WORLD HEALTH ORGANIZATION FOOD AND AGRICULTURE
ORGANIZATION
ORGANISATION MONDIALE DE LA SANTE ORGANISATION POUR L'ALIMENTATION
ET L'AGRICULTURE
WHO/VBC/DS/88.68
ORIGINAL: ENGLISH
Distr.: LIMITED
DATA SHEETS ON PESTICIDES No. 68
1988
DISULFOTON
It must be noted that the issue of a Data Sheet for a
particular pesticide does not imply endorsement of the pesticide by
WHO or FAO for any particular use, or exclude its use for other
purposes not stated. While the information provided is believed to
be accurate according to data available at the time when the sheet
was compiled, neither WHO nor FAO are responsible for any errors or
omissions, or any consequences therefrom.
The issue of this document does Ce document ne constitue pas une
not constitute formal publication. Il ne doit faire
publication. It should not be l'objet d'aucun compte rendu ou
reviewed, abstracted or quoted résumé ni d'aucune citation sans
without the agreement of the l'autorisation de l'Organisation
Food and Agriculture des Nations Unies pour
Organization of the United l'Alimentation et l'Agriculture
Nations or of the World Health ou de l'Organisation Mondiale de
Organization. la Santé.
CLASSIFICATION:
Primary use: Insecticide, acaricide, miticide
Secondary use: None
Chemical group: Organophosphorus compound
Date issued: March 1988
1.0 GENERAL INFORMATION
1.1 COMMON NAME
disulfoton (BSI, E-ISO, F-ISO, ESA), ethylthiodemeton (JMAF),
M-74 (USSR)
1.1.1 Identity
IUPAC: O,O-diethyl S-2-ethylthioethyl phosphorodithioate
CAS: O,O-diethyl S-[2-(ethylthio)ethyl] phosphorodithioate
CAS Reg. No.: 298-04-4
Molecular formula: C8H19O2PS3
Relative molecular mass: 274.4
Structural formula:
Synonyms: Bay S276, Bay 19639, Bayer 19639, Dimaz, Disipton,
Disulfaton, Di-syston G, DisystonR, Di-syston, Disystox,
dithiosystox, ENT-23347, ethyl thiometon, ethylthiometon, Frumin,
Frumin ALR, Frumin G, Glebofos, M 74, Solvigran, SolvirexR,
thiodemeton, TwinSpan, Vuagt 1-4, Vuagt 1964.
1.2 SYNOPSIS
Disulfoton is a systemic insecticide and acaricide used as a
seed coating and for soil application to protect from insect attack.
Control for up to seven weeks may be obtained. Disulfoton is
metabolized to potent inhibitors of cholinesterases, and has an
extremely high acute toxicity in mammals.
1.3 SELECTED PROPERTIES
1.3.1 Physical characteristics
The pure product is a colourless oil with a sulfurous odour,
m.p. > -25 °C, b.p. 128 °C at 1.33 hPa, density d20 1.14. The
4
technical product is a yellowish oil.
1.3.2 Solubility
In water 15 mg/L at 20 °C. Soluble in most organic solvents.
1.3.3 Stability
It is relatively stable under normal storage conditions.
Hydrolysis occurs in alkaline media.
1.3.4 Vapour pressure
24 mPa at 20 °C.
1.4 AGRICULTURE, HORTICULTURE AND FORESTRY
1.4.1 Common formulations
Granules (20-150 g/kg), emulsifiable concentrates (850 g/kg).
Also in combination with DasanitR, Ethimeton and Ekanon in spray
concentrates, granular (20-100 g/kg) and emulsifiable concentrates.
1.4.2 Susceptible pests
Used against aphids and mites on corn, sorghum, cotton,
vegetables, fruits, nuts, ornamentals, small grains and other field
crops; also used against leafhoppers, fleabeetles, lacebugs,
leafrollers, whiteflies, mealybugs, leafminers and Mexican bean
beetles.
1.4.3 Use pattern
Applied at 560 to 3 400 g per hectare on crops. Applied to soil
by drilling, side dressing or broadcasting; applied prior to
planting, prior to emergence or post-emergence. Work into the soi
and water thoroughly. May be used as a seed dressing and on fruit
trees by spreading from drip line to trunk of tree.
1.4.4 Unintended effects
High dosages may injure seeds. Some leafburn in alfalfa has
occurred, garden lily bulbs have been injured. Plant injury may be
enhanced when used with some pre-emergence herbicides. Disulfoton
may be toxic to insect pest predators and bees.
1.5 PUBLIC HEALTH USE
No recommended use.
1.6 HOUSEHOLD USE
No recommended use.
2.0 TOXICOLOGY AND RISKS
2.1 TOXICOLOGY- MAMMALS
2.1.1 Absorption route
Disulfoton may be absorbed from the gastrointestinal tract,
through the intact skin or by inhalation of fine dusts.
2.1.2 Mode of action
Acetylcholinesterase inhibition by some of the metabolites of
disulfoton.
2.1.3 Excretion products
Excretion is rapid, half of an oral dose of O-ethyl-14C-
labelled disulfoton was recovered in the excreta within six hours in
male rats, 32 hours in female rats. For either sex urinary excretion
accounted for 80% of the dose, expired air 9%. For both sexes the
major urinary metabolites diethylphosphate and diethylthiophosphate
accounted for >90% of the urinary excretion. These metabolites were
probably formed by hydrolysis of the products of oxidative
metabolism, namely: the sulfone and sulfoxide of disulfoton, and the
sulfone and sulfoxide of the oxygen analogue of disulfoton. Minor
proportions of the latter three metabolites were identified in rat
urine.
2.1.4 Toxicity, single dose
As for many other pesticides, the nature of the solvent or
carrier used to aid administration of the compound may affect the
magnitude of the observed LD50 values.
Oral LD50:
Rat (M) 6.2 - 12.5 mg/kg b.w.
Rat (F) 1.9 - 4.2 mg/kg b.w.
Mouse (M) 5.8 - 27.0 mg/kg b.w.
Mouse (F) 2.7 - 27.0 mg/kg b.w.
Guinea pig (M) 8.9 mg/kg b.w.
Guinea pig (F) 12.7 mg/kg b.w.
Dermal LD50:
24 hour exposure Rat (M) 15.9 - 25 mg/kg b.w.
24 hour exposure Rat (F) 3.6 - 6 mg/kg b.w.
4 hour exposure Rat 41 mg/kg b.w
Intraperitoneal LD50:
Rat (M) 7.5 mg/kg b.w.
Rat (F) 2.1 - 3.1 mg/kg b.w.
Mouse (M) 6.7 mg/kg b.w.
Mouse (M,F) 14.0 mg/kg b.w.
Inhalation LC50:
1 hour Rat (M) 290 mg/m3
1 hour Rat (F) 63 mg/m3
4 hour Rat (M,F) 15 - 60 mg/m3
Most susceptible species: Among the mammals tested, the rat
and mouse appear equally to be the most susceptible to disulfoton
poisoning, and in both species the female is more susceptible than
the male.
2.1.5 Toxicity, repeated doses
Tolerance to continued exposure of sub-lethal amounts of
disulfoton has been demonstrated following gavage, dietary exposure
or intraperitoneal injection. Although the cholinergic symptoms
(tremors, fasciculations, excessive salivation) may disappear as the
duration of exposure increases, the acetylcholinesterase activity
remains depressed. (See 2.1.7 for biochemical interpretation.) The
rate and extent of adaptation are dependent on the route of
administration, the magnitude of the dose and the animal species, or
even the strain.
Female rats receiving disulfoton during 30 days 1.0 mg/kg/day
intraperitoneally fully recovered from symptoms of cholinergic
poisoning and weight loss which had been evident for the first seven
days of administration. Although symptomless, the brain and serum
cholinesterase activities in these rats, and in rats receiving 0.25
mg/kg/day (intraperitoneally), remained low throughout the 30 day
period.
Histopathological changes in the optic nerve and retina were
observed in all dogs receiving a gelatin capsule dose of 0.5, 1.0 or
1.5 mg/kg/day, five days/week for two years. Retinal lesions
observed were mild.
2.1.6 Dietary Studies
Short term: No mortality or effect on body weight gain,
haematology, urinalysis, clinical chemistry or gross and microscopic
tissue and organ analyses were observed in studies on rats fed on a
diet of > 5 ppm disulfoton for 90 days, in mice fed on a diet
containing 10 ppm for 16 weeks, nor in mongrel dogs on a diet
containing 10 ppm for 12 weeks. Cholinesterase activity wa
depressed in brain tissue, measured in rats and mice only, generally
more severely in females than males and in erythrocytes and in
plasma of all three species. In dogs plasma cholinesterase activity
rapidly returned to normal after cessation of dosing, but
erythrocyte cholinesterase remained inhibited for more than four
weeks. The no observed effect level (NOEL) for cholinesterase
inhibition was determined as 1 ppm for all three species.
Dietary administration of disulfoton at a dose of 7.5 ppm to
male albino rats for 30 days resulted in 4/71 deaths, decreased
weight gain and inhibition of cholinesterase activity in the brain,
stomach and diaphragm. Cholinesterase activity of the stomach and
diaphragm regain pre-treatment values after 19 days but the brain
cholinesterase activity remained depressed. Dietary administration
of disulfoton at a dose of 7.5 ppm to female Holtzman rats for 62
days produced no overt signs of toxicity. At a dose of 20 ppm,
diarrhoea, excessive urination and tremors were seen initially. The
severity of the symptoms decreased with duration of exposure but
some tremors, fasciculations and reduced weight gain were apparent
at 62 days.
Long term: In a two year dietary study in rats at 1, 4 and 16
ppm the no observed adverse effect level (NOAEL) for cholinesterase
depression in both sexes was observed to be 1.0 ppm while body
weight decrease was reported at 16 ppm in both sexes. No other
significant adverse effects were observed at any dose level.
Beagle dogs received a diet of 0.5 or 1.0 ppm for two years. An
additional dose group was fed on a diet of 2.0 ppm, for 69 weeks,
increased to 5.0 ppm from week 70-72, and increased again to 8.0 ppm
from week 73-104. No adverse effect on mortality, behaviour, growth,
ophthalmological, clinical chemistry or haematology parameters, or
urinalysis were recorded. Plasma and erythrocyte cholinesterase
activity were depressed in a group fed on a diet of 2.0 ppm. The
effect was accentuated by increased magnitude and duration of
dosing. Brain cholinesterase activity was inhibited by 8.0 ppm diet
at week 104. NOAEL for beagle dogs is 1.0 ppm.
2.1.7 Supplementary studies of toxicity
Carcinogenicity: No evidence of carcinogenicity was observed
in a two year rat dietary study up to and including 16 ppm, the
highest dose tested.
Teratogenicity: No teratogenic effects were observed in rats
treated by gavage with 0.1, 0.3 or 1.0 mg/kg/day, embryotoxicity was
observed at the highest dose and the NOAEL for cholinesterase
activity in the dams was 0.1 mg/kg/day.
In rabbits, doses of 1.5 mg/kg/day and above were found to be
maternally toxic, causing clinical signs of poisoning and death i
some animals. No teratogenic, fetotoxic nor embryotoxic effects were
observed at any dose level, up to aud including 1.5 mg/kg/day.
Reproduction: In a rat dietary study at 1, 3 and 9 ppm the
NOAEL was reported to be 1 ppm for reproductive effects including
reduced litter size, pup weight and pup viability at 3 ppm and
above. Maternal toxicity, weight loss and clinical signs of
cholinesterase depression, were observed in the high dose group.
In another study dietary administration of disulfoton at doses
of 2, 5 and 10 ppm had no adverse effect on rat reproduction
parameters. At 10 ppm an increased mortality at weaning was observed
in the first generation, and some fatty changes in the liver, (males
especially) of the third generation. Erythrocyte cholinesterase
activity was decreased in all treatment groups.
Inhalation: In a three week study with rats the NOAEL was
reported to be 0.02 mg/m3 (6 hours/day) for both sexes for signs
of toxicity due to cholinesterase depression at higher doses.
Mutagenicity: Disulfoton was not mutagenic in metabolically
activated or unactivated systems with Saccharomyces cerevisiae D3
and D7, nor in metabolically activated systems with several
Salmonella typhimurium strains, Escherichia coli strains or
Bacillus subtilus strains. However, other workers report that
disulfoton was mutagenic without metabolic activation in several S.
typhimurium and E. coli strains. Disulfoton did not induce
sister chromatid exchange in vitro with three mammalian cell
lines. In a mouse micronucleus test, and also in a dominant lethal
test in mice, mutagenic potential was not demonstrated.
Neurotoxicity: No clinical nor histopathologic evidence of
delayed neurotoxicity was observed in a study with hens.
Following oral administration of 0.5-1.5 mg/kg/day to dogs for
two years (Section 2.1.5) no degeneration of the optic nerves was
observed.
Miscellaneous effects: Induction of microsomal multisubstrate
oxygenases and particularly cytochrome P-450 have been demonstrated
in the liver of mice. Barbiturate sleeping times were reduced in
mice receiving 1/2 LD50 doses for 10 days. Phenobarbital pre-
treatment protected rats or mice against the lethal effects of oral
or intraperitoneal administration of LD50 doses of disulfoton.
2.2 TOXICOLOGY - MAN
2.2.1 Absorption
Disulfoton may be absorbed from the gastrointestinal tract,
through the intact skin and by inhalation of fine dusts or mist
2.2.2 Dangerous doses
No published information available.
2.2.3 Observations in occupationally exposed workers
Between 1966 and June 1978, incidents of human exposure to
disulfoton alone were reported in the United States of America: 48
involved agricultural, industrial or transportation accidents. The
majority of the incidents arose from container damage, failure to
decontaminate skin and clothing after exposure and failure to wear
adequate protective equipment. Hospitalization was necessary in some
cases, but there were no fatalities from exposure to disulfoton
alone. The majority of urine samples collected daily for 25 weeks
from 10 male formulators of disulfoton contained significant
concentrations of the metabolites diethylphosphate,
diethylthiophosphate and diethylphosphorothiolate. Plasma and
erythrocyte cholinesterase activities were not, however,
significantly reduced.
2.2.4 Observations on exposure of the general public
Several instances of contamination of people during aerial
application were reported in the United States of America between
1966 and 1978, none requiring hospitalization.
2.2.5 Observations on volunteers
Five volunteers received an oral dose of 0.75 mg/day for 30
days without an adverse effect on plasma or erythrocyte
cholinesterase.
2.2.6 Reported mishaps
In two separate incidents in the United States of America,
drums or pesticide bags contaminated with disulfoton residues
resulted in symptoms of severe poisoning and coma in three children
playing with the containers. Hospitalization and atropine therapy
gave slow but continuing recovery, the children were fully recovered
after two or five days treatment. Alleged incidents of disulfoton
ingestion were generally asymptomatic.
2.3 TOXICITY TO NON-MAMMALIAN SPECIES
2.3.1 Fish
Disulfoton is highly toxic to fish and crustaceans, however,
there are no reported environmental killings of fish or other
aquatic organisms. Disulfoton has no effect upon the hatchability of
brine shrimp at 10 mg/L
2.3.2 Birds
Oral LD50:
Starlings 133.O mg/kg b.w.
Mallards 6.54 mg/kg b.w.
Bobwhite quail (M) 31.0 mg/kg b.w.
Bobwhite quail (F) 28.0 mg/kg b.w.
Oral LC50 (five days):
Bobwhite 715 ppm
Japanese quail 333 ppm
Ring-necked pheasant 634 ppm
Mallard 510 ppm
Dermal LD50:
Mallard (M) 192 mg/kg b.w.
2.3.3 Other species
Disulfoton is toxic to bees and terrestrial wildlife.
3.0 FOR REGULATORY AUTHORITIES: RECOMMENDATIONS ON REGULATION OF
COMPOUND
3.1 RECOMMENDED RESTRICTIONS ON AVAILABILITY
(For definition of categories, see introduction to Data
Sheets).
Liquid formulations greater than 130 g/L and solid formulations
greater than 500 g/kg, Category 1.
All other formulations, Category 2.
3.2 TRANSPORTATION AND STORAGE
All formulations
Should be transported or stored in clearly labelled rigid and
leakproof containers, and away from containers of food and drink.
Storage should be under lock and key and secure from access by
children and other unauthorized persons.
3.3 HANDLING
All formulations: Full protective clothing (see part 4)
should be used by those handling the compound. Adequate washing
facilities should be available close at hand. Eating, drinking and
smoking should be prohibited during handling and before washing
after handling.
3.4 DISPOSAL AND/OR DECONTAMINATION OF CONTAINER
Empty containers should not be re-used. After decontamination
the container must be either burned or crushed and buried below
topsoil. Care must be taken to avoid subsequent contamination of
water sources.
3.5 SELECTION, TRAINING AND MEDICAL SUPERVISION OF WORKERS
All formulations: Pre-employment medical examination for
workers is necessary. Workers suffering from active hepatic or renal
diseases should be excluded from contact with disulfoton. Pre-
employment and periodic blood cholinesterase tests for workers is
desirable. Special account should be taken of the worker's mental
ability to comprehend and fol!ow instructions. Training of workers
in techniques to avoid contact is essential.
3.6 ADDITIONAL REGULATIONS RECOMMENDED IF DISTRIBUTED BY AIRCRAFT
All formulations: Pilots and loaders should have special
training in application methods and early symptoms of poisoning, an
they must wear protective clothing. It is not advisable to employ
flagmen, but if essential they must wear protective gloves,
overalls, boots, a respirator and an impermeable hat and be located
well away from the dropping zone.
3.7 LABELLING
All formulations
"DANGER - POISON"
(skull and cross-bones insignia)
Disulfoton is an organophosphorus compound which inhibits
cholinesterases. It has an extremely high mammalian toxicity.
Contact with the skin, inhalation of dust or spray, or swallowing
may be fatal. Wear protective gloves, clean protective clothing, and
a respirator of the organic-vapour type when handling this material.
Bathe immediately after work. Ensure that containers are stored
under lock and key. Empty containers must be decontaminated and
disposed of in such a way as to prevent all possibility of
accidental contact with them. Keep the material out of reach of
children and well away from foodstuffs, animal feed and their
containers. Do not tank mix with phosalone. In case of contact,
immediately remove contaminated clothing and wash the skin
thoroughly with soap and water; for eyes, flush with water for 15
minutes. If poisoning occurs, call a physician. Atropine sulfate is
an effective drug if applied in time, repeated doses may be
necessary. Artificial respiration also may be needed.
3.8 RESIDUES IN FOOD
Maximum residue levels
Maximum residue levels have been recommended by the FAO/WHO
Joint Meeting on Pesticide Residues.
4.0 PREVENTION OF POISONING IN MAN AND EMERGENCY AID
4.1 PRECAUTIONS IN USE
4.1.1 General
Disulfoton, an organophosphorus pesticide, is extremely toxic
by the oral route. It is also readily absorbed through the intact
skin, and by inhalation of dust or spray mist. Repeated exposure may
have a cumulative effect on cholinesterase activity.
4.1.2 Manufacture and formulation - T.L.V.
0.1 mg/m3. Closed systems and forced ventilation are required
to reduce, as much as possible, the exposure of workers to the
chemical.
4.1.3 Mixers and applicators
When opening the container and when mixing, protective
impermeable hoots, clean overalls, gloves and a respirator should be
worn. Mixing, if not mechanical, should always be carried out with a
paddle of appropriate length. When spraying tall crops or during
aerial application, a respirator should be worn, as well as an
impermeable hat, overalls, boots, and gloves. The applicator should
avoid working in spray mist and avoid contact with the mouth.
Particular care is needed when equipment is being washed after use.
All protective clothing should be washed immediately after use,
including the insides of gloves. Splashes must be washed immediately
from the skin, or eyes, with large quantities of water. Before
eating, drinking or smoking, hands and any other exposed skin should
be washed.
4.1.4 Other associated workers (including flagmen in aerial
operations)
Persons exposed to disulfoton and associated with its
application should wear protective clothing and observe the
precautions described above in 4.1.3 under "Mixers and applicators".
4.1.5 Other populations likely to be affected
With good agricultural practice, other persons should not be
exposed to hazardous amounts of disulfoton.
4.2 ENTRY OF PERSONS INTO TREATED AREA
Unprotected persons should be kept out of treated areas for at
least one day
4.3 DECONTAMINATION OF SPILLAGE AND CONTAINERS
Re-use of containers should not be permitted. Residues in
containers should be emptied in a diluted form into a deep pit,
taking care to avoid contamination of ground waters. The empty
container should be rinsed with 5% sodium hydroxide, which should be
left in the container overnight. The rinse should be emptied into a
deep pit, and the container crushed and buried, avoiding
contamination of ground waters. Impermeable groves should be worn
during this work. Spillage of disulfoton and its formulations should
be removed by washing with 5% sodium hydroxide solution and then
rinsing with large quantities of water.
4.4 EMERGENCY AID
4.4.1 Early symptoms of poisoning
Early signs and symptoms of poisoning may include excessive
sweating, headache, weakness, giddiness, nausea, vomiting,
hypersalivation, stomach pains, blurred vision, slurred speech, and
muscle twitching. Later there may be convulsions and coma in cases
of severe poisoning.
4.4.2 Treatment before person is seen by a physician if these signs
and symptoms appear following exposure
The person should stop work immediately, remove contaminated
clothing and wash the affected skin with soap and water, and flush
the area with large quantities of water. If swallowed, and if the
person is conscious, vomiting should be induced. In the event of
respiratory difficulty ventilatory support should be given, bearing
in mind that if mouth-to-mouth resuscitation is used, vomit may
contain dangerous amounts of disulfoton.
5.0 FOR MEDICAL AND LABORATORY PERSONNEL
5.1 MEDICAL DIAGNOSIS AND TREATMENT IN CASES OF POISONING
5.1.1 General information
Disulfoton, an organophosphorus pesticide, is extremely toxic
to mammals. It is readily absorbed from the gastrointestinal tract
through the intact skin and from the lungs following inhalation of
dust or spray mist. It is metabolized to the oxygen analogues of
disulfoton which are potent inhibitors of cholinesterases. It does
not accumulate in body tissues.
5.1.2 Symptoms and signs
Initial symptoms and signs of poisoning may include excessive
sweating, headache, weakness, giddiness, nausea, hypersalivation,
vomiting, stomach pains, blurred vision, slurred speech and muscle
twitching. More advanced symptoms of poisoning may be convulsions,
coma, loss of reflexes and loss of sphincter control.
5.1.3 Laboratory
The most important finding is reduction of activity of blood
cholinesterases. Urinary levels of organic phosphorus containing
metabolites may also be used as a measure of exposure. Neither
method is specific for disulfoton.
5.1.4 Treatment
If the pesticide has been ingested, unless the patient is
vomiting, rapid gastric lavage should be performed using 5% sodium
bicarbonate. Care should be taken to avoid pulmonary complications
from solvents which may be present in emulsifiable concentrate
formulations. For skin contact, the skin should be washed with soap
and water. If the compound has entered the eyes, they should be
washed with large quantities of isotonic saline or water. Care must
be taken by the victims attendants to avoid their own intoxication
from contaminated clothing, skin or vomit.
Persons without signs of respiratory insufficiency but with
manifest peripheral symptoms, should be treated with 2-4 mg of
atropine sulfate by intravenous injection followed by 1 000 mg
pralidoxime chloride in split doses or 250 mg of toxogonin (adult
dose) by slow intravenous injection. the additional therapy with
pralidoxime or toxogonin is most effective if given within 24 hours
of the onset of intoxication. However, treatment should continue for
as long as benefits are observed. More atropine may be given as
needed. Persons with severe intoxication, with respiratory
difficulties, cyanosis, convulsions, or who are unconscious should
immediately be given oxygen followed by atropine sulfate and the
pralidoxime chloride. In such severe cases 4-6 mg of atropine
sulfate should be given initially followed by repeated doses of 2 mg
at 5-10 minute intervals until atropinization. Symptoms will
reappear if tissue concentrations of disulfoton remain high when the
effect of atropine wears off. Rales in the lung bases, myosis,
nausea, or bradycardia may indicate inadequate atropinization;
overdosage with atropine (pulse rate over 140, dry mouth, flushed
face) is rarely serious, but under-dosage may be fatal. Diazepam may
be given to control convulsions. The patient's condition including
respiration, blood pressure, pulse rate, salivation and convulsions
should be carefully observed as a guide to further administration of
atropine.
The airways should be kept free and artificial resuscitation
should be applied if required, preferably by mechanical means. If
necessary, intubation should be performed.
Application of morphine, aminophylline, phenothiazines,
reserpine and central nervous system stimulants is contraindicated.
Return to work should be delayed until blood cholinesterase activity
reaches at least 80% of the pre-exposure value.
5.1.5 Prognosis
If the acute toxic effect is survived, and if adequate
artificial resuscitation (if needed) has been given, the chances of
complete recovery are good. However, in very severe cases,
particularly if artificial resuscitation has been inadequate,
prolonged anoxia may give rise to permanent brain damage.
5.1.6 References of previously reported cases
US EPA (1978) "Summary for Reported Incidents Involving
Disulfoton". Report No. 105, Office of Pesticide Programs,
Environmental Protection Agency, United States of America.
5.2 SURVEILLANCE TESTS
Test Normal Action Symptomatic
level* level* level*
Plasma 100% 50% variable
cholinesterase
Whole blood or 100% 70% usually 40%
erythrocyte
cholinesterase
* Expressed as percentage of pre-exposure activity
5.3 LABORATORY METHODS
5.3.1 Detection and assay of compound
Analysis of metabolites in urine may be performed by several
methods:
Abbot, D.C., Crisp, S.S., Tarrant, V.R., Tatton, J.O'G. (1970),
Pestic. Sci., 1, 10-13.
Bowman, M.C., Beroza, M. (1969,) J. Assoc. Offic. Anal.
Chem., 52, 1231-1237.
Brokopp, C.D., Wyatt, J.L., Gabica, J. (1981), Bull. Environ.
Contam. Toxicol., 26, 524-529.
Jensen, T.L. (1980), J. Assoc. Offic. Anal. Chem., 64,
869-872.
5.3.2 Other tests in case of poisoning
Acetylcholinesterase activity in blood, provide the most useful
diagnosis of poisoning.
Ellman, G.L., Courtney, D., Andres, V., Featherstone, R.M.
(1961), Biochem. Pharmacol., 7, 88-95.
Fleischer, J., Woodson, S., Simet, L. (1956), Arch. Indust.
Hyg., 14, (6), 510-520.
Michel, N.O., (1949), J. Lab. Clin. Med., 34, 1564-1568.
Wilhelm, D., Reiner, E. (1973), Bull. Wld. Health Org., 48,
235-238.
REFERENCES
1. ACGIH (1984), Supplementary documentation. American Conference
Governmental Industrial Hygienists, Cincinnati, Ohio 45211,
United States of America.
2. Dreisbach, R.H., (1983), Handbook of Poisoning: Prevention,
Diagnosis and Treatment. Eleventh Edition, Lange Medical
Publications, California 94022, United States of America.
3. FAO/WHO (1974) - 1973 Evaluations of some Pesticide Residues in
Food. AGP 1973/M/9/1: WHO, Pesticide Residue Series, No. 3,
Rome, Italy.
4. FAO/W-HO (1976) - 1975 Evaluations of some Pesticide Residues
in Food. AGP 1975/M/13: WHO, Pesticide Residue Series No. 5,
Rome, Italy.
5. Hayes, W.J. (1982), Pesticides Studied in Man. Williams and
Williams, Baltimore, United States of America.
6. Farm Chemicals Handbook (1984), Meister Publishing Co.,
Willoughby, Ohio 44040, United States of America.
7. Hartley D., Kidd, H. (1983), The Agrochemicals Handbook, Royal
Society of Chemistry, Unwin Bros. Ltd., Surrey, United
Kingdom.
8. Thomson, W.T. (1982), Agricultural Chemicals. Book I
Insecticides, 1982-1983 Revision. Thomson Publications,
California 93791, United States of America.
9. USEPA (1982), Recognition and Management of Pesticide
Poisonings, Third edition, EPA 540/9-80-005.
10. WHO (1986), Environmental Health Criteria 63, Organophosphorus
Insecticides: A General Introduction. UNEP/ILO/WHO, Geneva,
Switzerland.
11. Worthing, C.R. (1987), The Pesticide Manual. A World
Compendium, Eighth Edition, British Crop Protection Council,
United Kingdom.