Metaldehyde
METALDEHYDE
International Programme on Chemical Safety
Poisons Information Monograph 332
Chemical
1. NAME
1.1 Substance
Metaldehyde
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
pain.
Convulsions, coma and respiratory failure.
Liver and renal injury at a later stage.
Hyperthermia.
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
ingestion.
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
intubation
Give activated charcoal and a saline cathartic.
Treat convulsions with intravenous (IV) diazepam.
3. PHYSICO-CHEMICAL PROPERTIES
3.1 Origin of the substance
Synthetic.
3.2 Chemical structure
Molecular formula:
acetaldehyde homopolymer
(C2H4O)n
(CH3CHO)n
tetramer
(C2H4O)4
C8H16O4
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;
non-corrosive.
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
Gardeners.
5. ROUTES OF EXPOSURE
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. TOXICOLOGY
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
7.2.1.1 Adults
Minimum oral LD human = 100 mg/kg
(Booze & Oehme, 1985)
Minimum oral LD human = 43 mg/kg (Dreisbach,
1987)
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,
1979).
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,
hyperreflexia.
150 to 200 Muscle twitching.
400 Coma, death.
7.2.1.2 Children:
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
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. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS
8.1 Material sampling plan
8.1.1 Sampling and specimen collection
8.1.1.1 Toxicological analyses
8.1.1.2 Biomedical analyses
8.1.1.3 Arterial blood gas analysis
8.1.1.4 Haematological analyses
8.1.1.5 Other (unspecified) analyses
8.1.2 Storage of laboratory samples and specimens
8.1.2.1 Toxicological analyses
8.1.2.2 Biomedical analyses
8.1.2.3 Arterial blood gas analysis
8.1.2.4 Haematological analyses
8.1.2.5 Other (unspecified) analyses
8.1.3 Transport of laboratory samples and specimens
8.1.3.1 Toxicological analyses
8.1.3.2 Biomedical analyses
8.1.3.3 Arterial blood gas analysis
8.1.3.4 Haematological analyses
8.1.3.5 Other (unspecified) analyses
8.2 Toxicological Analyses and Their Interpretation
8.2.1 Tests on toxic ingredient(s) of material
8.2.1.1 Simple Qualitative Test(s)
8.2.1.2 Advanced Qualitative Confirmation Test(s)
8.2.1.3 Simple Quantitative Method(s)
8.2.1.4 Advanced Quantitative Method(s)
8.2.2 Tests for biological specimens
8.2.2.1 Simple Qualitative Test(s)
8.2.2.2 Advanced Qualitative Confirmation Test(s)
8.2.2.3 Simple Quantitative Method(s)
8.2.2.4 Advanced Quantitative Method(s)
8.2.2.5 Other Dedicated Method(s)
8.2.3 Interpretation of toxicological analyses
8.3 Biomedical investigations and their interpretation
8.3.1 Biochemical analysis
8.3.1.1 Blood, plasma or serum
"Basic analyses"
"Dedicated analyses"
"Optional analyses"
8.3.1.2 Urine
"Basic analyses"
"Dedicated analyses"
"Optional analyses"
8.3.1.3 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
interpretation
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
useful).
- 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
value.
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. CLINICAL EFFECTS
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,
1987).
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
Irritation.
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
9.4.3.1 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).
9.4.3.2 Peripheral nervous system
No data available.
9.4.3.3 Autonomic nervous system
Urinary incontinence can occur in
children (Booze & Oehme, 1986).
9.4.3.4 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,
1999).
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
9.4.6.1 Renal
Kidney injury has been observed in
animals and urinary incontinence in children
(Booze & Oehme, 1986).
9.4.6.2 Other
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
9.4.12.1 Acid-base disturbances
Metabolic acidosis may be severe.
Respiratory alkalosis has been reported
(Longstreth & Pierson, 1982).
9.4.12.2 Fluid and electrolytes
Dehydration is often observed (Olson, 1999).
9.4.12.3 Other
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. MANAGEMENT
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
induced.
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
ingestion.
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
persists.
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. ILLUSTRATIVE CASES
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
bicarbonate.
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
tablet.
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,
1928).
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,
1958).
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
recovered.
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
hands.
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. ADDITIONAL INFORMATION
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
pesticides.
Appropriate protective and hygienic measures should be
applied in the workplace where the product is being
manufactured, packaged, or stored.
12.2 Other
None.
13. REFERENCES
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14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES)
Author: Elsa Wickstrom
National Poison Information Centre
P.O. Box 89991 DEP
0034 Oslo 1
Norway
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.