WORLD HEALTH ORGANIZATION FOOD AND AGRICULTURE
ORGANIZATION
ORGANISATION MONDIALE DE LA SANTE ORGANISATION POUR L'ALIMENTATION
ET L'AGRICULTURE
VBC/DS/83.53
ORIGINAL: ENGLISH
DATA SHEET ON PESTICIDES No. 53
ALDICARB
CLASSIFICATION:
Primary use: Insecticide
Secondary use: Acaricide, nematicide
Chemical group: Carbamate
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.
1. GENERAL INFORMATION
1.1 COMMON NAME: Aldicarb (BSI, ISO, ANSI, exception - Germany)
1.1.1 Identity:
IUPAC: 2-methyl-2-(methylthio)propionaldehyde O-(methylcarbamoyl)
oxime
CAS No. 1: Propionaldehyde,2-methyl-2-(methylthio)-,O-
(methylcarbamoyl)oxime
CAS Reg. No.: 116-06-3
Molecular formula: C7H14N2O2S
Structural formula:
Molecular weight: 190.29
1.1.2 Synonyms: Aldicarb, aldicarbe, carbanolate, Ent 27093, NCI
08640, OMS 771, TernicR, TemikR, UC-21149
1.2 SYNOPSIS - Aldicarb is a broad spectrum carbamate pesticide; a
fast-acting cholinesterase inhibiting agent with effective direct
contact and stomach action; and, a plant systemic of extremely
high acute toxicity to mammals. It is non-cumulative and rapidly
metabolized in both plants and animals, the initial degradation
products are also highly toxic to mammals. Aldicarb is a
persistent carbamate compound with excellent residual and
knock-down properties.
1.3 SELECTED PROPERTIES
1.3.1 Physical characteristics - The pure compound is a white
crystalline solid with a slight sulfurous odour; a melting point
of 98-100°C; and a specific gravity of 1.195 at 25/20°C.
Aldicarb is non-corrosive to most metals and plastics. The
technical product is 94.7-97.7% pure aldicarb.
1.3.2 Solubility - (30°C) 9.0 g/kg water
430.0 g/kg acetone
240.0 g/kg benzene
50.0 g/kg carbon tetrachloride
440.0 g/kg chloroform
240.0 g/kg methyl isobutyl ketone
120.0 g/kg toluene
(20°C) 250.0 g/kg ethanol
200.0 g/kg methanol
1.3.3 Stability - Aldicarb is a relatively stable compound, it is
heat labile and decomposes above 100°C, it is stable in acidic
aqueous solution but rapidly decomposes in alkaline media.
1.3.4 Vapour pressure - 0.133 x 10-4 kPa (1 x 10-4 mm Hg) at 25°C.
1.4 AGRICULTURE, HORTICULTURE AND FORESTRY
1.4.1 Common formulations - To reduce handling hazards aldicarb is
prepared in granular formulations only; on corn cob grits at 50,
100 and 150 g a.i./kg; on coal at 100 g a.i./kg; and, on gypsum
at 100 and 150 g a.i./kg.
1.4.2 Susceptible pests - Aldicarb is effective against various
insects (especially aphids, whiteflies, leaf miners, flea
beetles and ground beetles), mites and nematodes on field
crops, some vegetable and fruit crops, cotton and
ornamentals in commercial plantings.
1.4.3 Use pattern - Aldicarb is applied only as a soil dressing at
rates of 0.56-11.25 kg a.i./ha depending upon the crop. For
most effective use, aldicarb should be incorporated into the
soil 2.5-5.0 cm below the surface. It may be applied
in the seed furrow, in band or broadcast applications;
preplanting, at planting or after crop emergence.
Formulated aldicarb may be used concurrently with many
fertilizers or other pesticides. It should not be applied
at the same time with alkaline compounds nor mixed with
fertilizers or other pesticides prior to application. The
active ingredient is released from the granules by water
action, for best effect the soil moisture content should be
increased immediately following application. Aldicarb
should not be used on stored crops or products.
1.4.4 Unintended effects - Applied as directed aldicarb is not
phytotoxic.
1.5 PUBLIC HEALTH PROGRAMMES (NO RECOMMENDED USAGE REPORTED)
1.6 HOUSEHOLD USE (NO RECOMMENDED USAGE REPORTED)
2. TOXICOLOGY AND RISKS
2.1 TOXICOLOGY MAMMALS
2.1.1 Absorption route - Aldicarb may be absorbed from the
gastrointestinal tract; through moist, intact skin; and, by
inhalation of dust. The presence of a binding agent in the
granular product, the only formulation available, reduces the
inhalation hazard in normal use.
2.1.2 Mode of action - Toxicity is primarily due to inhibition of
cholinesterase activity which is spontaneously reversible.
2.1.3 Excretion products - Within 48 hours of administration of
carbonyl-14C labelled aldicarb rats eliminated over 60% of the
14C as carbondioxide, less than 30% was found in the urine. In
other 14C-studies rats excreted more than 80% of the degradation
products in urine and less than 10% in faeces (an excretion
pattern favoured by enterohepatic cycling of glucuronides which
may also serve to extend the systemic activity of the toxic
metabolites). The major urinary metabolites were aldicarb
sulfoxide (40% of the dose), its oxime and nitrile forms (over
30%); the sulfone and related oxime and nitrile; and, the
aldehyde and acid analogues. Aldicarb is not commonly found in
the excreta. Bound residues of ingested plant tissues are not
absorbed and therefore are found in the faeces. In single dose
and short-term diet studies, lactating cows eliminated aldicarb
metabolites as rapidly as rats and in the same array of
metabolites. Approximately 1% of the dose was excreted in the
milk, sulfone and sulfoxide were the major metabolites at 15 and
4% of the total milk residue content respectively.
2.1.4 Toxicity, single doses
Oral LD50:
technical material, Rat (M), 0.67-1.23 mg/kg b.w. (corn oil)
Rat (F), 0.62-1.07 mg/kg b.w. (corn oil)
Rat (F), 1.0 mg/kg b.w.
(glycerol formal: ethanol 9:1)
Mouse (M), 0.38-0.50 mg/kg b.w. (corn oil)
Mouse (F), 1.5 mg/kg b.w. (cotton seed
oil)
Guinea-pig, 1.0 mg/kg b.w. (corn oil)
Rabbit 1.3 mg/kg b.w. (propylene
glycol)
formulated product, Rat (M), 0.81 mg/kg b.w. (50% W.P.,
water)
Rat (M), 0.67-1.23 mg/kg b.w. (50% W.P.,
corn oil)
Rat (M), 7.07 mg/kg b.w. (10% on
gypsum,
neat)
Rat (M), 7.9 mg/kg b.w. (5.5% with
fungicides,
corn oil)
Rat (F), 0.62 mg/kg b.w. (50% W.P.,
water)
Rat (F), 0.77-1.07 mg/kg b.w. (50% W.P.,
corn oil)
Rat (F), 6.7 mg/kg b.w. (5.5% with
fungicides,
corn oil)
Rabbit (F), 7.9-17.8 mg/kg b.w. (10% on
gypsum,
neat)
Rabbit (F), 5.3-10.6 mg/kg b.w. (15% on
gypsum,
neat)
Rabbit (F), 8.4 mg/kg b.w. (15% on corn
cob grits,
neat)
Dermal LD50:
technical material, Rat (M), 38.1-44.9 mg/kg b.w. (water)
Rat (M), >10 mg/kg b.w. (corn oil)
Rat (M), 3.2-7.0 mg/kg b.w. (DMP)
Rabbit (M), 144-200 mg/kg b.w. (corn oil)
Rabbit (M), 20 mg/kg b.w. (water)
Rabbit (M), 5.0 mg/kg b.w. (propylene
glycol)
Rabbit (M), 10.0 mg/kg b.w. (corn oil)
Guinea-pig (M), 24.0 mg/kg b.w. (organic
solvent)
formulated product, Rat (M,F), 2100-5000 mg/kg b.w. (10% gypsum,
dry)
Rat (M,F), 283- 673 mg/kg b.w. (10% gypsum,
water)
Rat (M,F), 1980-6320 mg/kg b.w. (15% gypsum,
dry)
Rat (M,F), 283-1010 mg/kg b.w. (15% gypsum,
water)
Rabbit (M), 4800 mg/kg b.w. (10-15%
gypsum, dry)
Rabbit (M,F), 2000 mg/kg b.w. (5.5% with
fungicide,
neat)
Intraperitoneal LD50:
technical material, Rat (M,F), 0.44-7.1 mg/kg b.w. (corn oil)
Rat (M), 0.28-0.44 mg/kg b.w. (PEG 400)
Rat (M), 0.57 mg/kg b.w. (ethanol)
Mouse (F), 0.3 mg/kg b.w. (cotton seed
oil)
Intravenous LD50:
technical material, Rat (M), 0.47 mg/kg b.w. (water)
Inhalation - Aldicarb does not produce toxic fumes, all test rats
survived an eight-hour exposure to aldicarb granules (no direct
contact) showing no acute or delayed ill effects. Inhalation of
aldicarb dust has been shown to be lethal at high concentrations
or with prolonged exposure to low levels. All test rats, mice
and guinea-pigs died from exposure to 200 mg/m3 for five minutes,
five of six female rats died from exposure, to 6.7 mg,/m3 for 30
minutes whereas all test animals survived 15 minutes of 6.7 mg/m3
of aldicarb dust. See section 2.2.1.
2.1.5 Toxicity, repeated doses
Oral - See sections 2.1.6 and 2.1.7.
Dermal - Aldicarb applied to male rabbits on abraded skin, with
moist dressings for six hours a day in a three-week study
produced reduced body weight gains and clinical signs of toxicity
at the lowest dose (5(mg/kg b.w.)/day) and depressed plasma
cholinesterase activity at the two highest doses only (10 and
20(mg/kgb.w.)/day). There were no mortalities, and no
histopathologic or haematologic signs of toxicity. Adverse
effects were rapidly reversed when the treatment stopped.
Aldicarb similarly applied to non-abraded skin with dry dressings
produced no adverse effects at 20 mg/kg b.w.
Dermal irritation and sensitization - Aldicarb applied to shaved
intact skin of rabbits produced no signs of irritation at the 20
mg/kg level of treatment. Wet preparations were absorbed more
readily than dry preparations but they were not more effective.
Multiple subdermal applications of 0.7 mg/kg b.w. did not
sensitize the animals.
Cumulation of compound - Aldicarb does not acclumulate in body
tissues, it is rapidly metabolized rnd excreted.
Cumulation of effect - Repeated exposure to sublethal amounts
does not produce a cumulation effect.
2.1.6 Dietary studies
Short-term - In several studies male and female rats were fed
aldicarb in diets for one week at dose levels ranging from 0.3 to
16.0 mg/kg b.w. Treatment related mortality was 100% and 40%
among males and females respectively at the 16.0 mg/kg level and
20% of the females only, at 8.0 mg/kg b.w. Growth rates were
depressed in both sexes at 3.2 mg/kg and above. There were
treatment related depressions gross organ weights and organ to
body weight ratios in both males and females at 1.6 mg/kg and
above. Plasma and erythrocyte cholinesterase activities were
depressed at 1.5 mg/kg and above in both sexes.
In several studies of one week to six months duration, aldicarb
sulfoxide and sulfone were fed to rats of both sexes at dosage
levels of 0.4-1.6 mg/kg b.w. and 0.4-20.0 mg/kg b.w.
respectively. There were no treatment related deaths, changes in
gross organ weights or organ to body weight ratios. The
sulfoxide metabolite significantly reduced growth at 0.8 mg/kg
b.w. and above in both sexes, the sulfone at 5.0 mg/kg and above
in males and, 0.6 mg/kg and above in females. The sulfoxide
depressed plasma and erythrocyte cholinesterase activity at 0.8
mg/kg level, the sulfone at 5.0 mg/kg and above. Brain
cholinesterase activity was depressed by sulfone at 20 mg/kg b.w.
The rat no-adverse-effect dose of aldicarb was estimated to be
0.125 (mg/kg)/day.
Mice fed dietary aldicarb at dosage levels ranging from 0.1 to
1.2 mg/kg b.w. for seven days showed no treatment related signs
of toxicity among the survivors, treatment related mortalities
occurred at the 1.2 mg/kg level only. Mice fed a 1:1 ratio of
aldicarb and aldicarb sulfone at dose levels from 2 to 36 mg/kg
b.w. showed no treatment related mortality. Growth rates were
depressed in both sexes at 18 and 36 mg/kg levels, liver weights
were lower in males at 18 and 36 mg/kg and in females at the 36
mg/kg dose, kidney weights were depressed in both sexes at 36
mg/kg dose. Male mice showed severe cholinergic signs at the 36
mg/kg level.
No adverse effects were observed in male and female beagles fed
aldicarb in diets at dosage levels of 0.2, 0.3 and 0.7 mg/kg b.w.
for seven-day and 100-day studies. In both studies the animals
were returned to the control diet for 24 hours at the end of the
study, therefore no useful cholinesterase information was
obtained. Beagles fed sulfoxide and sulfone metabolites at diet
dosage levels of 0.0625-0.5 mg/kg and 0.2-5.4 mg/kg respectively
showed no ill-effects attributable to treatment.
Long-term - No significant treatment related ill-effects were
observed in several two-year studies of rats fed aldicarb in
diets at dose levels of 0.005-0.3 mg/kg b.w.
No significant treatment related ill-effects were observed in
two-year studies of dogs on diets containing aldicarb at 0.025,
0.05 and 0.1 mg/kg b.w. dose levels.
In a two-year study of mice fed aldicarb in the diet at dosages
of 0.10 and 0.30 mg/kg b.w., no adverse effects were observed.
In a similar mouse study mortalities occurred among the males at
the 0.4 mg/kg dose and above, among the females at the 0.2 mg/kg
dose and above.
In CD-1 mice fed aldicarb at 0.7 mg/kg b.w. for 18 months, the
incidence of hepatomas among the surviving treated males was
significantly higher than among the surviving controls or the
dead males. Among the treated dead males the increase of lymphoid
neoplasms was significant. However, the incidence of both
hepatomas and lymphoid neoplasms among controls was unusually
high and in a similar follow-up study there was no significant
increase in carcinogenic response among the treated animals.
2.1.7 Supplementary studies of toxicity
Carcinogenicity - Aldicarb is classified as a tumorogen with no
carcinogenic potential (NCI-GI-TR-136, 7-). In the dietary
studies described in section 2.1.6 neither aldicarb nor its
metabolites were implicated in the development of neoplastic
lesions. It was also found to be carcinogenically negative in a
transplacental host-mediated hamster cell culture assay and a
mouse dermal application study.
Nitrosoaldicarb on the other hand, was found to be strongly
carcinogenic in rats following oral administration of cumulative
doses of 40 mg/kg b.w. over two weeks and 90 mg/kg b.w. over nine
weeks. It produced carcinoma and/or benign tumours of the non-
glandular stomach tissue of all survivors. It was also active in
a transplacental host-mediated hamster cell culture assay. There
is no evidence that the n-nitrosamide derivative of aldicarb is a
naturally occurring product.
Teratogenicity - No evidence of teratogenicity was presented in
the literature surveyed. Aldicarb injected into hen's eggs at a
dose of 1.0 mg/egg produced no teratogenic effects. Aldicarb
given to pregnant rats at doses of 0.4-1.0 mg/kg b.w. for the
duration of pregnancy, for the first seven days, or from day five
to day 15 produced no changes in the standard indices of
reproductive behaviour or performance and no teratogenic
manifestations in the pups.
Mutagenicity - No evidence of mutagenicity was presented in the
literature surveyed. Aldicarb was found to be a weak mutagen in
only one of several microbial pre-screening tests for
mutagenicity, in all other tests it was negative. It was also
found to be negative in two DNA alteration tests with human skin
fibroblast cultures; in an ICR mouse micronucleus assay; and, in
a rat dominant lethal study. Metabolism of aldicarb by rat liver
microsomal enzyme systems did not activate aldicarb mutagenicity.
Reproduction - No evidence of modifaction of reproductive
behaviour or performance was presented in the literature
surveyed. (See also the sections above.) Single oral doses of
aldicarb as low as 1.0 µg/kg b.w. given to pregnant rabbits on
day 18 of gestation had a greater effect on the foetuses than the
dams. Foetal blood cholinesterase activity was significantly
decreased by aldicarb, there was evidence of a rapid and
prolonged placental transfer of the compound and/or its
metabolites. Foetal brain cholinesterase activity was depressed
at the 100 µg/kg level. In a three-generation study, rats fed
1.0 and 2.0 mg/kg diets for 90 days showed no treatment-related
adverse changes in standard reproduction indices when mated.
There were no observed treatment-related adverse changes in
standard reproductive indices or in gross and microscopic
abnormalities in the pups. In another three-generation study,
rats fed 4, 6 and 14 mg/kg diets for 100 days prior to mating
showed no ill-effects of treatment save a significant decrease in
growth rate at the highest dose. There were no observed
treatment-related adverse changes in standard reproductive
indices, gross or microscopic abnormalities in the foetuses.
Neurotoxicity - No ataxia, hind limb paralysis or delayed
neurotoxicity was observed in hens given a single dose of
aldicarb (45 mg/kg b.w.) or, in the diet (0, 2.25 and 4.5
mg/kg b.w.) for 30 days. A positive control study (TOCP)
was carried out for comparison. In the dietary study, a dose-
related weight loss occurred and acute clinical signs of toxicity
were observed on days 2 and 3 of treatment.
Behaviour - In a study of rats trained and evaluated in standard
avoidance tests, the lowest behaviourally effective aldicarb dose
was found to be 0.266 mg/kg b.w. (i.p.) suggesting that the level
required to produce significant alteration in behaviour is close
to the fatal dose and unlikely to be achieved in suggested use
patterns.
2.1.8 Modifications of toxicity - Aldicarb showed no synergistic
effects when used in combination with a number of
organophosphorus pesticides.
2.2 TOXICOLOGY - MAN
2.2.1 Absorption route - Aldicarb may be absorbed from the
gastrointestinal tract; through moist, intact skin; and by
inhalation of dust.
2.2.2 Dangerous doses
Single - The lowest lethal dose of aldicarb is unknown. However,
human volunteer studies indicate that an oral dose of 0.1 mg/kg
b.w. will induce mild, transient clinical signs of toxicity, 0.26
mg produced acute poisoning requiring atropine treatment.
Repeated - No published information available.
2.2.3 Observations of occupationally exposed workers - There has been
only one reported fatality involving aldicarb since its
introduction. A field worker in California became ill after a
day's work in fields treated with aldicarb and an organophosphate
pesticide; he died en route to the hospital.
Between 1966 and 1982 over 108 incidences of confirmed and/or
suspected aldicarb poisonings were reported in the literature.
Illnesses resulting from exposure during loading, application and
handling of treated plants and soils were the result of gross
misuse of the product. Carelessness, failure to wear protective
clothing or premature entrance into the treated areas were the
causes cited in most incidents. Most cases involved systemic
illness, some with skin or eye irritation. The signs and symptoms
were cholinergic and recovery was rapid when the symptomatic
patients vere treated with atropine. Blood cholinesterase was
depressed and toxic degradation products were detected in urine.
There were no reports of chronic effects.
2.2.4 Observations on exposure of the general public - See section
2.2.6. With good agricultural practices exposure of the general
public to harmful quantities of aldicarb is unlikely.
2.2.5 Observations of volunteers - Male volunteers were given an
aqueous solution of aldicarb orally at dose levels of 0.025,
0.05, 0.1, and 0.25 mg/kg b.w. Acute signs of toxicity were
observed at the two highest doses one hour after administration,
blood cholinesterase activity was depressed at all dose levels.
The clinical and cholinesterase effects diminished within six
hours of atropine treatment. Approximately 10% of the dose was
excreted in the urine within eight hours of administration, toxic
residues were present.
2.2.6 Reported mishaps - A report of two episodes of aldicarb poisoning
a year apart, in a small community in Nebraska, United States of
America, demonstrates the difficulties encountered in successful
diagnosis and etiologic investigation. Each incident of
poisoning immediately followed ingestion of locally grown
hydroponic cucumbers. Although collectively the clinical signs
and symptoms were typically cholinergic, their similarity to
those of influenza and food allergy reaction led to incorrect
diagnoses in some cases. Neither vomitus nor urine were analysed
for toxicity potential or metabolite content. Also, although the
rapid onset and recovery patterns suggested an anticholinesterase
agent, the time lapse between onset of illness and blood analysis
precluded finding cholinesterase depression. It was this absence
of cholinesterase depression in a total review of clinical
evidence that eventually indicated carbamate involvement. The
suspect cucumbers had been either completely consumed or the
remaining portions were too small and aged to permit specific
identification. However, aldicarb was found in the water and
gravel (1.8 mg/l and 0.6 mg/kg respectively), of the hydroponic
system, and in cucumbers (6.6-0.7 mg/kg), produced in that
system. The contamination was deemed to be accidental and
represents a gross misuse of the product.
2.3 TOXICITY TO NON-MAMMALIAN SPECIES
2.3.1 Fish - Toxic to fish.
LC50: (24 h) Channel catfish, 1.6 mg/l
(96 h) Rainbow trout, 8.8 mg/l
The sequence of toxic signs is hyperactivity, lethargy, body
paralysis, scoliosis, loss of equilibrium, opercular and mouth
paralysis followed by death.
2.3.2 Birds - Toxic to birds.
Oral LD50: Peking duck, 3.4 mg/kg b.w.
Japanese quail, 6.0 mg/kg b.w.
Domestic hen, 9.0 mg/kg b.w.
Pigeon, 12.5 mg/kg b.w.
Pheasant, 15.2 mg/kg b.w.
Dietary LD50: Bob-white quail, 2400 mg/kg diet of seven days
duration.
3. FOR REGULATORY AUTHORITIES - RECOMMENDATIONS ON REGUIATION OF
COMPOUND
3.1 RECOMMENDED RESTRICTIONS ON AVAIIABILITY (For definition of
categories, see the Introduction to Data Sheets) - Only granular
formulations are available. All formulations are placed in
Category 2.
3.2 TRANSPORTATION AND STORAGE
Formulations in Category 2 - Should be transported or stored in
clearly labelled containers and away from containers of food and
drink. Storage should be under lock and key and secure from
access by unauthorized persons and children.
3.3 HANDLING
Fomulations in Category 2 - Protective clothing (see part 4)
should be provided for workers. 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 OF CONTAINER - Do not reuse containers. Container must
be either burned or buried below topsoil. Care must be taken to
avoid subsequent contamination of water sources.
3.5 SELECTION, TRAINING AND MEDICAL SUPERVISION OF WORKERS
Formulations in Category 2 - Pre-employment medical examination
for workers desirable. Workers suffering from active hepatic or
renal diseases should be excluded from contact. Pre-employment
and periodic cholinesterase tests for workers desirable. Training
of workers in techniques to avoid contact is essential.
3.6 ADDITIONAL REGULATIONS RECOMMENDED IF DISTRIBUTED BY AIRCRAFT -
Not to be applied by aircraft.
3.7 LABELLING - "DANGER - POISON" (skull and cross bones insignia).
Precautionary statements - Hazard to Humans and Domestic Animals.
- Poisonous if swallowed. May be fatal or harmful by skin or eye
contact or by breathing dust. Rapidly absorbed through skin or
eyes. Do not get on skin or eyes. Do not breathe dust. Antidote
is atropine sulfate. See statement of practical treatment and
other detailed warnings on the package. Read the entire label
before using this pesticide. Wear long-sleeved clothing and
protective gloves when handling. Wash hands and face before
eating or smoking. Bathe at the end of work day, washing entire
body and hair with soap and water. Change contaminated clothing
daily and wash in strong washing soda solution and rinse
thoroughly before reusing.
3.8 RESIDUES IN FOOD - Maximum residue levels have been recommended by
the joint FAO/WHO Meeting on Pesticide Residues.
4. PREVENTION OF POISONING IN MAN AND EMERGENCY AID
4.1 PRECAUTIONS IN USE
4.1.1 General - Aldicarb is a carbamate insecticide of extremely high
acute toxicity which is quickly metabolized and therefore acts
only as an acute poison. It can be absorbed by inhalation of the
dust and also through the intact skin. It is important that
formulations be washed immediately from the skin and eyes.
4.1.2 Manufacture and formulation - Aldicarb is available only as a
formulated product. The manufacturer does not sell concentrates
for formulation.
4.1.3 Applicators - When opening the container, care should be taken to
avoid contact with the mouth, eyes and skin. If necessary a
facial visor and gloves should be worn. The applicator should
avoid contact with the mouth, eyes and skin. Granules must be
washed immediately from the skin or eyes with large quantities of
water. Before eating, drinking or smoking, hands and other
exposed skin should be washed.
4.1.4 Other associated workers - Persons exposed to aldicarb and
associated with its application should observe the precautions
described in 4.1.3 under "applicators".
4.1.5 Other populations likely to be affected - With correct use in
agriculture, the general population should not be exposed to
hazardous amounts of aldicarb.
4.2 ENTRY OF PERSONS INTO TREATED AREAS - No re-entry restrictions
have been established for agricultural uses.
4.3 DISPOSAL OF SPILLAGE - If a container is broken, handle with
rubber gloves. Do not get dust or granules on the skin or in the
eyes. Do not breathe dust. Sweep up and bury any small spills or
excess aldicarb formulation at least 45 cm deep in the soil
isolated from water supplies and food crops. Spillage of aldicarb
formulations should be removed by cleaning up granules, 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 symptoms may include
excessive sweating, headache, weakness, nausea, vomiting, stomach
pains, salivation, tightness of the chest, blurred vision,
slurred speech and muscle twitching.
4.4.2 Treatment before a person is seen by a physician, if these
symptoms appear following exposure - The person should stop work
immediately, remove contaminated clothing, wash the affected skin
with soap and water if available, and flush the area with large
quantities of water. If swallowed, vomiting should be induced if
the person is conscious.
5. FOR MEDICAL AND LABORATORY PERSONNEL
5.1 MEDICAL DIAGNOSIS AND TREATMENT IN CASES OF POISONING
5.1.1 General information - Aldicarb is a carbamate insecticide of
extremely high toxicity. It is absorbed from the
gastrointestinal tract and through the intact skin. Its mode of
action is by reversibly inhibiting acetyl cholinesterase.
Erythrocyte cholinesterase is more inhibited than plasma
cholinesterase. Symptoms of poisoning are short lasting and in
the case of occupational overexposure, occur without delay at a
dose well below the fatal dose. Because of its rapid metabolism
and excretion it does not accumulate in the tissues.
5.1.2 Symptoms and signs - Symptoms of poisoning include excessive
sweating, headache, chest tightness, weakness, nausea, vomiting,
stomach pains, salivation, blurred vision, slurred speech, and
muscle twitching. Paraesthesia and mild skin reaction have also
been reported.
5.1.3 Laboratory - Because aldicarb is a reversible inhibitor of
cholinesterase, measurements of cholinesterase activity should be
made by a method which minimizes the reactivation of inhibited
enzyme.
Erythrocyte cholinesterase determination is more informative than
measuring either plasma or whole blood cholinesterase, but the
enzyme will only be inhibited for a short time (few hours) after
exposure. The presence of metabolites of aldicarb in urine is
also indicative of exposure.
5.1.4 Treatment and information for physician - This product is a
carbamate pesticide containing 2-methyl-2-
(methylthio)propionaldehyde O-(methyl-carbamoyl)oxime. It is a
spontaneously reversible cholinesterase inhibitor causing
parasympathetic nerve stimulation. Preferred treatment of
poisoning in adults is atropine sulfate given intravenously. As
much as 2-4 mg may be needed every 10-12 minutes until the
patient is fully atropinized. Dosage for children is
appropriately reduced. Atropinization should be maintained for
12 hours by intramuscular administration of atropine in lower
doses given at appropriate time intervals. Do not administer
opiates or cholinesterase inhibiting drugs. Artificial
respiration or oxygen may be necessary. Observe the patient
continuously for at least 24 hours. Allow no further exposure to
any cholinesterase inhibitors until cholinesterase level is
normal by blood test.
5.1.5 Prognosis - If the acute effects are survived, the chances of
complete recovery are very good.
5.1.6 References of previously reported cases
Goses, E. A. et al. (1980) American Jour. Epidemiology, 111 (2),
254. Peoples, S. A. et al. (1978) Calif. Dept. Food Agric. Sci.
Rep., pp. 321-324
5.2 SURVEILLANCE TESTS - Due to the rapid reactivation of inhibited
enzyme, determination of blood cholinesterase level is of little
if any practical value in detemining when workers should be
withdrawn to prevent overexposure. Minor complaints, such as
headache and nausea, cause the worker to stop work and thus
prevent further overexposure. The worker quickly recovers,
particularly if appropriate decontamination procedures are
followed.
5.3 LABORATORY METHODS
5.3.1 Detection and assay of compound - Aaronson, M. J. et al. (1980)
Jour. Food Safety, 2, 171. Davies, R. D. (1979) Jour. of
Chromatography, 1970, 453. Galoux, M. (1979) Jour. of
Chromatography, 177, 245. Johnson, D. P. et al. (1966) J. Assoc.
Off. Anal. Chem., 49, 399. Lee, D. F. & Rougham, J. A. (1971)
Analyst (London), 96, 798. Maitland, J. C. et al. (1968) J.
Agric. Food Chem., 16, 549. Romine, R. R. et al. (1973) Anal.
Methods Pestic. Plant Growth Regul., 7. 143. Tewari, S. N. &
Singh, R. (1979) Jour. of Chromatography, 1972, 528. Tewari, S.
N. & Singh, R. (1979) Fresenius Z. Anal. Chem., 294, 287.
Woodham, D. W. et al. (1973) J. Agric. Food Chem., 21 (4), 604.
5.3.2 Other tests in cases of poisoning - Cholinesterase levels in
blood are unreliable as a routine test to detect poisoning by
aldicarb. However, shortly after absorption, inhibition of
erythrocyte cholinesterase may be demonstrated by an appropriate
method. Plasma cholinesterase activity: Ellman, G. L. et al.
(1969) Biochem. Pharmacol., 7, 88.
Whole blood cholinesterase activity: Fleischer, J. et al. (1956)
Arch. Indust. Hyg., 14, 510; Wilhelm, K. et al. (1973) Bull.
Wld Hlth Orig., 48, 235
Note: This data sheet was drafted in the Bureau of Chemical Standards,
Environmental Health Directorate, Health and Welfare, Canada, and
subsequently underwent medical, scientific, and industrial review.
See Also:
Aldicarb (EHC 121, 1991)
Aldicarb (IARC Summary & Evaluation, Volume 53, 1991)
Aldicarb (ICSC)