Camphor (UK PID)

Monograph for UKPID

CAMPHOR

Sarah McCrea

National Poisons Information Service (London Centre)
Medical Toxicology Unit
Guy's & St Thomas' Hospital Trust
Avonley Road
London
SE14 5ER
UK

This monograph has been produced by staff of a National Poisons
Information Service Centre in the United Kingdom. The work was
commissioned and funded by the UK Departments of Health, and was
designed as a source of detailed information for use by poisons
information centres.

Peer review group: Directors of the UK National Poisons Information
Service.

1. SUBSTANCE/PRODUCT NAME

Camphor

last updated: 17 March 1996

1.1 Origin of substance

Steam distillation of communited Cinnamomum camphora trees (which
should be at least 50 years old) and purification by sublimination.
Also found in the plant Lippia dulcis Trev (not a major industrial
source) (Compadre et al 1986). Can also be produced synthetically,
modern processes start with vinyl chloride and cyclopentadiene to
obtain important intermediate dehydronorbornyl chloride. The naturally
occurring form is dextrorotatory and the synthetic form optically
inactive (Budavari 1989, Reynolds 1993).

1.2 Name

1.2.1 Brand/trade name

Balmosa Cream (camphor 4%, menthol 2%, methyl salicylate 4%, capsicum
oleoresin 0.035%) (Pharmax Healthcare)
Boots Vapour Rub (Boots)
Earex (almond oil 33.33%, arachis oil 33.33%, camphor oil 33.33%)
(Seton Healthcare)
Mentholatum Vapour Rub (camphor 9%, menthol 1.35%, methyl salicylate
0.33%) (Mentholatum)
Nasciodine (iodine 1.26%, menthol 0.59%, methyl salicylate 3.87%,
turpentine oil 3.87%, camphor 3.87%)
Nicobrevin (methyl valerate 100mg, quinine 15mg, camphor 10mg,
eucalyptus oil 10mg) (Intercare Products)
PR Heat Spray (camphor 0.62%, methyl salicylate 1.24%, ethyl
nicotinate 1.1%) (Crookes Healthcare)
Radian-B (liniment and spray: menthol 1.4%, camphor 0.6%, ammonium
salicylate 1%, salicylic acid 0.54%. rub: menthol 2.54%, camphor
1.43%, methyl salicylate 0.42%, capsicin 0.042%. cream: camphor 1.43%,
menthol 2.54%, methyl salicylate 0.42%, oleoresin capsicum 0.005%)
(Roche Consumer Health)
Tixylix inhalant (camphor 60mg, menthol 25mg, turpentine oil 50mg,
eucalyptus oil 20mg) (Intercare Products)
Vicks Inhaler (camphor 41.54%, menthol 41.54%, siberian pine needle
oil 4.65%) %) (Procter and Gamble)
Vicks Sinex (oxymetazoline 0.05%, menthol 0.025%, camphor 0.015%,
eucalyptus oil 0.0075%) %) (Procter and Gamble)
Vicks Vaporub (menthol 2.82%, camphor 5.46%, eucalyptus oil 1.35%,
turpentine oil 4.71%) (Procter and Gamble)

Non-proprietary preparations:

Camphor Linctus compound (APF): Camphor spirit compound 1ml, glycerol
1.5ml, tolu syrup to 5ml.

Camphor Liniment (BP 1973): Camphor 20% w/w in arachis oil (AKA Camph.
Lin; Camphorated oil).
Camphor Spirit (USP): Camphor 10g, alcohol to 100ml.
Camphor Spirit Compound (APF): Camphor 300mg, benzoic acid 500mg,
anise oil 0.3ml, alcohol (60%) to 100ml.
Concentrated Camphor Water (BP) Camphor 4g, alcohol (90%) 60ml, water
to 100ml.

1.2.2 Generic name

Camphor

1.2.3 Synonyms

1,7,7-Trimethylbicyclo[2.2.1]heptan-2-one; 2-bornanone; 2-oxobornane;
2-camphanone; 2-keto-1,7,7-trimethyl-norcamphane;
2-keto-1,7,7-trimethylnor-camphane; 1,7,7-trimethylnorcamphor;
gum camphor; Japan camphor; Formosa camphor; laurel camphor;
camphor-natural, camphor-synthetic; huile de camphre (French); kampfer
(German); matricaria camphor; anemone camphor.

1.2.4 Common names/street names

1.3 BNF pharmacotherapeutic group

None.

1.4 Reference numbers

Camphor

CAS 76222
RTECS EX1225000
EINECS 2009450

Camphor-l-

CAS 464482
RTECS EX1250000
EINECS 2073547
UN 2717

Camphor (1R, 4R)(+)

CAS 464493
RTECS EX1260000
EINECS 2073552

1.5 Manufacturer of camphor containing products

Crookes Healthcare, PO Box 57, Central Pk, Lenton Lane, Nottingham,
NG7 2LJ.
Tel: 0115 950 7431 Fax: 0115 968722

Intercare Products Ltd, 7 The Business Centre, Molly Millars Lane,
Wokingham, Berks, RG11 2QZ.
Tel: 01734 79345 Fax: 01734 772114

Mentholatum Co Ltd, 1 Redwood Ave, Peel Park Campus, East Kilbride,
Glasgow, G74 5PF.
Tel: 01355 848484 Fax: 01355 263387

Pharmax Ltd, Bourne Rd, Bexley, Kent, DA5 1NX.
Tel: 01322 550550 Fax: 01322 558776.

Procter and Gamble (Health and Beauty Care) Ltd, The Heights,
Brooklands, Weybridge, Surrey, KT13 0XP.
Tel: 01932 896000 Fax: 01932 896200

Roche Consumer Health, P.O Box 8, Broadwater Rd, Welwyn Garden City,
Herts, AL7 3AY.
Tel: 01707 366000 Fax: 01707 338297

Seton Healthcare Group Plc, Tubiton Hse, Medlock St, Oldham, Lancs,
OL1 3HS.
Tel: 0161 652 2222 Fax: 0161 626 9090

1.6 Supplier/importer/agent/ licence holder

Not relevant

1.7 Presentation

1.7.1 Form

1.7.2 Formulation details

1.7.3 Pack sizes available

1.7.4 Packaging

1.8 Physico-chemical properties

Chemical structure C₁₀H₁₆O

Physical state Crystalline solid.

Colour Colourless or white.

Odour Pungent

Solubility in water and organic solvents

Slightly soluble in water, soluble in alcohol, ether, benzene,
acetone, oil of turpentine, glacial acetic acid, chloroform, carbon
disulphide, solvent naphtha and fixed and volatile oils. Also soluble
in aniline, nitrobenzene, tetralin, decalin, methylhexalin, petroleum

ether, higher alcohols, concentrated mineral acids, phenol, liquid
ammonia and liquid sulphur dioxide.

Autoignition temperature 871°F (466°C)

Important chemical interactions

Liquefies when triturated with chloral hydrate, menthol, resorcinol,
salol, B-napthol, thymol, phenol, urethan (Budavari 1989). Camphor can
diffuse through polyethylene (Polythene) (Reynolds 1989).

Major products of combustion/pyrolysis

Carbon monoxide may be formed

Flammability Moderate
Boiling point 204°C
Density d=0.992 @ 25°C/4°C
Relative vapour density 5.24
Flash point 150°F (65.5°C)

1.9 Uses

1.9.1 Indications

Camphor acts as a counter-irritant, rubefacient and mild analgesic and
is included in liniments for relief of fibrositis, neuralgia and
similar conditions. By ingestion camphor has irritant and carminative
properties and has been used as a mild expectorant and to relieve
griping. Camphor has been used as a circulatory and respiratory
stimulant (as a solution in oil given subcutaneously or
intramuscularly), this use is considered hazardous. It has been used
in combination with menthol and chenodeoxycholic acid to aid dispersal
of bile duct stones, although this is no longer recommended (Reynolds
1989).

Also used as a plasticizer for cellulose nitrate; chemical
intermediate, other explosives and lacquers, insecticides, moth and
mildew proofings, tooth powders, flavouring, embalming, pyrotechnics
(Saks and Lewis 1987).

1.9.2 Therapeutic doses

1.9.2.1 Adults

In the past, when camphor was used medicinally, the oral doses ranged
from 120-300mg (Wade 1977). The parenteral dose range was from 60-
200mg (not recommended any more).

1.9.2.2 Children

1.9.3 Contraindications

Camphor and camphor containing products should be avoided in children
who have a history of febrile convulsions or other predisposing
factors for convulsions (Galland et al 1992).

1.9.4 Abuses

Abuse of camphor for its stimulant properties has been reported
(Koppel et al 1982). Vicks VapoRub and Vicks Sinex have reportedly
been used, by inhalation and skin application, by nightclubbers to
enhance the effects of MDMA (Rayner 1991). It has been used,
historically, to procure abortion (Vasey and Karayannopoulos 1972),
and the plant Lippia dulcis Trev., which contains camphor, may still
be used for this purpose in South America (Compadre et al 1986).

1.10 Pharmacokinetics

1.10.1 Absorption

Camphor is well absorbed after inhalation, ingestion or dermal
exposure (Baselt and Cravey 1990). Peak plasma levels reached by 1
hour post-ingestion when 200mg camphor was ingested with a solvent
(Tween 80), and 3 hours post-ingestion when taken without a solvent
(Koeppel et al 1988).

1.10.2 Distribution

Volume of distribution 2-4 L/kg (Koeppel et al 1988). Plasma protein
binding has been estimated as 61% (Koppel et al 1982).

1.10.3 Metabolism

Hydroxylation in the 3-, 5-, 8-, and 9-position. 5- and 8- (or 9-)
hydroxycamphor further oxidised to a ketone and carbonic acid. The
carbonic acid VI is conjugated with glucoronic acid (Koppel et al
1982).

1.10.4 Elimination

The glucoronide is excreted in the urine, some camphor is excreted
unchanged in urine and from the lungs.

1.10.5 Half-life

167 minutes (200mg camphor ingested alone); 93 minutes (200mg camphor
ingested with a solvent - Tween 80) (Koppel et al 1988).

1.10.6 Special populations

No data available.

1.10.7 Breast milk

No data available. It seems likely that camphor will be excreted in
breast milk.

1.11 Toxicokinetics

1.11.1 Absorption

Peak plasma levels of camphor were reached within an hour of ingestion
of an unknown quantity of 10% camphor spirit (10% camphor, 70%
isopropanol, 20% water) by an adult female (Koppel et al 1988).

1.11.2 Distribution

Camphor crosses the placental barrier. An infant born prematurely to a
woman who had ingested 50ml of camphorated oil was healthy, but its
mouth and skin smelt of camphor, as did the amniotic fluid (she gave
birth within 20 hours of the ingestion) (Weiss and Catalano 1973).

Camphor was found in the liver, kidneys and brain of an infant who
died within 30 minutes of birth, whose mother had ingested about 12g
of camphor 17 hours previously (Riggs et al 1965).

1.11.3 Metabolism

1.11.4 Elimination

Six metabolites of camphor were detected in the urine of two men who
had ingested 6-10g of camphor (5-hydroxycamphor; 5-ketocamphor;
9-hydroxycamphor; 8-hydroxycamphor; 3-hydroxycamphor; 8 or 9-camphor
carbonic acid trimethylsilylester). Camphor was also detected in its
unchanged form (Koppel et al 1982).

1.11.5 Half-life

No data.

1.11.6 Special populations

No data.

1.11.7 Breast milk

No data.

2 ADVERSE EFFECTS AND INTERACTIONS

Convulsions were reported in a small child following skin exposure to
camphor spirit, and recurred a year later on brief inhalation exposure
(Skoglund et al 1977). Deafness has been reported in association with
camphor (Davies 1985). Ulceration of the mucous membranes has been
reported following the use of toothache solutions containing camphor
(along with menthol, phenol, clove oil and chloroform) (Davies 1985).

3 SUMMARY

4 EPIDEMIOLOGY OF POISONING

Most severe cases are associated with the ingestion of camphorated
oil, either deliberately or in mistake for other medication e.g.
castor oil. Camphorated oil has now been removed from the market in
both the UK and the US (Reynolds, 1993) but may still be present in
some households. Abuse of camphor for its stimulant properties has
been reported (Koppel et al 1982).

A review of 182 cases of camphor ingestion reported to two poisons
centres between 1980-1983 found that the 101 cases who ingested less
than 2mg/kg remained asymptomatic. 90% of the patients ingesting over
2mg/kg remained asymptomatic, 4% developed minor clinical effects
(sleepy but rousable, gagging, crying - mean dose 15mg/kg), and 6%
developed major clinical effects (syncope, cyanosis, hypotension,
arryhthmias, mental status changes - mean dose 152mg/kg). There were
no deaths in this series. The authors also reviewed the literature
from 1964 -1983, and found the mean dose ingested by patients with
major symptoms to be 124mg/kg, with the mean dose in fatal cases being
199mg/kg (Geller et al 1984).

From 1985-1989, 32,362 human exposures to camphor were reported to the
American Association of Poison Control Centres (AAPCC). Of these,
life-threatening toxicity occurred in 33 children, but there were no
paediatric deaths. In 5 of the cases the products contained more than
11% camphor, although products of that strength had been discontinued
in 1983, at the request of the FDA. In 14 cases the products involved
contained between 10-11% camphor, and in 4 cases 6-10% camphor. Major
toxic symptoms were seen in 7 cases where the camphor content of the
product ingested was less than 5% (Committee on Drugs 1994).

Three of 23 children who had been reported to the Poison Control
Centre and Pharmacovigilance Centre of Marseilles as suffering from
febrile convulsions had been recently treated with medications
containing camphor. The authors also reported the case of two
epileptics who developed non-febrile convulsions following dermal use
of VicksVaporub. They suggested that camphor and camphor containing
products should be avoided in children who had a history of febrile
convulsions or other predisposing factors for convulsions (Galland et
al 1992).

5 MECHANISM OF ACTION/TOXICITY

5.1 Mechanism

Camphor has been described as a counter-irritant, but when applied to
the skin of volunteers as a 20% solution in alcohol it produced no
significant sensation of irritation or pain at normal skin
temperatures. It did appear to have a slight sensitising effect on the
perception of temperature change during heating and cooling, and
increased the sensation of burning at high temperatures (Green 1990).

5.2 Toxic dose

A review of 182 cases of camphor ingestion reported to two poisons
centres between 1980-1983 found that the 101 cases who ingested less
than 2mg/kg remained asymptomatic. 90% of the patients ingesting over
2mg/kg remained asymptomatic, 4% developed minor symptoms (mean dose
15mg/kg), and 6% developed major symptoms (mean dose 152mg/kg). There
were no deaths in this series. The authors also reviewed the
literature from 1964-1983, and found the mean dose ingested by
patients with major symptoms to be 124mg/kg, with the mean dose in
fatal cases being 199mg/kg. They suggested, based on their analysis of
these figures, that patients ingesting less than 10mg/kg of camphor
and displaying no symptoms required no treatment (Geller et al 1984).

Adults have survived ingestions of up to 42g, but usually doses in
excess of 2g produce dangerous effects. Fatal doses in children have
ranged from 0.7-1.0g (Committee on Drugs 1994).

6 FEATURES OF POISONING

6.1 Acute

6.1.1 Ingestion

Most common route of exposure. Nausea, vomiting, convulsions, coma and
respiratory depression may occur.

6.1.2 Inhalation

Convulsions were reported in a small child following skin exposure to
camphor spirit, and recurred a year later on brief inhalation exposure
(Skoglund et al 1977). A 3 month old infant became pale, collapsed,
stopped breathing and had convulsions immediately after a single
inhalation of Vicks Inhaler (40% camphor [sic]) (Bavoux et al 1985).

6.1.3 Dermal

Camphor applied to the skin of volunteers as a 20% solution in alcohol
produced no significant sensation of irritation or pain at normal skin
temperatures (Green 1990).

Table 1

Blood levels Dose Author

1.95mg/100ml 7h pi
undetectable 21h pi 0.7g (convulsions) Phelan 1976
0.0015mg/100ml 0.5-1g (asymptomatic) Phelan 1976
300 + 400ng/ml (nk time) 6-10g (symptomatic) Koppel et al 1982
ND 3g/kg (24.5) over 6 months Jimenez et al 1983
ND 9g/24h (dermal/symptomatic) Mercier et al 1984
0.3µg/ml (9h pi) 1.5g (symptomatic) Bavoux et al 1985
>2µg/ml NK (symptomatic) Bavoux et al 1985
0.45µg/ml (17h post exposure) 160mg/kg/24h (dermal/symptomatic) Bavoux et al 1985
ND 112mg/18h (symptomatic) Bavoux et al 1985
5.5µg/ml (1h pi) NK Koppel et al 1988
ND 1g (approx) (symptomatic) Gibson et al 1989
ND 1g (19months/death) Smith and Margolis 1954
Present, not measured 12g (symptomatic and baby died) Riggs et al 1965
ND 12g (symptomatic) Ginn et al 1968
ND 30g (symptomatic) Vasey and Karayannopoulos 1972
ND 10g (symptomatic) Weiss and Catalano 1973
ND 0.5g (asymptomatic) Aronow and Spigiel 1976
ND 6g (symptomatic) Aronow and Spigiel 1976
ND 23g (symptomatic) Aronow and Spigiel 1976
ND 12g (symptomatic) Trestrail and Spartz 1977
ND 6-12g (asymptomatic) Trestrail and Spartz 1977
ND 12g (symptomatic) Trestrail and Spartz 1977
ND 6g (symptomatic) Reid 1979
ND 6g (symptomatic) Reid 1979
3.1mg/l (3h pi) 5g (symptomatic) Mascie-Taylor et al 1981

Table showing relationship between blood levels and reported ingested dose of camphor in humans.

Note: ND=Not Done; pi=post ingestion; NK=Not Known

Convulsions were reported in a small child following skin exposure to
camphor spirit, and recurred a year later on brief inhalation exposure
(Skoglund et al 1977).

A 30 month old child with burns to 45% of body surface area developed
vomiting, drowsiness, coma and convulsions after the application of
camphor containing dressings (total dose 9g). The symptoms gradually
disappeared after the removal of the dressings (Mercier et al 1984).

Convulsions were reported in 4 children who had had burns dressed with
camphor-containing gauze (9.6% camphor) for periods of time ranging
from 4 hours to 3 weeks, the extent of the burns ranged from 5-50%
(all second degree) (Bavoux et al 1985).

6.1.4 Ocular

No data.

6.1.5 Other routes

Application of Vicks Vaporub (5% camphor) to the nostrils, lips and
chin of a 6 month old infant over a 3 day period resulted in 4 apnoeic
episodes (2 following generalised convulsions) from 48 hours into the
exposure (Bavoux et al 1985).

6.2 Chronic toxicity

6.2.1 Ingestion

An illness initially resembling Reye's syndrome with coma and
hepatomegaly, resulting in death was described in a 6 month old child
who had been chronically administered a home-made remedy containing
camphor 29.2 mg/ml in 33.3% alcohol (Jimenez et al 1983). Weakness,
fever, anorexia, intense pruritis and weight loss developed in a woman
who regularly ingested an ointment containing camphor. On examination,
hepatomegaly was found, with granulomas, necrosis and eosinophils
apparent on biopsy (McClollam et al 1989).

6.2.2 Inhalation

Corneal erosions have been reported in association with the use of
inhalant capsules containing camphor (Soen et al 1992).

6.2.3 Dermal

No data.

6.2.4 Ocular

No data.

6.2.5 Other routes

No data.

6.3 Systematic description of clinical effects

6.3.1 Cardiovascular

Peripheral circulatory shock has been seen (in association with severe
vomiting and dehydration) (Vasey and Karayannopoulos 1972).
Tachycardia and hypotension may occur (Koppel et al 1988). An adult
female who ingested 12g had a period of asystole (with apnoea) for
30-45 seconds following a convulsion (Riggs et al 1965).

6.3.2 Respiration

Respiratory depression (Benz 1919), apnoea (Smith and Margolis 1954)
and collapsed lung secondary to aspiration of stomach contents
(Kopelman et al 1979) may occur. Respiratory arrest been reported
(Aronow and Spigiel 1976). Apnoea has been described in young children
following exposure, often in conjunction with convulsions, and in one
case from a single inhalation in a 3 month old (Bavoux et al 1985). An
adult female who ingested 12g had a period of apnoea (with asystole)
for 30-45 seconds following a convulsion (Riggs et al 1965).

6.3.3 Neurological

Convulsions (tonic-clonic and grand-mal) are relatively common
following exposure to camphor (Benz 1919, Antman et al 1978, Kopelman
et al 1979, Koppel et al 1988, Gibson et al 1989). Convulsions, with,
on postmortem examination, neuronal death in the hippocampus, cerebral
cortex and ischaemic necrosis in the medulla have been reported (Smith
and Margolis 1954). Convulsions were reported in a small child
following skin exposure to camphor spirit, and recurred a year later
on brief inhalation exposure (Skoglund et al 1977).

Hyperexciteable emotional state (Antman et al 1978), irritability,
confusion, (Phelan 1976, Ginn et al 1968), somatic hallucinations,
restlessness (Aronow and Spigiel 1976), anxiety and agitation (Koppel
et al 1982) and coma (Kopelman et al 1979) have also been reported.
Coma with, on postmortem examination, cerebral oedema, neuronal
degeneration and frank necrosis in the hippocampus and frontal cortex
was seen in a 6 month old with chronic oral exposure to camphor
(Jimenez et al 1983).

6.3.4 Gastrointestinal

Increased salivation has been reported (Smith and Margolis 1954).
Abdominal pain, nausea, vomiting (Benz 1919, Kopelman et al 1979) and
coffee-ground vomiting (Smith and Margolis 1954) may occur. Epigastric
pain has been reported (Riggs et al 1965).

6.3.5 Hepatic

Liver function test changes suggestive of acute parenchymal liver
necrosis have been reported (Trestrail and Spartz 1977). Hepatomegaly
with abnormal LFTs and prolonged prothrombin time was seen in a 6
month old child following chronic oral dosing of camphor. On
postmortem the liver was swollen, discoloured and friable, with fatty
deposits within hepatocytes (Jimenez et al 1983). Hepatomegaly was
found, with granulomas, necrosis and eosinophils apparent on biopsy,
in a woman who regularly ingested an ointment containing camphor
(McClollam et al 1989).

Central zonal congestion of the liver was observed on postmortem
examination in 19 month old child who had ingested 5ml camphorated oil
(Smith and Margolis 1954).

6.3.6 Urinary

Changes in renal function, resolving spontaneously may occur
(Trestrail and Spartz 1977). Albuminuria has been reported (Smith and
Margolis 1954).

6.3.7 Endocrine and reproductive system

No data.

6.3.8 Dermatological

Camphor applied to the skin of volunteers as a 20% solution in alcohol
produced no significant sensation of irritation or pain at normal skin
temperatures (Green 1990).

6.3.9 Eye, ears, nose and throat

Camphor administered in doses of 60mg-4g was reported to cause
flickering, darkening or veiling of vision along with noises in the
ears (Grant and Schuman 1993). Corneal erosions have been reported in
association with the use of inhalant capsules containing camphor (Soen
et al 1992).

6.3.10 Haematological

A rise in white blood cell count has been reported in acute poisoning
(Koppel et al 1982, Smith and Margolis 1954).

6.3.11 Immunological

No Data

6.3.12 Metabolic

6.3.12.1 Acid-base disturbances

No Data

6.3.12.2 Fluid and electrolyte disturbances

Severe dehydration due to vomiting has been reported (Vasey and
Karayannopoulos 1972).

6.3.12.3 Other

No Data

6.3.13 Allergic reactions

No Data

6.3.14 Other clinical effects

The breath, vomitus and urine may smell of camphor following
ingestion. The breath, skin and amniotic fluid of a baby born to a
woman who ingested 50 ml of camphorated oil smelt of camphor (Weiss
and Catalano 1973).

6.4 At risk groups

6.4.1 Elderly

No Data

6.4.2 Pregnancy

An infant born 36 hours after its mother had ingested 12g of
camphorated oil failed to initiate respiration and was declared dead
30 minutes post delivery. Camphor was found in its bloodstream, liver,
kidneys and brain (Riggs et al 1965). The breath, skin and amniotic
fluid of a baby born to a woman who ingested 50 ml of camphorated oil
smelt of camphor (although the child was healthy) (Weiss and Catalano
1973).

6.4.3 Children

No data.

6.4.4 Enzyme deficiencies

No data.

6.4.5 Enzyme induced

No data.

6.4.6 Others

No data.

7 MANAGEMENT

7.1 Decontamination

As camphor is rapidly adsorbed, gastric decontamination is likely to
only be of benefit within 2 hours of ingestion. Ipecac and other
emetics are not recommended due to the risk of convulsions. If more
than 10mg/kg has been ingested, gastric lavage should be performed (or
stomach contents aspirated via a nasogastric tube if a liquid
preparation has been ingested). Activated charcoal, 1g/kg body weight
(max 50g), should be administered (charcoal in haemoperfusion columns
has been shown to adsorb camphor).

7.2 Supportive care

Camphor may cause severe vomiting and it is important to ensure
adequate hydration. Diazepam should be used to control convulsions.
The airway should be protected to prevent aspiration of stomach
contents during convulsions.

7.3 Monitoring

The liver function, renal function and hydration status of the patient
should be monitored.

7.4 Antidotes

None.

7.5 Elimination techniques

Charcoal haemoperfusion, amberlite haemoperfusion and lipid dialysis
have all been shown to remove camphor from the serum (Mascie-Taylor et
al 1981, Koppel et al 1988, Kopelman et al 1979, Ginn et al 1968,
Antman et al 1978).

7.6 Investigations

A smell of camphor is usually apparent on the breath of poisoned
patients. It can be measured in serum and urine (eg Riggs et al 1965,
Phelan 1976).

7.7 Management controversies

None.

8 CASE DATA

Convulsions

A 3 year old girl with a history of confusion, irritability,
projectile vomiting and, 2 hours later, a generalised convulsion was
brought to hospital. The convulsion was controlled by 25mg
secobarbitone given IM, oxygen was administered because of respiratory
depression following the barbiturate, she was then given 0.2g of
caffeine sodium benzoate and transferred to a paediatric hospital. On
admission there she was drowsy and had an odour of camphor on her
breath. It then transpired that she had been found with an open jar of
Vicks Vaporub 2 hours before the convulsion, and may have ingested
about a tablespoonful of it (approx. 0.7g of camphor). She was
asymptomatic by 21 hours after admission, and required no further
anticonvulsants or respiratory support. No abnormalities in liver or
renal function tests were found, and she was discharged home 24 hours
after admission on phenobarbitone 5mg/kg/day. Blood levels of camphor
measured 7 hours post-ingestion were 1.95mg/100ml, and undetectable by
21 hours post-ingestion. EEG at about 18 hours post-ingestion showed
diffuse neuronal disturbance with excessive slow activity in the
bianterior and bicentral areas and no specific paroxysmal discharges.
This pattern was still apparent on the EEG 15 days after discharge,
but it had returned to normal on review after 3 months.

A 15 month old crawled through a spill of spirits of camphor (10%
camphor). Over the next 48 hours he became progressively ataxic and
had some brief, generalised motor seizures. The convulsions recurred
over a 2 day period, despite anticonvulsant therapy. He recovered
slowly over the next 15 days, and appeared to be completely well, with
no further convulsions. However, a year later he suffered a brief
convulsion when exposed to camphor from a vaporiser (camphor content
of preparation being used 4.81%) (Skoglund et al 1977).

Hallucinations

Two 22 year old men ingested 6-10g of camphor as a substitute for
hashish, and were admitted to hospital two hours later in a state of
anxiety with agitation. They were both having hallucinatory feelings,
one described a floating sensation, the other the feeling that his
legs no longer belonged to him. The only physical findings were a
slight tachycardia and leukocytosis. The patients were given 2 litres
of tea, and given 10mg diazepam. They were both discharged well 24
hours post admission. Their blood levels taken at an unspecified time
were 300 and 400ng/ml (Koppel et al 1982).

Fatal liver damage in a child

A 6 month old male with a 2-day history of cough, nasal discharge and
fever was prescribed ampicillin for presumed pneumonia. By the next
day the child was lethargic but rouseable, with diffuse rales and
wheezing in both lungs. Chest X-ray showed hyperinflation with diffuse

interstitial infiltrates, and bronchiolitis was diagnosed. Within 6
hours the child became unrousable and the liver was palpable 3cm below
the costal margin, and the child was transferred to a paediatric
hospital with presumed Reye's syndrome. On admission there, the child
was comatose, with abnormal lung sounds, hepatomegaly and hyperactive
reflexes, but normal white blood cell count and haematocrit. AST, ALT,
urea and bilirubin levels were elevated, and prothrombin time
increased (20.5 seconds). Supportive therapy for Reye's syndrome was
commenced, with administration of hypertonic dextrose, IV mannitol as
indicated by the intra-cranial pressure, and imposed respiratory
alkalosis. 6 hours post-admission an EEG showed diffuse slowing with
no seizure activity, and liver biopsy showed changes not
characteristic of Reye's syndrome. On further questioning the family
admitted to the use of a home-made remedy containing camphor in
whiskey (33.3% alcohol, 29.2mg/ml camphor). This mixture had been
administered to the child on a daily basis, in dropperful quantities,
from the age of about a month, the total quantity administered was
about 28 fl oz (828ml), of which 4 fl oz (118.4ml) had been given in
the 3 days before hospitalisation (total dose of camphor approx. 24.5g
or 3g/kg). The child's liver function improved, but his neurological
status deteriorated, and by the fifth day in hospital deep tendon,
corneal and ocular-vestibulo-cephalic reflexes were all absent, and
repeat EEG showed an absence of any electrical activity. The child
suffered a cardiac arrest and died later that day. On postmortem the
brain was symmetrically swollen, with flattening of the gyri and
narrowing of the sulci, it weighed 1250g (normal 660g).
Microscopically there was diffuse oedema with patchy individual
neuronal degeneration and areas of frank necrosis, mainly in the
hippocampus and frontal cortex. The liver was enlarged (weight 354g
compared with normal 200g), friable and discoloured yellow.
Histologically there were fat deposits within the hepatocytes,
irregular in size and distribution, with the majority of hepatocyte
nuclei located peripherally rather than centrally. The classical
changes characteristic of Reye's syndrome, such as decreased succinic
dehydrogenase and cytochrome oxidase activity, were not found, neither
were swollen mitochondria. There was no inflammation, bile stasis,
Mallory bodies or cellular necrosis, which would be expected in
alcohol-induced hepatitis (Jimenez et al 1983).

Camphorated gauze

Three cases of poisoning were associated with the use of camphorated
gauze (9.6% camphor). A 14 month old child with 2nd degree burns to 5%
of body area was treated with regular application of the gauze for 3
weeks. The child was ataxic within 3-4 days of starting treatment, and
developed convulsions by the third week. The serum level of camphor at
the time the gauze was removed was >2µg/ml, 32µg of camphor was
recovered from the urine during the first 12 hours following exposure.
A 13 year old boy with 2nd degree burns covering 35% of body surface
was treated with camphor gauze dressings, for 50 hours, with the
dressings changed at 24 and 48 hours. The total quantity of camphor
applied was estimated to be 160mg/kg/24h. He began to have convulsions

50 hours into this treatment, the dressings were removed, and he
recovered. His blood camphor level was 0.452µg/ml 17 hours after the
dressings were removed, and urinary levels of metabolites were still
rising by 4 days post termination of exposure. A 29 month old with 2nd
degree burns to 50% of body surface area had camphor dressings applied
for 4 hours until he began to have convulsions, with a respiratory
arrest. He recovered. No serum or urinary camphor concentrations were
measured.

Poisoning from nasal and/or dermal application

Two cases of poisoning were associated with nasal and/or dermal
application of camphor; a 3 month old went pale, collapsed, stopped
breathing and had a convulsion following one inhalation of Vicks
Inhaler (40% camphor). The child was treated with phenobarbitone, on a
continuing basis. A 6 month old was treated for 3 days with
application of VicksVaporub to the nostrils, the lips and the chin. 48
hours into this treatment he had 4 apnoeic episodes, 2 of which
followed generalised convulsions.

Two cases were associated with the use of a talcum powder containing
0.3% camphor: an 8 month old with mild chicken-pox was exposed to an
unknown quantity of this powder and developed convulsions with apnoea
a few hours after the last exposure, but recovered. A 24 month old,
again with mild chickenpox, was exposed to about 112mg worth of
camphor in 18 hours (3/4 bottles of the powder). The child had
convulsions after the 6-7th application of the powder, when re-exposed
had another convulsion, and yet more convulsions one hour after the
last application. In between the child was agitated, and the
chickenpox worsened. Recovery took place over 48 hours (Bavoux et al
1985).

Camphor spirit

A 54 year-old, alcoholic, diabetic woman drank an unknown quantity of
10% camphor spirit (10% camphor, 70% isopropanol and 20% water) and
was discovered comatose half an hour later suffering grand-mal
convulsions and respiratory failure. She was given 10mg diazepam IV
and intubated and ventilated, then transferred to intensive care. On
arrival there she was in coma grade II, with hyporeflexia,
tachycardia, and grand-mal convulsions which could be precipitated by
light touch to the arms or legs. She was washed out with liquid
paraffin, then haemoperfusion with amberlite XAD4 was carried out for
4 hours. Although the convulsions ceased during the haemoperfusion the
patient's level of consciousness did not improve. She gradually came
round over the next few days and she was extubated and transferred to
an ordinary ward six days post-ingestion. One of the authors
voluntarily ingested 200mg of camphor with and without a solvent in
order to determine the absorption kinetics and plasma half-life. When
ingested with a solvent peak plasma levels were reached by one hour
post-ingestion, when ingested alone peak levels were reached by 3
hours. The elimination half life in the volunteer was 93 minutes when

camphor was ingested with a solvent, and 167 minutes when ingested
alone. The plasma elimination half life measured in the patient during
haemoperfusion was 128 minutes (Koppel et al 1988).

Chronic ingestion of camphor containing rub

A 72 year old woman presented to hospital with a history of weakness,
fever, pruritis, anorexia and weight loss. On examination she was
found to have hepatomegaly, on biopsy the liver displayed granulomas
with necrosis and eosinophils. This pattern of symptoms and liver
damage was seen again 4 months later at another hospital. The patient
claimed to have ingested Vicks Vaporub regularly over a period of
about 5 years, consuming about one jar a year. The patient was
instructed to discontinue her use of the rub, and the liver damage and
other symptoms resolved slowly (McCollam et al 1989).

Eye exposure to inhalant preparation

A 4 month old girl was brought to hospital with a 2 day history of
fever, nasal congestion and bilateral eye irritation. An hour earlier
she had been placed, lying face-up, on a pillow which had been
sprinkled with a decongestant mixture (Rhino-Caps: camphor 25mg,
eucalyptol 125mg, menthol 55mg, terpineol 120mg and chlorothymol 5mg),
but the parents denied any direct contact of the substance to her
eyes. On examination she had bilateral corneal erosions,
conjunctivitis, and a burn to the temporal conjunctiva, but had no
other symptoms other than nasal congestion. The eyes were irrigated
with saline, and antibiotic and steroid drops applied. By 12 hours
post the initial admission she was noticed by her parents to be
lethargic and weak, and was re-admitted. On the second examination she
was drowsy and hypotonic, with marked head lag. She was observed for 8
hours, by the end of which time she was alert. The corneal erosions
healed within 2 days (Soen et al 1992).

Ingestion of camphorated oil

A 15 month old infant ingested 1.5g of camphor in the form of
camphorated oil and had two convulsions 45 minutes post ingestion. The
stomach was washed out (the first washing smelt strongly of camphor),
and phenobarbitone and diazepam administered. The blood level of
camphor was 0.30µg/ml 9 hours post ingestion, 12µg of camphor was
recovered from the urine during the first 16 hours, and 220µg of the
glucuronide metabolite; in the following 24 hours urinary excretion
increased to 165µg of camphor and 1540µg of the metabolite.

An unspecified number of children (aged from 4-10 years) were each
given between 1-1.5 tablespoons of camphorated oil, in place of castor
oil. The first child to become unwell developed symptoms 45 minutes
later, and by the time a physician arrived on the scene the children
were displaying "all kinds of symptoms, from...nausea to convulsions".
Twenty of the children were in fact convulsing. The most severely
affected child was unconscious and rigid, cold to the touch, with
blue-black lips, tachycardia and slow, shallow respirations. The child

had dilated pupils, the eyes were fixed staring straight ahead, the
jaws were locked, with tetanic contraction of the masseters, cervical
rigidity and tonic contraction of the arms, extension of the legs.
This child remained unconscious for 20 hours, but had recovered by 29
hours post-ingestion. The treatments which the children received
included administration of mustard water as an emetic, and immersion
in hot mustard water (for the more severely ill children) followed by
oral mustard water (given forcibly). Most of the children were
reportedly well within 3-4 hours of treatment, and all survived (Benz
1919).

A 19 month old male ingested about 5ml of camphorated oil and vomited
within minutes, then remained well until 3 hours later when he
developed salivating and rigidity. A local doctor then administered
pethidine 50mg, caffeine and sodium benzoate, with little effect, the
child was therefore transferred to hospital. On admission he was
pyrexial, tachycardic, with a raised white blood cell count and
albuminuria. Shortly after admission the child vomited coffee-ground
material which smelt of camphor and he then went into a coma, with
repeated tonic convulsions and hyperreflexia. He was given penicillin,
fluid by hypodermoclysis (subcutaneous administration) and
intermittent phenobarbitone, nasal oxygen and sponge baths. By 3 days
post admission the right pupil was fixed and dilated, and the blood
pressure had risen to 150/100 mmHg. Recurrent periods of apnoea
developed, which increased in severity, and required artificial
ventilation. Tracheotomy was performed, but the child died 5 days
post-ingestion. On postmortem examination the lungs were oedematous,
with congestion of both lower lobes, and the right side of the heart
was dilated. The liver, spleen and kidneys were congested. The brain
was swollen and soft, weighing 1350g (350g more than expected). There
was extensive neuronal degeneration, spread throughout the cerebral
cortex and basal ganglia, most severe in Sommer's section of the
hippocampus, where almost all the pyramidal cells were necrotic. There
was a small area of ischaemic necrosis in the medulla, but the
cerebellar Purkinje cells were unchanged. There was no glial or
vascular injury apparent, nor any inflammatory changes (Smith and
Margolis 1954).

A 20 year old pregnant woman (40 weeks) ingested 12g of camphorated
oil in mistake for castor oil while being observed in hospital for
mild pre-eclampsia. She was found 15 minutes later prostrate, agitated
and irrational. She had dilated pupils, her eyes were undergoing slow,
rhythmic divergent and convergent movements, she had fine tremors of
the hands and feet and general hyperreflexia. The woman's blood
pressure was 140/70 and the foetal heart rate was 140/minute. Stomach
washout was performed, but the patient developed opisthotonus and had
tonic-clonic movements of the extremities, within 30 minutes of the
ingestion. She then suffered a period of apnoea and asystole lasting
30-45 seconds, the convulsion terminated spontaneously 2 minutes after
it had started. The mothers blood pressure and the foetal heart rate
remained unchanged. Sodium amytal 500mg IV and phenobarbitone 60mg IM
were given and the tremors of the hands and feet and the abnormal eye

movements gradually disappeared. Stomach washout was continued until
the odour of camphor was no longer detectable in the return washings.
The tremors, hyperreflexia and ocular movements returned about 8 hours
post ingestion, but disappeared again on the administration of another
60mg of phenobarbitone. The patient remained rational and awake, but
had epigastric pain relieved by antacids. Labour began spontaneously
17 hours after the ingestion. Amniocentesis was performed 19.5 hours
post ingestion, and produced bright red blood, believed to be
placental in origin. 18.5h after the start of labour vaginal bleeding
and foetal bradycardia were noticed. When the child was delivered 1.5
hours later it was limp and cyanosed, with a heart rate of 80/minute
and no respiratory effort. Aspiration of nose, pharynx, and stomach
was performed, and positive pressure ventilation with a paediatric
face mask was instituted, with no response. The heart rate gradually
dropped, and the child was pronounced dead 30 minutes after delivery.
The mother remained well apart from transient changes in liver
function tests (elevation of bilirubin and alkaline phosphatase
levels). On postmortem examination the infant was small (2250g), with
marked congestion of all organs, and severe pulmonary atelectasis with
many air-filled blebs on the pleural surface of the lungs. Within the
central nervous system there was general congestion and neuronal
necrosis. Camphor was found to be present in maternal blood samples
taken just prior to the convulsion, but not 8 hours post ingestion or
later. No camphor was found in the blood obtained during amniocentesis
(and presumed to be placental), but it was detected in amniotic fluid
taken at that time. Camphor was detectable in the amniotic fluid, cord
blood, and foetal blood at 36 hours post ingestion. The liver, kidneys
and brain of the infant also contained camphor (Riggs et al 1965).

A 77 year old man ingested 60ml of camphorated oil (dispensed in error
instead of cough mixture). Thirty minutes post-ingestion he vomited
and had a grand-mal convulsion, and was brought to hospital. The
vomitus smelt strongly of camphor. On admission he was post-ictal, but
became progressively more agitated, disorientated and had two further
convulsions despite being given IV barbiturates. His breath and urine
smelt of camphor, but urinalysis, whole blood count, blood sugar, urea
and electrolytes and liver function tests were all normal.
Haemodialysis using soya bean oil as the dialysate was initiated
within 4 hours of the ingestion. The procedure was carried out for 4.5
hours, and the patient became alert and orientated after 3 hours of
dialysis. He was discharged the next day, asymptomatic. The soybean
oil had removed 6.56g of camphor (on analysis by gas chromatography)
(Ginn et al 1968).

An adult male who had deliberately ingested 150ml of camphorated oil
(B.P. 20%) was admitted to a regional Poisons Unit in peripheral
circulatory shock and severely dehydrated due to vomiting. He was
resuscitated and then stomach washout was performed under general
anaesthetic, with a cuffed ET tube in place. Shortly after admission
he developed 3 severe, prolonged grand mal convulsions, which were
controlled with diazepam IV. He required intensive supportive
treatment, but was discharged well 36 hours post admission (Vasey and
Karayannopoulos 1972).

A pregnant woman who ingested 50 ml of camphorated oil in mistake for
castor oil had a total of three grand-mal convulsions, and went into
labour prematurely (20 hours post-ingestion). The infant was healthy,
but its breath and skin, and the amniotic fluid, smelt of camphor
(Weiss and Catalano 1973).

A 2 month old girl was given 2.5ml of camphorated oil by mistake, and
taken immediately to hospital. There gastric washout was performed,
and she was admitted for observation. No symptoms developed, and she
was discharged within 24 hours. A 12 year old boy who was given 1 fl
oz (29.6ml) of camphorated oil complained of the taste, was given a
glass of milk and immediately vomited. He was taken straight to
hospital, but appeared to lose consciousness for ten minutes on the
way. On admission, about 2 hours post-ingestion, he was convulsing. He
was given diazepam IV which controlled the convulsions, and remained
alert for the next 48 hours with only mild, intermittent abdominal
cramps. He was discharged 3 days post-ingestion(Aronow and Spigiel
1976).

A 19 year old woman ingested 2 fl oz (59.2ml) of camphorated oil in
mistake for castor oil was found 45 minutes later unresponsive with
stiff arms and legs, hands stiffly pronated bilaterally, salivating,
and with eyes rolled back. She was vomiting and had a grand mal
convulsion in the first hospital she was taken to, and on admission to
the second hospital was semi-conscious and agitated, requiring
restraint. She was transferred to ITU and where she was managed
conservatively, slowly improved and was discharged 13 days after
admission. During her stay she developed liver function test changes
suggestive of acute parenchymal liver necrosis, also slightly deranged
renal function, both of which resolved. A 15 year old male ingested 2
fl oz (59.2ml) of camphorated oil, again in mistake for castor oil,
and shortly thereafter had a convulsion and vomited. The patient was
admitted to hospital within 2 hours of the ingestion, but the mistake
was not realised until 10 hours post-ingestion, by which time he was
complaining of blurred vision. He was managed conservatively and
discharged after 2 days (Trestrail and Spartz 1977).

A 56 year old female ingested 12 ml of 20% camphor oil, and developed
epigastric burning, nausea and vomiting 45 minutes later, and was
brought to the emergency room. On admission she had no symptoms other
than a smell of camphor on the breath, but rapidly developed a
hyperexcitable emotional state, neuromuscular hyperactivity, and jerky
movements of the extremities. She had a transient mild elevation in
serum glutamic oxaloacetic transaminase and lactic dehydrogenase and
nasogastric aspirate was positive for blood. Haemodialysis with
soy-bean oil dialysate was carried out for 4.5 hours. The odour of
camphor cleared from her breath and became noticeable in the dialysate
compartment; the patient recovered and remained well during 2.5 years
of follow-up (Antman et al 1978).

A 37 year old man was brought to hospital 1 hour and 40 minutes after
ingesting up to 90ml of camphorated oil (18g camphor). He was
complaining of abdominal pain, and had vomited twice, the first time
twenty minutes post-ingestion. Although he was conscious and alert on
presentation, grand mal convulsions developed within minutes of
arrival, and the patient aspirated stomach contents. He was then
intubated, and gastric lavage performed. His breath, vomitus and urine
all smelt strongly of camphor. Recurrent convulsions occurred during
his first 12 hours in hospital, and were treated with diazepam 100mg,
chlorpromazine 50mg, secobarbital 300mg and phenobarbitone 300mg (IV).
He was given IV fluids, and underwent bronchoscopy to reexpand the
right upper lobe of his lung at about 8 hours post-ingestion (it had
collapsed due to aspiration of stomach contents). The patient was
still comatose and having recurrent convulsions, and it was decided to
attempt to speed up the elimination of the camphor by instituting
haemoperfusion against an amberlite resin, followed by lipid dialysis
(connected in series, as the efficacy of amberlite haemoperfusion was
unproven). Combined haemoperfusion and lipid dialysis were carried out
for 45 minutes, until clotting occurred in the perfusion column and it
was discontinued; lipid dialysis alone was carried out for a further 3
hours 45 minutes. The patient had started to awaken by 2.5 hours after
the start of the extracorporeal elimination procedure, and was fully
alert by about 32 hours post-ingestion, and discharged about 60 hours
post-ingestion. The plasma camphor level measured before the start of
the elimination procedure was 1.7µg/ml. Samples taken after passage
through the haemoperfusion column showed no detectable camphor, while
when the lipid dialysis system was operating alone it extracted about
60% of the camphor (Kopelman et al 1979).

A 60-year old woman accidentally drank about 25ml of camphorated oil
(about 5g or 100mg/kg camphor), and became nauseated and vomited once
shortly after ingestion. She then suffered two grand mal convulsions,
the second witnessed by medical personnel during her journey to
hospital. On admission (about 1 hour post-ingestion) the patient was
responsive only to pain. A stomach washout was performed, and the
patient was intubated. She was treated with combined charcoal
haemoperfusion and lipid dialysis arranged in series, starting from
about 3 hours post-ingestion and continuing for 4 hours. At the end of
this time the patient had recovered, however the total amount of
camphor removed from the bloodstream was calculated to be only 48.7mg
(less than 1% of the ingested dose). The initial plasma level of
camphor in this patient was 3.1mg/L (at about 3 hours post-ingestion),
and the clearance rate using the charcoal haemoperfusion column was
240ml/min. The lipid dialysis column induced haemolysis, and so was
disconnected, clearance rates for it were therefore not measured
(Mascie-Taylor et al 1981).

NPIS (L) Cases

100 cases on file where adequate follow-up information was received,
covering the period 1964-1991. Most of the cases involved children
(89%), and the source of the camphor was most commonly camphorated oil
(95% of cases). There were no fatalities reported.

Example cases

84/2625 Male, 4 years old ingested a mouthful of camphorated oil,
vomited twice and had a convulsion 15 minutes post-ingestion. He was
well after overnight observation.
84/12478 A schizophrenic, 43 year old female ingested an unknown
amount and suffered grand-mal convulsions and hallucinations, she was
treated with diazepam and observed in ITU.
84/13439 A 4 year old male ingested about 25ml and developed rolling
eyes and twitching within 1.5 hours, also vomiting and abdominal pain.
He was given activated charcoal and an irritant laxative, and observed
overnight.
84/3873 A 1 year old female ingested 50ml camphorated oil and
developed vomiting and drowsiness, and had a minor epileptic fit. She
was given activated charcoal 2 hourly and recovered by 24 hours.

9 ANALYSIS

9.1 Agent/toxin/metabolite

9.2 Sample containers to be used

9.3 Optimum storage conditions

9.4 Transport of samples

9.5 Interpretation of data

9.6 Conversion factors

9.7 Other recommendations

10 OTHER TOXICOLOGICAL DATA

10.1 Carcinogenicity

No evidence of carcinogenicity has been found in human tests (ACGIH
1986).

10.2 Genotoxicity

10.3 Mutagenicity

Sister chromatid exchange has been reported in mice given 80mg/kg
doses of camphor intraperitoneally (RTECS 1996).

10.4 Reprotoxicity

Camphor crosses the placental barrier (Weiss and Catalano 1973). It
has been used, historically, to procure abortion (Vasey and
Karayannopoulos 1972), and the plant Lippia dulcia Trev., which
contains camphor, may still be used for this purpose in South America
(Compadre et al 1986).

10.5 Teratogenicity

None to minimal risk (TERIS 1993).

10.6 Relevant animal data

Camphor was administered to rabbits and mice, to examine the changes
(if any) occurring in their brain as a result, and to see if
barbiturates had a protective effect. All rabbits administered
camphorated oil via oral tube developed convulsions within 5-40
minutes of administration, with convulsions occurring later in those
receiving the lower doses. The animals who died had intermittent
convulsions up to the time of death, those which recovered stopped
convulsing by 4 hours post-ingestion. Mice were administered camphor
by intraperitoneal (IP) injection, and again, convulsions occurred. On
post-mortem examination, the rabbit brains showed no significant
changes, but some of the mice had necrosis of neurons in the brain
stem, basal ganglia, medulla, hippocampus and cerebral cortex. The
experiment was repeated in mice, the test group being given camphor
and pentobarbitone IP and the controls camphor alone. The animals
given camphor and pentobarbitone all became stuporose within 10
minutes, but recovered within about 1.5 hours and developed no
convulsions, whereas the control group all developed convulsions, and
7/10 died. The mice who had received pentobarbitone as well as camphor
showed no cerebral changes when examined after death (Smith and
Margolis 1954).

10.7 Relevant in vitro data

Amberlite haemoperfusion resin was found to be superior to an
activated charcoal column - relative clearance of camphor by amberlite
was 98% compared with 59% for the charcoal (Koppel et al 1982).

Author

Sarah McCrea

National Poisons Information Service (London Centre)
Medical Toxicology Unit
Guy's & St Thomas' Hospital Trust
Avonley Road
London
SE14 5ER
UK

This monograph was produced by the staff of the London Centre of the
National Poisons Information Service in the United Kingdom. The work
was commissioned and funded by the UK Departments of Health, and was
designed as a source of detailed information for use by poisons
information centres.

Peer review was undertaken by the Directors of the UK National Poisons
Information Service.

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