POISONOUS PLANTS
    1. NAME
     1.1 Scientific name
       Ricinus communis
     1.2 Family
       Euphorbiaceae (Spurge family).
     1.3 Common name(s)
       African coffee tree (USA)
       Carrapateiro  (Brazil)
       Castor (Argentine)
       Castor bean  (USA)
       Castor-oil  (USA)
       Higuereta  (Cuba, Puerto Rico)
       Koli, Pa'aila  (Hawaii)
       La'au-'aila  (Hawaii)
       Mamona  (Brazil)
       Mamoneiro  (Brazil)
       Palma de Cristo (Uruguay)
       Palma-cristi  (Brazil)
       Ricin  (France)
       Ricino  (Argentine)
       Steadfast  (USA)
       Tartago (Uruguay)
    2. SUMMARY
     2.1 Main risks and target organs
       Intense gastroenteritis and acute dehydration.  Renal and 
       hepatic  insufficiency have been reported.
     2.2 Summary of clinical effects
       Burning sensation of the mouth and throat occurs after chewing 
       the  seeds.  After a latent period of 3 to 6 h, nausea, 
       vomiting, severe stomach  pains, diarrhoea, and excessive 
       thirst developed leading to acute  dehydration, hypotension 
       and circulatory failure.  Prostration, blurring of  vision, 
       loss of consciousness, convulsions, haemolysis, uraemia and 
       liver  necrosis have also occurred.
     2.3 Diagnosis
       Blood gases and electrolytes.
       
       Close monitoring of renal, hepatic and haematologic systems.
          
       A sample of the plant should be obtained for botanical and 
       pharmacognostic  identification.
     2.4 First-aid measures and management principles
       Ingestion of any part of Ricinus communis is an indication for 
        admission to hospital for close observation.
       
       Immediate gastric lavage or emesis should be performed.  
       Activated charcoal  may be administered.
       
       Correct fluid and electrolyte imbalances immediately.
     2.5 Poisonous parts
       All parts of the plant are poisonous, especially the seeds. 
     2.6 Main toxins
       Ricin, a toxalbumin, is one of the most toxic substances of 
       plant  origin.
    3. CHARACTERISTICS

     3.1 Description of the plant
       3.1.1 Special identification features
             Shrublike herb, stems 1 to 4 metres high, branched, 
             green to  reddish or purple, leaves alternated, simple, 
             long-stalked, 20 to  80 cm wide and palmately lobed  
             with 5 to 11 long lobes which are  toothed on the 
             margins, green or reddish.  It has clusters of seed  
             pods, green or red, and covered with fleshy spines. The 
             seeds  contained in the pods are 3 per capsule, about 
             1.5 to 2.5 cm across,  elliptical glossy, black or white 
             or usually mottled with grey,  black, brown and white.  
             The seeds have a pleasant taste (Lampe,  1985; Hardin, 
             1974; Font-Quer, 1979). 
       3.1.2 Habitat
             Castor bean is cultivated as a decorative plant in 
             gardens.  It is very common in South America growing 
             wild in uncultivated  lands (Pronczuk, 1988).  It is 
             commercially cultivated mainly in Brazil and India and 
             in several other countries (Ecuador, Paraguay,  Tanzania,
             Rumania, Ethiopia, USA, USSR, South Africa) for its  
             industrial and medicinal use (Lampe, 1985; Cooper, 1989).
             
             Seeds are used to make ornamental necklaces and there 
             are commercially prepared packages of seeds available 
             in plant stores (Kinamore, 1980).
       3.1.3 Distribution
             Originally from tropical Africa, it is now growing in  
             tropical, subtropical and temperate areas.
             
             Ricinus communis is now worldwide in distribution.
     3.2 Poisonous parts of the plant
       If chewed, the seeds are the most toxic part of the plant 
       although the leaves are also poisonous. The seeds contain 0.2 
       to 3% ricin (Favarel-Carriques, 1978; Schvartsman, 1979)
       and one mg of pure ricin can be isolated from its grains 
       (Frohne, 1984).
     3.3 The toxin(s)
       3.3.1 Name(s)
             Ricin.  It must not be confused with ricine oil (Castor 
             oil) produced commercially as a cathartic.
       3.3.2 Description, chemical structure, stability
             Ricin 
             
             CAS: 9009-86-3
             
             A glycoprotein composed of two peptide chains of 
             differing molecular weights attached by a disulfide 
             bond (Wedin, 1986).
             
             It is destroyed by heat and light (Cooper, 1989; 
             Schvartsman, 1979).  The toxins are dimers of 30 000 to 
             33 000 mol. wt. (Budavari, 1989).
       3.3.3 Other physico-chemical characteristics
             Ricin is crystallizable, toxic, soluble in water and  
             chloroform and insoluble in alcohol.  Ricin resists 
             degradation by hydrochloric acid, pepsin, chemopepsine 

             and papaine.
     3.4 Other chemical contents of the plant
       A potent allergen that has not been identified (Knight, 1979).
       
       Castor oil contains about 80% of the trigliceride of rinoleic 
       acid (Martindale, 1982).
       
       Castor bean also has an agglutinating protein composed of four 
       polypeptide chains which are non-toxic orally (Wedin, 1986).  
       This protein shows decreased agglutinating activity at low 
       temperatures (Cooper, 1989).
    4. USES/CIRCUMSTANCES OF POISONING
     4.1 Uses
       Folk medicine: ricine oil is used as a cathartic (Font-
       Quer, 1979).
       
       Industry: castor oil is used as a lubricant in the 
       plastics, soap and paint industries.  The fibrous 
       residue (cake) left by castor oil extraction is  
       detoxified by steam treatment and used as a fertilizer 
       (Cooper, 1989; Schvarstman, 1979).
       
       Ricin is used as a tool in studies of cell surface 
       properties and experimentally used in cancer research 
       (Budavari, 1989).
     4.2 High risk circumstances
       Accidental or intentional poisoning occurs by ingestion if the 
       seeds  are chewed (Pronczuk, 1988).  Because of the hard, 
       water-impermeable coat,  the seed is considered harmless if 
       swallowed whole. In some countries, the  seeds are used as 
       beads for necklaces which could cause toxicity because the  
       seeds are already broken (Pronczuk, 1988; Kinamore, 1980).  
       Allergic  reactions have been reported among workers exposd to 
       R. communis in  commercial cultivation and gardening (Cooper, 
       1989; Schvartsman, 1979).   Also people living in the vicinity 
       of castor oil factories have developed  allergic reactions 
       (Schvartsman, 1979).  Severe allergies have been reported  
       from handling necklaces and other trinkets made from castor 
       bean.  Secondary  intoxication can occur from harvesting or 
       consumption of contaminated crops  (such as soy bean) (Cooper, 
       1984). 
     4.3 High risk geographical areas
       Ricin is widely distributed.  Poisoning cases have been known 
       to occur  in many countries.
    5. ROUTES OF ENTRY
     5.1 Oral
       Accidental ingestion can occur.
     5.2 Inhalation
       The allergen can produce asthma and rhinitis (Cooper, 1989, 
       Schvartsman,  1979).
     5.3 Dermal
       Prolonged exposures can induce dermatitis and eczemas 
       (Schvartsman,  1979).
     5.4 Eye
       Allergic conjunctivitis can occur through this route 
       (Schvartsman,  1979).

     5.5 Parenteral
       Subcutaneous administration of rincin has been reported in 
       experimental  studies (Knight, 1979).
     5.6 Others
       No data available.
    6. KINETICS
     6.1 Absorption by route of exposure
       After ingestion of the chewed seeds the toxins are rapidly 
       absorbed  through the gastrointestinal tract (Schvartsman, 
       1979).
     6.2 Distribution by route of exposure
       The fate of ricin in the human body is still not established  
       (Kopferschmitt, 1983).
     6.3 Biological half-life by route of exposure
       The biological half-life is not yet known.  The plasma  
       elimination  half-life has been estimated to be approximately 
       8 days (Kopferschmitt,  1983).
     6.4 Metabolism
       No data available.
     6.5 Elimination by route of exposure
       Two routes of excretion have been proposed: intestinal and 
       faecal  (Kopferschmitt, 1983).
    7. TOXICOLOGY/TOXINOLOGY/PHARMACOLOGY
     7.1 Mode of action
       Ricin binds to galactose-containing receptors on the cell 
       surface. This  is followed by uncoupling of the peptide chains 
       from the ricin molecule, and  the smaller chain is taken into 
       the cell by endocytosis. Ricin impairs chain  elongation in 
       protein synthesis, causing cell death (Olnes, 1974).
     7.2 Toxicity
       7.2.1 Human data
             7.2.1.1 Adults
                     The estimated lethal dose in man is 1 mg/kg  
                     (Kopferschmitt, 1983).  Two to four seeds may
                     cause severe poisoning in an adult, and 8 are 
                     generally  fatal (Wedin; 1986), Hardin, 1974). 
                     If seeds are swallowed  without chewing, 
                     poisoning is unlikely.
             7.2.1.2 Children
                     One to three seeds can be fatal to a child  
                     (Weding, 1986).
       7.2.2 Animal data
             The fatal dose by intravenous injection of ricin in  
             experimental animals (mice) has been reported to be as 
             low as 300  nanaogram/kg (Martindale, 1982).  The 
             ingestion of 2 g undetoxified  fibrous residue of castor 
             oil can determine toxic effects in large  animals 
             (Schvartsman, 1979). 
             
             Ricin - MLD ip mice: 0.001 microgram ricin nitrogen per 
             g body  weight (Budavari, 1989).  In animals, repeated 
             small doses result  in antibody production. Pretreated 
             animals can withstand up to 800  times the lethal dose 
             (Knight, 1979).
       7.2.3 Relevant in vitro data
             No data available.

     7.3 Carcinogenicity
       No data available.
     7.4 Teratogenicity
       No data available.
     7.5 Mutagenicity
       No data available.
     7.6 Interactions
       No data available.
    8. TOXICOLOGICAL/TOXINOLOGICAL 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)
                     Ricin can be measured by radioimmunassay.   Anti-
                     ricin antibodies can be labelled
                     with isotopic iodine (I 125) (Kopferschmitt, 
                     1983).
       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
                     Cases of ricin poisoning been described in which 
                     the serum concentration is 1.5 nanogram/l but there 
                     is no correlation between serum levels and evolution 
                     of the clinical signs (Kopferschmitt,  1983).
             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
             If chewed, the seeds are toxic; the leaves are less 
             toxic.   Ricin causes a burning sensation of the mouth 
             and throat  (Schvartsman, 1979).  After a latent period 
             of 3 to 6 h (or  sometimes several days), nausea, 
             vomiting, severe stomach pains,  diarrhoea (sometimes 
             bloody), excessive thirst, and acute  dehydration 
             develop.  Prostration, blurring of vision, mydriasis,  
             fever, necrosis of the liver, spleen and lymphatic 
             system,  nephritis, proteinuria, uremia, red cell 
             hemolysis, loss of  consciousness and convulsions occur 
             (Arena, 1981; Hardin, 1974;  Jouglard, 1977; Kinamore, 
             1980; Kopferschmitt, 1983; Pronczuk,  1988; Wedin, 
             1986).
       9.1.2 Inhalation
             The allergen can produce asthma and rhinitis.
       9.1.3 Skin exposure
             The allergen can produce dermatitis and eczema
       9.1.4 Eye contact
             The allergen can produce conjunctivitis.
       9.1.5 Parenteral exposure
             A case of subcutaneous injection which in a few hours  
             developed circulatory failure, hypothermia and high 
             leucocyte count  leading to death, was reported Knight, 
             1979).
       9.1.6 Other
             No data available.
     9.2 Chronic poisoning
       9.2.1 Ingestion
             No data available.
       9.2.2 Inhalation
             The allergen can produce asthma and rhinitis 
             (Schvartsman,  1979).
       9.2.3 Skin exposure
             Prolonged contact can produce allergic dermatitis and 
             eczema  (Schvartsman, 1979).
       9.2.4 Eye contact
             Allergic conjunctivitis (Schvartsman, 1979).
       9.2.5 Parenteral exposure
             No data available.
       9.2.6 Other
             No data available.
     9.3 Course, prognosis, cause of death
       Nausea and burning sensation of the mouth and throat appear 
       immediately  after ingestion of the chewed seed (Schvartsman, 
       1979).  Intense vomiting  and profuse watery or bloody 
       diarrhoea appear 3 to 6 h later.  In some cases,  symptoms may 
       be delayed for up to 15 h after ingestion (Schvartsman, 1979). 

        Other effects are secondary to extensive fluid and 
       electrolyte depletion.   Death can occur through dehydration 
       and electrolyte imbalance within a few  hours.  Convulsions 
       may precede death (Pronczuk, 1988; Knight, 1979).   However, 
       death due to uraemia may occur within 12 days.  The prognosis  
       epends on the promptness of treatment and the number of seeds 
       chewed and ingested.
     9.4 Systematic description of clinical effects
       9.4.1 Cardiovascular
             Hypotension is frequently observed due to fluid 
             depletion.   Tachycardia and ECG changes have been 
             described (Wedin, 1986).
       9.4.2 Respiratory
             Bronchial asthma and allergic rhinitis (Cooper, 1989;  
             Schvartsman, 1979).
       9.4.3 Neurological
             9.4.3.1 CNS
                     Vertigo, mydriasis, somnolence, stupor, and 
                     coma.   Convulsion may precede death 
                     (Kopferschmitt, 1983; Knight,  1979, Wedin, 
                     1986).
             9.4.3.2 Peripheral nervous system
                     No data available.
             9.4.3.3 Autonomic nervous system
                     No data available.
             9.4.3.4 Skeletal and smooth muscle
                     Muscular weakness and cramps are observed.
       9.4.4 Gastrointestinal
             Burning sensation of the mouth and throat almost 
             immediately  after ingestion.  Nausea, vomiting and 
             intense watery or bloody diarrhoea, stomach-ache follow 
             (Hardin, 1974; Jouglard, 1977; Arena,  1981; 
             Kopferschmitt, 1983; Wedin, 1986, Pronczuk, 1988).
       9.4.5 Hepatic
             Liver necrosis with elevation of SGPT, SGOT and and LDH 
             have  been described (Kinamore, 1980).
       9.4.6 Urinary
             9.4.6.1 Renal
                     Proteinuria and nephritis with elevation of BUN  
                     and poor urinary output have been reported
                     (Wedin, 1986).
             9.4.6.2 Others
                     No data available.
       9.4.7 Endocrine and reproductive systems
             No data available.
       9.4.8 Dermatological
             Prolonged contact can produce dermatitis and eczema  
             (Schvartsman, 1979).
       9.4.9 Eye, ears, nose, throat:  local effects
             Eyes: Allergic conjunctivitis and rhinitis (Schvartsman, 
              1979).
             
             Throat: Burning sensation is the first symptom of this 
             poisoning  (Schvartsman, 1979).
       9.4.10 Haematological
              Hyperplastic myelosis initially occurs followed by  

              haemolytic anaemia, neutropenia and eosinophilia 
              (Schvartsman,  1979).
       9.4.11 Immunological
              (see 9.4.13 - Allergic reactions).
       9.4.12 Metabolic
              9.4.12.1 Acid base disturbances
              9.4.12.2 Fluid and electrolyte disturbances
                       Severe dehyradation with various degrees of  
                       hypokalaemia and hyponatraemia.
              9.4.12.3 Others
       9.4.13 Allergic reactions
              Occur mostly among gardners; workers exposed to  
              agricultural cultivation of castor bean; and mill 
              workers exposed  to ricine oil.  
              
              Severe allergies have been reported from wearing or 
              handling  necklaces or other trinkets made from castor 
              bean.  The allergens  can produce bronchial asthama, 
              allergic rhinitis, dermatitis,  eczema, eosinophilia, 
              conjunctivitis, and anaphylactic shock  (Schvartsman, 
              1979; Knight, 1979; Cooper, 1989).  Other  agricultural 
              products such as coffee and soya bean contaminated  
              with ricin can produce allergic reactions among exposed 
              workers.
       9.4.14 Other clinical effects
              No data available.
       9.4.15 Special risks
              Ricin crosses the placenta and is excreted in breast 
              milk. 
     9.5 Others
     9.6 Summary
    10. MANAGEMENT
      10.1 General principles
         Any person ingesting any part of Ricinus communis should be  
         hospitalized for close observation.  Treatment is mainly 
         symptomatic with  gastric decontamination and correction
         of fluid and electrolyte disturbances (Lampe, 1985; Pronczuk,
          1988; Wedin,  1986; Kopferschmitt, 1983).
      10.2 Relevant laboratory analyses and other investigations
         10.2.1 Sample collection
                Blood and urine for biomedical analysis.
                
                Gastric contents for identification of the plant.
                
                The plant should be obtained for botanical and 
                pharmacognostic  studies.  
         10.2.2 Biomedical analysis
                Electrolytes and blood gases.
                
                Monitoring of renal, hepatic functions, haematology 
                and blood  clotting.
         10.2.3 Toxicological/toxinological analysis
                Ricin has been measured in plasma and urine by means 
                of radioimmunassay with antiricin antibodies 
                labelled with iodine 125  (Kopferschmitt, 1983).
         10.2.4 Other investigations

      10.3 Life supportive procedures and symptomatic treatment
         Symptomatic treatment: correction of fluid and electrolyte  
         disturbances.  Antispasmodics may be needed for colic.
         
         In case of bronchial asthma, oxygen, epinephrine or 
         aminophylline, and corticosteroids may be necessary.
         
         Antihistamines or corticosteroids may be beneficial in 
         treating skin  lesions.
         
         Renal insufficiency may require haemodialysis.  However, 
         ricin is not dializable (Kopferschmitt, 1983).
      10.4 Decontamination
         Induce emesis or perform gastric lavage immediately.  
         Activated charcoal may be administered.  Cathartics are 
         contraindicated (Wedin, 1986).
      10.5 Elimination
         Forced alkaline diuresis has not been proved to be effective 
         (Arena,  1981; Oladosu, 1979; Kopferschmitt, 1983)
      10.6 Antidote/antitoxin treatment
         10.6.1 Adults
         10.6.2 Children
      10.7 Management discussion
         The effectiveness of forced diuresis has not been proved.
         
         Ricin is not dialyzable.
    11. ILLUSTRATIVE CASES
      11.1 Case reports from literature
         Wedin et al. (1986) reported two cases with intense vomiting,
          diarrhoea, dehydration and transient elevation of serum 
         creatinine.  There  was no clinical or laboratory evidence 
         of liver necrosis or dysfunction.   One case had slight 
         abnormalities of haematological values either due to  
         dehydration or haemolysis.  Both patients recovered 
         uneventfully with  symptomatic treatment.
         
         Kopfershmitt et al. (1983) described the case of a 21-year-
         old man who  ingested 31 castor beans. Soon after ingestion 
         he developed vomiting and  profuse diarrhoea with marked 
         dehydration, circulatory collapse and elevated  BUN.  His 
         ricin plasma level reached up to 1.5 nanogram/l; urinary 
         excretion  began after 3 days at a rate of 0.72 nanogram/24 
         h. Recovery was rapid with  fluid administration.
      11.2 Internally extracted data on cases
         Ingestion of seeds of Ricinus communis is a common cause of  
         consultation at CIAT (Montevideo). Most are admitted with 
         vomiting,  diarrhoea and abdominal pain, but they never 
         develop the severe dehydration  and other complications 
         described in the literature.
         
         Early treatment was effective in preventing the appearance 
         of symptoms  (Pronczuk, 1988).
      11.3 Internal cases
    12. ADDITIONAL INFORMATION
      12.1 Availability of antidotes/antitoxins
      12.2 Specific preventive measures

      12.3 Other
    13. REFERENCES
      13.1 Clinical and toxicological
         Arena JM (1981)  Plants that poison.  Emergency Medicine, 
         June, 15:  22-.57.
         
         Budavari S (ed) (1989). The Merck Index: an encyclopedia of 
         chemicals, drugs  and biologicals. 11th ed. Rahway, New 
         Jersey. Merck & Co. Inc.
         
         Cooper WC (1989)  Castor oil.  Encyclopaedia of Occupational 
         Health and  Safety, IWO. Vol 1: 38-39.
         
         Favarel-Carrigues JC, Castaig Y, Obikpi-Benissan G, Gabinski 
         C (1978)  Les  intoxications d'origine végétal dans le sud-
         ouest.  Bordeaux Médicale,  28(11): 1617-1621.
         
         Font Quer P (1979)  Plantas medicinales.  Ed. Labor. 
         Barcelona.
         
         Hardin JN & Arena JM (1974)  Human poisoning from native and 
         cultivated  plants. 2nd Ed. Duke University Press, Durham, 
         North Carolina.
         
         Jouglard J (1977)  Intoxication d'origine végétale.  
         Encyclopédie  Médico-Chirurgicale.  Intoxications 16065 A 
         10.
         
         Kinamore PA, Jaeger R, Castro FJ (1980)  Abrus and Ricinus 
         ingestion.  Management of three cases.  Clinical Toxicology,
         17(3): 401-405.
         
         Kopferschmitt J, Flesh F, Lugnier A, Sauder PH, Jaeger A, 
         Mantz JM  (1983)   Acute voluntary intoxication by Ricin.  
         Human Toxicology, 2: 239-242.
         
         Lampe KF & McCann MA (1985)  AMA Handbood of poisonous and 
         injurious plants.  American Medical Association, Chicago, 
         Illinois.
         
         Martindale. The Extra-Pharmacopoeia (1982).  The 
         Pharmaceutical Press, 28th  Ed. 695 and 1751.
         
         Oladosu LA, Case AA (1979)  Large animal hepatoxic and 
         nephrotoxic plants.  Veterinary and Human Toxicology 21(4): 
         363-364.
         
         Olnes S, Refsnes K, Piohl A (1974)  Mechanism of action of 
         the toxic lectins  abrin and ricin.  Nature, 249: 627-631.
         
         Pronczuk J, Laborde A (1988)  Plantas Silvestres y de 
         Cultivo: riesgo de  intoxicacion para el hombre.  
         Universidad de la Republica.  Montevideo,  6f3-65.
         
         Schvartsman S (1979)  Plantas venenosas Sarvier.  Sao Paulo. 

         92-96.
         
         Wedin GP, Jeffrey SN, Everson GW, Krenzelok EP (1986)  
         Castor Bean  Poisoning.  American Journal of Emergency 
         Medicine, 4(3): 259-261.
      13.2 Botanical
    14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE 
    ADDRESS(ES)
    Author:   Dr Mosto
    Jefa Seccion Toxicologia
    Hospital de Clinicas "Jose de San Martin"
    Facultad de Medicina
    Universidad de Buenos Aires
    Cordoba 2351
    Buenos Aires
    Argentina
    
    Tel: 54-1-9621280
    Fax: 54-1-3318605
     
    Date:April 1989
    
    Reviewer: Dr A. Laborde
    CIAT 7° piso
    Hospital de Clinicas
    Av. Italia s/n
    Montevideo
    Uruguay
    
    Tel: 598 2 470300
    Fax: 598 2 470300
       
    Date:November 1989
    
    Peer Review: London, March 1990

    See Also:
       Toxicological Abbreviations