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Conium maculatum L.

1. Name
   1.1 Scientific name
   1.2 Family
   1.3 Common name(s)
2. Summary
   2.1 Main risk and target organs
   2.2 Summary of clinical effects
   2.3 Diagnosis
   2.4 First-aid measures and management principles
   2.5 Poisonous parts
   2.6 Main toxins
3. Characteristics
   3.1 Description of the plant
      3.1.1 Special identification features
      3.1.2 Habitat
      3.1.3 Distribution
   3.2 Poisonous parts of the plant
   3.3 The toxin(s)
      3.3.1 Name(s)
      3.3.2 Description, Chemical Structure (molecular weight),
      3.3.3 Other physico-chemical characteristics
   3.4 Other chemical contents of the plant
4. Uses / circumstances of poisoning
   4.1 Uses
   4.2 High risk circumstances
   4.3 High risk geographical areas
5. Routes of entry
   5.1 Oral
   5.2 Inhalation
   5.3 Dermal
   5.4 Eye
   5.5 Parenteral
   5.6 Others
6. Kinetics
   6.1 Absorption by route of exposure
   6.2 Distribution by route of exposure
   6.3 Biological half-life by route of exposure
   6.4 Metabolism
   6.5 Elimination by route of exposure
7. Toxicology / Toxinology / Pharmacology
   7.1 Mode of action
   7.2 Toxicity
      7.2.1 Human data
         7.2.1.1 Adults
         7.2.1.2 Children
      7.2.2 Animal data
      7.2.3 Relevant in vitro data
   7.3 Carcinogenicity
   7.4 Teratogenicity
   7.5 Mutagenicity
   7.6 Interactions
8. Toxicological/toxinological and biomedical investigations
9. Clinical effects
   9.1 Acute poisoning:
      9.1.1 Ingestion
      9.1.2 Inhalation
      9.1.3 Skin exposure
      9.1.4 Eye contact
      9.1.5 Parenteral exposure
      9.1.6 Other
   9.2 Chronic poisoning by:
      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 (acute, chronic,
      9.4.1 Cardiovascular
      9.4.2 Respiratory
      9.4.3 Neurologic
         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 Immunologic
      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: Pregnancy, breast feeding, enzyme
   9.5 Others
10. Management
   10.1 General principles
   10.2 Relevant laboratory analysis and other investigations
      10.2.1 Sample collection
      10.2.2 Biomedical analysis
      10.2.3 Toxicological/Toxinological analysis
      10.2.4 Other investigations
   10.3 Life supportive procedures and symptomatic treatment
   10.4 Decontamination
   10.5 Elimination
   10.6 Antidote treatment
      10.6.1 Adults
      10.6.2 Children
   10.7 Management discussion: alternatives, controversies, research
11. Illustrative cases
   11.1 Case reports from literature
   11.2 Internally extracted data on cases (from writer of monograph)
   11.3 Internal cases (added by the PC using monograph)
12. Additional information
   12.1 Availability of antidotes and antisera
   12.2 Specific preventive measures
   12.3 Other
13. References
   13.1 Clinical and toxicological
   13.2 Botanical
14. Author(S), Reviewer(S), Date(S) (including each update), complete addresses
    1.    Name

      1.1   Scientific name

            Conium maculatum L.

      1.2   Family

            Umbelliferae (Apiaceae)

      1.3   Common name(s)

            Bunk (Canada)
            Cashes (Canada)
            Cige (Canada, France)
            Poison hemlock (USA)
            Poison parsley (USA)
            Poison root (USA)
            Snake weed (USA)
            Spotted hemlock (USA)
            Spotted parsley (USA)
            Winter fern (USA)
            Cicuta (Spain, Uruguay, Argentina, Portugal)
            Perejil lobuno (Spain)
            Cicuta negra (Uruguay)

    2.    Summary

      2.1   Main risk and target organs

            The central nervous system is the main target organ: initial 
            stimulation is followed by severe CNS depression associated 
            with muscle paralysis and respiratory failure. 

      2.2   Summary of clinical effects

            Usually rapid onset of irritation of oral mucosa with 
            salivation, nausea, emesis and slight abdominal pain.  
            Diarrhoea is uncommon. Bradycardia, miosis and hypertension may 
            rapidly change to tachycardia, hypotension and mydriasis.  
            Seizures followed by ascendant muscle paralysis can be seen in 
            severe cases leading to respiratory failure. 

      2.3   Diagnosis

            Blood gases and electrolytes

            Sample of the plant should be obtained for botanical and
            pharmacognostic identification.


     2.4   First-aid measures and management principles


            Immediate gastric lavage or emesis followed by administration 
            of activated charcoal with a cathartic. Treatment is 
            supportive, mainly ensuringadequate respiratory function. 

      2.5   Poisonous parts

            The entire plant contains toxic alkaloids, especially the 
            root and seeds.

      2.6   Main toxins

            The main poisonous principle is coniine, a pyridine derivative 
            similar in structure and function to nicotine; there are also 
            four other structurally related alkaloids. 

    3.    Characteristics

      3.1   Description of the plant

            3.1.1 Special identification features

                  Conium maculatum is a herb growing up to nine feet high 
                  that resembles a carrot plant.  The leaves are large (may 
                  reach up to 4 feet) and lacy, with alternate 
                  distribution.  The small and white flowers are borne in 
                  flat clusters like an umbrella ("umbelliferae").  The 
                  stem is typically hollow and has purple spots.  The 
                  tuberous root is white.  The fruit is small, 3 to 4 
                  millimeters long and flattened on its sides.  When 
                  crushed, the leaves and flowers produce an offensive 
                  "mousy" odour. 

                  Conium maculatum blossoms in Spring and its fruits are 
                  ripe in Summer (Font-Quer, 1979; Pronczuk, 1988; Lampe, 
                  1985) 

            3.1.2 Habitat

                  Conium maculatum often grows abundantly on waste areas or 
                  on land not maintained either by cultivation or cutting, 
                  such as ditch banks, fence rows, low-lying rocky outcrops 
                  and timbered areas.  (Keeler, 1978; Pronczuk, 1988) 

            3.1.3 Distribution

                  Originally from Europe, conium maculatum has adapted to 
                  America and Asia.  Now it has a worldwide distribution, 
                  mostly in temperate areas below 5000 feet of altitude. 

      3.2   Poisonous parts of the plant

            The whole plant is toxic, but especially the root and seeds.


     3.3   The toxin(s)


            3.3.1 Name(s)

                  The whole plant contains coniine, N-methyl coniine, 
                  conhydrine, lambda-coniceine and pseudoconhydrine.

            3.3.2 Description, Chemical Structure (molecular weight), 
                  Stability 

                  Coniine is a piperidine alkaloid (2-propylpiperidine) 
                  (Keeler, 1978). 

                  No other data available.

            3.3.3 Other physico-chemical characteristics

                  The characteristic odour is at least in part attributable 
                  to coniine, which is a volatile a colourless liquid with 
                  a bitter taste (Schvarstman, 1979; Gosselin, 1976; 
                  Keelers, 1978). 

      3.4   Other chemical contents of the plant

            Other alkaloids related to coniine have been isolated from the 
            plant. According to Keeler and Balls (1978), over 98% of the 
            total alkaloid of the fresh vegetative Conium maculatum was 
            coniceine, and in the dry plant less than 20% was coniceine, 
            and one third was coniine.  Other authors believe that coniine 
            and coniceine are the main active principles.  Other alkaloids 
            include N-methylconniine, conhydrin and pseudoconhydrine, which 
            have a toxic action similar to that of coniine.  (Keeler, 1978; 
            Schvarstman, 1979) 

    4.    Uses / circumstances of poisoning

      4.1   Uses

            Preparations containing the active principle were used as an 
            analgesic or sedative by herbalists.  As the bromhydrate, the 
            recommended maximal dose is 15 mg per day.  Powder from the 
            dried fruits is also used; the maximal dose recommended is 1 g. 
            (Font Quer, 1979).  The recommended dose of a tea prepared from 
            dried leaves is 1 g in 100 cc water (Font Quer, 1979). 

      4.2   High risk circumstances

            A large number of the umbelliferae family are used as aromatics 
            or edible plants.  The fruits of Conium maculatum have been 
            confused with aniseed; the leaves can be confused with parsley, 
            or wild carrots; and the root with parsnip (Hardin, 1974).  In 
            mid-summer the whole plant exudes a fetid odour reminiscent of 
            mouse or cat urine (Gosselin, 1976). 



      4.3   High risk geographical areas


            It is found in Asia, Europe, North and South America. The plant 
            is widely distributed and grows mainly in moist waste areas not 
            maintained by cultivation or cutting.  Consequently, the stands 
            are dense along ditch banks, fence rows, low-lying rocky 
            outcrops, and timbered areas. 

    5.    Routes of entry

      5.1   Oral

            Pieces of the plant, medicinal preparations or teas can be 
            ingested accidentally, in suicide attempts, or because of 
            confusion with other plants.

      5.2   Inhalation

            Toxicity has been reported from prolonged inhalation of the
            vapour of coniine (Gosselin, 1976).

      5.3   Dermal

            Coniine and coniceine can be absorbed through the skin when the 
            plant is used as an analgesic "plaster" (Font Quer, 1979).

      5.4   Eye

            No data available.

      5.5   Parenteral

            No data available.

      5.6   Others

            No data available.

    6.    Kinetics

      6.1   Absorption by route of exposure

            Coniine is mainly absorbed orally.  It may rarely be absorbed 
            by inhalation and through the skin. 

      6.2   Distribution by route of exposure

            No data available.

      6.3   Biological half-life by route of exposure

            No data available.


      6.4   Metabolism

            Coniine is normally excreted rapidly after biotransformation
            (Geehr, 1984).

      6.5   Elimination by route of exposure

    7.    Toxicology / Toxinology / Pharmacology

      7.1   Mode of action

            Coniine produces muscular paralysis similar to that from 
            curare. Nicotine-like ganglionic blockade also occurs 
            (Dreisbach, 1987). 

      7.2   Toxicity

            7.2.1 Human data 

                  7.2.1.1 Adults
      
                        In man, 3 mg of coniine is said to have produced 
                        symptoms, but 150 mg have been tolerated without 
                        discomfort.  Perhaps 30-60 mg is dangerous and 
                        death may occur with doses greater than 100 mg.  It 
                        has been reported that a lethal dose may be 6 to 8 
                        fresh leaves (Gosselin, 1976; Pronczuk, 1988). 

                  7.2.1.2 Children

                        No data available.

            7.2.2 Animal data

                  Toxic doses in animals: cows 3.3 mg/kg, horses 15.5 mg/kg 
                  and sheep 44 mg/kg (Keeler, 1980).

            7.2.3 Relevant in vitro data

                  No data available.

      7.3   Carcinogenicity

            No data available.

      7.4   Teratogenicity

            Conium maculatum has caused congenital malformations when fed 
            to cattle, pigs and sheep (Poisindex, 1990). 

      7.5   Mutagenicity

            No data available.

      7.6   Interactions

            No data available.

    8. Toxicological/toxinological and biomedical investigations


    9. Clinical effects

      9.1   Acute poisoning:

            9.1.1 Ingestion

                  The clinical effects are mainly neurological and when 
                  death occurs it is probably secondary to respiratory 
                  paralysis with hypoxia.  The most prominent signs are due 
                  to peripheral paralysis and loss of sensation. 

                  Symptoms include irritation of the mucous membranes, 
                  nausea, vomiting and profuse salivation.  Abdominal pain 
                  is usually minimal and diarrhoea is infrequent.  
                  Drowsiness, paresthesiae, ataxia and gradually increasing 
                  muscular weakness followed by ascending paralysis leads 
                  to respiratory failure.  Bradycardia, miosis, 
                  hyperventilation may rapidly change to tachycardia, 
                  hypotension, mydriasis and respiratory paralysis.  
                  Seizures may occur terminally (Lampe, 1985; Geehr, 1984; 
                  Gosselin, 1976; Dreisbach, 1987). 

            9.1.2 Inhalation

                  Inhalation of vapours may occur rarely and clinical 
                  effects would be predicted to be similar to those seen 
                  following ingestion. 

            9.1.3 Skin exposure

                  Skin contact can result in a burning sensation, 
                  numbness, dermatitis and possible systemic absorption 
                  (Poisindex, 1990, Font Quer, 1979).

            9.1.4 Eye contact

                  Because conium can cause dermal irritation conjunctivitis 
                  might occur following eye exposure.  However, no such 
                  cases have been reported. 

            9.1.5 Parenteral exposure

                  No data available.

            9.1.6 Other
            
                  No data available.

      9.2   Chronic poisoning by:

            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

            In non-fatal cases, the effects are relatively transient 
            (Gosselin, 1976).

            In severe cases, there is usually a rapid onset of symptoms;  
            death occurs rapidly (in less than 3 hours) if no treatment is 
            given. Death is due to respiratory arrest from paralysis of 
            respiratory muscles, although central depression may play a 
            role after ingestion of very large doses (Lampe, 1985). 


     9.4   Systematic description of clinical effects (acute, chronic, 
           etc.) 

            9.4.1 Cardiovascular

                  Tachycardia or bradycardia and vasoconstriction may 
                  occur. 

            9.4.2 Respiratory

                  Respiratory failure is due to muscular paralysis.

            9.4.3 Neurologic

                  9.4.3.1 CNS

                        Drowsiness, ataxia and seizures in severe cases.

                  9.4.3.2 Peripheral nervous system

                        Numbness, paresthesiae and ascending paralysis.

                  9.4.3.3 Autonomic nervous system

                        Initial symptoms of coniine poisoning resulting 
                        from transitory stimulation of autonomic ganglia. 

                  9.4.3.4 Skeletal and smooth muscle

                        Progressive muscular paralysis.

            9.4.4 Gastrointestinal

                  Irritation of oral mucosa, nausea, vomiting and slight
                  abdominal pain.

            9.4.5 Hepatic

                  No data available.

            9.4.6 Urinary

                9.4.6.1 Renal

                9.4.6.2 Other

            9.4.7 Endocrine and reproductive systems

                  No data available.

            9.4.8 Dermatological

                  Dermal absorption can result in a burning sensation, 
                  numbness, dermatitis and possibly systemic absorption 
                  (Poisindex, 1990, Font Quer, 1979).

            9.4.9 Eye, ear, nose, throat: local effects

                  Because conium can cause dermal irritation, 
                  conjunctivitis might occur following eye exposure.  
                  However no such cases have been reported. 

            9.4.10 Haematological

                  No data available.

            9.4.11 Immunologic

                  No data available.

            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

                  No data available.

            9.4.14 Other clinical effects 

                  No data available.

            9.4.15 Special risks: Pregnancy, breast feeding, enzyme
                        deficiencies

                  Conium maculatum is a known animal teratogen.  No human 
                  data are available. 

      9.5 Others

            No data available.

    10.   Management

      10.1 General principles

            Immediate induction of emesis or gastric lavage and 
            administration of activated charcoal and a cathartic are 
            indicated.  Treatment is otherwise symptomatic.  Provision of 
            adequate respiratory care is the main treatment measure (Lampe, 
            1985; Geehr, 1984). 

      10.2 Relevant laboratory analysis and other investigations

            10.2.1 Sample collection

                  Plant specimen should be collected for botanical and
                  pharmacognostic identification if possible.  Plant 
                  portions found in vomitus should be stored in a plastic 
                  bag (see 8.1.1). 
      
            10.2.2 Biomedical analysis

                  Blood gases and ECG provide valuable data.

            10.2.3 Toxicological/Toxinological analysis

                  (In preparation)

            10.2.4 Other investigations

                  As required by patients' clinical condition.

      10.3 Life supportive procedures and symptomatic treatment

            Immediate induction of emesis gastric lavage and administration 
            of activated charcoal and cathartic are indicated.  Treatment 
            is otherwise symptomatic.  Provision of adequate respiratory 
            care is the main treatment measure (Lampe, 1985; Geehr, 1984). 

      10.4 Decontamination

            Immediate induction of emesis or gastric lavage and 
            administration of activated charcoal and cathartic are 
            indicated. 

      10.5 Elimination

            No data available.

      10.6 Antidote treatment

            10.6.1 Adults

                  No data available.

            10.6.2 Children

                  No data available.

      10.7 Management discussion: alternatives, controversies, research 
           needs 

            Alternatives and controversies.

    11.   Illustrative cases

      11.1  Case reports from literature

      11.2  Internally extracted data on cases (from writer of monograph)

            No cases have been registered at CIAT (Uruguay PCC).


      11.3  Internal cases (added by the PC using monograph)

            To be added by the centre.

    12.   Additional information

      12.1  Availability of antidotes and antisera

            Not relevant.

      12.2  Specific preventive measures

            Not relevant.

      12.3  Other

            Not relevant.

    13.   References

      13.1  Clinical and toxicological

            Dreisbach, RH; Robertson, WO, Handbook of Poisoning.  Appleton 
            Lange, Norwalk, Connecticut.  Twelfth edition. Page 4.99, 1987. 

            Font Quer, P.  Plantas medicinales Editorial Labour.  
            Barcelona. Page 484, 1979. 

            Geehr, E. Common Toxic Plant Ingestion.  Emergency Medicine 
            Clinics of North America 2 (3):  556, 1984.

            Gosselin, RE. et al.  Clinical Toxicology of Commercial 
            Products. Williams-Wilkins, Baltimore.  Fourth Edition 1976. 

            Hardin, JW; Arena, JM.  Human poisoning from native and 
            cultivated plants.  Duke University Press.  Second Edition.  
            Kingsport, Tennessee, 1974. 

            Keeler, RF; Balls, LD.  Teratogenic effects in cattle on Conium 
            maculatum and conium alkaloids and analogs.  Clinical 
            Toxicology 12 (1):  49-64, 1978. 

            Lampe, KF; McCann, MA.  AMA Handbook of poisoning and injurious 
            plants. American medical Association, Chicago, Illinois, 1985. 

            Pronczuk, J; Laborde, A.  Plantas silvestres y de cultivo: 
            riesgo de intoxicacion para el hombre.  Universidad de la 
            Republica. Montevideo, 1988. 

            Schvartsman, S.  Plantas venenosas.  Sarvier, Sao Pablo, 1979.

            Bowman, WC; Sanghvi, IS.  Pharmacological actions of hemlock
            alkaloids. J Pharm Pharmacol 1963; 15:1-25.

            Cromwell, BT.  The separation, micro-estimating and 
            distribution of the alkaloids of hemlock (Conium maculatum L).  
            Biochem J 1956; 64: 259-266. 

            de Boer, J.  The death of Socrates.  A historical and 
            experimental study on the action of coniine and conium 
            maculatum.  Arch Int Pharmacodyn 1950; 83:473-490. 

            Fairbairin, JW; Challen, SB.  The alkaloids of hemlock (conium
            maculatum L).  Biochem J 1958; 72:556-561.

            Hill, RK.  Stereochemistry of the hemlock alkaloids.  I. 
            conhydrine.  J Am Chem Soc 1958; 80: 1609-1611.

            Keeler, RF.  Coniine, a teratogenic principle from conium 
            maculatum producing congenital malformations in calves.  Clin 
            Toxicol 1974;  7:195-206.

            Keeler, RF; Balls, LD.  Teratogenic effects in cattle of Conium 
            maculatum and Conium alkaloids and analogs.  Clin Toxicol 1978; 
            12: 49-64. 

            Keeler, RF; Balls, LD; Shupe, JL et al.  Teratogenicity and 
            toxicity of coniine in cows, ewes and mares.  Cornell Vet 1980; 
            70:19-26.

            Mitchell, J; Rook, A.  Botanical Dermatology.  Greengrass Ltd,
            Vancouver, BC, 1979.

            Ober, WB.  Did Socrates die of hemlock poisoning?  NY State J 
            Med 1977; Feb: 254-258. 
            
            Panter, KE; Bunch, TD; Keeler, RF.  Maternal and foetal 
            toxicity of poison hemlock (Conium maculatum) in sheep.  Am J 
            Vet Res 1988;  49: 281-283. 

            Panter, KE; Keeler, RF; Buck, WB.  Induction of cleft palate in 
            newborn pigs by maternal ingestion of poison hemlock (conium 
            maculatum).  Am J Vet Res 1985; 46: 1368-1371. 

            Panter, KE; Keeler, RF; Buck, WB.  Congenital skeletal 
            malformations induced by maternal ingestion of Conium maculatum 
            (poison hemlock) in newborn pigs.  Am J Vet Res 1985a; 46: 
            2064-2066.

            Sollmann, T.  A Manual of Pharmacology, 8th ed, Saunders,
            Philadelphia, 1957.

      13.2 Botanical

    14.  Author(S), Reviewer(S), Date(S) (including each update), complete 
     addresses 

      J. Higa de Landoni
      Jefa de Seccion Toxicologia
      Hospital de Clinicas "Jose de San Martin"
      Facultad de Medicina
      Universidad de Buenos Aires
      Cordoba 2351
      Buenos Aires
      Argentina

      Tel: 54-1-7989552
      Fax: 54-1-3318605

      Reviewer:   Dr J. Pronczuk
                  CIAT 7
                  Hospital de Clinicas
                  Av Italia s/n
                  Montevideo
                  Uruguay

                  Tel: 598-2-470300
                  Fax: 598-2-470300

      Peer Review:      London, UK, March 1990



    See Also:
       Toxicological Abbreviations