1.1 Substance
   1.2 Group
   1.3 Synonyms
   1.4 Identification numbers
      1.4.1 CAS numbers
      1.4.2 Other numbers
   1.5 Main brand names:
   1.6 Main Manufacturers/Main Importers
   2.1 Main risks and target organs
   2.2 Summary of clinical effects
   2.3 Diagnosis
   2.4 First-aid measures and management principles
   3.1 Origin of the substance
   3.2 Chemical structure
   3.3 Physical properties
      3.3.1 Colour
      3.3.2 State/Form
      3.3.3 Description
   3.4 Hazardous characteristics
   4.1 Uses
      4.1.1 Uses
      4.1.2 Description
   4.2 High-risk circumstances of poisoning
   4.3 Occupationally exposed populations
   5.1 Oral
   5.2 Inhalation
   5.3 Dermal
   5.4 Eyes
   5.5 Parenteral
   5.6 Other
   6.1 Absorption by route of exposure
   6.2 Distribution by route of exposure
   6.3 Biological half-life by route of exposure
   6.4 Metabolism
   6.5 Elimination and secretion by route of exposure
   7.1 Mode of action
   7.2 Toxicity
      7.2.1 Human data Adults Children:
      7.2.2 Relevant animal data
      7.2.3 Relevant in vitro data
      7.2.4 Workplace standards
      7.2.5 Acceptable daily intake
   7.3 Carcinogenicity
   7.4 Teratogenicity
   7.5 Mutagenicity
   7.6 Interactions
   8.1 Material sampling plan
      8.1.1 Sampling and specimen collection Toxicological analyses Biomedical analyses Arterial blood gas analysis Haematological analyses Other (unspecified) analyses
      8.1.2 Storage of laboratory samples and specimens Toxicological analyses Biomedical analyses Arterial blood gas analysis Haematological analyses Other (unspecified) analyses
      8.1.3 Transport of laboratory samples and specimens Toxicological analyses Biomedical analyses Arterial blood gas analysis Haematological analyses Other (unspecified) analyses
   8.2 Toxicological Analyses and Their Interpretation
      8.2.1 Tests on toxic ingredient(s) of material Simple Qualitative Test(s) Advanced Qualitative Confirmation Test(s) Simple Quantitative Method(s) Advanced Quantitative Method(s)
      8.2.2 Tests for biological specimens Simple Qualitative Test(s) Advanced Qualitative Confirmation Test(s) Simple Quantitative Method(s) Advanced Quantitative Method(s) Other Dedicated Method(s)
      8.2.3 Interpretation of toxicological analyses
   8.3 Biomedical investigations and their interpretation
      8.3.1 Biochemical analysis Blood, plasma or serum Urine 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
   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 Central Nervous System Peripheral nervous system Autonomic nervous system Skeletal and smooth muscle
      9.4.4 Gastrointestinal
      9.4.5 Hepatic
      9.4.6 Urinary Renal Other
      9.4.7 Endocrine and reproductive systems:
      9.4.8 Dermatological
      9.4.9 Eyes, ears, nose, throat: local effects
      9.4.10 Haematological
      9.4.11 Immunological
      9.4.12 Metabolic Acid-base disturbances Fluid and electrolytes Other
      9.4.13 Allergic reactions
      9.4.14 Other clinical effects
      9.4.15 Special risks:
   9.5 Other
   10.1 General principles
   10.2 Life-supportive procedures and symptomatic treatment
   10.3 Decontamination
   10.4 Enhanced Elimination
   10.5 Antidote treatment
      10.5.1 Adults
      10.5.2 Children
   10.6 Management discussion
   11.1 Case reports from literature
   12.1 Specific preventive measures
   12.2 Other

    International Programme on Chemical Safety
    Poisons Information Monograph 332

    1.  NAME

        1.1  Substance


        1.2  Group

        1.3  Synonyms

             Metacetaldehyde; Meta

        1.4  Identification numbers

             1.4.1  CAS numbers

                    108-62-3 (tetramer)

             1.4.2  Other numbers

                    CAS Metaldehyde (homopolymer): 9002-91-9 
                    UN: 1332 
                    RTECS: AB3042000 (homopolymer)
                    XF9900000 (tetramer)

        1.5  Main brand names:

             Cekumeta (Cequisa); Halizan (Tamogan); Metason
             (Jewnin-Joffe); Helarion (Fisons); Ariotox (Sandoz); Mifaslug
             (Farmers Crop Chemical);  Namekil; Slug-Tox

        1.6  Main Manufacturers/Main Importers

             Manufactured by Meoc S.A. Charrat (Switzerland).
             A/S Plantevern-kjemi (Norway).

    2.  SUMMARY

        2.1  Main risks and target organs

             Convulsions, central nervous system depression, and
             liver and kidney injury.

        2.2  Summary of clinical effects

             Nausea, vomiting, salivation, diarrhoea and abdominal
             Convulsions, coma and respiratory failure.
             Liver and renal injury at a later stage.

        2.3  Diagnosis

             Acute metaldehyde poisoning by ingestion can cause
             severe abdominal pain, nausea, vomiting, salivation,
             diarrhoea, hyperthermia, rhabdomyolysis, convulsions,
             hypotension, tachycardia, respiratory arrest, and coma.  The
             onset of symptoms usually occurs 1 to 3 hours after
             Inhalation of metaldehyde fumes can cause drowsiness and
             depression of the central nervous system.
             Urine may be acidic and there may be casts and albumin. 
             Plasma levels of metaldehyde are not clinically useful.

        2.4  First-aid measures and management principles

             After inhalation:
                    Establish respiration and remove patient to fresh air,
                    administer oxygen.
                    Transfer patient to hospital.
             After ingestion:
                    Establish respiration.
                    Transfer patient to hospital.
                    Gastric emptying: perform gastric lavage after
                    Give activated charcoal and a saline cathartic.
                    Treat convulsions with intravenous (IV) diazepam.


        3.1  Origin of the substance


        3.2  Chemical structure

             Molecular formula:
             acetaldehyde homopolymer
             Molecular weight: 176.2 (tetramer)
             Structural name
             Tetramer:    2,4,6,8 - tetramethyl - 1,3,5,7 tetraoxocane

        3.3  Physical properties

             3.3.1  Colour

                    Colourless or white

             3.3.2  State/Form

                    Solid crystals.

             3.3.3  Description

                    Odour: mild characteristic odour.
                    Melting point:  246°C (in sealed tube)
                    Boiling point:  sublimes at 112 to 115°C with partial
                                    depolymerization above 80°C.
                    Flash point:    36 to 40°C
                    Relative density (water = 1): 1.27
                    Relative vapour density (air = 1): 6.06
                    Solubility in water:  200 mg/L at 17°C;
                    (practically insoluble)
                    Sparingly soluble in ethanol, ether.
                    Soluble in benzene, chloroform.
                    Insoluble in acetone, acetic acid.

                    Note:  In the USA, metaldehyde formulations are 
                           limited to 4% concentrations and occasionally 
                           contain other toxic components (e.g., carbaryl, 
                           arsenates, and organophospates). European
                           metaldehyde concentrations in molluscicides may
                           reach 50% (Ellenhorn  1997).

        3.4  Hazardous characteristics

             Flammable solid; can react with oxidizing materials;

    4.  USES

        4.1  Uses

             4.1.1  Uses

             4.1.2  Description

                    -  Molluscicide, slug and snail poison
                       (prepared as baits).
                    -  Solid fuel for small heaters (instead of alcohol)
                       in tablets.
                    -  Fire-starter (as tablets).

        4.2  High-risk circumstances of poisoning

             -    accidental ingestion of snail-killers by children,
                  of metaldehyde crystals, or of tablets mistaken for
                  sugar, cereal or candy.
             -    ingestion of the product in suicide attempts;
             -    occupational or accidental exposure to fumes.

        4.3  Occupationally exposed populations



        5.1  Oral

             Oral ingestion of molluscicide and fuel tablets is the
             most common route of exposure.

        5.2  Inhalation

             Inhalation of metaldehyde fumes from use as fire
             starters (eg. small heaters, barbeques)

        5.3  Dermal

             Dermal exposure to dust.

        5.4  Eyes

             Eye exposure to dust or fumes.

        5.5  Parenteral

             No data available.

        5.6  Other

             No data available.

    6.  KINETICS

        6.1  Absorption by route of exposure

             Metaldehyde is absorbed (1 to 2 hours) from the
             gastrointestinal tract and is also secreted back
             (enterohepatic circulation) into the gastrointestinal tract
             (Dreisbach, 1987).

        6.2  Distribution by route of exposure

             Metaldehyde was found in plasma and urine of dogs given
             a single oral dose of 600 mg/kg. 

        6.3  Biological half-life by route of exposure

             No data available.

        6.4  Metabolism

             Metaldehyde slowly hydrolyses to acetaldehyde in acid
             solutions (i.e., in the stomach).  Acetaldehyde is then
             oxidized to acetic acid.
             Acetaldehyde was not found in plasma and urine of metaldehyde
             treated dogs (Booze & Oehme, 1986).

        6.5  Elimination and secretion by route of exposure

             Renal (Dreisbach, 1987).
             The urinary excretion of metaldehyde was less than 1% of the
             dose (Booze & Oehme, 1986). Elimination half-life is 27 hours
             (Olson, 1999).


        7.1  Mode of action

             The toxicologically active substance in metaldehyde
             intoxication is mainly the degradation product acetaldehyde,
             which is formed at a low pH in the stomach.  Other toxic
             products are probably also formed.  Acetaldehyde acts as a
             releasing factor for 5-hydroxytryptamine (5-HT) and
             noradrenaline (NA).  It also competitively inhibits
             biogenic amine oxidation which, in turn, decreases
             5-hydroxyindoleacetic acid (5-HIAA), a metabolite of 5-HT by
             competitively inhibiting 5-HT-oxidation.  Acetaldehyde also
             increases monoamine oxidase activity and decreases central
             serotonin levels (Booze & Oehme, 1985).
             Its pesticidal action is due to contact with the foot of the
             mollusc, making it torpid and increasing the secretion of
             mucus leading to dehydration (RSC, 1987).

        7.2  Toxicity

             7.2.1  Human data


                             Minimum oral LD human = 100 mg/kg
                             (Booze & Oehme, 1985)
                             Minimum oral LD human = 43 mg/kg (Dreisbach,
                             Minimum oral LD human = 60 mg/kg (Sax, 1979).
                             Estimated human oral LD = 50 to  500 mg/kg
                             (Gosselin et al., 1984).
                             LD adults = 4 g (Moeschlin, 1980; Perkow,
                             As reported by Ellenhorn  (1997) and adapted
                             from Longstreth and Pierson (1982), the
                             relation between the dose ingested and the
                             clinical consequences is:
                             Dose mg/kg     Clinical effects
                             Traces (few)   Salivation, facial flushing,
                                            fever, abdominal cramps,
                                            nausea, vomiting.

                             Up to 50       Drowsiness, tachycardia,
                                            spasms, irritability,
                                            salivation, abdominal cramps,
                                            facial flushing, nausea.
                             50 to 100      Ataxia, increased muscle tone.
                             100 to 150     Convulsions, tremor,
                             150 to 200     Muscle twitching.

                             400            Coma, death.


                             LD children  = 2 g (Moeschlin, 1980:
                                                 Perkow, 1979)
                             LD child     = 3 g (Olson, 1999).

             7.2.2  Relevant animal data

                    Rat, acute oral LD50 = 630 mg/kg
                    Dog, acute oral LD50 = 600 mg/kg.
                    The paper by Booze and Oehme (1985) contains the
                    following data:
                    Minimum Oral Lethal Doses and Acute Oral Toxicity
                    of Metaldehyde for Various Animal Species
                    Species      Lethal dose    LD50 mg/kg
                    Dog          100            100 to 1000
                    Rat          227            927 to 690
                    Mouse        200
                    Guinea-pig   175            175 to 700
                    Rabbit       290            290 to 1250
                    Geese        800
                    Chicken      500
                    Duck         300
                    Cow          200
                    Sheep        300
                    Goat         783
                    Horse        60
                    Donkey       360

                    Toxicity of Metaldehyde to Fish
                    Species                 96 hour LC50 (ppm)
                    Rainbow trout           62
                    Bluegill                10

             7.2.3  Relevant in vitro data

                    No data available.

             7.2.4  Workplace standards

                    No data available.

             7.2.5  Acceptable daily intake

                    Not applicable.

        7.3  Carcinogenicity

             A 2-year feeding study, 5000 mg/kg metaldehyde in the
             diet of rats caused no carcinogenic effects (Verschuren et
             al., 1975).

        7.4  Teratogenicity

             Dietary levels of 1000 mg/kg and 5000 mg/kg  metaldehyde
             given to rats interfered with their reproductive process but
             were not teratogenic (Verschuren et al., 1975).

        7.5  Mutagenicity

             When tested in a salmonella microsome assay, metaldehyde
             was not mutagenic (Quinta et al. 1981).

        7.6  Interactions

             No data available.


        8.1  Material sampling plan

             8.1.1  Sampling and specimen collection

            Toxicological analyses

            Biomedical analyses

            Arterial blood gas analysis

            Haematological analyses

            Other (unspecified) analyses

             8.1.2  Storage of laboratory samples and specimens

            Toxicological analyses

            Biomedical analyses

            Arterial blood gas analysis

            Haematological analyses

            Other (unspecified) analyses

             8.1.3  Transport of laboratory samples and specimens

            Toxicological analyses

            Biomedical analyses

            Arterial blood gas analysis

            Haematological analyses

            Other (unspecified) analyses

        8.2  Toxicological Analyses and Their Interpretation

             8.2.1  Tests on toxic ingredient(s) of material

            Simple Qualitative Test(s)

            Advanced Qualitative Confirmation Test(s)

            Simple Quantitative Method(s)

            Advanced Quantitative Method(s)

             8.2.2  Tests for biological specimens

            Simple Qualitative Test(s)

            Advanced Qualitative Confirmation Test(s)

            Simple Quantitative Method(s)

            Advanced Quantitative Method(s)

            Other Dedicated Method(s)

             8.2.3  Interpretation of toxicological analyses

        8.3  Biomedical investigations and their interpretation

             8.3.1  Biochemical analysis

            Blood, plasma or serum

                             "Basic analyses"
                             "Dedicated analyses"
                             "Optional analyses"


                             "Basic analyses"
                             "Dedicated analyses"
                             "Optional analyses"

            Other fluids

             8.3.2  Arterial blood gas analyses

             8.3.3  Haematological analyses

                    "Basic analyses"
                    "Dedicated analyses"
                    "Optional analyses"

             8.3.4  Interpretation of biomedical investigations

        8.4  Other biomedical (diagnostic) investigations and their

        8.5  Overall interpretation of all toxicological analyses and
             toxicological investigations

             Sample collection:
                   -  Blood and urine sampling for biomedical analysis
                      (metaldehyde plasma levels are not clinically
                   -  Keep samples of gastric content.
                   -  Obtain samples of ingested product.
             Biomedical analysis:
                   -  Routine blood and urine analysis should be
                      performed, but with special emphasis on:
                   -  Complete urinalysis: the urine may be very acid in
                      spite of intensive alkali therapy; casts and albumin
                      may be found and persist for several days after
                      symptomatic recovery.
                   -  Arterial blood gas analysis (for assessment of
                      metabolic acidosis).
                   -  Monitoring of fluids and electrolytes.
                   -  Liver function tests.
                   -  Renal function tests.
                   -  Serum creatine kinase (may indicate muscle damage
                      from convulsions) (Dreisbach, 1987).
             Toxicological analysis
                    Metaldehyde plasma levels are of no clinical
                    Significant amounts of metaldehyde were detected in
                    both serum and urine by gas chromatography, in a case
                    where a 37-year-old man took an overdose of a liquid
                    containing metaldehyde (Moody & Inglis, 1992). The
                    serum levels remained elevated for 35 hours.
                    Metaldehyde can be identified in gastric lavage.

             Other investigations
                    Metaldehyde can be detected in baits by placing the
                    baits in a test tube and warming it slowly. 
                    Metaldehyde sublimes to form large amounts of
                    artificial snow.


        9.1  Acute poisoning

             9.1.1  Ingestion

                    Ingestion is the most common route of
                    poisoning.  One to three hours after ingestion the
                    following can occur: severe abdominal pain, nausea,
                    salivation, vomiting, facial flushing,
                    gastroenteritis, diarrhoea, metabolic acidosis, a
                    marked rise in body temperature, drowsiness,
                    convulsions, muscular rigidity, spasms, rhabdomyolysis
                    and coma (Perkow, 1979).
                    Pulse and respiratory rate become progressively slower
                    (Windholz, 1983; Gosselin et al., 1984). Liver and
                    kidney injury occurs at a later stage (Dreisbach,

             9.1.2  Inhalation

                    Metaldehyde fumes may cause somnolence,
                    uncoordinated movements, nausea, dizziness,
                    CNS-depression, convulsions, and coma.
                    This has been a particular problem when metaldehyde
                    has been used in small heaters in tents and igloos
                    with bad ventilation (Moeschlin, 1980).

             9.1.3  Skin exposure


             9.1.4  Eye contact

                    Irritation or corrosion (Sax, 1979).

             9.1.5  Parenteral exposure

                    No data available.

             9.1.6  Other

                    No data available.

        9.2  Chronic poisoning

             9.2.1  Ingestion

                    Chronic poisoning is practically impossible;
                    amounts less than those that cause acute poisoning
                    have no effect (Dreisbach, 1987).

             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

             Mental deficiencies after metaldehyde poisoning such as
             disorientation and loss of memory, may persist for 1 year or
             more (Dreisbach, 1987).
             Death may occur up to 48 hours after ingestion from paralysis
             of the respiratory centre.
             Liver and kidney injury also occur.

        9.4  Systematic description of clinical effects

             9.4.1  Cardiovascular

                    Hypotension, tachycardia (Booze & Oehme, 1985).

             9.4.2  Respiratory

                    Increased tracheobronchial secretions.
                    Respiratory failure may occur up to 48 h after
                    ingestion (Longstreth & Pierson, 1982).

             9.4.3  Neurological

            Central Nervous System

                             Inhalation of metaldehyde fumes may
                             cause CNS-depression.  Drowsiness occurs
                             first, followed by coma up to 24 to 40 hours
                             after inhalation.  Temporary memory loss and
                             psychomotor impairment have been reported
                             (Longstreth & Pierson, 1982).

                             Metaldehyde may cause convulsions and muscle
                             spasms. The convulsions may continue for 3
                             days or more depending on the amount
                             ingested. Coarse tremor, increased tendon
                             reflexes and irritability have also been
                             observed (Longstreth & Pierson, 1982).

            Peripheral nervous system

                             No data available.

            Autonomic nervous system

                             Urinary incontinence can occur in
                             children (Booze & Oehme, 1986).

            Skeletal and smooth muscle

                             Spasm and hypertonia may occur
                             (Wilkinson, 1968, Longstreth &
                             Pierson, 1982).

             9.4.4  Gastrointestinal

                    Initial effects include salivation, nausea,
                    vomiting, abdominal pain, and diarrhoea  (Olson,

             9.4.5  Hepatic

                    Liver damage has been reported in animals
                    (Booze & Oehme, 1985).
                    Liver injury occurs in human beings (Dreisbach, 1987).

             9.4.6  Urinary


                             Kidney injury has been observed in
                             animals and urinary incontinence in children
                             (Booze & Oehme, 1986).


                             No data available.

             9.4.7  Endocrine and reproductive systems:

                    No data available.

             9.4.8  Dermatological

                    Skin, mucous membrane irritation (Sax, 1979).

             9.4.9  Eyes, ears, nose, throat: local effects

                    Mydriasis and conjunctivitis have been reported
                    (EPA, 1980).
                    Reversible blindness in poisoned animals has been
                    reported (Grant 1993).

             9.4.10 Haematological

                    No data available.

             9.4.11 Immunological

                    No data available.

             9.4.12 Metabolic

           Acid-base disturbances

                             Metabolic acidosis may be severe. 
                             Respiratory alkalosis has been reported
                             (Longstreth & Pierson, 1982).

           Fluid and electrolytes

                             Dehydration is often observed (Olson, 1999).


             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:
                    No data available.

        9.5  Other

             No data available.


        10.1 General principles

             If recently ingested or if the patient's condition
             allows, remove  by  gastric lavage, administer activated
             charcoal and, later, a saline cathartic.
             NB: There is a high risk of seizures when vomiting is
             If the patient is already symptomatic, treat the seizures,
             re-establish ventilation, administer oxygen, correct
             acidosis, restore fluid and electrolyte balance, detect and
             treat renal and hepatic failure by the usual means. 
             Elimination of the poison is indicated only after life-saving
             procedures have been performed.
             Wash the skin thoroughly with soap and water.
             -  Irrigate eyes with large amounts of water for 10 to 15
                minutes (consult ophthalmologist if pain persists).

        10.2 Life-supportive procedures and symptomatic treatment

             Make a proper assessment of airway, breathing,
             circulation and neurological status of patient
             Maintain a clear airway
             Perform cardio-pulmonary resuscitation as necessary
             Monitor vital signs
             Control convulsions with appropriate drug regimen
             Administer Oxygen
             Monitor blood pressure and ECG
             Correct hypotension as required
             Administer intravenous fluids
             Monitor fluid and electrolyte balance
             Monitor acid-base balance

        10.3 Decontamination

             Measures to eliminate the substance from the
             gastrointestinal tract should be especially emphasized
             because metaldehyde is slowly absorbed and eliminated in the
             gastrointestinal tract.
             Perform gastric lavage.
                    A 2% to 5% sodium-bicarbonate solution administered
                    orally is recommended, because it reduces the
                    conversion of metaldehyde to acetaldehyde.
                    Gastric lavage may be effective up to 12 to 24 h after
                    Administer activated charcoal.

                    Activated charcoal should be given after emesis or
                    lavage: 30 to 100 g in adults, and 15 to 30 g in
                    children (it may be administered with sorbitol). 
                    Charcoal should be given repeatedly due to secretion
                    to the gastrointestinal tract
                    Wash the skin thoroughly with soap and water.
                    Emesis is contraindicated.
                    Eyes: Irrigate with large amounts of water for 10 to
                          15 min.  Consult an ophthalmologist if pain

        10.4 Enhanced Elimination

             Forced diuresis probably does not significantly enhance
             the renal elimination of metaldehyde. Haemoperfusion and
             dialysis are ineffective.

        10.5 Antidote treatment

             10.5.1 Adults

                    There is no specific antidote (Dreisbach, 1987).

             10.5.2 Children

                    There is no specific antidote (Dreisbach, 1987).

        10.6 Management discussion

             Sorbitol has been suggested for use as an alternative
             carthartic to saline to help prevent absorption. Alternative
             agents for treatment of metaldehyde poisoning that have been
             recommended on the basis that they lower blood acetaldehyde
             levels include D-penicillamine, N-acetylcystein, ascorbic
             acid, or thiamine. Other agents that have been recommended to
             help control intractable seizures include calcium gluconate,
             clonidine and naloxane (though human usage is very limited).


        11.1 Case reports from literature

             A 20-month-old child was admitted to hospital after
             swallowing an unknown quantity of metaldehyde. Gastric lavage
             was performed within ´ hour of ingestion, and an intravenous
             (IV) infusion of 5% dextrose in 0.2 M saline was given for 12
             hours; a good diuresis followed. There were no symptoms for
             48 hours. On day 3, the child developed coarse tremor,
             generalized hypertonia, increased tendon reflexes and
             irritability.  The intravenous (IV) infusion was resumed and
             phenobarbital, 30 mg twice daily was given together with oral
             By day 5, all symptoms had resolved and the child was
             discharged perfectly well on the day 8 (Wilkinson, 1968).
             A 3´-year-old girl came home complaining of a sudden pain in
             her arms.  A few minutes later nausea, intense retching, and
             repeated vomiting, and then respiratory distress and cyanosis
             occurred.  Her extremities went into cramp-like flexion and
             became very cold.  She lost consciousness and her pupils
             constricted and did not react to light.  Her muscles became
             completely flaccid and she went into deep shock.  Her blood
             pressure could not be recorded, and her pulse rate was 120
             per min. On admission to hospital, she was still vomiting
             mucus and perspiring. Her skin was pale and reddish-blue, as
             in peripheral vasoconstriction. Her reflexes were normal with
             some hyper-reflexia.
             Treatment consisted of gastric lavage and colonic irrigation,
             oxygen and a caffeine-glucose infusion, and later 150 mL of
             intravenous (IV) plasma. Her legs were warmed by a light box.
             Penicillin, streptomycin,and 0.4 mg atropine were given to
             prevent aspiration pneumonia and to counteract the
             muscarinic-like symptoms. Later in the evening, her blood
             pressure rose to 170/90 mmHg and her temperature to 40.9°C. 
             Vomiting continued. The next morning she was in an agitated
             coma. Her conjunctivae were injected, and her pupils were
             still contracted and did not react to light. There was some
             fibrillary twitching of muscles. The fever had subsided.  The
             systolic blood pressure was 150 mmHg. Within another 48
             hours, the girl recovered completely, except from amnesia
             from before and during the illness. Only after her recovery
             was it found that the intoxication was due to the intake of
             metaldehyde-sprayed strawberries (Spighel, 1958).

             Lewis (1939) describes in detail the death of a 2´-year
             old-child who had ingested one tablet (5 g) of metaldehyde
             (Locket, 1957).  After 1¨ hours, the child awoke from sleep
             crying, retching, and complaining of abdominal pain. 
             Retching persisted for a further 3´ hours and the abdominal
             pain recurred.  The first convulsions began and then
             recurred, at first only about 1 hour later, but then rapidly
             at more frequent intervals. About 6 hours after taking the
             tablet, the child lost consciousness, and 2 hours later was
             in a state of constant convulsion, rather like "status
             epilepticus" with "risus sardonicus", opisthotonus, pyrexia,
             and increased respiration and pulse rates. Her pupils were
             small.  This convulsive state persisted for another 24 hours. 
             The child died about 33 hours after ingesting the single
             A greater delay in the onset of symptoms and a milder course
             are characteristic of non-fatal cases.  For example, a
             16-year-old boy who mistook a metaldehyde tablet for candy
             remained well for 7 hours, and had no convulsions for another
             additional 3 hours. He had only six episodes of convulsions
             within a 14 hour period; he never became fully unconscious,
             and his temperature only rose only to 38.3°C. A striking
             feature of this case was his loss of memory of the illness
             and other recent events; even 3 months after the episode, his
             memory was poor for 2 months after the ingestion (Miller,
             Most metaldehyde poisoning has resulted from accidental
             ingestion by children or from suicide by adults. Metaldehyde
             has, however, been used in at least two murders (Ludin,
             Dosage response: many doctors did not report the weight of
             the tablets that their patients had swallowed, so there is no
             way to know if the tablets were all of the same size and
             weight.  Belfrage (1927) estimated that half a tablet
             equalled approximately 2000 mg. This amount was ingested by a
             2.8-year-old child who survived the dosage which, for his
             weight, was 136 mg/kg.
             A 53-year old man with a history of chronic cardiopulmonary
             disease and alcoholism died approximately 38 hours after
             ingesting six tablets, about a total of 24 000 mg (Vischer,
             1935). However, a woman who also swallowed six tablets
             vomited immediately and completely recovered (Lewis et al.,
             1939). Several other adults survived after attempted suicide
             by ingesting one to three tablets (Vischer, 1935).

             Two females, 30 and 32 years of age, ingested 16 to 19 g
             metaldehyde as liquid slug bait. Their signs included
             convulsions for 3 days, fever, coma (of 7-days duration in
             one case), and memory loss. Memory loss has been reported
             before. Longstreth et al. (1982) reported the following
             additional signs and symptoms:
             One patient was in a comatose state and unresponsive to
             painful stimuli several hours after metaldehyde ingestion. 
             Her temperature was 38.1°C, respirations were 20/min, and
             blood pressure was 130/90.  Her pupils were reactive: 
             corneal reflexes and Chvostek's sign were present.  A high
             anion gap (23 mEq/litre) and a urine pH of 5.5 with ketones
             present indicated a metabolic acidosis.  However, the
             arterial blood gas measurements (pH 7.57, PaCO2=21 mmHg)
             indicated that respiratory alkalosis was also present. 
             Pneumonia, increased oral and tracheobronchial secretions,
             and elevated serum transaminase and creatine kinase 
             activities (4x normal) all occurred during the course of her
             51-day hospital stay. The patient had severe impairment of
             memory in verbal and visual-spatial areas and an adaptive
             problem-solving impairment. Her memory had almost returned to
             normal 1 year after the metaldehyde ingestion. In addition to
             the same signs, the second patient also had respiratory
             depression, frontal lobe damage, regression to infant-like
             reflexes, and general apathy.  It is not known if she
             Other reported signs and symptoms reported have included
             nausea, vomiting, blurred vision, dilated pupils, confusion,
             agitation, fainting, dermatitis, conjunctival irritation,
             lethargy, itching, tenderness, erythema, and swelling of the
             Poisoning by metaldehyde has also been described in cats,
             dogs, sheep, goats, birds, cattle and horses. Toxicology is
             described by Booze and Oehme (1985, 1986).


        12.1 Specific preventive measures

             Keep the metaldehyde slug and snail baits, as well as
             the solid fuel tablets out of the reach of children and
             irresponsible people.
             Follow the instructions carefully for the safe use of
             Appropriate protective and hygienic measures should be
             applied in the workplace where the product is being
             manufactured, packaged, or stored.

        12.2 Other



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        Booze, TF & Oehme, FW (1985). Metaldehyde toxicity - a review.
        Vet. Hum. Tox., 27(I): 11-19.
        Booze, TF & Oehme, FW (1986). An investigation of metaldehyde and
        acetaldehyde toxicities in dogs. Fund. Appl. Toxicol., 6:
        Dreisbach, RH (1987). Handbook of poisoning. 12th ed. p. 185,
        Connecticut, Appleton & Lange.
        Ellenhorn, MJ (1997). Medical Toxicology - Diagnosis and Treatment
        of Human Poisoning. 2nd. Ed. New York, Elsevier.
        EPA (1980) Summary of reported pesticide incidents involving
        metaldehyde pesticide. Incident monitoring report no.285, March
        Gosselin, BE, Smith, R, Hodge, HC (1984). Clinical Toxicology of
        Commercial Products.  5th ed. blue; section, Nr. 485, Williams &
        Wilkins, Baltimore.
        Grant WM, Schuman JS (1993). Toxicology of the eye, 4th ed.
        Springfield, IL, Charles C. Thomas
        Lewis, DB, Madel GA, Drury, J (1939). Fatal poisoning by meta fuel
        tablets. Br. Med. J., 1, 1283-1284.
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        Longstreth, WT Jr., Pierson, DJ (1982). Metaldehyde poisoning from
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        Ludin VN (1958) Mord mit metaldehyde. Med. Wochenschr 88(16),
        Miller, R (1928) Poisoning by meta fuel tablets (metacetaldehyde).
        Arch. Dis. Child, 3: 292-295.
        Moeschlin, S (1980). Klinik und Terapie der Vergiftungen, 6th ed. 
        p. 284. Stuttgart, Georg Thierve Verlag.
        Moody JP, Inglis FG (1992) Persistence of metaldehyde during acute
        molluscicide poisoning. Human & Experimental Toxicology, 11:
        361 - 362.
        Olson K (1999) Poisoning and drug overdose. 3rd ed. Appleton and
        Lange. Paramount Publishing Business and Professional Group.

        Perkow, W (1979). Wirksubstanzen der Pfanzenschuts- und
        Schädlings- bekampfungsmittel, Molluskizide, Berlin & Hamburg,
        Verlag Paul Parey.
        Quinta I, Martire G (1981) Screening of 24 pesticides by
        salmonella microsome assay. Mut. Res. 85:265
        RSC. The Agrochemical Handbook. Royal Society of Chemistry, 2nd
        ed. Nottingham, UK, 1987.
        Sax, NI (1979). Dangerous Properties of Industrial Materials. 5th
        ed. p. 799. New York, Van Nostrand Reinhold.
        Spighel, A, Alroy-Spiegel, M (1958). Metaldehyde Poisoning.
        Lancet, 2, p: 1017.
        Verschuuren, HG, Dentonkekler, EM, Bertiverns, JM, Helleman, PW,
        Van Esch, GJ (1975). Long-term Toxicity and Reproduction Studies
        with Metaldehyde in Rats. Toxicology, 4: 97-115.
        Vischer, A. (1935). Beitrag zum krankheitsbild der meta
        vergiftung. Med. Wochenschr., 65: 827.
        Wilkinson, RA (1968). Metaldehyde. Practitioner, 200: 320.
        Windholz M (1983) The Merck Index: an encyclopedia of chemicals,
        drugs, and biologicals. 10th ed. Rahway, New Jersey, Merck & Co.,
        Inc. p 847.


        Author:  Elsa Wickstrom
                 National Poison Information Centre
                 P.O. Box 89991 DEP
                 0034 Oslo 1
                 Tel:     47-2-33 40 30
                 Fax:     47-2-33 40 34
        Date:             June 1990
        Peer Review:      London, UK, March 1990
        Internal review
        IPCS:             June, 1995
        Updated and Peer Reviewed,  Sao Paulo INTOX-11, October 21, 1999.
        Dr N. Besbelli (co-ordinator), Dr S. Kluge, Dr N. Langford, Dr Y.
        Cesaretli and Dr L. Querino.

    See Also:
       Toxicological Abbreviations