available
5.5 Parenteral
No data available
5.6 Others
No data available
6. KINETICS
6.1 Absorption by route of exposure
Gastrointestinal absorption is rapid. It is lipid
soluble and absorption is likely to be enhanced with foods
such as milk. Bioavailability is unknown.
6.2 Distribution by route of exposure
No data available
6.3 Biological half-life by route of exposure
No data available
6.4 Metabolism
No data available
6.5 Elimination and excretion
It is excreted via the lungs, urine, skin and faeces
(MacPherson, 1925). Yet, this has not been quantitatively
determined in humans.
7. PHARMACOLOGY AND TOXICOLOGY
7.1 Mode of action
7.1.1 Toxicodynamics
See 7.1.2
7.1.2 Pharmacodynamics
Cellular mode of action is unknown. Its medical
use as a decongestant, or skin rubefucient is
traditional but with no fairly established
bases.
7.2 Toxicity
7.2.1 Human data
7.2.1.1 Adults
Probable lethal dose 0.05 mL to 0.5
mL/kg (Hindle, 1994).
7.2.1.2 Children
Although many children remain
asymptomatic after ingestions clinically
significant symptoms have been reported
following ingestion of less than one
teaspoonful (Craig, 1953; Owen, 1885).
Anticipate minor depression of consciousness
after ingestion of 2 mL to 3mL of pure
eucalyptus oil and significant depression
after more than 5 mL (Tibballs, 1995).
Severe poisoning has occurred after ingestion
of 4 mL to 5 mL (Allan, 1910; Foggie, 1911).
Children have recovered after 14 mL and 24 mL
(Sewell, 1925; Benjamin, 1906).
7.2.2 Relevant animal data
LD50 (ORAL) rat of cineole (Eucalyptol) 2480
mg/kg (Jenner et al., 1964)
7.2.3 Relevant in vitro data
No information available.
7.3 Carcinogenicity
Eucalyptus oil appeared to have weak tumour promoting
activity on mouse skin (Roe & Field, 1965).
7.4 Teratogenicity
No information available
7.5 Mutagenicity
No information available
7.6 Interactions
No information available
8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS
9. CLINICAL EFFECTS
9.1 Acute poisoning
9.1.1 Ingestion
Poisoning affects the central nervous system
(loss of consciousness, hypoventilation, depression of
reflexes and convulsions), the gastrointestinal system
(abdominal pain, vomiting and diarrhoea) and the
respiratory system (respiratory depression, dyspnoea,
pneumonitis and bronchospasm) (Tibballs, 1995).
Gastrointestinal effects are frequently the initial
effects (Foggie, 1911) although drowsiness may occur
in a few minutes and coma within 10 minutes (Craig,
1953). The patient may vomit while drowsy or
unconscious and aspiration is a major risk.
Tachycardia and weak irregular pulse has been noted
(Kirkness, 1910). Muscle weakness and ataxia may occur
(MacPherson, 1925). Nephritis is rare but has been
recorded (Gurr & Scroggie, 1965). Both miosis and
mydriasis can occur(miosis being more common) (Webb &
Pitt, 1993). CNS depression or vomiting have been
delayed up to four hours (Wood, 1900; Foggie, 1911).
Recovery is often within 24 hours.
9.1.2 Inhalation
Inhalation of eucalyptus oil either as liquid
or aerosol may result in pneumonitis (Krueger, 1967).
Inhalation of vapour may be used medicinally and there
is no data available on toxicity by this route
(Tibballs & James, 1995).
9.1.3 Skin exposure
Possible irritant.
9.1.4 Eye contact
Possible irritant.
9.1.5 Parenteral exposure
No data available.
9.1.6 Other
Not relevant.
9.2 Chronic poisoning
9.2.1 Ingestion
No data available.
9.2.2 Inhalation
No data available.
9.2.3 Skin contact
No data available.
9.2.4 Eye contact
No data available.
9.2.5 Parenteral exposure
Not relevant.
9.2.6 Other
Not relevant.
9.3 Course, prognosis, cause of death
The toxic effects are rapid in onset and extensive
(Patel & Wiggins, 1980).
Gastrointestinal symptoms may occur initially followed by
unconsciousness. However in some patients central nervous
system (CNS) effects occur first and aspiration is a risk if
the patient vomits.
The initial gastrointestinal effects are: Burning sensation
in the mouth, vomiting, diarrhoea and epigastric pain.
Vomiting may be delayed for periods varying from minutes up
to four hours.
The initial CNS effects may be giddiness, ataxia,
disorientation within minutes of ingestion (Kirkness, 1910)
loss of reflexes and unconsciousness within 10 to 15 minutes.
Vertigo and ataxia may be indicative of a relatively mild
degree of poisoning, the more serious cases being quickly
overcome by stupor (Craig, 1953). Onset of coma may be from
several minutes (Sewell, 1925) up to two hours (Wood, 1900).
Coma may last from half an hour (Orr & Edin, 1906), to eight
hours (Benjamin,1906) and up to three days (Gurr & Scroggie).
Convulsions are rare in the adult but may be prominent in the
child (Chun, 1951).
The respiratory system can respond be exhibiting
bronchospasm, pulmonary oedema, tachypnoea or irregular
shallow respirations. The non comatose patient often
complains of a feeling of suffocation. Aspiration pneumonia
is a distinct possibility.
Prognosis:
Permanent sequelae following recovery from the acute phase
have not been reported although symptoms such as drowsiness,
ataxia and fatigue may occasionally persist for one to two
weeks (Gurr & Scroggie, 1965; Kirkness, 1910).
Those patients who suffered severe gastric irritation who
promptly vomited fared better but almost all made an
uneventful recovery within 24 hours (Polson & Tattersall,
1973). Recovery may be interrupted or reversed by
bronchopneumonia (Myott, 1906).
Death has occurred from within 15 minutes to 15 hours after
ingestion. One patient died 40 hours after taking the oil
relapsing after apparent recovery (MacPherson, 1925).
9.4 Systematic description of clinical effects
9.4.1 Cardiovascular
Tachycardia and hypotension have been reported.
Evidence of cardiovascular collapse has been reported
with severe intoxication (Gurr & Scroggie, 1965).
EKG abnormalities have been reported (Spoerke et al.,
1989).
9.4.2 Respiratory
Respiratory problems include bronchospasm,
tachypnoea, pulmonary oedema, respiratory depression
(Patel & Wiggins, 1980) and pneumonitis following
aspiration of the oil (Webb & Pitt, 1993).
9.4.3 Neurological
9.4.3.1 Central nervous system
Dizziness, slurred speech, ataxia,
headache and drowsiness are common
features.Serious poisoning is usually marked
by progression to loss of consciousness with
diminution or absence of reflex activity and
evidence of medullary depression (Gurr &
Scroggie, 1965).
Seizures have been reported and are more
frequent in children than adults (Chun,
1951).
9.4.3.2 Peripheral nervous system
Muscle weakness, paresis or
paralysis have been reported (MacPherson,
1925).
Deep tendon reflexes may be decreased or even
absent (Patel & Wiggins, 1980).
9.4.3.3 Autonomic
Pupils typically pin-point but may
remain active or dilated and fixed
(MacPherson, 1925).
9.4.3.4 Skeletal and smooth muscle
No information available.
9.4.4 Gastrointestinal
Acute ingestion may result in a burning
sensation in the mouth and throat, abdominal pain,
nausea, vomiting (the most common feature) and
diarrhoea (MacPherson, 1925).
9.4.5 Hepatic
No data available
9.4.6 Urinary
9.4.6.1 Renal
Urinary tract symptoms are only
occasionally mentioned and there is little
evidence of direct nephrotoxicity following
doses of up to 30 mL in an adult or older
child.
9.4.6.2 Other
Not relevant
9.4.7 Endocrine and reproductive systems
No data available
9.4.8 Dermatological
Topical exposure may cause redness, irritation
and burning sensation that cleared in an hour after
washing (Spoerke et al., 1989).
Pruritis and an itchy maculopapular rash have been
reported (Webb & Pitt, 1993).
9.4.9 Eye, ear, nose, throat: local effects
Burning sensation in the throat is commonly
reported after ingestion (Sewell, 1925).
Eucalyptus oil inadvertently given intranasally has
caused irritated nasal mucous membranes (Melis et al.
1989).
9.4.10 Haematological
There have been isolated reports of changes to
PT time (Gurr & Scroggie, 1965) and epistaxis (Spoerke
et al. 1989).
9.4.11 Immunological
No data available
9.4.12 Metabolic
9.4.12.1 Acid-base disturbances
No data available
9.4.12.2 Fluid and electrolyte disturbances
No data available
9.4.12.3 Others
Not relevant
9.4.13 Allergic reactions
No data available
9.4.14 Other clinical effects
Not relevant
9.4.15 Special risks
Pregnancy:
No data available
Breast feeding:
No data available
Enzyme deficiencies:
No data available
9.5 Other
Not relevant
9.6 Summary
10. MANAGEMENT
10.1 General principles
Management is mainly symptomatic and supportive. The
main risk is aspiration because the principle toxic effects
are vomiting and depression of conscious state. Therefore
aggressive gastrointestinal decontamination without airway
protection may in itself be harmful. Attempts to induce
vomiting must be avoided. The best option for treating minor
or moderate poisoning is close observation.
Asymptomatic patients should be observed for six hours . If
respiratory manifestations develop after ingestion,
aspiration may have occured.An initial chest examination
(including chest x-ray) is indicated. If no abnormalities are
detected on initial chest examination, repeat six hours after
ingestion.
Careful gastric lavage and instillation of activated charcoal
or colonic washout solution should only be attempted under
general anaesthesia with endotracheal intubation (Tibballs,
1995).
10.2 Life supportive procedures and symptomatic/specific treatment
Make a proper assessment of airway, breathing,
circulation and neurological status of the patient.
Symptomatic and supportive measures should be undertaken
(Tibballs, 1995).
10.3 Decontamination
Emesis is contraindicated.
Activated charcoal is indicated if the patient is unconscious
or a large ingestion is suspected. Aspiration of eucalyptus
and/or charcoal is a major risk. Therefore careful gastric
lavage and instillation of activated charcoal or colonic
washout solution should only be attempted under general
anaesthesia with endotracheal intubation.
The role of catharsis has not been adequately
assessed.
10.4 Enhanced elimination
No data available. However, although peritoneal and
hemodialysis has been reported for the management of
eucalyptus oil ingestion- its routine use has not been
established.
10.5 Antidote treatment
10.5.1 Adults
There is no specific antidote
10.5.2 Children
There is no specific antidote
10.6 Management discussion
The efficacy of activated charcoal in eucalyptus oil
poisoning has yet to be proved.
All patients should be medically assessed regardless of the
amount ingested, particularly children.
11. ILLUSTRATIVE CASES
11.1 Case reports from the literature
After evening supper an adult male took a large
teaspoonful of eucalyptus oil. He immediately experienced
oesophageal pain followed by gasping for breath,
restlessness, convulsive movements of his hands and was
semicomatose passing to coma. Vomiting was induced prior to
him becoming comatose and he gradually recovered
consciousness being quite well by next morning
(Taylor,1905).
An adult male who took 10 mL to 15 mL of eucalyptus oil
became ataxic and faint within ten minutes. He soon had
distressing dyspnoea, weak pulse and violent vomiting. His
skin was greenish -yellow. Half an hour after ingestion he
was very drowsy, had painful and excessive micturition and
was experiencing violent diarrhoea. For three days he was
drowsy, ataxic and his skin retained the chlorotic hue. For
nearly a fortnight his breathe, faeces and skin smelt of the
oil and it was a clear fortnight before he felt really well
again (Kirkness, 1910).
An adult male took approximately 25 mL of eucalyptus oil.
Within two hours he was dazed and friends successfully
induced vomiting. Four hours after ingestion he was cyanosed
with laboured breathing, foam in the mouth, congestion,
rhonchi and moist rales throughout both lungs. He was given
oxygen with a stimulant and five to six hours later was
restored enough to answer questions. However 13 hours after
ingestion he complained of difficulty and pain in drawing his
breathe. Breathing became more rapid and laboured, the pulse
quick and thready and he died forty hours after taking the
oil (Myott, 1906). Presumably death was due to
bronchopneumonia.
An adult who ingested 120 mL to 220 mL had severe poisoning
and was successfully treated with mannitol, haemodialysis and
peritoneal dialysis (Gurr & Scroggie, 1965).
A 7 month old boy was offered a teaspoonful of eucalyptus
oil. He coughed, choked and some of the oil was spilled. He
was pale, collapsed with rapid shallow respirations and
feeble pulse 25 minutes later. Limbs were flaccid, pupils
pin-point, rhonchi being heard at both bases. His stomach was
washed out and three hours later he was showing spontaneous
movement. At 24 hours his general state was good. The odour
stayed on his breath for 72 hours (Craig, 1953).
This case is mentioned because it is often the source of the
quote that as little as 1 mL can cause transient coma in an
infant. From the history this may or may not be the case but
is hardly certain.
A six year old boy took 4 mL to 5 mL of eucalyptus oil and
within two hours severe vomiting had set in. Five hours later
he was semi-comatose. There was no cough and breathing was
shallow. After approximately eight hours the heavy comatose
condition appeared to pass off. He slept well but beyond
being tired the next day was quite well. The breathe smelt of
eucalyptus oil for three days. In summary the poisoning
manifest itself as gastrointestinal irritation and cerebral
paresis (Foggie, 1911).
A 10 year old boy took approximately 15 mL of eucalyptus oil.
In a few minutes he was gasping for air and vomited heavily.
He breathed well for about an hour when the struggle for air
increased until his death 15 hours after ingestion of the
oil. He spoke rationally several times up to within an hour
of death. There was only one vomit (Neale, 1893).
A 3 year old boy took 10 mL of eucalyptus oil. Within 30
minutes he was deeply comatose and his breath smelt strongly
of eucalyptus. Pupils were constricted, muscle tone markedly
reduced and tendon reflexes could not be elicited.
Respirations were shallow and irregular. Blood pressure was
75/40 mmHg. Respiratory rate, blood pressure and pulse
returned to normal after two and a half hours. After five
hours consciousness had gradually been regained and by 24
hours physical examination was normal apart from a faint
smell of eucalyptus on the breathe (Patel & Wiggins,
1980).
A 6 year old was given approximately 15 mL of eucalyptus oil
and experienced only slight drowsiness (Atkinson, 1909).
12. ADDITIONAL INFORMATION
12.1 Specific preventive measures
No data available.
12.2 Other
Other sources of information:
Dayal R & Ayyar KS (1986) Analysis of medicinal oil from
Eucalyptus globulus.ssp. bicostata leaves. Planta Medica, 52:
162.
Ryan DC (1951) Acute accidental poisoning in children: its
incidence, diagnosis and treatment. Med J Aust, 2: 702-708.
Sheaf E (1888) Toxic action of extract of eucalyptus. Br Med
J, 1: 849-850.
13. REFERENCES
Allan J (1910) Poisoning by oil of eucalyptus. Br Med J, 1:
569
Atkinson TR (1909) Eucalyptus oil. Br Med J, 2: 1656.
Benjamin J (1906) Eucalyptus poisoning. Br Med J, 1: 1020.
Brophy JJ, Lassak EV & Toia RF (1985) The steam volatile leaf oil
of Eucalyptus pulverulenta. Planta Medica, 51: 170-171.
Budavari S ed. (1996) The Merck Index: an encyclopedia of
chemicals, drugs and biologicals, 12th ed. Rahway, New Jersey,
Merck and Co., Inc.
Chun LT (1951) Accidental poisoning in children with special
reference to kerosene poisoning. Hawaii Med J, 11(2) Nov-Dec:
83-87.
Craig JD (1953) Poisoning by the volatile oils in childhood.
Arch Dis Child, 28: 475-483.
Foggie WE (1911) Eucalyptus oil poisoning. Br Med J, 1: 359-
360.
Gurr RW & Scroggie JG (1965) Eucalyptus oil poisoning treated by
dialysis and mannitol infusion. Aust Ann Med, 4: 238-249.
Hindle RC (1994) Eucalyptus oil ingestion. N Z Med J, May:
185-186.
Jenner PM, Hagan EC, Taylor JM, Cook EL & Fitzhugh OG (1964) Food
flavourings and compounds of related structure. Fd Cosmet Toxicol,
2: 327-343.
Kirkness WR (1910) Poisoning by oil of eucalyptus. Br Med J, 1:
261.
Krueger RP (1967) Chemical pneumonitis from medicated vapour
aerosol spraying. Clin Ped, Aug: 465-467.
MacPherson J (1925) The toxicology of eucalyptus oil. Med J Aust,
2: 108-110.
Melis K, Bochner A & Janssens (1989) Accidental nasal eucalyptol
and menthol installation. Eur J Pediatr, 148: 786-787.
Myott MB (1906) Case of eucalyptus poisoning. Br Med J, 1:
558.
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14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE
ADDRESS(ES)
Author: James Magarey
Victorian Poison Information Centre
Flemington Rd,
Parkville
Victoria 3052
Australia
Telephone: 61-3-93455680
Fax: 61-3-93491261
E Mail: poison@cryptic.rch.unimelb.edu.au
Written: June, 1997
Reviewer: Ms R. McKeown
ACT Poisons Information Service
Canberra Hospital
Garran ACT 2605
Australia
Telephone: 61-6-2852852
Fax: 61-6-2443334
Email: actpic@leprosy.anu.edu.au
Peer review: INTOX Meeting, London UK, March 1998
Editor: Dr M. Ruse (September, 1998)