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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): 176C to 177C.
                    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 25C 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

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        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:
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        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.
    
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        2: 108-110.
    
        Melis K, Bochner A & Janssens (1989) Accidental nasal eucalyptol
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        Myott MB (1906) Case of eucalyptus poisoning. Br Med J, 1:
        558.
    
        Neale A (1893) Case of death following blue gum (eucalyptus
        Globulus) oil. Aust Med Gazette, 12: 115-116.
    
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        1st ed. London, The Pharmaceutical Press
    
        Orr J & Edin S (1906) Eucalyptus poisoning. Br Med J, 1: 1085.
    
        Owen FJ (1885) Notes on a case of poisoning by eucalyptus. Med J
        Aust, Sept 15: 394-397.
    
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        Child, 55: 405-406.
    
        Polson CJ & Tattersall RN (1973) Clinical Toxicology, 2nd ed. New
        York, N.Y. Pitman Medical Publishing Company Ltd.
    
        Reynolds JEF ed. (1982) Martindale:the extra pharmacopoeia, 28th
        ed. London, The Pharmaceutical Press
    
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        ed. London, Royal Pharmaceutical Society
    
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        certain other products of natural origin. Fd Cosmet Toxicol, 3:
        331-324
    
        Sewell JS (1925) Poisoning by eucalyptus oil. Br Med J, 1:
        922.
    
        Spoerke DG, Vandenberg SA, Smolinske SC, Kulig KK & Rumack BH
        (1989) Eucalyptus oil: 14 cases of exposure Vet Hum Toxicol,
        31:166-168.
    
        Taylor HS (1905) A case of acute poisoning by eucalyptus oil.
        Lancet, 2: 963-964.
    
        Tibballs J (1995) Clinical effects and management of eucalyptus
        oil ingestion in infants and young children. Med J Aust, 163: 177-
        180.
    
        Tibballs J & James A (1995) Eucalyptus oil-medicinal therapy or
        folk remedy? Aust J Hosp Pharm, 25(6): 516-519.

        Webb NJA & Pitt WR (1993) Eucalyptus oil poisoning in childhood:
        41 cases in south-east Queensland. J Paediatr Child Health, 29:
        368-371.
    

        Wood FC (1900) Poisoning by oleum eucalypti. Br Med J, 1: 194

    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)
    


    See Also:
       Toxicological Abbreviations