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Camphor

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 Brand names, Trade names
   1.6 Manufacturers, Importers
2. SUMMARY
   2.1 Main risks and target organs
   2.2 Summary of clinical effects
   2.3 Diagnosis
   2.4 First aid measures and management principles
3. PHYSICO-CHEMICAL PROPERTIES
   3.1 Origin of the substance
   3.2 Chemical structure
   3.3 Physical properties
      3.3.1 Properties of the substance
      3.3.2 Properties of the locally available formulation
   3.4 Other characteristics
      3.4.1 Shelf-life of the substance
      3.4.2 Shelf-life of the locally available formulation
      3.4.3 Storage conditions
      3.4.4 Bioavailability
      3.4.5 Specific properties and composition
4. USES
   4.1 Indications
   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 Other
6. KINETICS
   6.1 Absorption by route of exposure
   6.2 Distribution by route of exposure
   6.3 Biological half-life by route of exposure
   6.4 Metabolism
   6.5 Elimination by route of exposure
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
   7.7 Main adverse effects
8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS
   8.1 Material sampling plan
      8.1.1 Sampling and specimen collection
         8.1.1.1 Toxicological analyses
         8.1.1.2 Biomedical analyses
         8.1.1.3 Arterial blood gas analysis
         8.1.1.4 Haematological analyses
         8.1.1.5 Other (unspecified) analyses
      8.1.2 Storage of laboratory samples and specimens
         8.1.2.1 Toxicological analyses
         8.1.2.2 Biomedical analyses
         8.1.2.3 Arterial blood gas analysis
         8.1.2.4 Haematological analyses
         8.1.2.5 Other (unspecified) analyses
      8.1.3 Transport of laboratory samples and specimens
         8.1.3.1 Toxicological analyses
         8.1.3.2 Biomedical analyses
         8.1.3.3 Arterial blood gas analysis
         8.1.3.4 Haematological analyses
         8.1.3.5 Other (unspecified) analyses
   8.2 Toxicological Analyses and Their Interpretation
      8.2.1 Tests on toxic ingredient(s) of material
         8.2.1.1 Simple Qualitative Test(s)
         8.2.1.2 Advanced Qualitative Confirmation Test(s)
         8.2.1.3 Simple Quantitative Method(s)
         8.2.1.4 Advanced Quantitative Method(s)
      8.2.2 Tests for biological specimens
         8.2.2.1 Simple Qualitative Test(s)
         8.2.2.2 Advanced Qualitative Confirmation Test(s)
         8.2.2.3 Simple Quantitative Method(s)
         8.2.2.4 Advanced Quantitative Method(s)
         8.2.2.5 Other Dedicated Method(s)
      8.2.3 Interpretation of toxicological analyses
   8.3 Biomedical investigations and their interpretation
      8.3.1 Biochemical analysis
         8.3.1.1 Blood, plasma or serum
         8.3.1.2 Urine
         8.3.1.3 Other fluids
      8.3.2 Arterial blood gas analyses
      8.3.3 Haematological analyses
      8.3.4 Interpretation of biomedical investigations
   8.4 Other biomedical (diagnostic) investigations and their interpretation
   8.5 Overall Interpretation of all toxicological analyses and toxicological investigations
   8.6 References
9. CLINICAL EFFECTS
   9.1 Acute poisoning
      9.1.1 Ingestion
      9.1.2 Inhalation
      9.1.3 Skin exposure
      9.1.4 Eye contact
      9.1.5 Parenteral exposure
      9.1.6 Other
   9.2 Chronic poisoning
      9.2.1 Ingestion
      9.2.2 Inhalation
      9.2.3 Skin exposure
      9.2.4 Eye contact
      9.2.5 Parenteral exposure
      9.2.6 Other
   9.3 Course, prognosis, cause of death
   9.4 Systematic description of clinical effects
      9.4.1 Cardiovascular
      9.4.2 Respiratory
      9.4.3 Neurological
         9.4.3.1 CNS
         9.4.3.2 Peripheral nervous system
         9.4.3.3 Autonomic nervous system
         9.4.3.4 Skeletal and smooth muscle
      9.4.4 Gastrointestinal
      9.4.5 Hepatic
      9.4.6 Urinary
         9.4.6.1 Renal
         9.4.6.2 Other
      9.4.7 Endocrine and reproductive systems
      9.4.8 Dermatological
      9.4.9 Eye, ear, nose, throat: local effects
      9.4.10 Haematological
      9.4.11 Immunological
      9.4.12 Metabolic
         9.4.12.1 Acid-base disturbances
         9.4.12.2 Fluid and electrolyte disturbances
         9.4.12.3 Others
      9.4.13 Allergic reactions
      9.4.14 Other clinical effects
      9.4.15 Special risks
   9.5 Other
   9.6 Summary
10. MANAGEMENT
   10.1 General principles
   10.2 Relevant laboratory analyses
      10.2.1 Sample collection
      10.2.2 Biomedical analysis
      10.2.3 Toxicological analysis
      10.2.4 Other investigations
   10.3 Life supportive procedures and symptomatic/specific treatment
   10.4 Decontamination
   10.5 Elimination
   10.6 Antidote treatment
      10.6.1 Adults
      10.6.2 Children
   10.7 Management discussion
11. ILLUSTRATIVE CASES
   11.1 Case reports from literature
   11.2 Internally extracted data on cases
   11.3 Internal cases
12. Additional information
   12.1 Availability of antidotes
   12.2 Specific preventive measures
   12.3 Other
13. REFERENCES
14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE ADDRESS(ES)
    PHARMACEUTICALS
    1. NAME
     1.1 Substance
       Camphor
     1.2 Group
       Rubefacient/counter-irritant
     1.3 Synonyms
       1,7,7-trimethyl bicyclo (2,2,1)-heptan-2-one
       2-bornanone
       2-camphanone
       2-keto-1,7, 7-trimethylnorcamphane
       2-oxo-bornane
       alcanfor
       camfora
       camphor-natural
       camphor-synthetic
       formasa-camphor
       Gum camphor
       Japan camphor
       l,7,7-trimethy1norcamphor
       laurel camphor
       matricaria camphor
       root bark oil
       spirit of camphor
       tramfer
     1.4 Identification numbers
       1.4.1 CAS number
             76-22-2
       1.4.2 Other numbers
             U.N. Number: 2717
     1.5 Brand names, Trade names
       Camphora synthetic tablets, camphora (see Section 4).
     1.6 Manufacturers, Importers
       NMD (Norwegian Medicinal Depot).
    2. SUMMARY
     2.1 Main risks and target organs
       Central nervous system (CNS) and kidney: convulsions followed 
       by depression, and renal damage may occur after intake of 
       relatively small amounts of camphor may occur.  The main risks 
       are apnoea, asystole, and severe post-convulsive coma.  Toxic 
       effects appear after the ingestion of approximately 2 g 
       (lethal dose LD adults: 4 g;  children: 1 g of pure camphor).
     2.2 Summary of clinical effects
       Clinical effects are:  gastric irritation, colic, nausea, 
       vomiting, and diarrhoea; anxiety, excitement, delirium, and 
       epileptiform convulsions; apnoea and asystole.  CNS depression 
       follows the excitatory phase, and may result in coma or, 
       rarely, death.  Anuria may occur.  The breath has the 
       characteristic odour of camphor.
     2.3 Diagnosis
       Poisoning by camphor is associated with an initial excitatory 
       phase, with vomiting, diarrhoea and excitement, followed by NS 
       depression and death. A characteristic odour of camphor is 
       present on the breath.
       
       The symptoms may appear 5 to 90 min after ingestion depending 

       on the product ingested (solid or liquid).  Oral and 
       epigastric burning sensations, nausea, and vomiting usually 
       occur early.  The onset of convulsions may be sudden and 
       without warning, or may be preceded by confusion and 
       irritability, neuromuscular hyperactivity, and jerky movements 
       of the extremities.
            
       Convulsions may be followed by coma, apnoea, and death.  
       Camphor is irritating to the eyes, skin and mucous membranes.
       
       Blood and urine samples should be taken for routine analysis 
       and follow-up.
       
       No specific laboratory analyses are indicated: camphor levels 
       are not clinically useful.
       
       Camphor is recognized by its characteristic odour on the 
       patient's breath.
     2.4 First aid measures and management principles
       Camphor induces convulsive states which may be life-
       threatening and must be considered before attempting emesis or 
       gastric lavage.
       
       If camphor has been ingested recently, and the condition of 
       the patient allows, perform gastric lavage with warm water (38
       C to 40 C).  If only small amounts have been ingested, 
       administer cathartics. Administration of vaseline oil 
       (laxative mineral oil) is controversial. 
       
       If camphor has been inhaled, remove patient from exposure, 
       administer fresh air or oxygen, and establish respiration.
       
       If there has been external contact with camphor, wash skin 
       thoroughly with soap and water.  Irrigate eyes with large 
       amounts of water.
       
       Send patient immediately to hospital.
       
       In case of severe poisoning:
       
       Establish respiration if depressed - artificial respiration 
       may be necessary.
       
       Treat convulsions (e.g., with diazepam).
       
       With the airway protected (endotracheal intubation), gastric 
       lavage may be performed, followed by activated charcoal, and 
       then a saline cathartic.
       
       Resin and charcoal haemoperfusion may be used in severe cases.
    3. PHYSICO-CHEMICAL PROPERTIES
     3.1 Origin of the substance
       Camphor may be natural or synthetic.  It occurs naturally in 
       the wood of the camphor tree (cinnamonum camphora), and is  
       xtracted by steam distillation and crystallization.  Natural 
       camphor is dextrorotatory.  Synthetic camphor may be made from 

       pinene which is converted into camphene by treatment with 
       acetic acid and nitrobenzene.  Synthetic camphor is optically 
       inactive.
     3.2 Chemical structure
       C10H16O
       
       Molecular Weight = 152.2
                                     CH3
       
                                           = O
       
                                     H3C-C-CH3
     3.3 Physical properties
       3.3.1 Properties of the substance
             Normal state at room temperature: solid, 
             translucent
             crystals.
             
             Colour: white crystals.
             
             Odour:  penetrating, aromatic.
             
             There are dangers associated with the vapour, its dispersion,
             and possible ignition.  There is a moderate risk of fire if 
             camphor is exposed to heat or flame, but spontaneous 
             combustion does not occur.
             
             Boiling point: 204 C
             
             Melting point: 176 to 180 C
             
             Sublimes appreciably at room temperature and normal 
             atmospheric pressure
             
             Flash point: 65C
             
             Autoignition temperature: 466C
             
             Relative density: 0.99 (specific gravity)
             
             Relative vapor density: 5.2
             
             Vapour pressure: 20 PA at 20C
             
             Solubility in water: 0.125 g/100 m1 (25 C)
             
             Soluble in ethanol, ethylether, turpentine, and 
             essential oils
             
             Explosive limits: 0.6 to 3.5 vol% in air
             
             Relative molecular mass: 152.2.
       3.3.2 Properties of the locally available formulation
             No data available.
    3.4 Other characteristics
       3.4.1 Shelf-life of the substance

             Five years.
       3.4.2 Shelf-life of the locally available formulation
             No data available.
       3.4.3 Storage conditions
             Store in airtight containers at a temperature not above 
             25C.
       3.4.4 Bioavailability
             No data available.
       3.4.5 Specific properties and composition
             Strong aromatic odour.
    4. USES
     4.1 Indications
       Camphor is used:

       as a rubefacient
       as a plasticizer for cellulose esters and ethers
       in the manufacture of plastics (especially celluloid)
       in lacquers and varnishes
       in explosives and pyrotechnics
       as a moth repellent
       in the manufacture of cymene
       as a preservative in pharmaceuticals and cosmetics.
              

       When camphor is applied on the skin, it is analgesic.  It is also 
       used in liniments as a counter-irritant in fibrositis, neuralgia, 
       and similar conditions.

       In dermatology, when it is applied as lotion (0.1 to 3%), it is
       an anti-pruritic and surface anaesthetic (when applied gently, 
       it creates a feeling of coolness).

       In dentistry, it is prepared with parachlorophenol 35% (and 65% 
       camphor) and used as an antibacterial for infected root canals.

       Taken internally, it is an irritant and carminative. It has been 
       used as a mild expectorant and to relieve griping (abdominal 
       discomfort) (this use is now discouraged because of toxicity).

       Camphor was formerly administered as a solution in oil by 
       subcutaneous or intramuscular injection to act as a circulatory 
       and respiratory stimulant, but there is no evidence of its value 
       for this purpose (Reynolds, 1982).

       According to the Dutch Information Medicamentorum (1986), camphor
       is used:

       For pruritus: lotion with 1 to 70 mg/g

       For muscular pains: oil with 40  to  250 mg/g or alcohol solution 
       with 100 mg/ml

       For colds: chest liniment, with 20 to 100 mg/g;  nose ointment, 
       with 20 to 50 mg/g:  nose drops/spray, with 0.15 mg/ml.

     4.2 Therapeutic dosage

       4.2.1 Adults
             The dosage varies according to its uses (see section 
             4.1).
       4.2.2 Children
             The dosage varies according to different uses (see 
             section 4.1).
     4.3 Contraindications
       Internal use is discouraged because of its toxicity.
       
       It is dangerous to place camphor into infants' nostrils, since 
       it can cause instant collapse (Reynolds, 1982).
       
       As with all rubefacients, it should not be applied to abraded, 
       irritated skin.
    5. ROUTES OF ENTRY
     5.1 Oral
       Ingestion of camphor, camphorated oils, spirits, or other 
       preparations is the main route of poisoning.
     5.2 Inhalation
       Camphor fumes may be inhaled.
     5.3 Dermal
       Camphor liniments, spirits, or oil can be applied in excessive 
       amounts.
     5.4 Eye
       Splash or fumes may cause irritation.
     5.5 Parenteral
       Subcutaneous or intramuscular injections.
     5.6 Other
       No data available.
    6. KINETICS
     6.1 Absorption by route of exposure
       Camphor is readily and rapidly absorbed from the skin, and 
       gastrointestinal and respiratory tracts.  Camphor in oil 
       solutions is absorbed slowly from subcutaneous or 
       intramuscular depots.
     6.2 Distribution by route of exposure
       After oral ingestion, peak blood levels are reached in 5 to 90 
       min.  The high lipid solubility of camphor suggests that it 
       accumulates in adipose and other tissues.  Camphor crosses the 
       placenta (Kresel, 1982), and has a large volume of  
       distribution.
     6.3 Biological half-life by route of exposure
       No data available.
     6.4 Metabolism
       Camphor is rapidly oxidized to campherols (2-hydroxycamphor 
       and 3-hydroxycamphor), and then conjugated in the liver to the 
       glucuronide form (Kresel, 1982).  Camphor-related metabolites 
       are relatively fat-soluble and may accumulate in fatty tissue.
     6.5 Elimination by route of exposure
       Campherol conjugated to glucuronic acid is eliminated mainly 
       in the urine as an inactive compound (Kresel, 1982).  Trace 
       amounts are eliminated by the lungs.
    7. PHARMACOLOGY AND TOXICOLOGY
     7.1 Mode of action
       7.1.1 Toxicodynamics
             Camphor is a CNS stimulant whose effects range from mild 

             excitation to grand-mal convulsions or status 
             epilepticus.  These effects result from excitation of 
             the cerebrum and lower structures of the CNS.
             
             Gastric irritation, together with cortical and medullary 
             stimulation, frequently causes vomiting and diarrhoea.
             
             It is not clear whether camphor toxicity is due to the 
             parent compound, a metabolite (secondary alcohols, 
             including borneol and isomers of hydroxy-camphor), or 
             both (Kresel, 1982).
       7.1.2 Pharmacodynamics
             Camphor is used exclusively because of its local 
             effects. When rubbed on the skin, it acts as a 
             rubefacient and causes localized vasodilatation 
             (mediated by way of an axon reflex), which gives 
             feelings of comfort and warmth.
             
             As an anti-pruritic gent, when applied gently on the 
             skin, it may create a feeling of coolness, and a mild, 
             local anaesthetic effect, which may be followed by 
             numbness.
             
             When ingested in small amounts, it creates feelings of 
             warmth and comfort in the stomach, but given in large 
             doses it acts as an irritant (Goodman et al 1985).
     7.2 Toxicity
       7.2.1 Human data
             7.2.1.1 Adults
                     The probable oral lethal dose is 50 to 500 
                     mg/kg.  A dose of 2 g generally causes toxic 
                     effects in adults.  The potential lethal oral 
                     dose in adults is 4 g pure camphor.
             7.2.1.2 Children
                     The lethal dose for children is estimated to be 
                     0.5 to 1.0 g (Siegel & Wason, 1986); for infants,
                      the oral LDLo is 70 mg/kg.
       7.2.2 Relevant animal data
             
             
             
             Species   Route              Effect   Dose mg/kg
             
             
             Rat      Intraperitoneal      LDLo      900 
             
             
             Mouse    Intraperitoneal      LD50     3000
             
             
             Mouse    Subcutaneous         LDLo     2200
             
             
             Dog        Oral               LDLo      800
             
             

             Cat      Intraperitoneal      LDLo      400
             
             
             Rabbit     Oral               LDLo     2000 
             
             
             Frog     Subcutaneous         LDLo      240
             
             
             Guinea-pig  Oral              LDLo     1800
             
       7.2.3 Relevant in vitro data
             Not relevant.
     7.3 Carcinogenicity
       Carcinogenicity tests have been negative.
     7.4 Teratogenicity
       No data available.
     7.5 Mutagenicity
       Not mutagenic with the Ames test.
     7.6 Interactions
       Oils, alcohols, and fats promote gastrointestinal absorption. 
       Although vaseline oil has been used for gastric 
       decontamination, its use is controversial.
     7.7 Main adverse effects
       There have been reports of instant collapse in infants after 
       camphor has been applied to their nostrils (Reynolds, 1982).
    8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS
     8.1 Material sampling plan
       8.1.1 Sampling and specimen collection
             8.1.1.1 Toxicological analyses
             8.1.1.2 Biomedical analyses
             8.1.1.3 Arterial blood gas analysis
             8.1.1.4 Haematological analyses
             8.1.1.5 Other (unspecified) analyses
       8.1.2 Storage of laboratory samples and specimens
             8.1.2.1 Toxicological analyses
             8.1.2.2 Biomedical analyses
             8.1.2.3 Arterial blood gas analysis
             8.1.2.4 Haematological analyses
             8.1.2.5 Other (unspecified) analyses
       8.1.3 Transport of laboratory samples and specimens
             8.1.3.1 Toxicological analyses
             8.1.3.2 Biomedical analyses
             8.1.3.3 Arterial blood gas analysis
             8.1.3.4 Haematological analyses
             8.1.3.5 Other (unspecified) analyses
     8.2 Toxicological Analyses and Their Interpretation
       8.2.1 Tests on toxic ingredient(s) of material
             8.2.1.1 Simple Qualitative Test(s)
             8.2.1.2 Advanced Qualitative Confirmation Test(s)
             8.2.1.3 Simple Quantitative Method(s)
             8.2.1.4 Advanced Quantitative Method(s)
       8.2.2 Tests for biological specimens
             8.2.2.1 Simple Qualitative Test(s)
             8.2.2.2 Advanced Qualitative Confirmation Test(s)
             8.2.2.3 Simple Quantitative Method(s)

             8.2.2.4 Advanced Quantitative Method(s)
             8.2.2.5 Other Dedicated Method(s)
       8.2.3 Interpretation of toxicological analyses
     8.3 Biomedical investigations and their interpretation
       8.3.1 Biochemical analysis
             8.3.1.1 Blood, plasma or serum
                     General:  Serum camphor levels are not 
                     clinically useful.
                          
                     A level of 15 mg/l within 20 minutes of 
                     ingestion caused no symptoms.
                          
                     A level of 19.5 microgram/l 7 h after ingestion 
                     caused convulsions (Phelan,1976).
             8.3.1.2 Urine
             8.3.1.3 Other fluids
       8.3.2 Arterial blood gas analyses
       8.3.3 Haematological analyses
       8.3.4 Interpretation of biomedical investigations
     8.4 Other biomedical (diagnostic) investigations and their 
       interpretation
     8.5 Overall Interpretation of all toxicological analyses and 
       toxicological investigations
     8.6 References
    9. CLINICAL EFFECTS
     9.1 Acute poisoning
       9.1.1 Ingestion
             The symptoms that occur within 5 to 90 min after 
             ingestion are:  oral and epigastric burning sensations, 
             nausea, vomiting and feeling of warmth.
             
             Mydriasis and impairment of vision have been reported.
             
             Other symptoms are: headache, confusion, vertigo, 
             excitement, restlessness, delirium, and hallucinations; 
             increased muscular excitability, tremors, and jerky 
             movements; epileptiform convulsions followed by 
             depression; convulsions sometimes occur early in cases 
             of poisoning and may be severe; coma; CNS depression may 
             at times be the primary clinical response.
             
             Death results from respiratory failure or from status 
             epilepticus.
       9.1.2 Inhalation
             Inhalation of concentrations above 2 ppm irritates the 
             nose and throat (mucous membranes). Respiratory 
             depression and apnoea may occur.  Very large exposures 
             will cause the same clinical features as ingestion.
       9.1.3 Skin exposure
             Camphor may be a skin irritant.  Acute poisoning may 
             occur after skin absorption.  (Symptoms may be the same 
             as those that occur after ingestion, see section 9.1.1).
       9.1.4 Eye contact
             Camphor may be somewhat irritating to the eyes, but no 
             serious injuries have been reported.
       9.1.5 Parenteral exposure

             Camphor was formerly used parenterally as a circulatory 
             and respiratory stimulant;  therefore, there is a 
             theoretical possibility of overdose or
             poisoning by the parenteral route (clinical features as 
             in section 9.1.1).
       9.1.6 Other
             No data available.
     9.2 Chronic poisoning
       9.2.1 Ingestion
             Symptoms include viral illness, rapid neurological 
             deterioration, liver injury, prolonged prothrombin time, 
             and low blood glucose were observed in a 6-month-old 
             male child who received a total dose of 3 g/kg over a 5 
             month period (Jimenez et al 1983).
       9.2.2 Inhalation
             No data available.
       9.2.3 Skin exposure
             No data available.
       9.2.4 Eye contact
             No data available.
       9.2.5 Parenteral exposure
             No data available.
       9.2.6 Other
             No data available.
     9.3 Course, prognosis, cause of death
       If the patient survives for 24 h, recovery is likely.  Death 
       results from respiratory failure during a convulsion or from 
       status epilepticus, and may also result from exhaustion and 
       circulatory collapse.  Death may occur during an early 
       convulsion or as late as 20 h after ingestion.
     9.4 Systematic description of clinical effects
       9.4.1 Cardiovascular
             Peripheral circulatory collapse and shock have been 
             reported (Vasey & Karayannopoulus, 1972).
       9.4.2 Respiratory
             Respiratory depression and apnoea may occur.  Death 
             usually results from post-convulsive respiratory 
             depression.
             
             The odour of camphor may be detected on the breath.
       9.4.3 Neurological
             9.4.3.1 CNS
                     Seizures are characteristic of camphor toxicity 
                     and may occur suddenly,  even without previous 
                     symptoms.  Confusion, hallucinations, tremors, 
                     agitation, and irritability can also be 
                     observed.  Convulsions may be followed by CNS 
                     depression and coma.
             9.4.3.2 Peripheral nervous system
                     There is neuromuscular hyperactivity.
             9.4.3.3 Autonomic nervous system
                     No data available.
             9.4.3.4 Skeletal and smooth muscle
                     Increased muscular activity and tremor 
                     (Ellenhorn & Barceloux, 1988).
       9.4.4 Gastrointestinal

             Oral and epigastric burning sensations, nausea, and 
             vomiting usually occur shortly after ingestion.
             
             Symptoms may be delayed for several hours if food is 
             present in the stomach (Ellenhorn & Barceloux, 1988).
       9.4.5 Hepatic
             Mild and transient hepatic derangement may occur with 
             elevation of serum concentrations of SGOT, ALAT, SGPT, 
             and lactic dehydrogenase.
       9.4.6 Urinary
             9.4.6.1 Renal
                     Urinary retention, albuminuria, and anuria have 
                     been described (Smith & Margolis, 1954).
             9.4.6.2 Other
                     No data available.
       9.4.7 Endocrine and reproductive systems
             No data available.
       9.4.8 Dermatological
             Camphor may be a skin irritant when applied in excessive 
             amounts or too vigorously.
       9.4.9 Eye, ear, nose, throat: local effects
             Eyes:  Camphor is an eye irritant.  Keratitis is 
             normally transient.
             
             Ear:   No data available (but camphor is probably 
             irritating).
             
             Nose:  Camphor irritates the nose at concentrations 
             above 2 ppm or when applied directly on mucous 
             membranes.
             
             Throat:  Camphor may irritate mucous membranes and cause 
             burning pain in the mouth or throat.
       9.4.10 Haematological
              No data available.
       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
                       No data available.
       9.4.13 Allergic reactions
              No data available.
       9.4.14 Other clinical effects
              No data available.
       9.4.15 Special risks
              Pregnancy:  Camphor crosses the placenta and has been 
              implicated in fetal and neonatal death.  It has been 
              used to induce abortions.  Camphor poisoning during 
              pregnancy was reported in four cases and, in each case, 
              camphorated oil was mistaken for castor oil (Weiss & 
              Capalano, 1973).  The topical use of camphorated oil in 
              pregnancy was not associated with teratogenic effects.

                             
              Breast feeding:  no data available .
     9.5 Other
       No data available.
     9.6 Summary
    10. MANAGEMENT
      10.1 General principles
         If 10 mg/kg has been ingested and no symptoms appear within 
         4 h there is no need for hospital admission (Blodgett 
         Regional Poison Centre, 1987).
         
         If 30 mg/kg have been ingested, the patient must be admitted 
         to hospital for gastric lavage if indicated (see section 
         10.4) (Geller et al 1984).
         
         Establish respiration
         
         Treat convulsions
         
         Initiate gastric lavage only after airway has been 
         protected.
         
         Do not induce vomiting
         
         Administer activated charcoal and then a cathartic
         
         Resin or charcoal haemoperfusion may be indicated in very 
         severe cases.
      10.2 Relevant laboratory analyses
         10.2.1 Sample collection
                Blood and urine for biomedical analysis
                
                Sample of the product for identification.
         10.2.2 Biomedical analysis
                Routine blood and urine analysis
                
                In particular:
                
                Hepatic transaminases and LDH
                
                Albuminuria
                
                EEG (Phelan, 1976).
         10.2.3 Toxicological analysis
                Tests for qualitative and quantitative determination 
                of camphor levels in serum/blood are generally not 
                available.  They can be performed by gas 
                chromatography (Phelan, 1976).
         10.2.4 Other investigations
      10.3 Life supportive procedures and symptomatic/specific 
         treatment
         Support respiratory and cardiovascular functions
         
         Treat seizures with:
         
         Diazepam IV 

         
         Adults:  5 to 10 mg initially, which may be repeated every 
         10 to 15 min to a maximum of 30 mg.
         
         Children: 0.25 to 0.4 mg/kg up to a maximum of 5 mg in 
         children aged 30 days to 5 years, and a maximum of 10 mg in 
         children over 5 years old.
         
         If seizures cannot be controlled or if they recur, 
         administer phenytoin or phenobarbital.
         
         Phenytoin
         
         Adults:  150 to 250 mg of phenytoin-sodium by slow 
         intravenous injection at a steady rate of not more than 50 
         mg/min.  An additional 100 to 200 mg may be given 30 min 
         later if necessary (Reynolds, 1982).
         
         Children: 5 mg/kg in one dose or divided into two doses 
         (Reynolds, 1982).
         
         Phenytoin administered intravenously can prevent a relapse 
         into a convulsive state.  It should be administered very 
         slowly in order to avoid cardiac arrhythmias.
         
         Phenobarbital
         
         Adults: initially 200 mg intramuscularly that can be 
         repeated after 6 h if necessary (Reynolds, 1982).
         
         Children:  initially 3 to 5 mg/kg intramuscularly (Reynolds, 
         1982).
         
         Doubts have been expressed as to the efficacy of 
         henobarbitone by intramuscular injection in an emergency 
         because of the slowness of absorption.
         
         Control renal function.
      10.4 Decontamination
         Ingestion
         
         Camphor is a convulsant: do not induce vomiting. Gastric 
         lavage is contraindicated unless it is performed immediately 
         after ingestion or after the airway has been protected 
         (endotracheal intubation), and when the camphor ingested is 
         in solid form (Bozza-Marrubini et al 1987).
         
         If the amount of ingested camphor is small, give a saline 
         cathartic. 
         
         Activated charcoal should be administered in the usual doses 
         of 30 to 100 g in adults and 15 to 30 g in children.
         
         Saline carthartics are indicated a few minutes after 
         activated charcoal has been given, and should be stopped 
         when a charcoal stool appears.

         
         Dose of sodium sulfate:  20 to 30 g in adults and 250 mg/kg 
         in children
         
         Dose of sorbitol:  30 to 50 g orally in adults.
         
         Eye contact
         
         Keep eyelids apart using your finger and flush eyes with 
         large amounts of water for at least 15 min.  Keratitis is 
         normally transient, but if it persists, an opthalmic 
         examination should be performed.
         
         Skin contact
         
         Wash exposed area very thoroughly with soap and water.
      10.5 Elimination
         Both lipid haemodialysis and resin haemoperfusion have been 
         helpful in lowering blood camphor concentrations (Kopelman 
         et al, 1979).
         
         Aqueous haemodialysis is ineffective in removing camphor.  
         In one patient lipid dialysis with soyabean oil removed 
         camphor effectively, but it is not routinely recommended 
         (Ginn et al, 1968).
         
         Amberlite resin haemoperfusion was used in 1 patient; 
         camphor was cleared from the blood and the patient had a 
         good recovery (Kopelman et al, 1979).
         
         Charcoal haemoperfusion has proven effective (Mascie-Taylor 
         et al, 1981)
      10.6 Antidote treatment
         10.6.1 Adults
                There is no specific antidote.
         10.6.2 Children
                There is no specific antidote.
      10.7 Management discussion
    11. ILLUSTRATIVE CASES
      11.1 Case reports from literature
         Camphor has occasionally been used in attempts to induce 
         abortion (Briggs et al 1965):  it was detected in maternal 
         blood 15 min after ingestion, but not after 8 h.  At 
         delivery 36 h later, however, it was present in the amniotic 
          fluid, the umbilical cord, and in the fetal blood.  This 
         distribution might reflect immature hepatic glucuronic 
         conjugation in the fetus - a major detoxication process for 
         camphor in adults.  The infant appeared viable at birth, but 
         failed to initiate respiration.  Post-mortem examination 
         revealed severe atelectasis and CNS-necrosis (Gosselin et al,
          1984).
         
         A patient who ingested approximately 60 g of camphorated oil 
         (i.e., 12 g pure camphor) was successfully treated by lipid 
         haemodialysis (Ginn et al, 1968).
         

         A 3 year-old girl swallowed 1 tablespoon of camphor-
         containing salve and developed violent vomiting, convulsions,
          and respiratory depression (Anon, 1975).
         
         A 2-year-old girl swallowed 2 teaspoons of a camphor 
         preparation and had violent vomiting but no convulsions 
         (Anon, 1975).
         
         A 19-month-old infant died after ingesting 1 g of a camphor 
         product; autopsy showed haemorrhage and brain cell 
         degeneration (Anon, 1975).
         
         A man attempted suicide with 150 ml of camphorated oil, i.e.,
          30 g pure camphor (the potential lethal dose in an adult is 
         4 g pure camphor).  He had peripheral circulatory shock and 
         severe dehydration because of vomiting.  Severe and 
         prolonged grand-mal attacks occurred.  The patient was fit 
         and well 36 h after intensive treatment.  This is one of the 
         largest camphor overdoses of camphor associated with 
         survival (Vasey & Karayannopoulus, 1972; Reynolds, 1982).
         
         A 12-year-old boy given approximately 30 g camphorated oil 
         (20% camphor) developed coma and convulsions.  After 
         treatment with diazepam, his condition improved, and he was 
         discharged from hospital on the 3rd day (Aronow & Spigiel, 
         1976).
                   
         A 33-year-old woman ingested 115 g camphorated oil (20%  
         camphor); she had several convulsions in hospital, but was 
         discharged after 4 days in the intensive care unit (Aronow & 
         Spigiel, 1976).
         
         A 37-year-old man ingested 18 g pure camphor and developed 
         grand-mal seizures.  He was treated by haemoperfusion; an 
         amberlite system was more effective than lipid dialysis in 
         extracting camphor from the blood (Kopelman et al, 1979).
         
         A 19-year-old girl ingested 60 g camphorated oil (20% 
         camphor) and had grand-mal seizures; she was discharged from 
         hospital after 13 days of treatment (Kopelman et al, 1979).
         
         A 15-year-old boy ingested 60 g camphorated oil (20% 
         camphor) and had grand-mal seizures; he was discharged from 
         hospital after 2 days of treatment (Kopelman et al, 1979).
         
         A 61-year-old man ingested 60 g camphorated oil (20% 
         camphor) and developed status epilepticus and coma; after 
         treatment in hospital he fully recovered (Antman et al, 
         1978).
         
         A 56-year-old woman ingested 12 ml camphorated oil (20% 
         camphor).  She had nausea, vomiting, and convulsions.  The 
         odour of camphor on her breath helped to diagnose her 
         condition.  Lipid haemodialysis with soybean oil dialysate 
         was performed for 4 to  5 h and she recovered fully (Antman 
         et al, 1978).

         
         A 6-month-old boy received a total dose of 3 g/kg camphor 
         over a 5-month period and developed clinical symptoms 
         consistent with a diagnosis of Reye's syndrome (Jimenez et 
         al, 1983).
         
         A 3-year-old girl ingested 7OO mg camphor from 1 tablespoon 
         of Vicks VapoRub (R).  This product had also been placed in 
         her nostrils twice daily for 5 months.  Grand-mal seizures 
         occurred 2 h after ingestion. Coma and respiratory 
         depression lasted 21 h.  Full recovery ensued (Phelan, 
         1976).
      11.2 Internally extracted data on cases
      11.3 Internal cases
         (to be added by PC using the monograph).
    12. Additional information
      12.1 Availability of antidotes
      12.2 Specific preventive measures
         Keep pharmaceutical preparations and moth-repellents out of 
         the reach of children and irresponsible people.
         
         Label camphorated oil appropriately to avoid mistaking it 
         for castor oil and cough syrups.
         
         Do not place camphor ointments into infants' nostrils.
         
         Do not use the rubefacient on abraded skin.
         
         In the workplace, the maximum permissible atmospheric 
         concentration is 2 ppm.
       12.3 Other
         No data available.
    13. REFERENCES
    Abdernalden's Handbuck der Biologischen Arbveitsmetoden (1935) 
    Vol 4, p l289 Leipzig, Germany.
    
    Anon (1975)  Camphor may do more harm than good. J Am Med Assoc 
    234: No 2, p l45.
    
    Antman E, Jacob G, Volpe B, Finkel S & Savona M (1978)  Camphor 
    Overdosage: therapeutic considerations.  NY State J Med, 6: 896-
    897.
    
    Arena JM (197O)  Poisoning.  Toxicology, Symptoms, Treatments.  
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    Aronow R (1976).  Camphor Poisoning.  J Am Med Assoc, 235: l26O.
    
    Aronow R & Spigiel RW (1976)  Implications of Camphor Poisoning.  
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    Baselt RC (1982)  Disposition of toxic drugs and chemicals in 
    man. 2nd ed, pll2.  California, Biomedical Publications.
    
    Bozza-Marrubini ML, Ghezzi R, Ucelli P (1987)  Intossicasioni 
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    Briggs GG, Freeman RK & Yaffe SJ (1986)  Drugs in pregnancy and 
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    "Documentation of Threshold Limit Values for Substances in 
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    Dupeyron IP, Quattrocchi F, Castaing H & Fabiani P (1976)  Child 
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    Fuhner H (1932)  Beitrage zer vergleichenden Pharmakologie I. Die 
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    Geller RJ, Spyker DA, Garrettson LK & Rogol AD (1984)  Camphor 
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    Goodman LS, Gilman AG, Rall TW & Murad F (1985)  Goodman and  
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    Saunders & Co.
    
    Hawley, GG (1981).  The Condensed Chemical Dictionary. 10th ed 
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    Jimenez JF, Brown AL, Arnold WC (1983).  Chronic camphor 
    ingestion mimicking Reye's syndrome.  Gastroenterology 84: 394-
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    Kelly RC, Kopelman RC, Sunshine I (1976)  A simple gas 
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    Kopelman R, Miller S, Kelly RC & Sunshine I (1979).  Camphor 
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    Poisindex, February 1988.
    
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    Reynolds EF (ed) (1982). Martindale, The Extra Pharmacopoeia, 
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    14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE 
    ADDRESS(ES)
    Author:   Elsa Wickstrom
              National Poison Center
              P.O. Box 8189 DEP
              0034 Oslo
              Norway
    
              Tel: 47-2-456063
              Fax: 47-2-454374  
    
    Date:     29 February 1988.
         
    Peer review: Hamilton, Canada, May 1989




    See Also:
       Toxicological Abbreviations
       Camphor (ICSC)
       Camphor (UKPID)