Dieldrin
1. NAME
1.1 Substance
Dieldrin
1.2 Group
1.3 Synonyms
Common name
HEOD;dieldrine;
1.4 Identification numbers
1.4.1 CAS number
60-57-1
1.4.2 Other numbers
UN 1093
IUPAC
1.5 Brand names, Trade names
Dieldrin
Alvit
Octalox
Panoram
Quintox
Cömpound-497
ENT-16,225
OMS-18
To be completed by each centre.
1.6 Main manufactures/main importers
The manufacture and import of dieldrin has
ceased. Formerly importer for Suriname:
Shell Suriname Verkoopmaatschappij, Sir W.
Churchillweg, Paramaribo, Suriname.
2. SUMMARY
2.1 Main risks and target organs
Dieldrin is highly hazardous by the oral and
dermal routes. The most common form of human
exposure occur through the ingestion of contaminated
foodstuff or water, inhalation of vapor, or
absorption through skin. The later being an
important factor leading to occupational poisoning
by dieldrin.
Dieldrin is persistent in the environment and is not
readily biodegradable.
Dieldrin is a central nervous system stimulant.
No data are available on the teratogenity
risks.
2.2 Summary of clinical effects
Symptoms of poisoning are general malaise,
headache, sweating, dizziness, nausea and vomiting,
cardiac arrhythmias, muscular weakness, motor
hyperexcitability, hyperreflexia, myoclonic jerking,
and convulsions in severe poisoning. Convulsions may
be delayed for 48 hours following exposure. Death
may result from cardiac or respiratory arrest.
Chronic poisoning may only produce convulsions.
2.3 Diagnosis
Clinical features
Shortly after ingestion toxic doses of dieldrin will
cause nausea and vomiting, followed by effects of
neuronal hyperactivity: apprehension, excitability,
parasthesias, dizziness, headache, disorientation,
and tremor progressing to stupor, coma and
convulsions in severe cases. Arrhythmias may occur
owing to myocardial sensitivity to catecholamines.
Signs of hepatitis or renal injury may develop.
Intoxication from acute oral exposure generally
begins within 45 minutes to several hours. Although
convulsions may be delayed for 48 hours following
exposure.
Pharmacological criteria
Not relevant
Laboratory analysis
The determination of the concentration of dieldrin
in blood is useful for the confirmation of the
diagnosis of dieldrin intoxication, but not of
importance for clinical management.
2.4 First-aid measures and management principles
Treatment is symptomatic, aimed at controlling
convulsions, coma, and respiratory depression.
Cardio-circulatory function need to be observed.
To control convulsions use clonazepam IV or diazepam
IV or per rectum. Once convulsions are controlled
further treatment with Phenytoin or Sodium
Valporate should be continued for a further two to
four weeks.
Do not give fats, oils or milk since these will
assist absorption in the intestinal tract.
If the patient is conscious perform gastric lavage
for large ingestions, avoiding aspiration into the
lungs. Followed by intragastic administration of a
large amount of activated charcoal powder with water
and a laxative.
In the case of skin contact remove and discard
contaminated clothing and wash exposed skin with
(soap and) copious amounts of water, including hair
and nails.
Opiates and adrenaline and nor-adrenaline
should only be given with extreme caution.
Aminophylline, atropine or oily laxatives
should not be administered.
Rescuers must take precautions to avoid personal
exposure.
3. PHYSICO-CHEMICAL PROPERTIES
3.1 Origin of the substance
Synthetic
3.2 Chemical structure
STRUCTURAL PICTURE:
Molecular formula:C12H8Cl6O
Molecular weight 380.93
Structural names:
(IUPAC)
(1R,4S,4aS,5R,6R,7S,8S,8aR)-1,2,3,4,10,10-hexachloro-
1,4,4a,5,6,7,8,8a-octahydro-6,7,-epoxy-1,4:5,8-
dimehanonaphthalene
(C.A.)
(1a-alpha,2-beta,2a-alpha,3-beta,6-beta,6a-alpha,7-
beta,7a-alpha)-3,4,5,6,9,9-hexachloro-
1a,2,2a,3,6,6a,7,7a-octahydro-2,7:3,6-
dimethanonaphth[2,3-b]oxirene(9CI)
(Dieldrin is a stereoisomer of endrin and a
metabolite of aldrin).
3.3 Physical properties
3.3.1 Colour
white
3.3.2 Form
Solid-crystals
3.3.3 Description (Worthing 1988; Windholz 1983;
Hayes and Laws 1991)
Melting point °C: 176-177
Solubility in water: 0.17mg/L at 20 °C:
soluble in aromatic and halogenated
solvents; moderately soluble in acetone;
slightly soluble in mineral oils, other
aliphatic hydrocarbons, and
alcohols.
Vapour Pressure: 400 µPa at 20 °C
Density: 1.70 at 20 °C
Stability: stable to alkali, mild acids and to light
Reactivity: react with concentrated
mineral acids, acid catalysts, acid
oxidizing agents, phenols and active
metals (iron, copper)
Flammability: nonflammable
Technical dieldrin contains 85% dieldrin
and 15% insecticidally active related
products. Minimum concentration is 95%
of the 85%/15% mixture (not less than
80.75% dieldrin).
Colour: buff to light brown
Melting point: °C: 95
3.4 Hazardous characteristics
Combustion: with sufficient burning or
external heat dieldrin will decompose whilst
emitting toxic fumes. The smoke and fumes could
be hazardous through inhalation, or absorption
through the skin (Ellenhorn and Barceloux
1988).
Corrosiveness: noncorrosive
Environmental risks: dieldrin is persistent in
the environment and is not readily
biodegradable. Care must be taken in handling
and use and particularly with waste disposal to
avoid environmental contamination (Shell
Agriculture 1990). Is should not be applied to
any crops, and be kept away from animals and
all forms of wild life (Shell Agriculture
1990).
Dieldrin is not readily decomposed chemically
and waste material must be burned in a proper
incinerator (minimum requirements: operating
temperature of > 1000 °C and residence time in
the flame of at least 2 seconds) (3).
4. USES
4.1 Uses
4.1.1 Uses
4.1.2 Description
Formerly used to control locusts
and tropical disease vectors, such as
Glossina spp. and mosquitoes (Worthing
1988).
Former industrial uses include timber
preservation, termite proofing of
plastic and rubber coverings of
electrical and telecommunications
cables, of plywood and building boards
and as termite barrier in building
construction (Worthing 1988).
4.2 High risk circumstances of poisoning
The most common form of human exposure
occur through the ingestion of contaminated
foodstuff or water, inhalation of vapor, or
absorption through skin (Ellenhorn and
Barceloux 1988). Undoubtedly, relatively
extensive absorption by the dermal route has
been an important factor leading to
occupational poisoning by dieldrin (Hayes and
Laws 1991).
4.3 Occupational exposed populations
Agriculture workers, structural insect
control, and malaria control programs.
5. ROUTES OF EXPOSURE
5.1 Oral
Oral ingestion is the commonest route of
poisoning, usually by the ingestion of
contaminated foodstuffs or water.
Oral ingestion may also occur through placing
contaminated objects in the mouth during
eating, drinking or smoking, or through
violation of proper procedures, e.g. blowing
out clogged spray nozzles by mouth.
Intentional ingestion may also occur in suicide
attempts.
5.2 Inhalation
Exposures occur through the inhalation of dust
from powder concentrates, or aerosols from spray of
liquid formulations while applying.
5.3 Dermal
Absorption through intact or damaged skin
is a significant route of exposure, especially
when applying.
5.4 Eye
Exposure to vapours, dust and aerosols is
possible.
5.5 Parenteral
No data available.
5.6 Others
No data available.
6. KINETICS
6.1 Absorption by route of exposure
Dieldrin is absorbed from the
gastrointestinal tract, the lungs and through
intact skin (Windholz 1983, Ellenhorn and
Barceloux 1988, Moffat 1986).
Both dieldrin powder and solutions are readily
absorbed after oral ingestion (Moffat 1986).
Dieldrin is absorbed from the gastrointestinal
tract via the hepatic portal vein in rats
(Heath and Vandekar 1964).
The intestinal absorption will be enhanced by
the fat content of the diet. It is also
influenced by the fibre content of the diet as
well as by the total food intake. The
absorption of dieldrin is enhanced by
starvation in rats (Heath and Vandekar
1964).
Owing to the relatively low vapour pressure
dieldrin seldom reaches levels in the air above
those permitted. The extent of absorption by
inhalation (dust or aerosol), depends on the
appropriate particle size (Hayes and Laws
1991).
Dieldrin is readily and effectively absorbed
through intact skin (Hayes and Laws 1991). Its
high dermal toxicity does not depend on
solution. Solid dieldrin, if very finely
ground, is absorbed through the skin (Hayes and
Laws 1991).
Dermal penetration involves not only partition
coefficients but also binding to various
dermal, epidermal, and serum sites (Hayes and
Laws 1991).
6.2 Distribution by route of exposure
Dieldrin is selectively stored in body fat
(Moffat 1986), and may be found in fat of
people in the general population (Hayes and
Laws 1991). It persists in body fat for several
year after cessation of exposure (Moffat 1986,
Nair et al 1992). Dieldrin may also be found in
blood and in various organs of people in the
general population (Hayes and Laws 1991).
The plasma: whole blood ratio is about 1.5, and
the protein binding in plasma is more than 99 %
(Moffat 1986).
The storage of dieldrin is influenced by other
chlorinated hydrocarbon insecticides (Hayes and
Laws 1991). In starvation stored chlorinated
hydrocarbon insecticides may be released into
the circulation, sometimes with marked effects
(Hayes and Law 1991).
6.3 Biological half-life by route of exposure
The reported half-life in blood is 50 to
170 days (mean 97) (Moffat 1986).
In chronic human exposure to dieldrin a
half-life of about 1 year may be seen (Hunter
et al 1969, Jager 1970).
6.4 Metabolism
Most organochlorines are metabolised
slowly (Ellenhorn and Barceloux 1988). In
common with other lipophilic xenobiotics,
chlorinated hydrocarbon insecticides can be
metabolised by the microsomal cytochrome P-450
system in the liver to mainly unknown
hydrophilic metabolites (Hayes and Laws 1991,
Moffat 1986). At least one metabolite of
dieldrin excreted in the feces has been
identified (9-hydroxydieldrin) (Richardson and
Robinson 1971).
Hepatic enzyme induction can result from
exposure to dieldrin (Ellenhorn and Barceloux
1988).
6.5 Elimination and Excretion
Dieldrin is eliminated from humans in
urine and faeces. In urine it is excreted as at
least two neutral polar metabolites. In faeces
it may be excreted unchanged, or metabolised.
At least one metabolite has been identified
(9-hydroxydieldrin) (Richardson and Robinson
1971).
Chlorinated hydrocarbon insecticides are
excreted in milk, because of the lipid content
of the milk and high bloodflow to breast tissue
considerable concentration of these chemicals
can be present compared to that in tissues.
Contamination of both cow's and human milk is a
form of excretion, but also an unique one that
could lead to toxic effects in the recipient
(Hayes and Laws 1991).
Dieldrin or its metabolites are excreted
rapidly in the bile of rats, with a rate of
excretion three time greater in males than in
females (Klevay 1970).
When dieldrin is given orally to rats it is
metabolised to compounds that are excreted in
both faces and urine (respectively
approximately 90 and 10 %) (Robinson and
Roberts 1969).
7. TOXICOLOGY
7.1 Mode of action
Chlorinated hydrocarbon insecticides act
by altering the electrophysiological and
associated enzymatic properties of nerve cell
membranes, causing a change in the kinetics of
Na+ and K+ ion flow through the membrane.
Disturbances of calcium transport or Ca2+
- ATPase activity may also be involved, as well
as phosphokinase activities (Hayes 1991). A
major site of action of dieldrin appears to be
at the synapse in the rat (Hayes and Laws
1991).
7.2 Toxicity
7.2.1 Human data
7.2.1.1 Adults
The acute adult lethal
dose is approximately 1.5-5 g
(Steentoft 1979).
Although a clinical case is
published of a man who survived
drinking 9 g (120 mg/kg) of
dieldrin in toluene (Black
1974). An oral dosage of
0.21mg/person/day or 0.0031
mg/kg/day was tolerated by
volunteers (Hunter and Robinson
1967). The estimated absorbed
intake corresponding to the
safe threshold is 3.6
mg/person/day (Hayes and Law
1991).
A NOEL of 105-200 micrograms/L
has been reported (Hayes and
Curley 1968; Jager
1970).
7.2.1.2 Children
Toxic doses of approximately
29 mg/kg has been reported (Fry 1964).
A dosage of 23 mg/kg led to convulsion
in a child (Princi 1954).
7.2.2 Relevant animal data
Acute oral LD50: for rats 24-167
mg/kg; for birds 10-500 mg/kg.
Acute percutaneous LD50: for rats
50-120 mg/kg.
7.2.3 Relevant in vitro data
Sufficient human data is available.
7.2.4 Workplace standards
OSHA PEL, ACGIH TLV: Time Weighted
Average 0.25 mg/m3 (skin)
DFG MAK: 0.25 mg/m3
In Great Britain: 0.25 mg/m3 (long
term), 0.75 mg/m3 (short term).
7.2.5 Acceptable daily intake (ADI)
Dieldrin was last reviewed at the
FAO/WHO JMPR 1977 when 0-0.0001 mg/kg
was confirmed as the estimate of the ADI
in man (Worthing 1988).
RfD 0.00005mg/kg/day.
7.3 Carcinogenicity
Dieldrin has been reviewed by the IARC. Orally
given to the mouse dieldrin can produce liver tumors
(Hayes and Law 1991). The significance of the
marginal increase in incidence of hepatic tumors in
mice, following lifetime exposure to dieldrin, is
doubtful (Worthing 1988). In the rat, dog and monkey
dieldrin is respectively negative and inconclusive
for the oral hepatocarcinogenicity. The IARC has not
stated that dieldrin pose no carcinogenic risk to
humans (Hayes and Law 1991).
7.4 Teratogenicity
No data available
7.5 Mutagenicity
Chlorinated hydrocarbon insecticides are,
in general, negative in mutagenicity tests
(Wildemauwe et al 1983).
7.6 Interactions
With chronic exposure, hepatic enzyme
induction can result (Hayes and Law 1991).
8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS
9. CLINICAL EFFECTS
9.1 Acute poisoning
9.1.1 Ingestion
Toxic doses of dieldrin will
cause nausea and vomiting, shortly after
ingestion, followed by effects of
neuronal hyperactivity: apprehension,
excitability, parasthesias, dizziness,
headache, disorientation, and tremor
progressing to stupor, coma and
convulsions in severe cases. Convulsions
may be delayed for 48 hours following
exposure (Shell Agriculture 1990).
Arrhythmias may occur owing to
myocardial sensitivity to catecholamines
(Olsen 1994). (The solvent for dieldrin
may also contribute to these symptoms).
Prolonged or repeated exposure may cause
convulsions without earlier symptoms
(Shell Agriculture 1990).
9.1.2 Inhalation
Dieldrin is well absorbed, the
extent depends on the appropriate
particle size. Symptoms are basically
the same as by ingestion.
9.1.3 Skin exposure
Is a significant route of
exposure. Symptoms are basically the
same as by ingestion.
9.1.4 Eye contact
Irritation may result. No further
data available.
9.1.5 Parenteral exposure
No data available.
9.1.6 Other
No data available.
9.2 Chronic poisoning
9.2.1 Ingestion
Chronic intoxication may produce
convulsions and muscular jerking alone,
without prominent signs of poisoning.
Headache, dizziness, hyperexcitability,
psychological disorders, chest pains,
arthralgia, ataxia and incoordination
(especially in the Romberg and other
tests), nystagmus, tremor of hands,
sweating, dermatographia, loss of recent
memory, tachycardia and severe
impairment of spermatogenesis, may be
detected in some patients (Hayes and Laws
1991; Cassertt and Doull`s 1996).
9.2.2 Inhalation
No data available.
9.2.3 Skin exposure
Skin rashes may occur.
9.2.4 Eye contact
Irritation may result. No further
data available.
9.2.5 Parenteral exposure
No data available.
9.2.6 Other
No data available.
9.3 Course, prognosis, cause of death
Intoxication from acute oral exposure
generally begins within 45 minutes to several
hours. In mild poisoning headache, dizziness
and nausea occur. Severe poisoning progresses
to vomiting, muscular weakness, coma and
convulsions.
Since chlorinated hydrocarbons are highly
lipid-soluble, the duration of toxicity may be
prolonged.
Recurrent or delayed-onset seizures have been
reported. Also severe poisoning producing coma
without observed convulsions has been reported.
Signs of hepatitis or renal injury may develop
without earlier symptoms. Death may result from
cardiac arrest.
Chronic intoxication may produce convulsions alone
(Shell Agriculture 1990; Ellenhorn and Barceloux 1988;
Olsen 1994).
9.4 Systemic description of clinical effects
9.4.1 Cardiovascular
Arrhythmias (eg tachycardia) may occur
owing to myocardial sensitivity to
catecholamines (Olsen 1994).
9.4.2 Respiratory
No data available.
9.4.3 Neurological
9.4.3.1 Central Nervous System
Dieldrin is a CNS
stimulator resulting in
apprehension, excitability,
parasthesia, dizziness,
disorientation, tremor, and
convulsions in severe
cases.
A temporary change of
personality characterised by
fear, weeping, difficulty in
sleeping, bad dreams, mania, or
other inappropriate behaviour
has been reported in a few
accidental and occupational
cases.
Abnormal performance of various
psychological tests
administered to sprayers has
been reported (Ibanez-Peterson
and DeFranzanetti 1957).
9.4.3.2 Peripheral nervous system
Paraesthesia. No further
data available.
9.4.3.3 Autonomic nervous system
No data available.
9.4.3.4 Skeletal and smooth muscle
Some persons poisoned
by dieldrin have experienced
sudden contraction of a major
muscle, sometimes sufficient to
move a part of the body or
cause a person to fall. In
extreme cases, these movements
were accompanied by momentary
loss of consciousness (Hayes
and Laws 1991).
9.4.4 Gastrointestinal
The only, non specific clinical
effects, reported shortly after acute
ingestion are nausea and vomiting.
9.4.5 Hepatic
It is still inconclusive if
dieldrin can induce hepatocellular
carcinoma in humans (Hayes and Laws
1991).
After ingestion, signs of hepatitis may
develop (Olsen 1994).
9.4.6 Urinary
9.4.6.1 Renal
After ingestion signs
of renal injury (haematuria and
albuminuria) may develop (Olsen
1994).
9.4.6.2 Others
No data available.
9.4.7 Endocrine and reproductive systems
No data available.
9.4.8 Dermatological
Dieldrin may cause a nonspecific
dermatitis. Persons with chronic skin disease
may be in special danger from occupational
exposure to dieldrin (Hayes and Laws 1991).
9.4.9 Eye, ear, nose and throat: local effects
No data available.
9.4.10 Hematological
Aplastic anaemia.
9.4.11 Immunological
A rare case of an autoimmune
haemolytic anaemia cured by splenectomy,
with the presence of antidieldrin IgG
antibodies in the serum and on the red
cell membrane is reported (Hayes and
Laws 1991).
9.4.12 Metabolic
9.4.12.1 Acid-base disturbances
Metabolic acidosis.
9.4.12.2 Fluid and electrolyte disturbances
No data available.
9.4.12.3 Others
No data available.
9.4.13 Allergic reactions
Dieldrin may cause a dermagrapghia and
dermatitis.
9.4.14 Other clinical effects
A case resembling radiculomyelitis
was attributed to dieldrin. It's the only
case described and so far reported
(Urbanska-Bonenberg and Langauer-Lewowicka 1966).
Case report also exists were the temperature has
reduced.
9.4.15 Special risks
Pregnancy: No data available.
Breast feeding: Chlorinated hydrocarbon
insecticides are excreted in milk. The
lipid content of the milk and high
bloodflow to breast tissue can lead to
considerable concentration of these
chemicals compared to that in tissues.
Infants in countries with a large use of
insecticides can be at particular risk,
especially since breast feeding is
recommended by the WHO and other
agencies (Hayes and Laws 1991).
Enzyme deficiencies: No data available.
9.5 Others
No data available.
9.6 SUMMARY
10. MANAGEMENT
10.1 General principles
Whether first attention is given in a
particular case to removal of the poison or to
sedation must depend on the condition of the
patient at the time.
Treatment is symptomatic, aimed at controlling
convulsions, coma, and respiratory
depression.
Cardiovascular function needs to be observed.
If ingested, gastric lavage may be indicated,
followed by activated charcoal powder.
Opiates should only be administered with
extreme caution because of their depressive
effects on the respiratory centre. Adrenaline
and nor-adrenaline should only be
administered with extreme caution, because they
may sensitise the myocardium and thus provoke
serious cardiac arrhythmias. Aminophylline,
atropine or oily laxatives should not be
administered.
10.2 Life supportive procedures and symptomatic/specific
treatment
Make a proper assessment of airway,
breathing, circulation and neurological status
of the patient.
Maintain a clear airway. Support ventilation
using appropriate mechanical device. Administer
oxygen.
Control convulsions with appropriate drug
regimen. Drugs of choice are clonazepam IV or
diazepam IV or per rectum.
Monitor blood pressure and ECG. Control cardiac
dysrrhythmias with proper drug regimen (proper
means).
10.3 Decontamination
Skin contact:
Remove and discard contaminated clothing.
Wash exposed skin with (soap and) copious
amounts of water, including hair and nails.
Eye contact:
Irrigate exposed eyes with copious amounts of
water (or saline).
Ingestion:
Emesis is contraindicated because of the risk
of abrupt onset of seizures. If the patient is
conscious perform gastric lavage for large
ingestion, avoiding aspiration into the lungs.
This should be followed by intragastric
administration of a large amount of activated
charcoal powder (50-200g) with water and a
water soluble cathartic. Do not give fats, oils
or milk as these will assist absorption in the
intestinal tract.
Gastric lavage is indicated if patient seen
within 4 hours of ingestion.
In the case of ingestion of a solution, or an
emulsifiable concentrate, a risk of chemical
pneumonitis following aspiration exist.
10.4 Enhanced Elimination
Enhanced elimination is not indicated
because of the large volume of distribution of
chlorinated hydrocarbon insecticides.
10.5 Antidote treatment
10.5.1 Adults
There is no specific antidote.
10.5.2 Children
There is no specific antidote.
10.6 Management discussion
The use of activated charcoal in the
treatment of an acute dieldrin intoxication is
fully established. Repeated dosing may be
beneficial as it partially interrupts the
entero-hepatic circulation (Hayes and Laws
1991).
If clonazepam or diazepam are not available,
barbiturates administered slowly by intravenous
or intramuscular injection can be used, eg
phenobarbitone (Shell Agriculture 1990). Major
side effects of the treatment with barbiturates
are sedation, respiratory depression,
hypotension, shock, apnoea and laryngospasm
(KNMP 1996).
When convulsions are under control and do not
recur it is recommended that treatment is
continued with Phenytoin (or Sodium
Valporate), for 2 to 4 weeks (Shell
Agriculture 1990).
11. ILLUSTRATIVE CASES
11.1 Case reports from literature
A man who attempted suicide by drinking 9
g (120 mg/kg) of dieldrin in toluene did not
regain full consciousness until 5 days later;
headache and disturbance of short-term memory
persisted for several weeks, and there was
evidence of mild liver damage. Convulsions were
so severe and persistent in spite of
conventional treatment that it seems unlikely
that the patient would have survived without
heroic treatment, including profound muscular
paralysis induced by pancuroniumbromide,
intermittent positive pressure ventilation, and
ß-sympathetic blockade (Black 1974).
A foodborne outbreak affecting a large number
of people by dieldrin-contaminated rice in
Mali, of whom 79 were studied epidemiologically
was reported by the WHO. In most cases onset
was 0.5-1.5 hr after the rice was eaten, and
the delay never exceeded 6 hr. Signs and
symptoms included convulsions aching muscles,
vomiting, vertigo, and fainting. Contamination
of the rice was attributed to the use of
dieldrin to kill rats and insects in the
building where the grain had been stored (WHO
1977).
12. ADDITIONAL INFORMATION
12.1 Specific preventive measures
Rescuers must take precautions to avoid
personal exposure.
The manufacture of dieldrin has ceased.
Disposal of any remaining stocks should be done
with care to avoid contamination of the
environment. Disposal can be done by burning
the remaining stock in a proper incinerator
designed for chlorinated hydrocarbon
insecticides waste disposal. Seek further
advice from the local distributor or poisons
centre.
12.2 Other
No data available
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Princi 1954 from Hayes and Law 1991
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14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES),
COMPLETE ADDRESS(ES)
Author: J.F.M. de Kom
Drug and Poisons Information Centre
Diakonessen Hospital
Zinniastraat/Bodegravenlaan
Paramaribo
Suriname
Telephone: 597 499644
Fax: 597 499224
E-Mail: dekomj@sr.net
Date: March 1996