INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY
ENVIRONMENTAL HEALTH CRITERIA 121
This report contains the collective views of an international group of
experts and does not necessarily represent the decisions or the stated
policy of the United Nations Environment Programme, the International
Labour Organisation, or the World Health Organization.
Published under the joint sponsorship of
the United Nations Environment Programme,
the International Labour Organisation,
and the World Health Organization
First draft prepared by Dr. J. Risher and Dr. H. Choudhury,
US Environmental Protection Agency,
Cincinnati, Ohio, USA
World Health Orgnization
The International Programme on Chemical Safety (IPCS) is a
joint venture of the United Nations Environment Programme, the
International Labour Organisation, and the World Health
Organization. The main objective of the IPCS is to carry out and
disseminate evaluations of the effects of chemicals on human health
and the quality of the environment. Supporting activities include
the development of epidemiological, experimental laboratory, and
risk-assessment methods that could produce internationally
comparable results, and the development of manpower in the field of
toxicology. Other activities carried out by the IPCS include the
development of know-how for coping with chemical accidents,
coordination of laboratory testing and epidemiological studies, and
promotion of research on the mechanisms of the biological action of
WHO Library Cataloguing in Publication Data
(Environmental health criteria ; 121)
1.Aldicarb - adverse effects 2.Aldicarb - toxicity 3.Environmental
exposure 4.Environmental pollutants I.Series
ISBN 92 4 157121 7 (NLM Classification: WA 240)
The World Health Organization welcomes requests for permission
to reproduce or translate its publications, in part or in full.
Applications and enquiries should be addressed to the Office of
Publications, World Health Organization, Geneva, Switzerland, which
will be glad to provide the latest information on any changes made
to the text, plans for new editions, and reprints and translations
(c) World Health Organization 1991
Publications of the World Health Organization enjoy copyright
protection in accordance with the provisions of Protocol 2 of the
Universal Copyright Convention. All rights reserved.
The designations employed and the presentation of the material
in this publication do not imply the expression of any opinion
whatsoever on the part of the Secretariat of the World Health
Organization concerning the legal status of any country, territory,
city or area or of its authorities, or concerning the delimitation
of its frontiers or boundaries.
The mention of specific companies or of certain manufacturers'
products does not imply that they are endorsed or recommended by the
World Health Organization in preference to others of a similar
nature that are not mentioned. Errors and omissions excepted, the
names of proprietary products are distinguished by initial capital
ENVIRONMENTAL HEALTH CRITERIA FOR ALDICARB
1.1. Identity, properties, and analytical methods
1.2. Uses, sources, and levels of exposure
1.3. Kinetics and metabolism
1.4. Studies on experimental animals
1.5. Effects on humans
2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, AND ANALYTICAL
2.2. Physical and chemical properties
2.3. Conversion factors
2.4. Analytical methods
3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE
3.1. Natural occurrence
3.2. Anthropogenic sources
3.2.1. Production levels, processes, and uses
126.96.36.199World production figures
4. ENVIRONMENTAL TRANSPORT, DISTRIBUTION, AND TRANSFORMATION
4.1. Transport and distribution between media
4.1.2. Water and soil
4.1.3. Vegetation and wildlife
4.3. Interaction with other physical, chemical or biological
4.3.1. Soil microorganisms
5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE
5.1. Environmental levels
5.1.3. Food and feed
5.2. General population exposure
5.3. Occupational exposure during manufacture, formulation
6. KINETICS AND METABOLISM
6.3. Metabolic transformation
6.4. Elimination and excretion in expired air, faeces, and
7. EFFECTS ON LABORATORY MAMMALS AND IN VITRO TEST SYSTEMS
7.1. Single exposure
7.2. Short-term exposure
7.3. Skin and eye irritation; sensitization
7.4. Long-term exposure
7.5. Reproduction, embryotoxicity, and teratogenicity
7.6. Mutagenicity and related end-points
7.8. Other special studies
7.9. Factors modifying toxicity; toxicity of metabolites
7.10. Mechanisms of toxicity - mode of action
8. EFFECTS ON HUMANS
8.1. General population exposure
8.1.1. Acute toxicity; poisoning incidents
8.1.2. Human studies
8.1.3. Epidemiological studies
8.2. Occupational exposure
8.2.1. Acute toxicity; poisoning incidents
8.2.2. Effects of short- and long-term exposure;
9. EFFECTS ON OTHER ORGANISMS IN THE LABORATORY AND FIELD
9.2. Aquatic organisms
9.3. Terrestrial organisms
9.4. Population and ecosystem effects
10. EVALUATION OF HUMAN HEALTH RISKS AND EFFECTS ON THE
10.1. Evaluation of human health risks
10.1.1. Exposure levels
10.1.1.1 General population
10.1.1.2 Occupational exposure
10.1.2. Toxic effects
10.1.3. Risk evaluation
10.2. Evaluation of effects on the environment
11. CONCLUSIONS AND RECOMMENDATIONS
11.1.1. General population
11.1.2. Occupational exposure
11.1.3. Environmental effects
12. FURTHER RESEARCH
13. PREVIOUS EVALUATIONS BY INTERNATIONAL BODIES
EVALUATION DES RISQUES POUR LA SANTE HUMAINE ET DES EFFETS
CONCLUSIONS ET RECOMMENDATIONS
RECHERCHES A EFFECTUER
EVALUACION DE LOS RIESGOS PARA LA SALUD HUMANA Y DE LOS
EFFECTOS EN EL MEDIO AMBIENTE
CONCLUSIONES Y RECOMENDACIONES
WHO TASK GROUP ON ENVIRONMENTAL HEALTH CRITERIA FOR ALDICARB
Dr I. Boyer, The Mitre Corporation, McLean, Virginia, USA
Dr G. Burin, Health Effects Division, Office of Pesticide
Programs, US Environmental Protection Agency, Washington, DC, USA
Dr S. Dobson, Institute of Terrestrial Ecology, Monks Wood
Experimental Station, Abbots Ripton, Huntingdon, United Kingdom
Professor W. J. Hayes, Jr., School of Medicine, Vanderbilt
University, Nashville, Tennessee, USA (Chairman)
Professor F. Kaloyanova, Institute of Hygiene and
Occupational Health, Medical Academy, Sofia, Bulgaria
Dr S. K. Kashyap, National Institute of Occupational
Health, Indian Council of Medical Research, Meghani Nagar,
Dr H. P. Misra, University Center for Toxicology, Virginia
Polytechnic Institute and State University, Blacksburg, Virginia,
Mr D. Renshaw, Department of Health, Hannibal House,
London, United Kingdom
Dr J. Withey, Environmental & Occupational Toxicology
Division, Environmental Health Center, Tunney's Pasture, Ottawa,
Dr Shou-zheng Xue, School of Public Health, Shanghai
Medical University, Shanghai, China
Representatives of other organizations
Dr L. Hodges, International Group of National Associations
of Manufacturers of Agrochemical Products (GIFAP), Brussels,
Dr J. M. Charles, International Group of National
Associations of Manufacturers of Agrochemical Products (GIFAP),
Dr B. H. Chen, International Programme on Chemical Safety,
World Health Organization, Geneva, Switzerland (Secretary)
Dr H. Choudhury, Environmental Criteria and Assessment
Office, US Environmental Protection Agency, Cincinnati, Ohio, USA
Dr P. G. Jenkins, International Programme on Chemical
Safety, World Health Organization, Geneva, Switzerland
NOTE TO READERS OF THE CRITERIA MONOGRAPHS
Every effort has been made to present information in the criteria
documents as accurately as possible without unduly delaying their
publication. In the interest of all users of the environmental health
criteria monographs, readers are kindly requested to communicate any
errors that may have occurred to the Manager of the International
Programme on Chemical Safety, World Health Organization, Geneva,
Switzerland, in order that they may be included in corrigenda, which
will appear in subsequent volumes.
* * *
A detailed data profile and a legal file can be obtained from the
International Register of Potentially Toxic Chemicals, Palais des
Nations, 1211 Geneva 10, Switzerland (Telephone No. 7988400 or
ENVIRONMENTAL HEALTH CRITERIA FOR ALDICARB
A WHO Task Group on Environmental Health Criteria for Aldicarb
met in Cincinnati, USA, from 6 to 10 August 1990. Dr C. DeRosa opened
the meeting on behalf of the US Environmental Protection Agency. Dr
B.H. Chen of the International Programme on Chemical Safety (IPCS)
welcomed the participants on behalf of the Manager, IPCS, and the
three IPCS cooperating organizations (UNEP/ILO/ WHO). The Task Group
reviewed and revised the draft criteria monograph and made an
evaluation of the risks for human health and the environment from
exposure to aldicarb.
The first draft of this monograph was prepared by Dr J. Risher
and Dr H. Choudhury of the US Environmental Protection Agency. The
second draft was prepared by Dr H. Choudhury incorporating comments
received following the circulation of the first draft to the IPCS
Contact Points for Environmental Health Criteria documents. During the
Task Group meeting all the participants contributed to review the
large amount of information submitted by Rhône-Poulenc, and undertook
a substantial revision of the second draft. Dr B.H. Chen and Dr P.G.
Jenkins, both members of the IPCS Central Unit, were responsible for
the overall scientific content and technical editing, respectively.
The efforts of all who helped in the preparation and finalization
of the document are gratefully acknowledged. The Secretariat wishes to
thank Dr S. Dobson and Dr G. Burin for the significant contributions
and revisions of the draft document during the meeting.
Financial support for the meeting was provided by the US
Environmental Protection Agency, Cincinnati, USA.
ADI acceptable daily intake
ai active ingredient
CHO Chinese hamster ovary
FAD flavin adenine dinucleotide
FPD flame photometric detector
GC gas chromatography
GPC gel permeation chromatography
HPLC high-performance liquid chromatography
LC liquid chromatography
MATC maximum acceptable toxic concentration
MS mass spectroscopy
NADPH reduced nicotinamide adenine dinucleotide phosphate
NOEL no-observed-effect level
TLC thin-layer chromatography
1.1 Identity, properties, and analytical methods
Aldicarb is a carbamate ester. It is a white crystal-line solid,
moderately soluble in water, and susceptible to oxidation and
Several different analytical methods, including thin-layer
chromatography, gas chromatography (electron capture, flame
ionization, etc.), and liquid chromatography, are available. The
currently preferred method for analysing aldicarb and its major
decomposition products is high-performance liquid chromatography with
post-column derivatization and fluorescence detectors.
1.2 Uses, sources, and levels of exposure
Aldicarb is a systemic pesticide that is applied to the soil to
control certain insects, mites, and nematodes. The soil application
includes a wide range of crops, such as bananas, cotton, coffee,
maize, onions, citrus fruits, beans (dried), pecans, potatoes,
peanuts, soybeans, sugar beets, sugar cane, sweet potatoes, sorghum,
tobacco, as well as ornamental plants and tree nurseries. Exposure of
the general population to aldicarb and its toxic metabolites (the
sulfoxide and sulfone) occurs mainly through food. The ingestion of
contaminated food has led to poisoning incidents from aldicarb and its
toxic metabolites (the sulfoxide and sulfone).
Due to the high acute toxicity of aldicarb, both inhalation and
skin contact under occupational exposure conditions may be dangerous
for workers if preventive measures are inadequate. There have been a
few incidents of accidental exposure of workers due to improper use or
lack of protective measures.
Aldicarb is oxidized fairly rapidly to the sulfoxide, 48%
conversion of parent compound to sulfoxide occurring within 7 days
after application to certain types of soils. It is oxidized much more
slowly to the sulfone. Hydrolysis of the carbamate ester group, which
inactivates the pesticide, is ph dependent, half-lives in distilled
water varying from a few minutes at a pH of > 12 to 560 days at a pH
of 6.0. Half-lives in surface soils are approximately 0.5 to 3 months
and in the saturated zone from 0.4 to 36 months Aldicarb hydrolyses
somewhat more slowly than either the sulfoxide or the sulfone.
Laboratory measurement of the biotic and abiotic breakdown of aldicarb
have yielded very variable results and have led to extrapolations
radically different from field observation. Field data on the
breakdown products of aldicarb furnish more reliable estimates of its
Sandy soils with low organic matter content allow the greatest
leaching, particularly where the water table is high. Drainage
aquifers and local shallow wells have been contaminated with aldicarb
sulfoxide and sulfone; levels have generally ranged between 1 and
50µg/litre, although an occasional level of approximately 500 µg/litre
has been recorded.
As aldicarb is systemic in plants, residues may occur in foods.
Residue levels greater than 1 mg/kg have been reported in raw
potatoes. In the USA, where the tolerance limit for potatoes is 1
mg/kg, residue levels of up to 0.82 mg/kg have been reported from
controlled field trials using application rates recommended by the
manufacturer. An upper 95th percentile level of 0.43 mg/kg has been
estimated from field trial data, and upper 95th percentile levels of
up to 0.0677 mg/kg in raw potatoes have been determined from a
1.3 Kinetics and metabolism
Aldicarb is efficiently absorbed from the gastrointestinal tract
and, to a lesser extent, through the skin. It could be readily
absorbed by the respiratory tract if dust were present. It distributes
to all tissues, including those of the developing rat fetus. It is
metabolically transformed to the sulfoxide and the sulfone (both of
which are toxic), and is detoxified by hydrolysis to oximes and
nitriles. The excretion of aldicarb and its metabolites is rapid and
primarily via the urine. A minor part is also subject to biliary
elimination and, consequently, to enterohepatic recycling. Aldicarb
does not accumulate in the body as a result of long-term exposure. The
inhibition of cholinesterase activity in vitro by aldicarb is
spontaneously reversible, the half-life being 30-40 min.
1.4 Studies on experimental animals
Aldicarb is a potent inhibitor of cholinesterases and has a high
acute toxicity. Recovery from its cholinergic effects is spontaneous
and complete within 6 h, unless death intervenes. There is no
substantial evidence to indicate that aldicarb is teratogenic,
mutagenic, carcinogenic, or immunotoxic.
Birds and small mammals have been killed as a result of ingesting
aldicarb granules not fully incorporated into the soil as recommended.
In laboratory tests, aldicarb is acutely toxic to aquatic organisms.
There is no indication, however, that effects would occur in the
1.5 Effects on humans
The inhibition of acetylcholinesterase at the nervous synapse and
myoneural junction is the only recognized effect of aldicarb in humans
and is similar to the action of organophosphates. The carbamyolated
enzyme is unstable, and spontaneous reactivation is relatively rapid
compared with that of a phosphorylated enzyme. Non-fatal poisoning in
man is rapidly reversible. Recovery is aided by the administration of
2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, AND ANALYTICAL METHODS
Common name: Aldicarb
CH3S - C - CH = N - OCNHCH3
Molecular formula: C7H14N2O2S
Synonyms and Aldicarb (English); Aldicarbe (French);
common trade Carbanolate; ENT 27 093; 2-methyl-2-
NCI-CO8640; OMS-771; Propanal,
Temik; Temik G; Temik M; Temik LD; Sentry;
Temik 5G; Temik 10G; Temik 15G; Temik 150G;
Union Carbide UC 21 149.
RTECS no. UE2275000.
2.2 Physical and chemical properties
Some physical and chemical properties of aldicarb are given in
Aldicarb, for which the IUPAC name is
2-methyl-2-(methylthio)propionaldehyde O-methylcarbamoyloxime, is an
oxime carbamate insecticide that was introduced in 1965 by the Union
Carbide Corporation under the code number UC 21 149 and the trade name
Temik (Worthing & Walker, 1987).
Takusagawa & Jacobson (1977) reported that the molecular
structure of the aldicarb crystal, as determined by single-crystal
X-ray diffraction techniques, consists of an orthorhombic unit cell
with eight molecules per cell. The C-O single bond length in the
carbamate group was reported to be significantly greater than in
carboxylic acid esters. This supports the theory that interaction with
acetylcholinesterase involves disruption of this bond.
Aldicarb has two geometrical isomers as shown below:
The commercial product is a mixture of these two isomers. It is
not certain which isomer is the more active.
2.3 Conversion factors
In air at 25 °C and 101.3 kPa (760 mmHg):
1 ppm (v/v) = 7.78 mg/m3
1 mg/m3 = 0.129 ppm (v/v).
2.4 Analytical methods
The methods for analysing aldicarb include thin-layer
chromatography (Knaak et al., 1966a,b; Metcalf et al., 1966), liquid
chromatography (LC) (Wright et al., 1982), ultraviolet detection
(Sparacino et al., 1973), post-column derivatization and fluorometric
detection (Moye et al., 1977; Krause, 1979), and gas chromatography
(GC) with various detectors. These include the Hall detector (Galoux
et al., 1979), mass spectrometry (Muszkat & Aharonson, 1983), flame
ionization detection (Knaak et al., 1966a,b), and esterification and
electron capture detection (Moye, 1975). A multiple residue method
exists for detecting N-methylcarbamate insecticide in grapes and
potatoes. It involves separation by reverse phase liquid
chromatography and detection by a post-column fluorometric technique
Table 1. Some physical and chemical properties of aldicarba
Relative molecular mass: 190.3
Form: colourless crystals (odourless or slight
Melting point: 100 °C
Boiling point: unknown; decomposes above 100 °C
Vapour pressure (25 °C): 13 mPa (1 x 10-4 mmHg)
Relative density (25 °C): 1.195
Solubility (20 °C): 6 g/litre of water; 40% in acetone;
35% in chloroform; 10% in toluene
Properties: heat sensitive, relatively unstable
chemical; stable in acidic media but
decomposes rapidly in alkaline media;
non-corrosive to metal; non-flammable;
oxidizing agents rapidly convert it to
the sulfoxide and slowly to the sulfone
Impurities dimethylamine; 2-methyl-2-(methylthio)
O- (methylcarbamoyl) oxime;
Log octanol/water partition 1.359
a From: Kuhr & Dorough (1976), Worthing & Walker (1987), and FAO/WHO (1980).
Because of aldicarb's thermal lability, it degrades rapidly in
the injection port or on the column during GC analysis. Thus, short
columns have been used to facilitate more rapid analyses and prevent
thermal degradation (Riva & Carisano, 1969). A major drawback to using
GC methods is that aldicarb degrades to aldicarb nitrile during GC;
this degradation may also occur in the environment (US EPA, 1984).
During GC analysis by conventional-length columns, aldicarb nitrile
interferes with aldicarb analysis, thus necessitating a time-consuming
clean-up procedure. Furthermore, aldicarb nitrile cannot be detected
by LC with UV detection since absorption does not occur in the UV
range (US EPA, 1984). The post-column fluorometric technique used in
LC requires hydrolysis of the analyte, with the formation of
methylamine, which reacts with o-phthalaldehyde to form a
fluorophore. Since aldicarb nitrile does not hydrolyse to form
methylamine, it cannot be detected (Krause, 1985a).
US EPA (1984) reported that high-performance liquid
chromatography (HPLC) can be used to determine
N-methyl-carbamoyloximes and N-methylcarbamates in drinking-water.
With this method, the water sample is filtered and a 400-µl aliquot is
injected into a reverse-phase HPLC column. Compounds are separated by
using gradient elution chromatography. After elution from the column,
the compounds are hydrolysed with sodium hydroxide. The methylamine
formed during hydrolysis reacts with o-phthalaldehyde (OPA) to form
a fluorescent derivative, which is detected with a fluorescence
detector. The estimated detection limit for this method is 1.3 µg
Reding (1987) suggested that samples be kept chilled, acidified
with hydrochloric acid to pH 3, and dechlorinated with sodium
thiosulfate. Other procedures used were the same as those described in
the previous paragraph.
In a collaborative study, Krause (1985a,b) reported an LC
multi-residue method for determining the residues of
N-methylcarbamate insecticides in crops. The average recovery for 11
carbamates (which included aldicarb and aldicarb sulfone) from 14
crops was 99%, with a coefficient of variation of 8% (fortification
levels of 0.03-1.8 mg/kg), and for aldicarb sulfoxide, a very polar
metabolite, was 55% and 57% at levels of 0.95 and 1.0 mg/kg,
respectively. Methanol and a mechanical ultrasonic homogenizer were
used to extract the carbamates. Water-soluble plant co-extractives and
non-polar plant lipid materials were removed from the carbamate
residues by liquid-liquid partitioning. Additional crop co-extractives
(carotenes, chlorophylls) were removed with a Nuchar S-N-silanized
Celite column. The carbamate residues were then separated on a
reverse-phase LC column, using acetonitrile-water gradient mobile
phase. Eluted residues were detected by an in-line post-column
fluorometric detection technique. Six laboratories participated in
this collaborative study. Each laboratory determined all the
carbamates at two levels (0.05 and 0.5 mg/kg) in blind duplicate
samples of grapes and potatoes. Repeatability coefficients of
variation and reproducibility coefficients of variation for all
carbamates in the two crops averaged 4.7 and 8.7%, respectively. The
estimated limit of quantification was 0.01 mg/kg.
Ting & Kho (1986) discussed a rapid analytical method using HPLC.
They modified their previous method (Ting et al., 1984) by using a
25-cm CH-Cyclohexyl column instead of the 15-cm C-18 column. This
modification resulted in the separation of the interference peak found
in watermelon co-extractives. The separation of the interference peak
and the aldicarb sulfoxide peak was made possible by the additional 10
cm in the length of the column and the higher polarity of the
CH-Cyclohexyl. Acetonitrile and methanol were used in the extraction
and derivatization procedure before the HPLC determination. Water
melons fortified with aldicarb sulfoxide at 0.1, 0.2, and 0.4 mg/kg
showed a mean recovery of 74-76%.
Chaput (1988) described a simplified method for determining seven
N-methylcarbamates (aldicarb, carbaryl, carbofuran, methiocarb,
methomyl, oxamyl, and propoxur) and three related metabolites
(aldicarb sulfoxide, aldicarb sulfone, and 3-hydroxy-carbofuran) in
fruits and vegetables. Residues are extracted from crops with
methanol, and co-extractives are then separated by gel permeation
chromatography (GPC) or GPC with on-line Nuchar-Celite clean-up for
crops with high chlorophyll and/or carotene content (e.g., cabbage and
broccoli). Carbamates are separated on a reverse-phase liquid
chromatography column, using a methanol-water gradient mobile phase.
Separation is followed by post-column hydrolysis to yield methylamine
and by the formation of a flurophore with o-phthalaldehyde and
2-mercaptoethanol prior to fluorescence detection. Recovery data were
obtained by fortifying five different crops (apples, broccoli,
cabbages, cauliflower, and potatoes) at 0.05 and 0.5 mg/kg. Recoveries
averaged 93% at both fortification levels, except in the case of the
very polar aldicarb sulfoxide for which recoveries averaged around 52%
at both levels. The coefficient of variation of the method at both
levels was < 5% and the limit of detection, defined as five times the
baseline noise, varied between 5 and 10 µg/kg, depending on the
The International Register of Potentially Toxic Chemicals (IRPTC,
1989) reported a GLC-FPD method for aldicarb analysis in foodstuffs.
The limit of quantification was 0.01-0.03 mg/kg with a recovery rate
of 76-125%. In this method, the acetone/dichloromethane-extracted
sample is evaporated to dryness and the residue is dissolved in a
buffered solution of potassium permanganate in water in order to
oxidize the thioether pesticide and its sulfoxide metabolite to the
corresponding sulfone. Aldicarb sulfone is then extracted with
dichloromethane and the extract is evaporated to dryness. The residue
is dissolved in acetone and the solution is analysed by GC-FPD using
a pyrex column filled with 5% ov-225 on chromosorb W-HP, 150-180 U
(the column temperature is 175 °C and the carrier gas is nitrogen with
a flow rate of 60 ml/min).
3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE
3.1 Natural occurrence
Aldicarb is a synthetic insecticide; there are no natural sources
of this ester.
3.2 Anthropogenic sources
3.2.1 Production levels, processes, and uses
Aldicarb is a systemic pesticide used to control certain insects,
mites, and nematodes. It is applied below the soil surface (either
placed directly into the seed furrow or banded in the row) to be
absorbed by the plant roots. Owing to the potential for dermal
absorption of carbamate insecticides (Maibach et al., 1971), aldicarb
is produced only in a granular form. The commercial formulation,
Temik, is available as Temik 5G, Temik 10G, and Temik 15G, which
contain 50, 100, and 150 g aldicarb/kg dry weight, respectively. The
metabolite aldicarb sulfone is also used as a pesticide under the
common name aldoxycarb. Aldicarb is usually applied to the soil in the
form of Temik 5G, 10G, or 15G granules at rates of 0.56-5.6 kg ai/ha.
Soil moisture is essential for its release from the granules, and
uptake by plants is rapid. Plant protection can last up to 12 weeks
(Worthing & Walker, 1987), but actual insecticidal activity may vary
from 2 to 15 weeks, depending on the organism involved and on the
application method (Hopkins & Taft, 1965; Cowan et al., 1966; Davis et
al., 1966; Ridgway et al., 1966). The effective life of this
insecticide will vary, depending on the type of soil, the soil
moisture, the soil temperature, the rainfall and irrigation
conditions, and the presence of soil micro-organisms.
Aldicarb is approved for use on a variety of crops, which include
bananas, cotton plants, citrus fruits, coffee, maize, onions, sugar
beet, sugar cane, potatoes, sweet potatoes, peanuts, pecans, beans
(dried), soybeans, and ornamental plants (FAO/WHO 1980; Berg, 1981).
Its use in the home and garden has been proscribed by the
Since aldicarb is used in a granular form, this reduces the
handling hazards, as water is necessary for the active ingredient to
be released. Respirators and protective clothing should, however, be
used in certain field application settings (Lee & Ransdell, 1984).
188.8.131.52 World production figures
In the USA, a total of 725 tonnes was sold domestically for
commercial use in 1974 (SRI, 1984).
The US EPA (1985) estimated that aldicarb production from 1979 to
1981 ranged from 1360 to 2130 tonnes/year. In 1988, the US EPA
estimated that between 2359 and 2586 tonnes of aldicarb were applied
annually in the USA (US EPA, 1988a). More recent world production
figures are not available.
184.108.40.206 Manufacturing processes
Aldicarb is produced in solution by the reaction of methyl
isocyanate with 2-methyl-2-(methylthio)propanal-doxime (Payne et al.,
1966). During normal production, loss to the environment is not
4. ENVIRONMENTAL TRANSPORT, DISTRIBUTION, AND TRANSFORMATION
4.1 Transport and distribution between media
The fate and transport of aldicarb and its decomposition products
in various types of soil have been studied extensively under
laboratory and field conditions. Owing to the physical properties of
aldicarb such as its low vapour pressure, its commercial granular
form, and its application beneath the surface of the soil, the vapour
hazard of aldicarb is low. Thus the fate of aldicarb in the atmosphere
has not received much attention. Similarly, its fate in surface water
has not been extensively studied. However, the rates and mechanisms of
the hydrolysis of aldicarb have been studied in the laboratory in some
No studies on the stability or migration of aldicarb in the air
over or near treated fields have been reported. Laboratory migration
studies with radiolabelled aldicarb in various soil types showed a
loss of the applied substrate. This loss could not be explained unless
aldicarb or its decomposition products had been transferred to the
vapour phase (Coppedge et al., 1977). When 34 mg of 14C-aldicarb
granules was applied 38 mm below the surface of a column of soil
contained in a 63 x 128 mm poly-propylene tube, about 43% of the
radiolabel was collected in the atmosphere above the column.
Additional experiments showed that the transfer of radioactivity to
the surrounding atmosphere was inversely proportional to the depth of
application in the soil. When 14C- and 35S-labelled aldicarb were
used separately in similar experiments, only the experiments in which
the 14C-labelled compound was used led to a transfer of
radioactivity to the surrounding atmosphere, thus showing that the
volatile compound was a carbon-containing breakdown product rather
than aldicarb per se.
In a subsequent study with aldicarb using 14C at the
S-methyl, N-methyl, and tertiary carbon, Richey et al. (1977)
reported that 83% of the radiolabel was recovered as carbon dioxide
from a column of soil. The rate of degradation depended on the
characteristics of the soil, e.g., pH and humidity.
Supak et al. (1977) reported that when aldicarb (1 mg/g) was
applied to clay soil and placed in a volatilizer, its volatilization
was very limited. The authors stated that the possibility of aldicarb
causing an air contamination hazard when it is applied in the field is
negligible since it is applied at a rate of only 1.1-3.4 kg/ha and is
inserted to 5-10 cm below the soil surface.
4.1.2 Water and soil
There have been numerous studies on aldicarb, under field and
laboratory conditions, to investigate its movement through soil and
water, persistence, and degradation. While earlier studies suggested
that aldicarb degraded readily in soil and did not leach, later
identification of residues in wells indicated that persistence could
be longer than predicted and that mobility was greater. Laboratory
studies have given variable results and the only totally reliable data
are from full-scale field studies.
In one of the few studies conducted with natural water (Quraishi,
1972), rain overflow and seepage water were collected from ditches
near untreated fields, filtered, and then treated with aldicarb at a
concentration of 100 mg/litre. Solutions were stored in ambient
lighting at temperatures ranging from 16 to 20 °C. It took 46 weeks
for the aldicarb concentration to decrease to 0.37 mg/litre.
Following an extensive study under laboratory-controlled
conditions, Given & Dierberg (1985) reported that the hydrolysis of
aldicarb was dependent on pH. They found that the apparent first-order
hydrolysis rate over the pH range 6-8 and at 20 °C was relatively slow
(Table 2). Above pH 8 the increase in the hydrolysis rate showed a
first-order dependence on hydroxide ion concentration. The authors
stated that these studies probably represented a "worst-case"
situation with respect to the persistence of aldicarb in water, since
other means of aldicarb removal or decomposition (e.g.,
volatilization, adsorption, leaching, and plant and microbial uptake)
had been prevented.
Hansen & Spiegel (1983) showed that aldicarb hydrolyses at much
slower rates than aldicarb sulfoxide and aldicarb sulfone. Since
aldicarb oxidizes fairly rapidly to the sulfoxide and at a slower rate
to the sulfone, and subsequent hydrolysis of the oxidation products
usually occurs, aldicarb does not persist in the aerobic environment.
In his review, de Haan (1988) discussed leaching of aldicarb to
surface water in the Netherlands. Some of the factors favourable to
leaching are weak soil binding, high rainfall, irrigation practices,
and low transformation rates of the oxidation products of aldicarb.
Aharonson et al. (1987) reported that hydrolysis of aldicarb is
one of the abiotic chemical reactions that is linked to the detection
of the pesticide in the ground water. The hydrolysis half-life at pH
7 and 15 °C has been estimated by these authors to be as long as
Table 2. Apparent first-order rate constant (k), half-life (t´), and
coefficient of variation of the regression line (r2) for aldicarb
hydrolysis at 20 °C in pH-buffered distilled watera
pH Period k (day-1)b t´b r2
3.95 89 5.3 x 10-3 131 0.86
6.02 89 1.2 x 10-3 559 0.90
7.96 89 2.1 x 10-3 324 0.62
8.85 89 1.3 x 10-3 55 0.98
9.85 15 1.2 x 10-1 6 1.00
a Adapted from Given & Dierberg (1985).
b Rates and resulting half-life values for pH 6-8 represent
only estimates since the slopes of the log percentage
remaining versus time regression lines were probably not
significantly different from zero.
The products of aldicarb hydrolysis at 15 °C under alkaline
conditions (pH 12.9 and 13.4) are aldicarb oxime, methylamine, and
carbonate (Lemley & Zhong, 1983). The half-lives of hydrolysis at
these two pHs are 4.0 and 1.3 min, respectively. Other hydrolysis
data, determined at pH 8.5 and 8.2, yielded rates with half-lives of
43 and 69 days, respectively (Hansen & Spiegel, 1983; Krause, 1985a).
Lemley et al. (1988) reported that at pH values of 5-8 the sorption of
aldicarb, aldicarb sulfoxide, and aldicarb sulfone decreases as the
temperature increases from 15 to 35 °C.
Andrawes et al. (1967) applied the pesticide at the recommended
rate of 3.4 kg/ha to potato fields and found that < 0.5% of the
original dose remained at the end of a 90-day period. In fallow soil,
decomposition of aldicarb to its sulfoxide and sulfone was rapid, >
50% of the administered compound dissipating within 7 days after
application. Peak concentrations of the aldicarb sulfoxide (8.24
mg/kg) and aldicarb sulfone (0.8 mg/kg) were reached at day 14 after
Ou et al. (1986) investigated the degradation and metabolism of
14C-aldicarb in soils under aerobic and anaerobic conditions. They
found that under aerobic conditions, aldicarb rapidly disappeared and
aldicarb sulfoxide was rapidly formed; the latter in turn was slowly
oxidized to aldicarb sulfone. The sulfoxide was the principal
metabolite in soils under strictly aerobic conditions. Although the
parent compound aldicarb persisted considerably longer in anaerobic
soils, anaerobic half-lives for total toxic residue (aldicarb,
aldicarb sulfoxide, and aldicarb sulfone) in subsurface soils were
significantly shorter than under aerobic conditions.
A number of factors, including soil texture and type, soil
organic content, soil moisture levels, time, and temperature, affect
the rate of aldicarb degradations (Coppedge et al., 1967; Bull, 1968;
Bull et al., 1970; Andrawes et al., 1971a; Suspak et al., 1977). Bull
et al. (1970) reported that soil pH had no significant effect on the
breakdown of aldicarb, but Supak et al. (1977) noted an increase in
the rate of degradation when the pH was lowered.
Lightfoot & Thorne (1987) investigated the degradation of
aldicarb, aldicarb sulfoxide, and aldicarb sulfone in the laboratory
using distilled water, water extracted from soil, and water with soil
particles (Table 3). Degradation of all three compounds was greatest
in the uppermost "plough" layer of the soil profile and much higher in
the presence of soil particulates. Even after sterilization of the
soil, degradation was fast in this layer, indicating that the effect
of particulate matter is not entirely microbial. Degradation continued
in the saturated zone (ground water) at a slower rate (particularly
for the sulfoxide and sulfone). A further series of experiments
investigated the degradation of mixtures of aldicarb sulfoxide and
sulfone in soil and water from the saturated zone of two soil types
(Table 4). The half-life was longer in the acidic Harrellsville soil
than the alkaline Livingston soil. As in the case of laboratory
experiments, the presence of particulates considerably increased the
rate of degradation of the carbamates. Investigation of many variables
in the laboratory led the authors to conclude that pH, temperature,
redox potential, and perhaps the presence of trace substances can all
affect degradation rates. They believed that laboratory
experimentation could not provide definitive results without the
identification of critical variables and that field observation was a
more reliable indicator of aldicarb degradation
Table 3. Degradation rates for aldicarb, aldicarb sulfoxide,
and aldicarb sulfonea
Half-life at 25 °C (days)b
Aldicarb Total carbamatesc
sterilized 2.5 (2.3-2.6) 10 (7-16)
unsterilized 1.0 (0.9-1.1) 44 (39-50)
sterilized 1679 (1056-4064) 1924 (1133-6370)
unsterilized 156 (143-176) 175 (158-195)
Distilled water (no buffers) 671 (507-994) 697 (518-1064)
Saturated zone soil and water
sterilized 15 (14-16) 16 (15-18)
unsterilized 37 (33-42) 123 (115-132)
a From: Lightfoot & Thorne (1987).
b Values in parentheses represent 95% confidence intervals.
c Aldicarb, aldicarb sulfoxide, and aldicarb sulfone.
sterilized soil water: 6.6-7.0 for 238 days;
4.8-5.0 at day 368 unsterilized soil water: 6.6-6.7 for 56
days; 4.2-4.4 at day 238, 3.2 at day 368 distilled water:
7.3-7.5 for 238 days, 6.2-6.8 at day 368 saturated zone soil
and water: 4.1-4.5 throughout entire study.
Coppedge et al. (1977) studied the movement and persistence of
aldicarb in four different types of soil in laboratory and field
settings using a radiolabelled substrate. Samples of clay, loam,
"muck" (soil with high organic content), and sand were packed in
polypropylene columns (63 x 128 mm), saturated with water, and
maintained at 25 °C throughout the study. Radiolabelled aldicarb
granules (34 mg) were applied to each column at a point 38 mm below
the soil surface. Water was then applied to each soil column at a rate
of 2.5 cm/week for the next 7 weeks. The water eluted through the
columns was collected and analysed for radiolabel. At the end of the
7-week period, the soil was removed in layers 25 mm thick and analysed
for residual radiolabel. The results of this study are shown in Tables
5 and 6. The radiolabel (< 1%) in the loam and clay soils remained in
the upper layers of the column, close to where it had been applied. In
the sand, the residual radiolabel (2-3%) passed through to the lower
parts of the column. A much higher percentage (5-6%) of the
radiolabel was retained in the muck soil column and was evenly
distributed along the column. The radiolabel leached into the water
eluted from the sand was 8-10 times greater than that from the other
soil types. The nature of the decomposition products (ultimately shown
to be carbon dioxide) resulted in some loss to the atmosphere
surrounding the soils. The data in Table 6 indicate that most of the
radioactivity retained in clay and loam soils represented aldicarb,
sulfoxide whereas that in sand largely represented the parent
compound. Greater leaching through sand decreased loss to the
atmosphere by degradation to carbon dioxide.
Coppedge et al. (1977) also studied the persistence of aldicarb
using field lysimeters. Aldicarb (34 mg), labelled with 35S, was
added to columns (63 x 128 mm) containing Lufkin fine sandy loam soil
at a point 76 mm below the surface. The contents were moistened with
water and then buried in the same type of soil at a depth where the
insecticide granules were 152 mm below the surface. The experiment
lasted for 7 weeks and rain was the only other source of moisture. The
column recovered 3 days after the application yielded 71% of the
radiolabel, while the column recovered at the end of 7 weeks yielded
only 0.9%. This suggested an approximate half-life for the aldicarb of
< 1 week, and the label distribution suggested an upward movement
through volatilization of the decomposition products. The authors
therefore concluded that there was little danger that aldicarb would
move into the underground water supply in this type of soil.
Bowman (1988) studied the mobility and persistence of aldicarb
using field lysimeters containing cores (diameter, 15 cm; length, 70
cm) of Plainfield sand. Half of the cores received only rainfall,
while the remainder received rainfall plus simulated rainfall (50.8
mm) on the second and eighth days after treatment, followed by
simulated irrigation for the duration of the study. The results of
this study indicated that under normal rainfall about 9% of the
applied aldicarb leached out of the soil cores as sulfoxide or
sulfone, whereas, in cores receiving supplementary watering, up to 64%
of applied aldicarb appeared in the effluent principally as sulfoxide
Table 4. Degradation rates for aldicarb sulfoxide and aldicarb sulfone mixtures in groundwater degradation mechanism studiesa
Sterilized (25 °C) Unsterilized (25 °C)
Soil type and medium
Half-lifeb pHc Half-lifeb pHc
saturated zone soil and water 137 (117-165) 5
Harrellsville, NC (first set)
saturated zone soil and water 378 (287-550) 4.3 1910 (1170-5180) 4.2
coarse-filtered water 1100 (760-1970) 4.6 > 2000 4.6
fine-filtered water > 2000 4.6 > 2000 4.2
Livingston, CA (original data)
saturated zone soil and water 8 (7-10) 7
saturated zone soil and water 1.3 (1.2-1.4) 9.0 7.5 (6.9-8.1) 8.4
coarse-filtered water 19 (17-22) 7.7 6.0 (5.7-6.3) 8.3
a From: Lightfoot & Thorne (1987).
b Half-life (days) for carbamate residues. Values in parentheses represent 95% confidence intervals. Since the experiments
were conducted for only 1 year, half-life estimates greater than about 600 days are not as reliable as other estimates.
Half-lives longer than about 2000 days could not be determined.
c Approximate average value during experiment.
Table 5. Distribution and persistence of 14C-aldicarb equivalents in soil columnsa,b
Percentage of total dose in the various layers Percentage of total dose
Soil type Total Unextractable In leached
0-25 c 25-50 50-75 75-100 100-128 extracted residue from water d Recovered Lost
from soil soil
Houston clay 0.4 0.1 0.1 T T 0.6 2.5 12.5 15.6 84.4
Lufkin loam 1.2 0.3 0.1 0.1 T 1.7 3.0 3.9 8.6 91.4
Coarse sand T T 0.2 0.5 2.0 2.7 0.2 84.0 86.9 13.1
Muck 8.7 5.3 8.5 5.6 4.8 32.9 7.1 3.5 43.5 56.5
a From: Coppedge et al. (1977).
b Results are the average from triplicate samples. Trace amounts (T) = < 0.1% of total dose.
c Layers are indicated by the distance (in mm) from the surface.
d Water that passed through the columns after the weekly addition of moisture.
Table 6. 14C-labelled aldicarb and metabolites in water eluted through soil columnsa,b
Percentage of total dose recovered at indicated days after treatment
Soil type and compounds 3 10 16 23 29 35 41 47 53
aldicarb 0.5 0.2 T 0
sulfoxide 3.2 1.9 0.4 0.2
sulfone 0 T T 0
other metabolites 0.7 0.6 0.3 0.2
Total 0 3.2 4.4 2.7 0.8 0.7 0.4 0.3 0
Accumulative total 0 3.2 7.6 10.3 11.1 11.8 12.2 12.5 12.5
aldicarb 7.3 31.5 5.0 5.4 2.3
sulfoxide 0.9 2.6 1.6 2.0 2.1
sulfone 0 0 0 0 0
other metabolites 0.2 1.9 0.4 0.5 1.1
Total 0 3.5 8.4 36.0 9.2 7.0 7.9 5.5 6.7
Accumulative total 0 3.5 11.9 47.9 57.1 64.1 72.0 77.5 84.0
Table 6 (contd). 14C-labelled aldicarb and metabolites in water eluted through soil columnsa,b
Percentage of total dose recovered at indicated days after treatment
Soil type and compounds 3 10 16 23 29 35 41 47 53
aldicarb T T T 0
sulfoxide 0.9 0.3 0.2 0.3 0.2 0.3
sulfone 0 0 T T
other metabolites 0.2 T 0.2 T 0.1 0.2
Total 0 0.7 1.1 0.3 0.4 0.3 0.3 0.5 0.3
Accumulative total 0 0.7 1.8 2.1 2.5 2.8 3.1 3.6 3.9
other metabolites 0.2
Total 0 0.2 0.6 0.9 0.9 0.3 0.1 0.3 0.3
Accumulative total 0 0.2 0.8 1.7 2.6 2.9 3.0 3.3 3.6
a From: Coppedge et al. (1977).
b Results are the average from triplicate samples. Trace amounts (T) = < 0.1% of total dose. Where a "total" value is given
without values for each component, the volume of samples was insufficient for individual analyses.
Andrawes et al. (1971a) studied the fate of radio-labelled
aldicarb ( S-methyl-14C-Temik) in potato fields. The initial soil
concentration was 13.1 mg/kg, which fell to 25.6 and 9.5% of the
applied amount after 7 and 90 days, respectively. Samples taken as
early as 30 min after the application showed that 12.7% of the
aldicarb had already been converted to aldicarb sufoxide. By day 7 it
had increased to 48%. In fallow soil, aldicarb was applied as an
acetone/water solution at the same level as that used in the planted
field. The dissipation of 14C residues occurred at a relatively slow
rate for the first 2 weeks and then at a faster rate. The breakdown
products in both the fallow and planted fields were essentially the
LaFrance et al. (1988) studied the adsorption characteristics of
aldicarb on loamy sand and its mobility through a water-saturated
column in the presence of dissolved organic matter. The results of
these studies suggested that aldicarb does not undergo appreciable
complexation with dissolved humic materials found in the interstitial
water of the unsaturated zones. Thus the presence of dissolved humic
substances in the soil interstitial water should not markedly affect
the transport of the pesticide towards the water table.
Woodham et al. (1973a) studied the lateral movement of aldicarb
in sandy loam soil. They applied the granular commercial formulation
of the pesticide (Temik 10G) to irrigated and non-irrigated fields at
a rate of 16.8 kg/ha and placed it 15-20 cm to the side of cotton
seedlings and 12.5-15 cm deep. Soil samples were collected throughout
the growing season from a depth of 15 cm, from the bottom of a creek
adjacent to a treated field, and from sites 0.40 and 1.61 km
downstream. The aldicarb used in this study was found to have a short
residence time. Levels in the treated field fell to 15% within one
month. Only 8% remained after 47 days. No residues were found after 4
months and no aldicarb was detected either between rows or in the bed
of the creek that collected water drainage. The authors concluded
that aldicarb was translocated into crop plants and weeds but that
there would be no carry-over of aldicarb or its metabolites from one
growing season to another (Woodham et al., 1973b). The results of
studies by Andrawes et al. (1971a) and Maitlen & Powell (1982) agree
with the observations of Woodham and his colleagues. Gonzalez & Weaver
(1986) failed to detect aldicarb or its breakdown products in run-off
water from a field treated with aldicarb in California, USA.
The method and timing of application can also affect the
migration and degradation of aldicarb (Jones et al., 1986). Aldicarb
was applied in-furrow during the planting of potatoes and as a
top-dressing at crop emergence. At the end of the growing season the
residues from the first application were found primarily in the top
0.6 m of soil, and the residues from the emergence application were
found primarily in the top 0.3 m of soil.
In a three-year Wisconsin potato field study (sandy plain),
Fathulla et al. (1988) monitored aldicarb residues in the saturated
zone ground water under fluctuating conditions of temperature, pH, and
total hardness. Soils were well drained sands, loamy sands or sandy
loams (with 1 to 2% organic matter). The water table was high with a
depth to the saturated zone of between 1.3 and 4.6 m. Sampling wells
were bored to a maximum of 7.5 m for groundwater sampling. Rothschild
et al. (1982) had found all residues of aldicarb (and its breakdown
products) within the upper 1.5 m of the ground water in the same area
in an earlier study. This is consistent with the views of both groups
of authors that movement of aldicarb will occur in these aquifers. The
report of Fathulla et al. (1988) indicated that detection and
persistence of aldicarb in the ground water were dependent on
alkalinity and temperature. Movement of aldicarb was lateral as well
as vertical and the authors emphasized the importance of seasonal
changes in water table depth and precipitation as factors influencing
movement. Degradation by microorganisms in the upper layers of the
soil and ground water was noted and identified as a major factor in
the short-term fate of the aldicarb. Hegg et al. (1988) measured the
movement and degradation of aldicarb in a loamy sand soil in South
Carolina, USA, and found that it degraded at a rate corresponding to
a half-life of 9 days with essentially no residues present 4 months
after application. This was a faster loss of aldicarb from the soil
than in comparable studies in neighbouring areas. Using the
unsaturated plant root zone model (PRZM) with rainfall records from 15
years, aldicarb residues were predicted to be limited to the upper 1.5
m, regardless of year-to-year variations in rainfall.
Pacenka et al. (1987) sampled both soil cores and ground water
from sites on Long Island (New York, USA), where earlier surveys had
suggested contamination of wells with aldicarb and its breakdown
products (the sulfone and sulfoxide). Three study areas were chosen
with shallow (3 m), medium (10 m), and deep (30 m) water tables. All
were overlain with sandy soils. Soil cores, driven to the depth of the
water table, were taken from a field where aldicarb had been applied
to potatoes and from surrounding areas. Ground water was sampled from
188 wells of varying depth and at different distances from the
aldicarb source. Results indicated that the residence time of
aldicarb (including the sulfone and sulfoxide) in the soil depended on
the depth of the water table and, hence, the overlying unsaturated
zone. In the shallow and medium depth water table sites, all aldicarb
residues had disappeared within 3 years of the last use of the
compound. In deeper unsaturated layers, aldicarb residues were present
at increasing concentrations in soil water from 10 m down to the water
table at 30 m. The uppermost 10 m was free of residues. Analysis of
the groundwater samples showed lateral movement of residues extending
from 120 m to 270 m "downstream" of the source in a single year. It
was calculated that the relatively shallow aquifer in the area (which
lay over a deeper aquifer capped by an impervious layer of clay) would
flush residues from the area completely within 100 years and lead to
concentrations below the drinking-water guideline level (New York) of
7 µg/litre being attained between 1987 and 2010 (depending on
assumptions for dispersion and degradation). Pacenka et al. (1987)
revised this figure downwards on the basis of their more extensive
field observations, although no firm figure could be advanced.
Studies in other geographical areas of the USA, including those
showing some residues of aldicarb or the sulfoxide and sulfone in
wells, have demonstrated a shorter residence time and more rapid
degradation than in the Long Island study (Jones et al., 1986; Wyman
et al., 1987; Jones, 1986, 1987). In these studies there was little
lateral movement of the ground water in the saturated zone. Water
table levels in these areas were generally high and much of the
sampling of the ground water was in the top 4-5 m of the saturated
zone. Much greater lateral movement of ground water in the Florida
Ridge area at a shallower depth than similar movement in Long Island
also shifted the aldicarb residues away from the treated area.
However, degradation was sufficiently fast in these soils to reduce
the chance of contamination of wells used for drinking-water. An
impervious layer 6 m down would prevent deeper contamination in this
area (Jones et al., 1987a).
A review of well and groundwater monitoring of aldicarb residues
throughout the USA has been published by Lorber et al. (1989, 1990),
which indicates geographical areas at greatest risk of water
contamination and local restrictions on the use of aldicarb.
4.1.3 Vegetation and wildlife
The uptake of aldicarb and its residues by food crops and plants
has been reported in several studies (Andrawes et al., 1974; Maitlen
& Powell, 1982). Residue levels in plants and crops grown in
aldicarb-treated soil are given in Table 7. Of the many varieties and
species of birds and mammals studied, only the oriole had aldicarb
residues (0.07 mg aldicarb equivalents per kg) in its tissues (Woodham
et al., 1973b).
In a study by Iwata et al. (1977), aldicarb was applied to the
soil in orange groves at rates of 2.8, 5.6, 11.2, and 22.4 kg ai/ha.
Residues found on day 118 after application in the soil were 0.03,
0.16, 0.20, and 0.42 mg/kg, respectively. On day 193, samples were
taken from the pulp of oranges grown in soil that had been given the
highest amount (22.4 kg ai/ha) of aldicarb. The residues in these
samples ranged from 0.02-0.03 mg/kg.
After aldicarb was applied to the leaves of young cotton plants
under field conditions, it was not translocated to other parts of the
plant to any great extent (Bull, 1968). Two weeks after application,
93% of the recovered radiolabel was found at the application site. The
remainder was spread evenly throughout the plant, including the roots
In plants, aldicarb is metabolized by processes involving
oxidation to the sulfoxide and sulfone, as well as by hydrolysis to
the corresponding oximes and, ultimately, to the nitrile.
There have been several studies on the metabolism of aldicarb by
the cotton plant. Metcalf et al. (1966) found that aldicarb was
completely converted within 4-9 days to the sulfoxide, which was then
hydrolysed to the oxime. The subsequent oxidation of the sulfoxide to
the sulfone occurred more slowly and was found to lead to
bioaccumulation in aged residues (Coppedge et al., 1967).
When aldicarb (10 µl of an aqueous solution containing 10µg
aldicarb) was applied to the leaves of cotton plants, 7.1% of the
administered dose was converted to the sulfoxide within 15 min. Two
days later there was no residual aldicarb in or on the plant tissues,
and the principal metabolite (78.4% of the initial dose) was the
sulfoxide. After 8 days, 7.4% of the initial dose was found as the
sulfone while the nitrile sulfoxide and an unidentified metabolite
were the final products of decomposition (Bull, 1968).
4.3 Interaction with other physical, chemical or biological factors
4.3.1 Soil microorganisms
Kuseske et al. (1974) studied the degradation of aldicarb under
aerobic and anaerobic conditions and found that degradation was much
slower under anaerobic conditions. Jones (1976) studied the metabolism
of aldicarb by five common soil fungi. The potential for aldicarb
detoxification by these fungi (in decreasing order) was as follows:
Gliocladium catenulatum > Penicillium multicolor = Cunninghamella
elegans > Rhizoctonia sp. > Trichoderma harzianum . The major
organosoluble metabolites were identified as aldicarb sulfoxide, the
oxime sulfoxide, the nitrile sulfoxide, and smaller amounts of the
corresponding sulfones, indicating that the metabolic pathways were
similar to those found in higher plants and animals.
Spurr & Sousa (1966, 1974) tested the effects of aldicarb and its
metabolites on pathogenic and saprophytic microorganisms and found
that some of the microorganisms appeared to use aldicarb as a carbon
source. The various bacteria and fungi used in these tests showed no
growth inhibition when aldicarb was added at levels up to 20 times
those usually used in field conditions.
Table 7. Residues (in mg/kg) of aldicarb and its sulfoxide and sulfone metabolites found in various
crops grown in aldicarb-treated soila,b
Replicate Potato Potato Alfalfa Alfalfa Mint Mustard Radish Radish
no. leavesc leaves (transplanted) (seeded) foliage greens tops roots
(70)d (408) (456) (456) (408) (408) (408) (408)
3.4 kg ai/ha application
1 7.65 0.52 0.14 0.16 0.02 ND 0.08 ND
2 7.93 0.15 ND 0.04 0.01 O.03 0.07 ND
3 8.11 1.34 0.09 0.05 0.05 0.08 0.05 ND
4 8.74 1.27 0.24 0.14 0.10
5 9.60 1.03 0.13 0.24 0.06
Average 8.41 0.66 0.12 0.13 0.05 0.04 0.07 ND
15.0 kg ai/ha application
1 19.30 0.69 0.89 0.89 0.64 ND 0.27 0.04
2 14.90 1.10 0.34 1.47 0.92 0.26 0.27 0.05
3 20.80 1.12 0.43 0.26 0.37 0.40 0.18 0.03
4 19.40 0.50 0.76 0.61 0.23
5 22.60 1.96 1.37 8.37 1.55
Average 19.40 1.07 0.76 2.32 0.74 0.22 0.24 0.04
a From: Maitlen & Powell (1982).
b Residues in this table were determined by oxidizing the aldicarb, aldicarb sufoxide, and aldicarb sulfone and then
determining them as one combined compound, aldicarb sulfone. ND = none detected; the lower limit of reliable detection for
these samples was < 5.0 ng/aliquot analysed or < 0.02 mg/kg.
c These samples are from the crop of 1979. All others are from the crop of 1980.
d Figures in parentheses are the interval in days between treatment of soil and sampling of plants.
5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE
5.1 Environmental levels
Since aldicarb is applied in granular form to the soil surface,
it reaches the atmosphere only by upward migration and by
volatilization. Thus, it is not transported to the atmosphere to any
great extent and so is not expected to contribute a significant health
threat from this source. In a volatilization study (Supak et al.,
1977), a special apparatus was designed to determine the volatility of
aldicarb from the soil. The air eluted from the apparatus after it had
passed over soil samples containing dispersed aldicarb was analysed by
the method of Maitlen et al. (1970). This method allowed the
quantitative analysis of aldicarb and its two oxidation products, the
sulfoxide and sulfone, both of which are toxic. Nontoxic decomposition
products, such as the sulfoxide and sulfone oximes, both of which
interfere with the determination of aldicarb sulfone by this method,
were removed by LC. When aldicarb was mixed with soil to a
concentration of 1 mg/kg, only 2µg of aldicarb volatilized over the
first 9 days of the experiment and subsequent losses increased to a
steady-state rate of approximately 1µg/day. According to the authors,
this rate of volatilization was almost negligible and not high enough
to cause a potential health hazard.
Run-off to surface water and leaching to aquifers used as sources
of water for human consumption have been investigated. Aldicarb
residues have been found in drinking-water wells in New York
(Wilkinson et al., 1983; Varma et al., 1983), Wisconsin (Rothschild et
al., 1982), and Florida (Miller et al., 1985). The US EPA groundwater
team reported that they had found groundwater residues in 22 states
(US EPA, 1988b). In Canada, water samples taken from private wells
showed contamination with aldicarb up to 6.0 µg/litre; ground water
from Quebec (maximum of 28 µg/litre) and Ontario (maximum of 1.1
µg/litre) also contained detectable levels (Hiebsch, 1988).
Prince Edward Island, Canada, is wholly dependent upon ground
water from a highly permeable sandstone aquifer for domestic,
agricultural, and industrial use. Priddle et al. (1989) reported that
12% of monitored wells exceeded the Canadian drinking-water guideline
of 9µg/litre for aldicarb. The maximum level detected was 15 µg/litre.
Following extensive agricultural use of aldicarb and as a result
of a combination of environmental and hydro-logical conditions on
eastern Long Island, New York, in 1978 the insecticide
and its metabolites had leached into groundwater aquifers that
constitute the major source of drinking-water for local inhabitants.
In December 1978, detectable levels of aldicarb were found in 20 of 31
water sources; similar results were obtained in the following June.
When both private and community wells located near potato farms were
sampled in August 1979, analyses revealed detectable levels of
aldicarb in potable water. In March 1980, the Department of Health
Services in Suffolk County, New York, undertook an extensive sampling
programme that included nearly 8000 wells. Union Carbide performed the
analyses, with the New York Department of Health serving as the
quality control arm. Levels of aldicarb ranging from trace amounts to
> 400 µg/litre were detected in 27% of the wells sampled. Baier &
Moran (1981) reported that of 7802 wells sampled, 5745 (73.6%) did
not have detectable concentrations of aldicarb, 1025 (13.1%) had
concentrations in excess of the 7 µg/litre guideline of the New York
State Department of Health, and the remaining 1032 (13.3%) had trace
amounts of this insecticide.
Aldicarb has been found at levels of 1-50 µg/litre in the ground
water of the USA (Cohen et al., 1986; de Hann, 1988).
The contamination of the Long Island (New York) aquifer by
aldicarb at levels of up to 500 µg/litre (in one well) was attributed
by Marshall (1985) to a combination of circumstances (high rainfall,
coarse sandy soil, low soil temperatures, and a shallow water table)
that favoured leaching. There have been some predictions that this
undesirable situation would persist for only a year or two, but also
some suggestions that wells could remain contaminated for up to a
century. Marshall (1985) also voiced concern that under anaerobic
conditions in cool climates, such as those in northern regions, the
breakdown of aldicarb and its residues would be a much slower process.
Contamination would also be favoured by heavy usage of Temik.
During 1982, aldicarb was identified in several wells in the
state of Florida (Miller et al., 1985). The state Commission of
Agriculture and Consumer Services subsequently banned the use of Temik
on citrus crops in 1983. A University of Florida task force was
appointed to sample the 10 largest drinking-water systems that
obtained water from groundwater sources in 35 counties. Neither
aldicarb nor its oxidative sulfoxide or sulfone metabolites were
detected in any of the almost 400 samples collected.
During the application season of 1984 (January to April), 2040
tonnes of aldicarb was used on citrus fruits at a rate of 5.6 kg ai/ha
in more than 30 counties in Florida. No residues were detected in
samples taken from community water systems, but trace amounts of
aldicarb, aldicarb sulfoxide, and aldicarb sulfone were found in the
Calloosahatchee River from which Lee County draws its drinking-water.
(However, no residues were found in finished drinking-water in Lee
County). The authors stated that the persistence of aldicarb and its
metabolites in shallow ground water may also contaminate
drinking-water. The results of a monitoring study by the Union Carbide
Corporation (UCC) showed that in shallow ground water aldicarb can
move further from its application point than originally predicted.
5.1.3 Food and feed
Residues have been detected on a variety of crops for which
aldicarb is used (see section 3.2.1). In the USA, aldicarb
intoxication from eating contaminated watermelons has been reported in
California (Jackson et al., 1986) and in Oregon (Green et al., 1987),
and two episodes of poisoning from eating aldicarb-contaminated
cucumbers have been reported in Nebraska (Goes et al., 1980).
Store-bought cucumbers, grown hydroponically, were found to contain
between 7 and 10 mg aldicarb/kg (Aaronson et al., 1980). It should be
noted that aldicarb is not approved for use on these crops.
Laski & Vannelli (1984) reported the results of a survey of
potatoes grown in New York State in 1982. Fifty samples, each
consisting of 9 kg, were collected after harvest from four areas. In
each of these areas, except one (Long Island), aldicarb was applied at
rates of 14 to 22 kg/ha at planting stage. Samples were analysed for
aldicarb, aldicarb sulfoxide, and aldicarb sulfone by the method of
Krause (1980). Over 50% (23 out of 43) of potato samples obtained from
areas where aldicarb was applied were positive for aldicarb sulfoxide
(trace to 0.48 mg/kg) and/or sulfone (trace to 0.20 mg/kg), but
aldicarb itself was not detected. No residues were found in any of the
7 samples from Long Island. The maximum concentrations were detected
in samples from the North Eastern location, where there is sandy soil.
Potatoes with the maximum concentration (0.48 mg/kg) were found to
contain two and a half times higher concentrations (1.2 mg/kg) when
reanalysed by a more sensitive method (Union Carbide, 1983). The
investigators suggested that soil type and climatic conditions
influenced residues in the crops.
When Krause (1985b) analysed aldicarb and its oxidative
metabolites in "market basket" potatoes, he detected levels of
aldicarb sulfone ranging from < 0.01 to 0.18 mg/kg and of aldicarb
sulfoxide from < 0.01 to 0.61 mg/kg. All 39 samples collected
between 1980 and 1983 contained residues of aldicarb or its
Potato samples collected from farms in the north-central part of
New York, where soil is of the wet muck type, contained lower aldicarb
residues than did the rocky-sandy soil type found in the north-eastern
part of the state, even though application rates were the same in both
areas. These lower residue levels were the result of aldicarb
decomposition associated with moisture. Cairns et al. (1984) described
the persistence of aldicarb in fresh potatoes.
Peterson & Gregorio (1988) reported upper 95 percentile residue
levels of 0.0677 mg/kg in raw potatoes (tolerance = 1 mg/kg), 0.0658
mg/kg in fresh bananas (tolerance = 0.3 mg/kg), and 0.0212 mg/kg in
grapefruit (tolerance = 0.3 mg/kg) in a market basket survey conducted
in the USA (national food survey). These authors also reported a
maximum residue level of 0.82 mg/kg in raw potatoes obtained in
controlled field trials, as well as upper 95 percentile residue levels
as high as 0.43 mg/kg in raw potatoes, 0.12 mg/kg in bananas, and 0.17
mg/kg in citrus products, estimated from the distribution of residue
levels obtained in field trials.
5.2 General population exposure
The general population may be exposed to aldicarb and its
residues primarily through the ingestion of food containing aldicarb
and from contaminated water, as discussed in sections 5.1.2, 5.1.3.,
and section 8. The largest documented episode of foodborne pesticide
poisoning in North American history occurred in July 1985. This
resulted from the consumption of Californian watermelons contaminated
with up to 3.3 mg/kg of aldicarb sulfoxide (Ting & Kho, 1986).
Hirsch et al. (1987) reported 140 cases of poisoning incidences
in the Vancouver area of British Columbia, Canada. A review of the
onset of symptoms and food consumed suggested illness associated with
eating cucumbers contaminated with aldicarb. Analytical investigations
confirmed that the cucumbers from one producer contained residues of
total aldicarb up to 26 mg/kg.
Petersen & Gregorio (1988) reported the results of a
comprehensive analysis of aldicarb data from controlled field residue
studies and provided estimates of the upper 95 percentile of residues
in foods in the USA. The analysis showed that daily exposure at the
upper 95 percentile consumption rate for aldicarb-treated commodities
containing the estimated upper 95 percentile aldicarb residue levels
would be approximately one-quarter of the daily exposure calculated by
assuming that all of the aldicarb-treated commodities contained
residues at the tolerance levels (e.g., 1.77 µg/kg per day versus 6.38
µg/kg per day for the USA population). In addition, Petersen &
Gregorio (1988) presented the results of a statistically designed
national food survey on the five commodities that were estimated to
be responsible for more than 90% of the dietary exposure to aldicarb
residues in the USA (bananas, white potatoes, sweet potatoes, oranges,
and grapefruit). Daily exposure to aldicarb at the 95 percentile
consumption rate for aldicarb-treated commodities containing the
95 percentile aldicarb residue levels, as estimated from the national
food survey, would be approximately 6% of the daily exposure calculated
by assuming aldicarb residue levels at the tolerance levels
(e.g. 0.40 µg/kg body weight per day versus 6.38 µg/kg per day for the
The highest daily exposure estimated from the results of the
national food survey was 0.89 µg/kg per day for non-nursing infants
and children (1-6 years of age).
A US EPA survey indicated that the vast majority of wells
contained levels of aldicarb residues less than 10 µg/litre and noted
that heat treatment of water used in cooking would result in aldicarb
residues no higher than 5 µg/litre (Cohen et al., 1986).
Accidental leaks of several gases at a plant producing aldicarb
in Institute, West Virginia, USA, required 135 people to be the
hospitalized (Marshall, 1985).
5.3 Occupational exposure during manufacture, formulation or use
The dangers of inadequate safety precautions and improper dress
and handling procedures are discussed in section 8. People involved in
the manufacture and field application of aldicarb are potentially at
higher risk than the general population (Doull et al., 1980) and
should always take proper safety precautions.
6. KINETICS AND METABOLISM
A number of studies on various mammalian and non-mammalian
species have shown that aldicarb, as well as its sulfoxide and sulfone
metabolites, is absorbed readily and almost completely from the
gastrointestinal tract (Knaak et al., 1966a,b; Andrawes et al., 1967;
Dorough & Ivie, 1968; Dorough et al., 1970; Hicks et al., 1972; Cambon
et al., 1979). Andrawes et al. (1967) reported that the uptake of
aldicarb and aldicarb sulfoxide from the gastro-intestinal tract of
the rat was rapid and efficient. They recovered 80-90% of the
radiolabel in the urine during the first 24 h after administration.
Their observation was substantiated by Knaak et al. (1966a,b), who
also recovered > 90% of the administered oral dose in rats.
Cambon et al. (1979) reported the rapid uptake of aldicarb in
pregnant rats. The rats showed overt signs of depression of
cholinesterase activity < 5 min after they were given single oral
doses of aldicarb ranging from 0.001 to 0.10 mg/kg. At all dose
levels, acetylcholin-esterase activity was significantly decreased in
fetal blood, brain, and liver 1 h after dosing.
Dorough et al. (1970) recovered 92% of the doses (0.006-0.52
mg/kg per day) of aldicarb and aldicarb sulfone in the urine of
lactating Holstein cows dosed during a 14-day period. Dorough & Ivie
(1968) found that > 90% of a single dose of 0.1 mg/kg administered
orally to lactating Jersey cows was absorbed and excreted in the
urine. In laying hens, oral doses of aldicarb and aldicarb sulfone
were administered in a 21-day short-term feeding study and in a single
capsule dose study, respectively. In the short-term feeding study,
80-85% of each daily dose was excreted in the faeces during the
following 24 h, while 90% of the total dose consumed was excreted
within one week after the cessation of aldicarb intake. In the single
dose study, 90% of the single oral dose was excreted within 10 days
(Hicks et al., 1972).
Feldman & Maibach (1970) reported the relatively efficient dermal
uptake of carbamate insecticides in man (73.9% of a dermally applied
dose of carbaryl was absorbed over a period of 5 days compared with
10% for five other representative pesticides). The percutaneous uptake
of aldicarb in water or in toluene has also been demonstrated
qualitatively in rabbits (Kuhr & Dorough, 1976; Martin & Worthing,
1977) and in rats (Gaines, 1969).
The rapid depression of acetylcholinesterase activity in fetal
and maternal blood and tissues observed after the oral administration
of aldicarb to pregnant rats demonstrated that aldicarb or its toxic
metabolites (the sulfoxide and sulfone) are distributed to the tissues
by the systemic circulation (Cambon et al., 1979, 1980). The
quantitative distribution of radiolabelled aldicarb and its
metabolites in the tissues of female rats, given a single oral dose of
0.4 mg aldicarb/kg, is shown in Table 8 (Andrawes et al., 1967).
Aldicarb and its residues appeared to be distributed among the various
tissues examined with no tendency to be sequestered or accumulated in
any one tissue, since animals killed from 5 to 11 days after dosing
had no detectable radiolabelled residues.
Aldicarb and its metabolites were found to be concentrated in the
livers of cows fed 0.12, 0.6, or 1.2 mg aldicarb/kg diet for up to 14
days (Dorough et al., 1970). Levels of the radiolabel in muscle, fat,
and bone were low or below the detection levels. In a previous study,
Dorough & Ivie (1968) found that 3% of the radiolabel was excreted in
the milk of a lactating cow after a single oral dose of 0.1 mg/kg.
Hicks et al. (1972) conducted a study in which single oral doses
(0.7 mg/kg) of aldicarb or a 1:1 molar ratio of aldicarb and aldicarb
sulfone were administered to laying hens. The radiolabel equivalents
were greatest in the liver and kidneys for the first 24 h, much lower
levels being found in fat and muscle. In a second study,
aldicarb/aldicarb sulfone was administered at 0.1, 1.0, or 20 mg/kg
diet for 21 days. Distribution to the tissues after this multiple
dosing regimen was similar to that after the single dose, the highest
residue levels appearing in the liver and kidneys.
Table 8. Total aldicarb equivalents (mg/kg) in tissues of rats treated
orally with 35 S-aldicarba
Time period (days after dosing)b
Day 1 Day 2 Day 3 Day 4
W D W D W D W D
Heart 0.12 0.44 0.09 0.32 0.08 0.29 0.11 0.38
Kidneys 0.16 0.56 0.08 0.25 0.06 0.16 0.07 0.21
Brain 0.11 0.35 0.02 0.08 0.08 0.25 0.05 0.19
Lungs 0.15 0.60 0.02 0.48 0.04 0.14 0.06 1.19
Spleen 0.27 1.08 0.04 0.12 0.10 0.37 0.05 0.17
Liver 0.16 0.28 0.07 0.22 0.07 0.21 0.05 0.14
Leg muscle 0.16 0.61 0.02 0.07 0.05 0.20 0.04 0.12
Fat 0.23 0.72 0.11 0.12 0.09 0.11 0.03 0.04
Bone 0.11 0.15 0.09 0.13 0.06 0.08 0.02 0.04
Stomach 0.19 0.64 0.07 0.26 0.08 0.29 0.06 0.19
Stomach contents 0.18 0.94 0.14 1.05 0.10 0.65 0.03 0.09
Small intestine 0.18 0.74 0.13 0.45 0.10 0.30 0.06 0.16
Small intestine 0.25 1.20 0.19 1.03 0.08 0.49 0.06 0.24
Table 8 cont'd. Total aldicarb equivalents (mg/kg) in tissues of rats treated
orally with 35 S-aldicarba
Time period (days after dosing)b
Day 1 Day 2 Day 3 Day 4
W D W D W D W D
Large intestine 0.15 0.66 0.12 0.54 0.08 0.27 0.13 0.30
Large intestine 0.18 0.67 0.05 0.24 0.09 0.39 0.04 0.16
Blood 0.16 0.74 0.14 0.18 0.08 0.21 0.05 0.17
a From: Andrawes et al. (1967).
b W = wet weight; D = dry weight.
6.3 Metabolic transformation
Carbamates undergo a limited number of in vivo reactions:
oxidation, reduction, hydrolysis, and conjugation (Ryan, 1971). In
animals, the enzymes involved in these processes are found in the
microsomal fraction of the liver homogenate. In the case of aldicarb,
both oxidation of the sulfur to the sulfoxide and sulfone and
hydrolysis of the carbamate ester group are involved (Andrawes et al.,
1967). Although the hydrolysis reaction destroys insecticidal
activity, both the sulfoxide and sulfone are active anticholinesterase
agents (Andrawes et al., 1967; Bull et al., 1967; NAS, 1977). The
metabolic pathways for aldicarb in the rat are shown in Fig. 1
(Wilkinson et al., 1983). The metabolism of aldicarb in animals
usually results in the formation of the sulfoxide, sulfone, oxime
sulfoxide, oxime sulfone, nitrile sulfoxide, nitrile sulfone, and at
least five other metabolites (Knaak et al., 1966a,b; Dorough et al.,
1970). Aldicarb metabolites formed by incubation with liver microsomal
enzymes are similar to the metabolites formed in plants and insects
(Oonnithan & Casida, 1967). The rapid conversion to the sulfoxide and
sulfone has been demonstrated in plants (Metcalf et al., 1966;
Coppedge et al., 1967) and animals (Andrawes et al., 1967; Dorough &
In vitro studies by Oonnithan & Casida (1967) showed that the
first stage in the metabolism of aldicarb involves the microsomal
reduced nicotinamide adenine dinucleotide phosphate (NADPH) system to
form the sulfoxide, but that the subsequent oxidation to the sulfone
derivative occurs only to a small extent. Andrawes et al. (1967)
confirmed these findings and showed that in the presence of the NADPH
cofactor the production of metabolites increases by a factor of 15.
The same authors also demonstrated that the principal urinary
metabolites in the rat consist of hydrolytic products with only a
small amount of carbamate. In studies with pig liver enzymes, Hajjar
& Hodgson (1982) concluded that, under aerobic conditions and in the
presence of NADPH, the FAD-dependent monooxygenase is responsible for
the observed oxidation of the thio-ether in the primary metabolic
step. The same authors found that sulfoxidation is enhanced rather
than inhibited by n-octylamine, a known inhibitor of cyto-chrome
6.4 Elimination and excretion in expired air, faeces, and urine
Most studies on the elimination and excretion of aldicarb and its
metabolites have used the radiolabelled compound. No kinetic
coefficients have been reported, although studies in which rats (Knaak
et al., 1966a,b; Andrawes et al., 1967; Dorough & Ivie, 1968; Marshall
& Dorough, 1979), cows (Dorough & Ivie, 1968; Dorough et al., 1970),
and chickens (Hicks et al., 1972) were used gave some information
about the clearance rates, mechanisms, and routes of excretion. In all
species, the principal excretion route for aldicarb and its
metabolites (> 90%) is via the urine. A small amount of aldicarb and
its metabolic products is excreted via the faeces (which is in part
due to biliary excretion), or is exhaled as carbon dioxide.
The total excretion of S-methyl-C14-, tert-butyl-C14-,
and N-methyl-C14-labelled aldicarb by rats after oral dosing was
investigated by Knaak et al. (1966a). Within 24 h, the total excretion
of the S-methyl, tert-butyl, and N-methyl labels was
approximately 90, 90, and 60%, respectively. For the S-methyl- and
tert-butyl-labelled compounds, > 90% was excreted via the urine and
only 1.1% of the radiolabel was excreted as carbon dioxide. In a study
on rats dosed orally with aldicarb (labelled in a different position
and with different radioisotopes), Andrawes et al. (1967) showed that
> 80% of the applied dose (labelled with 14C) was excreted over 24
days, while 6.6% was excreted in the faeces within 4 days.
The biliary excretion of aldicarb and its metabolites was studied
by Marshall & Dorough (1979) in rats with cannulated bile ducts. A
single oral dose of 14C-thiomethyl aldicarb (0.1 mg/kg) in 0.2 ml of
vegetable oil was given by intubation, and urine, bile, and faeces
were collected over the next 72 h. Biliary excretion accounted for
2.6, 9.5, 22.9, 28.1, and 28.6% of the administered dose at 3, 6, 12,
24, and 48 h after dosing, respectively. More than 64% was excreted in
the urine over the 48-h period, and < 1% was recovered from the
In a study by Dorough & Ivie (1968), 83% of an oral dose of 0.1
mg/kg given to a lactating cow was recovered in the urine within 24 h,
this increasing to 90% over 22.5 days. Only 2.85% of the radiolabel
was recovered in the faeces within 8 days after dosing. All samples of
milk taken from 3 h to 22.5 days after dosing contained the radiolabel
and accounted for 3.02% of the administered dose.
Hicks et al. (1972) dosed laying hens with 35S-aldicarb or with
a 1:1 molar ratio of 14C-aldicarb and 14C-aldicarb sulfone. The
dose (0.7 mg/kg) was administered orally in a gelatin capsule. In both
cases, the label was excreted rapidly; 75% of the radiolabel was
recovered in the faeces within 24 h and > 80% was recovered within 48
h. Repeated dosing, twice a day for 21 days, resulted in a similar
pattern of excretion, 80-85% of the daily dose being excreted in the
faeces within 24 h after the administration of each dose.
7. EFFECTS ON LABORATORY MAMMALS AND IN VITRO TEST SYSTEMS
7.1 Single exposure
The acute oral and dermal toxicity of aldicarb has been studied
in several species (Table 9). Oral LD50 values appear to be fairly
consistent (0.3-0.9 mg/kg body weight in the rat) and not dependent on
the carrier vehicle. Oral administration of the granular formulation
of aldicarb gives LD50 values proportional to the active ingredient
content (Carpenter & Smyth, 1965). The oral LD50 values for aldicarb
sulfoxide and sulfone in rats are 0.88 mg/kg body weight and 25.0
mg/kg body weight, respectively (Weil, 1968). Dermal LD50 values
vary with the mode of application and the carrier vehicle used.
Several acute dermal toxicity studies using different carrier vehicles
have been reported. The dermal 24-h LD50 in rabbits for a single
application of aldicarb in water was 32 mg/kg body weight (West &
Carpenter, 1966). However, when aldicarb was tested in propylene
glycol, the observed dermal LD50 was 5 mg/kg body weight (Striegel
& Carpenter, 1962). A dermal LD50 of 141 mg/kg body weight was
reported in a 4-h exposure study on rabbits using dry Temik 10G
formulation. On the basis of results of acute oral and dermal toxicity
studies, aldicarb should be labelled as extremely hazardous (WHO,
Carpenter & Smyth (1965) reported 100% mortality within 5 min
when rats, mice, and guinea-pigs were exposed to aldicarb dust at a
concentration of 200 mg/m3. The rats and mice were more sensitive
than the guinea-pigs. Rats survived a dust concentration of 6.7
mg/m3 for 15 min, but five out of six died after 30 min. All rats
survived for 8 h when exposed to a saturated vapour concentration.
Rats were also less sensitive to aerosol concentrations than to
similar concentrations of the dust. Two of six rats survived an 8-h
exposure to an aerosol concentration of 7.6 mg/m3. Weil & Carpenter
(1970) determined an LD50 of 0.44 mg/kg body weight in rats by the
Table 9. Acute toxicity of aldicarb and its formulation products
Compound Route of Vehicle Species LD50 Reference
adminis (mg/kg body
Technical oral rat 0.93 Martin & Worthing
oral peanut oil rat M: 0.8 Gaines (1969)
oral corn oil rat M: 0.09 Carpenter & Smyth
oral corn oil rat F: 1.0 Weiden et al. (1965)
oral not specified mouse 0.3 Black et al. (1973)
skin xylene rat M: 3.0 Gaines (1969)
skin not specified rabbit 5.0 Weiden et al. (1965)
skin propylene glycol rabbit 5.0 Striegel & Carpenter
Temik 10G oral not specified rat 7.7 Weil (1973)
dermal water rat 400 Carpenter & Smyth
(4 h) (1965)
dermal none rat 200 Carpenter & Smyth
Table 9 cont'd. Acute toxicity of aldicarb and its formulation products
Compound Route of ad- Vehicle Species LD50 Reference
ministration (mg/kg body
dermal none rat 850 Weil (1973)
dermal water (50%) rabbit 32 West & Carpenter
dermal dimethyl rabbit 12.5 West & Carpenter
(4 h) phthalate (1966)
dermal toluene (5%) rabbit 3.5 West & Carpenter
(4 h) (1966)
a M = male; F = female.
Trutter (1989a) investigated the clinical effects and the effect
on plasma cholinesterase and erythrocyte acetylcholinesterase of a
single feeding of aldicarb residues (about 83.4% sulfoxide and 16.6%
sulfone). These residues were contained in a watermelon grown under
experimental conditions, aldicarb having been applied to the soil at
intervals beginning at the time of planting. Water-melon with a
residue concentration of 4.9 mg/kg was fed to three male and three
female cynomolgus monkeys at a dosage that provided a residue intake
of 0.005 mg/kg body weight. Additional groups of three male and three
female monkeys received untreated water-melon (20 g/kg body weight).
The test monkeys received supplemental untreated water-melon so that
their total intake of the fruit was the same as that of the controls.
Cholinesterase activity was measured 16, 9, and 3 days before and
immediately before the test. Peak inhibition of plasma cholinesterase
(31-46%) occurred 1 h after treatment. It was only slightly less at 2
h but was absent at 4 h after feeding. Observations continued at
intervals for 24 h. No inhibition of erythrocyte cholinesterase and no
clinical effects occurred (Trutter, 1989a).
A similar study with identical numbers of cynomolgus monkeys was
conducted using treated bananas. The total residue level (0.25-0.29
mg/kg) in six bananas was less than that in the water-melon, and the
average distribution of metabolites was different (91.8% sulfoxide and
8.2% sulfone). The dosage of aldicarb metabolites for the test monkeys
was 0.005 mg/kg body weight and the banana intake for both test and
control animals was 20 g/kg body weight. Inhibition of cholinesterase
was similar in male and female test monkeys, averaging 23% one hour
after dosing, increasing to 33% by the second hour, and decreasing to
24% by the fourth hour. No inhibition of erythrocyte cholinesterase
and no clinical effects occurred (Trutter, 1989b).
7.2 Short-term exposure
Short-term studies have been conducted in several species with
aldicarb and its principal metabolites (the sulfoxide and sulfone)
both alone and in combination.
In studies by Weil & Carpenter (1968b,c), male and female rats
were fed daily doses of aldicarb sulfoxide (0, 0.125, 0.25, 0.5, and
1.0 mg/kg body weight) or aldicarb sulfone (0, 0.2, 0.6, 1.8, 5.4, and
16.2 mg/kg body weight) in the diet for 3 and 6 months.
Acetylcholinesterase activities were depressed at the three highest
levels of each compound, and this was accompanied by some growth
retardation. No mortality or pathological effects (gross or
microscopic) were observed. In an earlier study, Weil & Carpenter
(1963) fed male and female rats daily with 0, 0.02, 0.10, or 0.50 mg
aldicarb/kg for 93 days. Plasma cholinesterase activity was depressed
in both males and females but erythrocyte cholinesterase activity was
depressed only in males. Male and female rats fed doses of either
aldicarb sulfoxide or the sulfone (0.4, 1.0, 2.5, or 5.0 mg/kg body
weight per day) for 7 days tolerated the lowest dose level of the
sulfoxide with no effects on body or organ weight (Nycum & Carpenter,
1970). There was no evidence of plasma, erythrocyte or brain
cholinesterase inhibition at that dose level. However, these
parameters were significantly affected at all higher dose levels.
Aldicarb sulfone caused a significant decrease in brain, plasma, and
erythrocyte cholinesterase activity at the highest dose level in rats
of both sexes. Reduction in brain cholinesterase activity also
occurred at the two intermediate dose levels for the sulfone in female
In a 13-week feeding study (NCI, 1979), there was 100% mortality
in rats exposed to 100 or 320 mg aldicarb/kg and body weight loss at
80 mg/kg in male rats.
DePass et al. (1985) exposed 8-week-old male and female Wistar
rats (10 of each sex per group) to a 1:1 mixture of aldicarb sulfoxide
and aldicarb sulfone in their drinking-water for 29 days. Their study
was based on a report by Wilkinson et al. (1983) that residues of
aldicarb in drinking-water consist essentially of a 1:1 mixture of the
sulfoxide and sulfone. The drinking-water levels were 0, 0.075, 0.30,
1.20, 4.80, and 19.20 mg/litre (0-1.67 mg/kg body weight per day for
males and 0-1.94 mg/kg body weight per day for females). The authors
concluded that 4.8 mg/litre (470µg/kg body weight per day) was the
no-observed-effect level (NOEL), based on erythrocyte
acetylcholinesterase and plasma cholinesterase inhibition observed at
the highest dose level.
Short-term dermal studies were conducted in which Temik 10G (with
10% ai) was applied with wetted gauze to the abraded skin of male
albino rabbits for 6 h/day for 15 days (Carpenter & Smyth, 1966). Dose
levels of 0.05, 0.10, and 0.20 g/kg body weight were applied daily,
and weight gain, food consumption, organ weights, cholinesterase
activity, and the histopathology of several tissues were examined.
Only plasma cholinesterase activity levels and weight gain at dose
levels of 0.1 and 0.2 g/kg per day were significantly altered.
In a 2-year study on beagle dogs, aldicarb was administered in
the diet at dose levels of 0, 0.025, 0.05, and 0.10 mg/kg body weight
per day (Weil & Carpenter, 1966). The same parameters as those
monitored in the rat study conducted by these authors were
investigated in this study, but none were significantly different from
controls. The authors concluded that the NOEL for rats and dogs was at
least 0.10 mg/kg body weight per day, since this was the highest level
In a study by Hamada (1988), male and female beagle dogs were fed
for one year a diet containing 0, 1, 2, 5 or 10 mg technical aldicarb
per kg to provide approximately 0, 0.025, 0.05, 0.13, or 0.25 mg/kg
body weight per day. No dogs died during the study, and there were no
effects on body weight, food and water consumption, organ weights, or
on haematological, ophthalmological, histopathological, and gross
pathological parameters. However, statistically significant increases,
compared to controls, in the combined incidence of soft stools, mucoid
stools, and diarrhoea were found in all groups treated with 0.05 mg/kg
per day or more, as well as in females treated with 0.025 mg/kg per
day. No statistically significant decrease in erythrocyte or brain
cholinesterase was found in groups treated with 0.025 or 0.05 mg/kg
body weight per day. However, plasma cholinesterase was inhibited in
male dogs treated with 0.05 mg/kg body weight per day or more
throughout the observation period of this study (weeks 5-52). In
addition, plasma cholinesterase was inhibited at the conclusion of the
study (week 52) in male dogs treated with 0.025 mg/kg body weight per
day. The author noted that plasma cholinesterase activity in the male
dogs treated with 0.025 mg/kg body weight per day was subsequently
determined to be within historical control values, and that the
statistically significant increase in soft stools and related effects
in females treated with 0.025 mg/kg body weight per day could be
attributable to an unusually high incidence of mucoid stools in one
dog during the last half of the experiment. The author concluded that
the NOEL in this study was 1 mg/kg (0.025 mg/kg body weight per day).
In a short-term study, Dorough et al. (1970) dosed lactating
Holstein cows with Temik (10% ai) at 0.042 mg ai/kg body weight per
day in their diet for 10 days and, in a second experiment, with a
mixture of aldicarb and aldicarb sulfone (Temik equivalents of 0.006,
0.027, and 0.052 mg/kg body weight per day) for a period of 14 days.
Although no alteration in blood cholinesterase activity levels or
other clinical effects were noted, aldicarb sulfoxide and sulfone were
detected in tissues. Milk production, feed consumption, and amount of
excreta were unaltered.
7.3 Skin and eye irritation; sensitization
Pozzani & Carpenter (1968) observed that aldicarb (0.7 mg/kg body
weight) in saline injected intradermally into male guinea-pigs had no
In male albino rabbits, application of aldicarb as a solution in
propylene glycol on covered clipped skin did not produce any
irritation. Instillation of 0.1 ml of a 25% suspension of aldicarb in
propylene glycol or 1 mg of dry compound did not cause corneal
irritation (Striegel & Carpenter, 1962).
The administration of 25 mg of aldicarb (Temik 5G) into the
conjunctival sac of rabbits resulted in conjunctival irritation, which
lasted for 24 h, in all the six test albino rabbits (Myers et al.,
In a study by Myers et al. (1982), the application of 500 mg
Temik 5G, moistened in saline solution, did not produce primary skin
irritation in rabbits. Similarly percutaneous administration to
abraded skin did not cause focal skin irritation.
Separate tests using aldicarb (75% wettable powder) and
technical aldicarb in saline resulted in no sensitization response in
male albino guinea-pigs following intradermal injections (Pozzani &
7.4 Long-term exposure
In a study by Weil & Carpenter (1972), male and female rats were
fed aldicarb (0.3 mg/kg body weight per day), aldicarb sulfoxide (0.3
or 0.6 mg/kg body weight per day), aldicarb sulfone (0.6 or 2.4 mg/kg
body weight/day), or a 1:1 mixture of the sulfoxide plus sulfone (0.6
or 1.2 mg/kg body weight per day) for 2 years. No effects were
observed at the low dose level with any of the treatments. At the high
dose level (except in the case of the sulfone), there was increased
mortality within the first 30 days and a reduction in plasma
cholinesterase activity, as well as decreased weight gain in the
males. The NOEL values determined for aldicarb, aldicarb sulfoxide,
aldicarb sulfone, and a 1:1 aldicarb sulfoxide/aldicarb sulfone
mixture were 0.3, 0.3, 2.4, and 0.6 mg/kg body weight per day,
When male and female rats were fed diets containing aldicarb
(0.005, 0.025, 0.05, or 0.1 mg/kg body weight per day) for 2 years,
there were no effects on food consumption, mortality, lifespan,
incidence of infection, liver and kidney weight, haematocrit,
incidence of neoplasms and pathological lesions, or on plasma, brain,
and erythrocyte cholinesterase levels (Weil & Carpenter, 1965).
7.5 Reproduction, embryotoxicity, and teratogenicity
Proctor et al. (1976) studied the effects of several methyl
carbamate and organophosphate insecticides on teratogenicity and
chicken embryo nicotinamide adenine dinucleotide (NAD) levels. Fertile
White Leghorn eggs (45-55 g) were used for the test. After the eggs
were incubated at 37 °C and 73% relative humidity for 4 or 5 days, 1
mg of aldicarb in a 30-µl methoxytriglycol solution was injected into
the yolk and the injection hole on the shell was then sealed with
paraffin wax. On day 12 after injection, some of the embryos were
removed and the NAD levels were examined. On day 19 after injection,
the remaining embryos (at least 10) were examined. NAD levels were
similar to those of controls. There were no terato-genic effects
(straight legs, abnormal feathers, or wry neck) in any of the embryos
exposed to aldicarb.
In a study by Weil & Carpenter (1964), pregnant rats were fed
with doses of 0, 0.04, 0.20, and 1.0 mg aldicarb per kg body weight
per day. One group was fed throughout the pregnancy and until the pups
were weaned, a second group was fed from the day of appearance of the
vaginal plug until the 7th day of gestation, and a third group
received aldicarb between days 5 and 15 of gestation. Although the
highest dose administered was near the reported LD50 for rats, no
significant effects on fertility, viability of offspring, lactation or
other parameters were observed.
In a teratology study, Harlan-Wistar rats were fed aldicarb
sulfone in their diets at dosages of 0.6, 2.4 or 9.6 mg/kg body weight
per day, administered either during the first 20 days of gestation,
during day 6 to day 15 of gestation, or during day 7 to day 9 of
gestation. No treatment-related teratogenicity occurred as a result of
any of the treatment regimes at any of the levels of exposure to the
sulfone (Woodside et al., 1977).
Groups of 16 pregnant Dutch Belted rabbits were given doses of 0,
0.1, 0.25 or 0.50 mg aldicarb/kg body weight per day by gavage on days
7-27 of gestation (IRDC, 1983). Fetuses were then removed by Caesarean
section. One spontaneous abortion was reported in each group given
0.25 or 0.50 mg/kg body weight per day. Although the number of viable
fetuses and total implantation values were lower in all treatment
groups than those in controls, they fell within historical control
ranges and no significant differences were recorded.
Developmental toxicity of aldicarb has been evaluated by Tyl &
Neeper-Bradley (1988). Four groups of pregnant CD Sprague-Dawley rats,
25 in each group, were administered aldicarb (0.125, 0.25 or 0.5 mg/kg
body weight per day) in water solution by gavage from gestation days
6 to 15. There were three treatment-related maternal deaths in the
high-dose group on day 7 of gestation (second day of administration).
Maternal toxicity at that dose level was indicated by reduced body
weight and food consumption and cholinergic signs. Body weight and
food consumption were also reduced in the rats given 0.25 mg/kg body
weight per day. The NOEL for maternal toxicity was 0.125 mg/kg body
weight per day. Litter weight was significantly reduced at 0.5 mg/kg
body weight per day. Fetotoxicity was indicated by body weight
reduction, increased skeletal variation, retarded ossification, and
ecchymosis on the trunk. No embryotoxicity was observed. An increased
incidence of dilation of the cerebral lateral ventricle was observed
at the highest dose level. However, due to the very high baseline
control value for such changes found in pooled historical review, this
increase was not considered to be significant.
In a 3-generation reproductive study on rats conducted by Weil &
Carpenter (1964), aldicarb was incorporated into the diet of the
parent generation at levels of 0.05 or 0.10 mg/kg body weight per day
for 84 days before mating. Similar doses were fed to the subsequent
F2 and F3 generations. No effects were noted.
In a further 3-generation reproductive toxicity study, Weil &
Carpenter (1974a) fed Harlan-Wistar rats aldicarb in their diet at
dosages of 0.2, 0.3 or 0.7 mg/kg body weight per day. No consistent
treatment-related effects were observed in any of the parameters
A 3-generation reproductive toxicity study was performed on
Harlan-Wistar rats that were fed aldicarb sulfone in their diets at
levels adjusted to give dosages of 0.6, 2.4, and 9.6 mg/kg body weight
per day (Woodside et al., 1977). Apart from occasional reductions in
maternal body weight gain at the medium and high dosage levels, there
were no treatment-related adverse effects on any of the parameters
Cambon et al. (1979) tested three carbamate insecticides
(aldicarb, carbaferran, and primicarb) on acetyl-cholinesterase
activity in tissues from pregnant Sprague-Dawley rats and fetuses.
Aldicarb was administered by gastric intubation (0.001, 0.01 or 0.1
mg/kg body weight) to the pregnant animals (eight per group) on day 18
of gestation, and acetylcholinesterase activity was measured in
maternal and fetal whole blood. Signs of poisoning occurred in animals
about 5 min after the administration of the medium and high doses.
There was significant inhibition of acetylcholinesterase in most
maternal and fetal tissues, and its activity in maternal and fetal
blood and liver was still lower than the control activity 24 h after
treatment at the medium and high dose levels.
7.6 Mutagenicity and related end-points
Ercegovich & Rashid (1973) evaluated the mutagenicity of aldicarb
in an Ames-type test using five strains of Salmonella typhimurium
(identity of strains not stated). Aldicarb was found to be weakly
mutagenic in the absence of a metabolic activation system.
Based on the results of four different laboratories that tested
aldicarb for mutagenicity in S. typhimurium (TA98, TA100, TA1535,
TA1537, and TA1538) and E. coli (WP2 uvrA ), both with and without
metabolic activation, Dunkel et al. (1985) reported that aldicarb did
not produce a mutagenic response in any of the bacterial strains
Rashid & Mumma (1986), reported that "technical grade aldicarb"
(500 µg/plate) induced DNA damage in S. typhimurium (TA1538). It did
not, however, have any lethal effect on the DNA-repair proficient
strain of S. typhimurium (TA1978). No DNA-damage was caused in E.
coli strains K-12 and WP2.
An in vitro gene mutation assay in L5178Y mouse lymphoma cells
gave inconclusive results for aldicarb in the absence of metabolic
activation, but aldicarb caused mutations in the presence of S9 mix
from Aroclor 1254- induced F-344 rat liver (Myhr & Caspary, 1988). In
an identical experiment performed at a different laboratory (Mitchell
et al., 1988), aldicarb was shown to be mutagenic in both the presence
and absence of induced S9 mix.
When aldicarb was tested in vitro in the CHO/HGPRT mammalian
cell forward gene mutation assay, there was no evidence of
mutagenicity either in the presence or absence of S9 mix from Aroclor
1254-induced male Sprague-Dawley rat livers (Stankowski et al., 1985).
Blevins et al. (1977) found no evidence of DNA damage in human
skin fibroblasts exposed in vitro to aldicarb.
No evidence that aldicarb caused any unscheduled DNA synthesis in
primary cultures of hepatocytes from male F- 344 rats was detected by
Godek et al. (1984).
Aldicarb caused increases in the numbers of chromatid and
chromosome breaks in human peripheral lymphocytes exposed in vitro
(Cid & Matos, 1987). This effect was greater in the presence of S9
mix from phenobarbital-induced livers of male Sprague-Dawley rats than
in its absence.
When Cid & Matos (1984) studied the effects of aldicarb on human
lymphocytes in vitro , they found that it caused a significant
increase in sister chromatid exchanges (SCE). Slightly higher SCE
values were found in the presence of S9 liver homogenate fractions
than in its absence.
The in vivo clastogenicity of aldicarb in bone marrow has been
investigated in rats and mice via the intraperitoneal route. Sharaf et
al. (1982) treated male albino rats (strain not stated) with
injections of aldicarb (0.00121, 0.00666 or 0.0121 mg/kg body weight)
dissolved in a 1:1 water/acetone vehicle. One group of animals served
as a control, a second group received one injection per day for 5
days, and a third group received one injection only. Increases in
structural and numerical aberrations were observed in bone marrow
cells in all groups of treated animals. Structural chromosomal
aberrations consisted of chromatid breaks or deletions, chromatid
gaps, centromeric attenuation, and (in the case of repeated exposure
only) centric fusions. Numerical aberrations were mainly due to
endomitosis, although there was also some evidence of increased
polyploidy. In mice, however, there was no evidence of any effect on
chromosomal aberration frequencies in bone marrow cells following a
single intraperitoneal injection of aldicarb (93.5% pure; 0.010 or
0.001 mg/kg body weight). In addition, no effects were seen when five
daily doses of 0.010 mg/kg body weight were given (Cimmino et al.,
Dominant lethal studies have been performed using Harlan-Wistar
rats (from the F2 generation of multi-generation studies) that had
been treated with aldicarb (Weil & Carpenter, 1974a) or aldicarb
sulfone (Woodside et al., 1977) given in the diet at dosages of 0.2,
0.3, and 0.7 mg/kg (aldicarb) and 0.6, 2.4, and 9.6 mg/kg (aldicarb
sulfone). The treated males were then mated with untreated virgin
females. The results of the studies gave no indication of an increased
incidence of dominant lethal mutations in rats treated orally with
aldicarb or aldicarb sulfone.
Although some of the mutagenicity tests performed on aldicarb
gave positive results, the results of the various in vitro and in
vivo tests, when considered together, indicate that aldicarb is not
an win vivow mutagen.
The mutagenic potential of N-nitroso aldicarb has also been
investigated. A bacterial spot test conducted with Salmonella
typhimurium his- G46 gave a weakly positive result (Seiler, 1977).
Blevins et al. (1977) investigated the interaction of N-nitroso
aldicarb with DNA in in vitro human skin fibroblasts and found
numerous single-strand breaks in the DNA of all the
nitroso-derivative-treated cells but not in the DNA from cells treated
with aldicarb itself. Cid et al. (1988) found that
N-nitroso-aldicarb caused an increase in the number of sister
chromatid exchanges in human lymphocytes in vitro.
Weil (1968) reported a skin-painting study of male mice in which
a 0.125% solution of aldicarb was applied to the hair-free skin on the
backs of animals twice a week for up to 28 months. There were no
substantial differences with respect to the incidence of tumours. Two
growths, a haemangioma and a thymoma, were noted in the animals
administered aldicarb. These internal growths were not accompanied by
cutaneous papillomas or carcinomas and were considered to be
spontaneous growths unrelated to any incidence of malignancy
(Wilkinson et al., 1983).
In a study by Weil & Carpenter (1974b), aldicarb was dissolved in
acetone prior to mixing with the diet, and dietary levels of 0.1, 0.3
or 0.7 mg/kg body weight were administered to groups of 50 male CD-1
mice for 18 months. Two control groups of 50 mice were used in
addition to a group of untreated mice from which one animal was killed
for comparison purposes each time a mouse in the aldicarb-treated
groups died during the experimental period. There was no
treatment-related effect on mortality. Furthermore, there were no
treatment-related effects on the incidence of any tumour type at any
site or on the total incidence of tumours.
In a study by Woodside et al. (1977), groups of CD-1 mice (50 of
each sex per group) were administered aldicarb sulfone (0, 0.15, 0.6,
2.4 or 9.6 mg/kg body weight) in the food for 18 months. Observations
included mortality, food consumption, and body weight determinations,
and gross and microscopic examinations were performed on all mice.
Body weight changes were sporadic and exhibited no trends.
Histological changes were not statistically different from those in
controls at any dose level for either sex.
In a 2-year feeding study on rats, Weil & Carpenter (1965, 1972)
reported no significant tumour increases in rats fed aldicarb (0.005,
0.025, 0.05, 0.10, or 0.30 mg/kg body weight per day) or its sulfoxide
and sulfone. In an NCI (1979) bioassay, male and female F-344 rats and
B6C3F1 mice were given technical aldicarb (2 or 6 mg/kg body weight)
in their diet for 103 weeks. No treatment-related tumours were
observed in either species.
Quarles et al. (1979) performed a series of experiments to
examine the transforming and tumorigenic activity of aldicarb and its
nitroso derivative. Pregnant hamsters were given intraperitoneal
injections of aldicarb (0.1 or 0.5 mg/kg) or nitroso-aldicarb (2
mg/kg) on day 10 of gestation. Fetal cell cultures were prepared and
plated on agar on day 13 of gestation. To test for tumorigenicity, 1
x 106 cells were injected subcutaneously into adult nude mice.
Aldicarb was found to be inactive and did not induce either
morphological transformations or cells that grew in agar, whereas
nitroso-aldicarb induced morphological transformations that were
tumorigenic in nude mice.
Weekly administration by oral gavage of N-nitroso-aldicarb
(nine doses of 10 mg/kg body weight or two doses of 20 mg/kg body
weight) to groups of 12 female Sprague-Dawley rats resulted in the
development, by the end of their natural lives, of forestomach
carcinomas in two of the rats from each treated group, compared with
none in control animals (Lijinsky & Schmahl, 1978). The nitroso
derivative of aldicarb may be formed in the laboratory when aldicarb
is in the presence of nitrite under the pH and temperature conditions
of the human stomach (Elespuru & Lijinsky, 1973; Lijinsky & Schmahl,
7.8 Other special studies
Farage-Elawar (1988) studied the functional consequences of
dosing six-day-old chicks orally with 0.2 mg aldicarb/kg body weight
per day for seven days. Both acetylcholinesterase and neuropathy
target esterase levels were determined during treatment and on days 1,
3, 6, 10, 20, 30, and 40 after treatment. Measurements of motor
function consisted of analysis of the gait at the same times. Six days
after the last treatment there was a significant weight reduction with
no recovery to the control weight. There were significant alterations
in three parameters of gait starting on post-treatment day 1 and
lasting until day 40. Aldicarb reduced the acetylcholin-esterase
levels significantly only 24 h after the first day of treatment, with
recovery to control levels thereafter. There were no significant
alterations in neuropathy target esterase levels at any time. The
authors concluded that motor function changes in the young chick can
be seen in the absence of alterations in acetylcholinesterase levels.
Olsen et al. (1987) conducted studies using low concentrations of
aldicarb (0, 1, 10, 100 or 1000 wµwg per litre) in the drinking-water
of inbred Swiss Webster mice for 34 days and measured the splenic
plaque-forming cells (PFC) response to sheep red blood cells. The mean
PFC count in the 1-µg/litre group was significantly less than in the
control group after 34 days. The authors stated that aldicarb
exhibited immunomodulatory capability.
Thomas et al. (1987) conducted experiments similar to Olson et
al. (1987), but used both Swiss Webster and B6C3F1 mice. The mean
PFC counts at 0.1 µg/litre were lower than the controls; at 1.0
µg/litre they exceeded the controls; and at 10µg/litre they were lower
than the controls. With B6C3F1 mice PFC counts exceeded control
values at both 100 and 1000µg/litre, whereas in the case of Swiss
Webster mice they were similar to control values at 100µg/litre but
lower at 1000µg/litre. The authors concluded that aldicarb at
environmentally relevant exposure concentrations is not immunotoxic in
Shirazi et al. (1990) studied the immunomodulation response of
mice to low levels of aldicarb in drinking-water (0.01 to
1000µg/litre). Compared to the mean PFC values of the control group,
the mean values of treated groups indicated a stimulatory effect for
30- and 60-day tests and an inhibitory effect for 90- and 180-days
tests. However, when the data were reanalysed using the distribution
of the relative PFC counts, a consistently inhibitory response was
observed. The authors concluded that the dose-response relationships
indicated a polyphasic and inhibitory response.
Selvan et al. (1989) observed that aldicarb selectively affected
macrophage-mediated cytotoxicity of tumor target cells without
affecting the cytotoxicity mediated by natural killer cells. However,
no dose-response relationship was found.
Dean et al. (1990) investigated the effect of aldicarb on
syngenic mixed lymphocyte reaction (SMLR). In this reaction CD4+
T-helper cells (autoreactive T cells) respond to syngenic Ia molecules
expressed on C3H mouse macrophages. The authors reported that
intraperitoneal treatment (0.1 ml per mouse of a solution containing
0.1 to 1000µg aldicarb per litre) suppressed the SMLR by selectively
decreasing the stimulatory activity of macrophages without affecting
directly the responsiveness of autoreactive T cells.
A significant suppression of macrophage-mediated cytotoxicity of
tumor cells was observed in C3H mice that received seven daily doses
of 0.1 to 10µg aldicarb per kg. The authors concluded that aldicarb
may selectively affect the macrophage function but not directly affect
other components of the immune response.
Thomas & Ratajczak (1988) reported that when aldicarb was
administered in the drinking-water (0.1, 1.0, 10, 100 or 1000µg/litre)
ad libitum for 34 consecutive days to both Swiss Webster and
B6C3F1 hybrid female mice, there were no effects in either strain on
body weight, organ weight, circulatory white blood cells or
microscopic pathology of the thymus, spleen, liver, kidneys or lymph
nodes. In vivo host resistance to infectious viral challenge was
unaffected by aldicarb treatment. Aldicarb was found to have no effect
in either strain on the number of antibody-forming cells in the spleen
or on the amount of circulating antibody in the blood. The capacity of
B and T lymphocytes to respond to nonspecific mitogens was unaltered,
as was the ability of T lymphocytes to recognize genetically different
cell types in a mixed lymphocyte culture (MLC). It was concluded that
aldicarb in drinking-water had no effect on any measured immunological
Thomas et al. (1990) exposed adult female B6C3F1 mice to
drinking-water containing 1.0, 10 or 100µg aldicarb per litre or to
distilled drinking-water alone for 34 consecutive days. The impact of
aldicarb exposure on the ability of splenic natural killer cells and
specifically sensitized cytotoxic T lymphocytes to lyse YAC-1 lymphoma
target cells and P 815 tumor cells was evaluated. The percentages and
absolute numbers of total T cells, T-suppressor, T-helper, and B cells
was also measured. The authors concluded that the absence of
statistically significant effects on any of these parameters indicated
that aldicarb treatment did not adversely affect the immune system of
7.9 Factors modifying toxicity; toxicity of metabolites
Of the metabolites that have been identified, only the sulfoxide
and sulfone have a mechanism of toxicity similar to aldicarb (as a
cholinesterase inhibitor in a carbamylation reaction). The sulfoxide
appears to be equally toxic and the sulfone considerably less toxic
than aldicarb in acute and long-term tests (Weil, 1968; Weil &
7.10 Mechanisms of toxicity - mode of action
Aldicarb and acetylcholine exhibit very close structural
CH3 O CH3 O
' " ' "
CH3S - C - CH = N - OCNHCH3 CH3 - N - CH2CH2OCCH3
The mechanism of toxic action of aldicarb and its metabolites
(sulfoxide and sulfone) involves their reaction with cholinesterase
enzymes. In particular, the carbamylation of acetylcholinesterase
interferes with hydrolysis of acetylcholine at synaptic and myoneural
junctions. This adversely affects neural transmission (Carpenter &
Smyth, 1965; Weil & Carpenter, 1968a,b,c, 1970; Dorough, 1970).
Various cholinesterase enzymes have been identified in the plasma, red
blood cells, liver, and brain (Kuhr & Dorough, 1976; Cambon et al.,
1980). The function of plasma cholinesterase is not fully understood,
but it is considered to play no role in cholinergic transmission.
Acetylcholinesterase in erythrocytes reflects the acetylcholinesterase
activity in the nerve synapses. Since acetylcholinesterase in
erythrocytes and in nerve synapses are considered to be biochemically
identical, erythrocyte cholinesterase activity may be taken as an
indicator of the biochemical effect of anti-cholinesterase pesticides
Carbamates, like organophosphates, inhibit esterases
(serine-esterases and/or beta-esterases) (WHO, 1986). Although the
inhibition of serine-esterases other than acetylcholinesterase is not
significant for the toxicity of the compound, it may have significance
for the potentiation of toxicity of other compounds after long-term
low level exposure (Sakai & Matsumara, 1968, 1971; Aldridge & Magos
1978). The site of carbamylation of the enzyme is the hydroxyl moiety
of the serine amino acid. The rate of reactivation of the
carbamylated enzyme to acetylcholinesterase is relatively rapid
compared to that of the enzyme phosphorylated by an organophosphorus
pesticide. Thus the inhibition of acetylcholinesterase by carbamate
pesticides is rapid and reversible. The chemistry of carbamate
pesticides is such that no aging reaction is possible, as occurs with
the phosphorylated enzyme. In order to permit an evaluation of
cholinesterase inhibition by carbamates in vivo , special care is
required. Carbamate cholinesterase inhibition studies should utilize
minimal dilution during the preparation of the assay, minimal
incubation times, and minimal time between blood sampling and assay
8. EFFECTS ON HUMANS
8.1 General population exposure
The symptoms that have been reported for accidental or
occupational poisoning and controlled human exposure to aldicarb are
cholinergic and subside spontaneously, usually within 6 h, unless
death intervenes. Clinical symptoms and signs include dizziness,
salivation, excessive sweating, nausea, epigastric cramps, vomiting,
diarrhoea, bronchial secretion, blurred vision, non-reactive
contracted pupils, dyspnoea, and muscular fasciculations. The
intensity of these symptoms varies with the extent of exposure.
8.1.1 Acute toxicity; poisoning incidents
The first reported case of accidental poisoning occurred in 1966
when aldicarb was being used as an experimental pesticide (Hayes,
1982). The wife of an experimental scientist used a small amount of a
10% granular formulation to treat the soil around a rose bush.
Twenty-four days later she ate a sprig of mint from a plant growing
nearby, which consisted of the terminal 4-6 leaves and the stem.
Thirty minutes later she vomited and had diarrhoea and involuntary
urination. On admission to the hospital, she was found to have
pinpoint pupils, muscle fasciculations, and difficulty in breathing.
Maximal signs were observed 2 h after onset. She was given 1 mg of
atropine with no observable effect. About 15 min later she was given
2 mg atropine and had transient opening of the pupils. A further 2 mg
atropine was followed by sustained opening of the pupils and gradual
improvement in the patient's condition. Three-and-a-half hours after
onset, she was resting comfortably and had no further signs or
symptoms. It was estimated that she had eaten between 0.5 and 1.0 g of
mint. Feeding 3.0 g of this mint to a rabbit resulted in its death
within 2 h; 2.4 g caused severe symptoms in a second rabbit.
Two minor incidents of aldicarb poisoning with moderately severe
symptoms occurred after hydroponically grown cucumbers were eaten
(CDC, 1979; Goes et al., 1980; Hayes, 1982). Although carbamates had
been used in both cases, there were no data on the aldicarb content of
the cucumbers in the first case. Levels of 6.6-10.7 mg aldicarb/kg
were found in the second case (the hydroponic nutrient solution
contained 1.8 mg aldicarb/litre). The symptoms lasted only 4.5-6.0 h,
and recovery from cholinergic symptoms occurred without specific
treatment (Aaronson et al., 1979).
Aldicarb food poisoning from contaminated melons was reported in
California, USA, in 1985. Of the 1358 cases reported, 692 were
classified as probable. The melons were tested for aldicarb
sulfoxide, and 10 (4%) of the 250 tests were positive. The most severe
signs and symptoms included loss of consciousness and cardiac
arrhythmia. Six deaths and two stillbirths were reported but no
analyses for aldicarb sulfoxide were reported (Jackson et al., 1986;
Ting & Kho, 1986).
Goldman et al. (1990a) analysed the same epidemic in California
in 1985. According to their result, 1376 cases of illness within
California were reported to the California Department of Health
Services of which 77% were classified as being probably or possible
carbamate-related illnesses. Seventeen individuals required
An outbreak of illness caused by aldicarb-contaminated
water-melons was reported in Oregon, USA, in 1985. About 264 cases of
poisoning were reported and 61 definite cases were confirmed. The
levels of residue in the water-melons ranged from 0.01 mg/kg (limit of
detection) to 6.3 mg/kg. (Green et al., 1987).
Goldman et al. (1990b) reviewed three outbreaks of poisoning due
to aldicarb-contaminated water-melons or cucumbers in California
between 1985 and 1988, and one outbreak due to contaminated cucumbers
in England. Estimated dosages of aldicarb sulfoxide that caused the
illnesses ranged between 0.0011 and 0.06 mg/kg body weight and most
were well below the 0.025 mg/kg for subclinical whole blood
Ramasamy (1976) reported an incident in which a 7-month-old
female baby ate some aldicarb powder. Recovery was complete after she
was given a total dose of 105.6 mg atropine.
8.1.2 Human studies
An experimental study was carried out on 12 men already involved
in the study of aldicarb and, therefore, familiar with its effects.
Four volunteers in each of three groups took aldicarb (99.2% purity;
dissolved in drinking-water) at concentrations of 0.025, 0.05, or 0.10
mg/kg body weight. Blood was collected for cholinesterase measurement
at 18 h and 1 h before ingestion of aldicarb and at 1, 2, 4, and 6 h
after ingestion. The samples of whole blood were analysed by the
radiometric method for whole blood, which has the advantage of
involving minimal dilution of the blood and a maximum of only 3 min
from the time the sample is taken until the chemical reaction is
complete (the period of storage of the samples until the radioactivity
in them is measured has no effect on the result). The compound
hydrolysed is acetylcholine and not, as in many methods, a substitute.
Urine samples were collected at 1, 2, 4, and 6 h after ingestion.
Analysis was by gas chromatography after all metabolites had been
oxidized to aldicarb sulfone. The highest dosage chosen was that
already found to be a no-observed-effect level in a 2-year rat feeding
study. This was done even though it was recognized that some symptoms
might occur if ingestion occupied less than 1 min rather than 24 h as
in the rat. Signs and symptoms did, in fact, occur at the highest
dosage and included nausea and vomiting, pinpoint non-reactive pupils,
malaise, weakness, epigastric pain, air hunger and yawning, sweating
of the hands, forearms and forehead, salivation, and slurred speech.
The authors stated that none of the signs and symptoms were severe and
they required no treatment. Cholinesterase activity was depressed in
proportion to the dosage. Based on the individual 18-h pre-dosing
samples, the average level 1 h after ingestion was reduced to 53.3,
38.8, and 34.6% of normal at 0.025, 0.05, and 0.1 mg/kg, respectively.
At the highest dosage, the activity was further decreased (28.1% of
normal) in the 2-h sample, but it was elevated at the two lower
dosages. At 4 h it was elevated in all groups but by 6 h it had almost
returned to normal. Urinary excretion of metabolites was proportional
to dosage; the total recovery varied from 3.4 to 10.7% during the 8 h
In a separate test of volunteers, one man took a dosage of 0.26
mg/kg body weight in the form of Temik 10G granules. He became ill and
took atropine. The carbamate concentration was greatest in a urine
sample collected 4.5 h after ingestion, but total recovery of aldicarb
was only 8.1% in 24 h (Cope & Romine, 1973).
8.1.3 Epidemiological studies
After aldicarb had been detected in well-water samples in Suffolk
County, New York, Varma et al. (1983) conducted a preliminary mail
survey of families who had consumed water from these wells in 1981.
The 1500 subjects had consumed water that contained from 8 to over 64
µg aldicarb/litre. They were asked to report any symptoms of 20
general health problems and the outcome of all pregnancies. A list of
25 randomly arranged neurological symptoms was also included. The
response rate (20%) was poor. No conclusive evidence of the
association of health problems with aldicarb exposure was obtained
from this study (for which there were no controls), although there
appeared to be an association between some neurological
symptoms/syndromes and the concentration of aldicarb in the well
water. The rate of spontaneous abortions was also high among women who
consumed water from wells that contained the highest aldicarb
concentrations (66 µg/litre or more).
In a cross-sectional study of exposed and unexposed residents of
Portage County, Wisconsin, Fiore et al. (1986) reported the effects of
chronic ingestion of ground water contaminated with levels of aldicarb
(< 61 µg per litre) on the immune function of 50 women aged 18 to 70
with no known underlying reason for immunodysfunction. Of these
exposed women, 23 consumed water from a source with detectable levels
of aldicarb, while 27 unexposed women consumed water from a source
with no detectable level of aldicarb. Exposed women showed an elevated
stimulation assay response to Candida antigen, an increase in the
number of T8 cells, and a decrease in the ratio of T4:T8 cells as
compared with unexposed women. Although the results of this study are
of interest, the T lymphocyte data fall within the normal range
indicated by Martin et al. (1985). The Candida response data are also
within normal limits that have been routinely observed at the
University of Wisconsin Medical Center. The results of this study,
because of the presence of other contaminants, present no evidence for
a causal relationship between consumption of water contaminated with
aldicarb and alteration of immunological parameters.
8.2 Occupational exposure
8.2.1 Acute toxicity; poisoning incidents
Peoples et al. (1978) reported on occupational exposure to
aldicarb in California during the period 1974-1976. They reviewed 38
illnesses, 31 of which were systemic, that were directly related to
occupational aldicarb (Temik) exposure. There were four cases of
contact dermatitis and one case of eye irritation in which dust from
Temik granules was blown directly into the eye causing chemical
Lee & Ransdell (1984) reported the death of a 20-year-old farm
worker who was run over by a tractor after he had been handling Temik
15G. Tissue samples taken at autopsy revealed an estimated body burden
of 18.2 mg aldicarb (0.275 mg/kg). This level is nearly 3 times higher
than that known to produce cholinergic symptoms in humans, and the
authors considered that pesticide intoxication contributed to the
Sexton (1966) reported the incapacitation of a foreman working in
an aldicarb mechanical bagging operation. Symptoms of cholinesterase
depression lasted longer than 6 h, but he returned to work the next
day. Griffith & Duncan (1985) surveyed Florida citrus fruit growers
over a 12-month period for aldicarb-related poisonings. Only one case,
that of a certified applicator who required hospitalization for
cholinergic symptoms, was directly related to the aldicarb exposure.
Aldicarb is one of the most potent and acutely toxic pesticides
in use. In most cases, excessive occupational exposure to aldicarb has
been due either to its improper application or to the improper use of
protective equipment. Its formulation as granules and its application
to the subsoil as a systemic pesticide have been recommended by the
manufacturer to reduce the hazards (SR1, 1984).
8.2.2 Effects of short- and long-term exposure; epidemiological
No controlled occupational exposure or epidemiological
studies have been reported.
9. EFFECTS ON OTHER ORGANISMS IN THE LABORATORY AND FIELD
Some aspects of the effects of microorganisms on aldicarb have
been discussed in section 4.3.1. In the study by Kuseske et al.
(1974), application rates of 5 and 500 ppm of a commercial formulation
of aldicarb (100 g/kg ai) caused a decrease in the population of
microflora for the first 16 days and then stimulated the population
growth, in proportion to the application rate, over the next 14 days.
The microorganisms used in this study were Actinomycetes,
Nitrosomonas europaea , and Nitrobacter agilis . When 5 ppm of the
insecticide was applied, depletion of Nitrosomonas resulted in
complete inhibition of the conversion of the ammonium ion to nitrite.
The oxidative capability of five common soil fungi (Jones, 1976) is
discussed in section 4.3.1. Spurr & Sousa (1966, 1967) found no
inhibition of bacterial or fungal growth by aldicarb. Indeed, in the
case of Rhizoctonia solani (a plant pathogen and soil saprophyte),
the addition of aldicarb to the medium doubled its growth rate. The
authors concluded that microorganisms probably used aldicarb as a
9.2 Aquatic organisms
The acute toxicity of aldicarb to freshwater aquatic organisms
varies greatly. The 96-h LC50 values for different species of fish
range between 52 and 2420 µg per litre at different temperatures and
water hardness (Table 10). Aquatic molluses are very insensitive to
the effects of aldicarb (Singh & Agarwal, 1981). For the adult water
flea, Daphnia laevis , the sulfoxide is more toxic than aldicarb by
a factor of two and the sulfone less toxic by a factor of five to six
(Foran et al., 1985). For the bluegill sunfish, Lepomis macrochirus
, the toxicity of aldicarb and the sulfoxide is comparable, but the
sulfone is less toxic (Clarkson, 1968b). For estuarine and marine
organisms, acute lethality is less variable with 96-h LC50 values
ranging between 13 and 170µg/litre for all species tested (Table 10).
Pant & Kumar (1981) studied the acute toxicity of aldicarb to the
Himalayan lake teleost Barbus conchonius in both hard and soft
water. Temperatures varied from 14 to 22 °C during the experiment, and
the tests were carried out under static conditions. Results indicated
that the toxicity of aldicarb to B. conchonius was considerably
greater in soft water (Table 10). Mortality data showed that
concentrations of 1.5 mg/litre in soft water and 6.0 mg/litre in hard
water resulted in 100% mortality within 96 h.
Table 10. Acute toxicity (LC50) of aldicarb to freshwater, estuarine, and marine organismsa
Organism Age/size Stat/ M/ Temperature Hardness pH Compound Duration Concentration Reference
flow N (°C) (mg/litre) (ug/litre)
Water flea adult stat M 21 58 6.9 A 48 h 209 (175-265) Foran et al. (1985)
laevis) M 21 58 6.9 AX 48 h 103 (36-142) Foran et al. (1985)
M 21 58 6.9 AN 48 h 1124 (993-1320) Foran et al. (1985)
(1-3 A 70 (61-84) Foran et al. (1985)
AX 84 (73-95) Foran et al. (1985)
AN 910 (821-1099) Foran et al. (1985)
(Daphnia A 48 h 410 US EPA (1988a)
Water snail adult stat A 24 h 30 000 Singh & Agarwal (1981)
acuminata) 96 h 11 500 Singh & Agarwal (1981)
240 h 7500 Singh & Agarwal (1981)
Water snail adult stat A 96 h 175 000 Singh & Agarwal (1981)
(Pila 240 h 78 000 Singh & Agarwal (1981)
Bluegill 1.3 g stat 24 44 7.4 A 24 h 103 (66-161) Mayer & Ellersieck
macro- 1.3 g stat 24 44 7.4 A 96 h 52 (34-79) Mayer & Ellersieck
3.9 g stat 18 44 7.4 A 24 h 160 (130-214) Mayer & Ellersieck
Table 10 (contd). Acute toxicity (LC50) of aldicarb to freshwater, estuarine, and marine organismsa
Organism Age/size Stat/ M/ Temperature Hardness pH Compound Duration Concentration Reference
flow N (°C) (mg/litre) (ug/litre)
3.9 g stat 18 44 7.4 A 96 h 71 (54-93) Mayer & Ellersieck
5.0 g stat A 72 h 100 Clarkson (1968b)
5.0 g stat AX 72 h 4000 Clarkson (1968b)
5.0 g stat AN 72 h 64 000 Clarkson (1968b)
Rainbow 0.5 g stat 12 44 7.4 A 24 h 1000 (727- Mayer & Ellersieck
trout 1376) (1986)
(Salmo 0.5 g stat 12 44 7.4 A 96 h 560 (394-796) Mayer & Ellersieck
2.7 g stat 18 44 7.4 A 24 h 780 (592-1027) Mayer & Ellersieck
2.7 g stat 18 44 7.4 A 96 h 660 (472-921) Mayer & Ellersieck
conchonius 4.8 cm stat 14-22 319 7.4 A 48 h 8990 (4265- Pant & Kumar (1981)
4.8 cm stat 14-22 319 7.4 A 96 h 2420 (2280- Pant & Kumar (1981)
4.8 cm stat 14-22 61 7.2 A 48 h 3296 (1116- Pant & Kumar (1981)
4.8 cm stat 14-22 61 7.2 A 96 h 459 (445-521) Pant & Kumar (1981)
Table 10 (contd). Acute toxicity (LC50) of aldicarb to freshwater, estuarine, and marine organismsa
Organism Age/size Stat/ M/ Temperature Hardness pH Compound Duration Concentration Reference
flow N (°C) (mg/litre) (ug/litre)
Estuarine & marine
Alga stat N 20 30 A 96 h > 50 000b Mayer (1987)
Mysid shrimp juvenile stat N 25 20 A 96 h 13 (10-15) Mayer (1987)
(Mysidopsis (1 day
adult flow M 22 28 A 96 h 16 (13-20) Mayer (1987)
Pink shrimp adult flow M 22 29 A 96 h 12 (7.5-18) Mayer (1987)
White shrimp juvenile stat N 25 20 A 96 h 72 (65-82) Mayer (1987)
Eastern embryo stat N 25 20 A 48 h 8800c Mayer (1987)
oyster (1400-56 000)
Sheepshead juvenile stat N 25 20 A 96 h 170 (100-320) Mayer (1987)
(Cyprinodon (28 days
adult flow M 28 28 A 96 h 41 (55-72) Mayer (1987)
Table 10 (contd). Acute toxicity (LC50) of aldicarb to freshwater, estuarine, and marine organismsa
Organism Age/size Stat/ M/ Temperature Hardness pH Compound Duration Concentration Reference
flow N (°C) (mg/litre) (ug/litre)
Pinfish adult flow M 22 30 A 96 h 80 (43-150) Mayer (1987)
Spot adult stat N 25 20 A 96 h 200 (120-290) Mayer (1987)
Snook juvenile stat N 26-30 35 A 48 h 100 Landau & Tucker (1984)
undecima- (0.23 g)
a M = measured concentration; N = nominal concentration; stat = static conditions; flow = flow-through conditions;
A = aldicarb; AX = aldicarb sulfoxide; AN = aldicarb sulfone. b LC50 for growth. c LC50 for metamorphosis.
Landau & Tucker (1984) exposed eggs of the estuarine snook
(Centropomus undecimalis) from 2 to 3 h after fertilization to
various aldicarb concentrations. Larvae were more sensitive than eggs
to aldicarb. Mortality over 14 to 25 h was 0, 17, 22, and 30% of
embryos and 0, 83, 78, and 70% of larvae at 0.025, 0.1, 0.25, and 0.5
mg per litre, respectively.
Pickering & Gilliam (1982) exposed eggs and newly hatched larvae
of the freshwater fathead minnow to aldicarb at 20, 38, 78, 156, and
340 µg/litre and monitored hatching and growth of juveniles over 30
days. None of the aldicarb concentrations affected embryo survival and
only the two highest levels reduced larval-juvenile survival (by 58%
and 80%, respectively) over 30 days. Growth of surviving young was
reduced significantly only at the highest exposure concentration.
Based on the acute maximum acceptable toxic concentration (MATC) of 78
to 156 µg per litre, the authors calculated a chronic MATC of 110 µg
9.3 Terrestrial organisms
Haque & Ebing (1983) conducted a 14-day laboratory toxicity test
of aldicarb using the earthworms Lumbricus terrestris and Eisenia
foetida as test species. The pesticide was homogeneously incorporated
into the test soil substrates. The authors noted a species-specific
variation in toxicity, L. terrestris showing an LC50 of 530
(490-565) and E. foetida of 65 (58-75) mg/kg dry soil substrate.
The acute oral LD50 for birds has been found to vary between
0.8 and 5.3 mg/kg body weight, while the dietary toxicity ranged from
approximately 250 to 800 mg/kg diet (Table 11). West & Carpenter
(1965) reported that the oral LD50 for White Leghorn cockerels was
9 mg/kg body weight (i.e. 10 times that of rats). Symptoms of aldicarb
poisoning in chickens were excessive salivation, dyspnoea, stiffness,
and twitching of leg, wing, and pectoral muscles (Schlinke, 1970).
When 28-day-old Japanese quail ( Coturnix coturnix japonica ) were
given analytical grade aldicarb in corn oil solution (in gelatin
capsules) at a dose of 30 mg/kg body weight (i.e. 3 times the LD50),
all birds died within 3 h (Martin et al., 1981). Balcomb et al. (1984)
measured the acute oral toxicity of aldicarb to two species of song
bird (house sparrow and redwinged blackbird) (Table 11). When birds
were dosed with varying numbers of aldicarb granules (Temik 15G), 40%
of blackbirds given a single granule died, and 80% of those given 5
granules died. In a study on the redwinged blackbird, technical and
granular (Temik 15G) aldicarb yielded similar LD50 values. However,
the oral LD50 of granular aldicarb for sparrows was 3.8 mg/kg body
weight whereas that for technical aldicarb was 0.8 mg/kg/body weight.
Hill & Camardese (1981) reported that dietary LC50 values in young
Japanese quail (Coturnix coturnix japonica) increased with the age of
the bird, the increase being reasonably predictable between 7 and 21
days of age. Five-day dietary LC50 values were 247, 355, 542, and
786 mg/kg diet at ages 1, 7, 14, and 21 days, respectively.
In studies by Schlinke (1970) on the toxic effects of aldicarb
and other nematocides in chickens, groups of five White Leghorn
chickens, 6-7 weeks old, were given oral doses of 1.0, 2.5 or 5 mg
aldicarb/kg per day. Individual doses were administered in gelatin
capsules or by an aqueous oral drench for 10 days. Groups of six to
eight chickens were used simultaneously as controls. Body weight gain
and mortality were determined. In the low-dose group, a slight
decrease in the percentage body weight gain (44% treated versus 49%
controls) was observed, but no adverse effects were reported at this
level. Body weight gain for the chickens given 2.5 mg/kg was 30%
versus 40% in controls. In addition one chicken died after receiving
a single dose of the compound and a second died after receiving three
consecutive daily doses. In the high-dose groups (5 mg/kg per day),
one chicken died after receiving a single dose (day 1 of
administration), one after the second dose, and the remaining three
chickens died after the third dose (day 3).
Farage-Elawar et al. (1988) compared the sensitivity of young and
adult chickens to aldicarb and carbaryl. Brain, liver, and plasma
cholinesterase levels were measured and histological examinations were
conducted. Adult chickens showed no changes in any of the parameters
measured. Brain acetylcholinesterase, plasma cholinesterase, plasma
carboxylesterase, and liver cholinesterase were all inhibited in young
chickens, but there were no histological changes or alterations in
neurotoxic esterase or liver carboxylesterase in the young birds.
In a study by Belal et al. (1983), aldicarb was administered in
the feed of 1-week-old chickens at a dietary level of 1 mg/kg. After
11 days of treatment, the mortality rate was 27%. Blood cholinesterase
activity levels were reduced by 74.3% during this treatment period.
Spierenburg et al. (1985) reported that six cows became ill and
two died after the accidental spill of Temik in a pasture. Chemical
analyses for aldicarb in the rumen of one of the dead animals revealed
the presence of aldicarb at a concentration above the lethal dose.
Examination for aldicarb residues showed the meat and organs to be
unfit for human consumption.
Schafer & Bowles (1985) found the approximate acute oral LD50
of aldicarb for the deermouse Peromyscus maniculatus to be 1-6 mg/kg
Table 11. Oral and dietary toxicity of aldicarb to birds
Species Age Exposurea Parameter Concentration Reference
House sparrow adult oral LD50 0.8 Balcomb et al. (1984)
Redwinged blackbird adult oral LD50 1.8 Balcomb et al. (1984)
Grackle oral LD50 0.8 d
Starling oral LD50 4.2 d
Pigeon oral LD50 3.2 d
California quail 10 months oral LD50 M: 2.6 (2-3.4) Hudson et al. (1984)
(Loportyx californica) F: 4.7 (3.3-6.6)
Table 11 (contd).
Species Age Exposurea Parameter Concentration Reference
Bobwhite quail mature oral LD50 2.8 Clarkson & Rowe
(Colinus virginianus) (1970)
Pheasant 3-4 months oral LD50 5.3 (3.9-7.4) Hudson et al. (1984)
Pheasant 10 days diet LC50 > 300 Hill et al. (1975)
Japanese quail 14 days diet LC50 387 (336-445) Hill & Camardese
(C. coturnix japonica) (1986)
Mallard duck 5 days diet LC50 594 (507-695) Hill et al. (1975)
(Anas platyrhynchos) 10 days diet LC50 < 1000c
a Oral dosing consisted of a single capsular dose. Dietary dosing consisted of 5 days feeding on a contaminated diet followed
by a 2-day observation period.
b LD50 = lethal dose for 50% of animals, expressed as mg/kg body weight. LC50 = lethal concentration for 50% of animals,
expressed as mg/kg diet. M = male; F = female.
c There was 70% mortality at 1000 mg/kg.
d Letter by E.W. Schafer, Jr, dated 28 April 1975: Summary of three data sheets on avian toxicity. Union Carbide Agricultural
9.4 Population and ecosystem effects
No studies have revealed effects at the population level
resulting from the recommended use of the pesticide aldicarb, nor has
significant introduction of aldicarb or its metabolites into the food
chain been reported in the limited information available (Woodham et
Of 48 bobwhite quail (Colinus virginianus) penned in treated
fields (34 kg/ha), only one died as a result of ingesting Temik 10G
granules. No effects were seen on the body weight of the test birds
compared to controls (Clarkson et al., 1968). In a second study,
Clarkson (1968a) misapplied Temik 10G to fields by surface broadcast
or "spilled" it in one corner of the pen as a small heap of granules.
No deaths of bobwhite quail were seen in the broadcast application,
but the birds consumed "spilled" granules and died. Chickens refused
to eat "spilled" granules even when hungry. Further studies were
reviewed by Clarkson et al. (1969) who concluded that broadcast Temik
10G granules could be toxic to bobwhite quail in the field under
conditions of confinement and food stress. Incorporation of the
granules into the soil and/or irrigation reduced or eliminated the
In a study in which Woodham et al. (1973b) examined total toxic
aldicarb residues in weeds, grasses, and wild-life in Texas after the
soil was treated with aldicarb, no evidence of mortality among mammal
or bird populations was observed in treated or adjacent areas. Of the
small mammals, coyotes, and birds examined, only one bird had
detectable levels of aldicarb residues (an oriole with a concentration
level of 0.07 mg/kg). In all, 8 mammals and 14 birds were sampled.
Bunyan et al. (1981) conducted an extensive field trial with
sampling of invertebrates, birds, and small mammals around fields of
sugar beet treated in furrow with aldicarb granules (10% ai) at 1.12
kg aldicarb per ha. A dead partridge and high levels of residues in
blackbirds and two small mammals trapped within the treated field
indicated to the authors that the most significant hazard of aldicarb
was from direct ingestion of non-incorporated granules by ground
feeders soon after application. A secondary hazard involved
aldicarb-poisoned earthworms that came to the surface of the soil
particularly in wet conditions. Moribund worms containing residues
were found 2-6 days after drilling. Low residues of aldicarb were
found in herbivores eating young plants that had systemically absorbed
aldicarb. Residues and reduced esterase activity in brain were found
in a number of bird species feeding on the ground, indicating that
exposure to aldicarb can be widespread in the case of granular
The death of 600 songbirds, poisoned following the surface
application of Temik granules without incorporation into the soil was
reported by Baron & Merrian (1988).
10. EVALUATION OF HUMAN HEALTH RISKS AND EFFECTS ON THE ENVIRONMENT
10.1 Evaluation of human health risks
Aldicarb is an extremely hazardous pesticide. The human health
risk arises mainly from the improper use of aldicarb and a failure to
use protective equipment during its manufacture, formulation, and
application. Aldicarb may contaminate food and drinking-water. The
effects of excessive exposure are acute and reversible. Although the
cholinergic effects may be severe and incapacitating and require
hospitalization, seldom have they been fatal.
10.1.1 Exposure levels
10.1.1.1 General population
The main possible sources for general population exposure are
food and water.
Some data are available in the USA to estimate daily dietary
intake of aldicarb (see section 5.2). Extensive data show that
residues in most harvested crops are generally low and do not exceed
the maximum residue limits if aldicarb is used according to good
agricultural practice and recommended pre-harvesting periods are
followed. However, even in this case, levels up to 1 mg/kg, and
occasionally more, have been found in potatoes.
High levels of aldicarb have been discovered in some food crops
treated illegally with aldicarb. One poisoning incident occurred after
the consumption of hydroponically grown cucumbers with levels of
6.6-10.7 mg aldicarb/kg. Two incidences of poisoning were reported in
the USA from contaminated watermelons where aldicarb levels ranged
from < 0.01 to 6.3 mg/kg. However, there is no certainty that this
range reflected the actual exposure.
Contamination of ground water by aldicarb has occurred. About 12%
of wells monitored in some regions of Canada exceeded 9 µg/litre. Of
7802 wells sampled in New York State, USA, in an area of aldicarb use
on potatoes, 5745 (73.6%) had no detectable residues, 1032 (13.3%) had
trace amounts; and 1025 (13.1%) had concentrations greater than 7
A nationwide survey of 15 000 private wells in the USA showed
levels of aldicarb in the water between 1 and 50 µg/litre in
approximately one-third of the positive samples. Occasional levels of
500 µg/litre in ground water have been reported in test bores.
10.1.1.2 Occupational exposure
Air concentrations of aldicarb during agricultural application
are minimized by the granular form of the product. However, some
operations, such as the loading process, may be hazardous if adequate
individual protection is not taken. Over-exposure to aldicarb leading
to a tissue level of 0.275 mg/kg contributed to the death of a young
worker loading formulated aldicarb. The main route of occupational
exposure is through the skin, especially when workers do not follow
recommended precautions and neglect the use of protective equipment.
10.1.2 Toxic effects
The effects or manifestations of aldicarb toxicity and its
metabolites (sulfoxide and sulfones) result from its inhibitory action
on acetylcholinesterase. The inhibition of cholinesterase is
reversible. The clinical signs and symptoms, depending upon the
magnitude and severity of exposure, include headache, dizziness,
anxiety, excessive sweating, salivation, lacrimation, increased
bronchial secretions, vomiting, diarrhoea, abdominal cramps, muscle
fasciculations, and pinpoint pupils. There is no substantial evidence
of carcinogenicity, mutagenicity, teratogenicity or immunotoxicity.
In human subjects, a single oral administration of 0.025 mg
aldicarb/kg body weight produced significant inhibition of whole blood
cholinesterase activity, but no symptoms. A dosage of 0.10 mg/kg body
weight led to cholinergic signs and symptoms and a dosage of 0.26
mg/kg body weight resulted in acute intoxication that needed
10.1.3 Risk evaluation
The risks from an extremely hazardous chemical can be evaluated
only in terms of different kinds of exposure and only in terms of the
safety measures available and the degree of certainty of their use.
By far the greatest risk from aldicarb is to those who
manufacture, formulate and use it. Aldicarb is manufactured in a
closed system. The use of aldicarb in granular form reduces the
generation of dust and the risk from occupational exposure. There have
been a few accidents associated with the formulation and use, but each
was the result of one or more clear violations of safety rules (see
section 8.2.1). However, although aldicarb is used in granules, there
can be a hazard to applicators if they do not follow all recommended
The sources of aldicarb residues in food include the legal
application of aldicarb to soil in which crops for which aldicarb use
has been approved are grown, as well as the illegal or improper use of
aldicarb. There is no evidence of a health risk from aldicarb in food
to the general population at recommended application rates and
employing current techniques. However, a substantial hazard exists
when aldicarb is used on non-approved crops, as indicated by reports
of several poisoning episodes. On the other hand, soil application
rates and tolerances for aldicarb residues have been set for approved
aldicarb use to protect the general population. The success of these
measures is suggested by the observation that no reports have been
found of adverse health effects attributable to aldicarb exposure from
commodities where aldicarb was used properly. The limited
market-basket survey data suggest that exposure to aldicarb will
probably not exceed 1 µg/kg body weight per day in the USA. This is
well below the acceptable daily intake (ADI) established by the Joint
FAO/WHO Meeting on Pesticide Residues (FAO/WHO, 1983).
Aldicarb has not been found in public water supplies derived from
deep aquifers or surface waters, and thus there is no anticipated risk
from aldicarb in water obtained from these sources. Aldicarb water
contamination has been reported in ground water, generally at levels
of 1-50 µg/litre in the USA with occasional findings of up to 500
µg/litre. However, most wells sampled in contaminated areas have
undetectable or trace amounts of aldicarb or its metabolites. Reduced
contamination of ground water has resulted from the restriction of use
in sandy soils.
Assuming an average daily water consumption of 2 litres and an
average body weight of 60 kg, the exposure of people consuming water
from locally contaminated shallow wells containing between 1 and 50
µg/litre would result in an exposure to metabolites of aldicarb
ranging from 0.033 to 1.7 µg/kg body weight per day. A well containing
water contaminated with aldicarb at a level of 500 µg/litre would
result in an exposure of 17 µg per kg body weight per day. The most
appropriate available study for the assessment of drinking-water risk
is a study in which aldicarb sulfoxide and sulfone were administered
to rats in drinking-water. The no-observed-effect-level for
acetylcholinesterase inhibition in this study was 480 µg/kg body
weight per day. The estimated exposure from contaminated ground water
is therefore well below this level.
10.2 Evaluation of effects on the environment
With full incorporation of aldicarb granules into soil at a depth
of 5 cm, as recommended by the manufacturer, there is minimal hazard
to birds and small mammals. Non-target soil invertebrates,
such as earthworms, can be killed when aldicarb is used at recommended
application rates. Kills of up to 600 songbirds have been reported
from misapplication of the granules on the soil surface, since birds
can die after ingesting a single granule. Small mammals would be
similarly at risk from surface-broadcast aldicarb.
There is no indication that aquatic organisms have been killed
from aldicarb poisoning despite its relatively high potential
toxicity. Aldicarb could contaminate drainage ditches when used in
areas where periodic torrential rainfall is likely, causing
substantial run-off of both water and surface soil. However, this is
unlikely to kill fish or aquatic invertebrates.
11. CONCLUSIONS AND RECOMMENDATIONS FOR PROTECTION OF HUMAN HEALTH
AND THE ENVIRONMENT
11.1.1 General population
Aldicarb is a highly toxic pesticide.
Accidental poisoning and a controlled laboratory study resulted
in cholinergic symptoms that included the following: malaise, blurred
vision, muscle weakness in arms and legs, epigastric cramping pain,
excessive sweating, nausea, vomiting, non-reactive contracted pupils,
dizziness, dyspnoea, air hunger, diarrhoea, and muscle fasiculation.
The symptoms disappeared spontaneously within 6 h. The highest oral
dose that produced no observable symptoms in a human study was 0.05
mg/kg body weight, although there was significant transient
whole-blood cholinesterase inhibition at this level.
The primary mechanism of aldicarb toxicity is
acetylcholinesterase inhibition. It is accepted that carbamate
insecticides interfere with the ability of acetylcholinesterase to
break down the chemical transmitter acetylcholine at synaptic and
myoneural junctions. The same mechanism of action is evident in both
target and non-target organisms. There is no substantial evidence of
carcinogenicity, mutagenicity, teratogenicity, or immunotoxicity.
11.1.2 Occupational exposure
Intoxication and poisoning due to occupational exposure are known
to have occurred as a result of a neglect of recommended safety
11.1.3 Environmental effects
Aldicarb will not cause effects on organisms in the environment
at the population level. Incidents of kills of individual birds and
small mammals will occur where granules are not fully incorporated
into the soil. Aquatic organisms are not at risk from aldicarb.
11.2 Recommendations for protection of human health and the
a) The handling and application of aldicarb should be undertaken by
b) The agricultural use of aldicarb should be restricted to
situations where less hazardous substitutes are unavailable.
c) Manufacturing of aldicarb is a hazardous process with possible
risk of exposure to toxic chemicals. Safety systems should be
adequate to prevent leaks and discharges.
d) To minimize or eliminate exposure of terrestrial vertebrates to
aldicarb, granules should be fully incorporated into soil to a
depth of 5 cm, as recommended by the manufacturer.
12. FURTHER RESEARCH
a) Additional pharmacokinetic studies, including uptake studies
following dermal application, are needed to allow physiologically
based pharmacokinetic modelling.
b) A case of intoxication resulting from the consumption of
aldicarb-containing mint demonstrated effects at what appeared to
be an unusually low dosage. A study of treated mint might reveal
a previously unknown metabolite or other factors relevant to this
c) Studies of the immunological effects of aldicarb are
inconclusive. Additional studies are needed to examine more
thoroughly the effects of aldicarb on the immune system.
d) A reproduction study in the rat is needed to investigate concerns
of fetal susceptibility. One such study is underway.
13. PREVIOUS EVALUATIONS BY INTERNATIONAL BODIES
The Joint FAO/WHO Expert Committee on Pesticide Residues (JMPR)
recommended an ADI of 1 µg/kg (FAO/WHO, 1980). In 1982, JMPR revised
the ADI upward to 5 µg per kg body weight per day. Aldicarb is
classified as an extremely hazardous pesticide (WHO, 1990b).
AARONSON, M.J., FORD, S.A., GOES, E.A., SAVAGE, E.P., WHEELER,
H.W., GIBBSONS, G., & STOESZ, P.A. (1979) Suspected carbamate
intoxications - Nebraska. Morb. Mortal. wkly Rep., 28: 133-134.
AARONSON, M.J., TESSARI, J.D., SAVAGE, E.P., & GOES, E.A. (1980)
Determination of aldicarb sulfone in hydroponically grown cucumbers.
J. food Saf., 2: 171-181.
AHARONSON, N., COHEN, S.Z., DRESCHER, N., GISH, T.J., GORBACH, S.,
KEARNEY, P.C., OTTO, S., ROBERTS, T.R., & VONK, J.W. (1987) Potential
contamination of groundwater by pesticides. Pure appl. Chem., 59(10):
ALDRIDGE, W.N. & MAGOS, L. (1978) Carbamates, thiocarbamates, and
dithio-carbamates, Luxembourg, Commission of the European Communities.
ANDRAWES, N.R., DOROUGH, H.W., & LINDQUIST, D.A. (1967) Degradation
and elimination of Temik in rats. J. econ. Entomol., 60: 979-987.
ANDRAWES, N.R., BAGLEY, W.P., & HERRETT, R.A. (1971a) Fate and
carryover properties of Temik aldicarb pesticide
[2-methyl-2-(methylthio)propionaldehyde O-(methylcarbamoyl)oxime] in
soil. J. agric. food Chem., 19: 727-730.
ANDRAWES, N.R., BAGLEY, W.P., & HERRETT, R.A. (1971b) Metabolism of
2-methyl-2-(methylthio)propionaldehyde O-(methylcarbamoyl)oxime (Temik
aldicarb pesticide) in potato plants. J. agric. food Chem., 19:
ANDRAWES, N.R., ROMINE R.R., & BAGLEY, W.P. (1974) Metabolism and
residues of Temik aldicarb pesticide in cotton foliage and seed under
field conditions. J. agric. food Chem., 21: 379-386.
AOAC (1990) 985.23. N-Methylcarbamate insecticide and metabolite
residues: Liquid chromatographic method. In: Helrich, K., ed. Official
methods of analysis, Arlington, Virginia, Association of Official
Analytical Chemists, pp. 292-294.
BAIER, J. & MORAN, D. (1981) Status report on aldicarb contamination
of ground water as of September 1981, Suffolk County Department of
BALCOMB, R., STEVENS, R., & BOWEN, C. (1984) Toxicity of 16 granular
insecticides to wild-caught songbirds. Bull. environ. Contam.
Toxicol., 33: 302-307.
BARON, R.L. & MARRIAM, T. (1988) Toxicology of aldicarb. Rev. environ.
Contam. Toxicol. 105: 1-69.
BELAL, M., RIAD, S., EL-HUSSEINY, O., & AWAAD, M. (1983) The toxicity
of some insecticides to Fayoumi chicks. Egypt. J. anim. Prod., 22:
BERG, G.L., ed. (1981) Farm chemicals handbook, Willoughby, Ohio,
Meister Publishing Co., p. C326.
BLACK, A.L., CHIU, Y.C., FAHMY, M.A.H., & FUKUTO, T.R. (1973)
Selective toxicity of N-sulfenylated derivatives of insecticidal
methylcarbamate esters. J. agric. food Chem., 21: 747-751.
BLEVINS, D., LIJINSKY, W., & REGAN, J.D. (1977) Nitrosated
methylcarbamate insecticides: Effect on the DNA of human cells. Mutat.
Res., 44: 1-7.
BOWMAN, B.W. (1988) Mobility and persistence of metolachlor and
aldicarb in field lysimeters. J. environ. Qual., 17(4): 689-694.
BULL, D.L. (1968) Metabolism of UC-21149
[2-methyl-2-(methylthio)propionaldehyde O-(methylcarbamoyl)oxime] in
cotton plants and soil in the field. J. econ. Entomol., 61:
BULL, D.L., LINDQUIST, D.A., & COPPEDGE, J.R. (1967) Metabolism of
2-methyl- 2(methylthio)propionaldehyde O-(methylcarbamoyl)oxime in
insects. J. agric. food Chem., 15: 610- 616.
BULL, D.L., STOKES, R.A., COPPEDGE, J.R., & RIDGWAY, R.L. (1970)
Further studies of the fate of aldicarb in soil. J. econ. Entomol.,
63: 1283- 1289.
BUNYAN, P.J., VAN DEN HEUVEL, M.J., STANLEY, P.I., & WRIGHT, E.N.
(1981) An intensive field trial and a multi-site surveillance exercise
on the use of aldicarb to investigate methods for the assessment of
possible environmental hazards presented by new pesticides. Agro
Ecosyst., 7: 239-262.
CAIRNS, T., SIEGMUND, E.G., & SAVAGE, T.S. (1984) Persistence and
metabolism of aldicarb in fresh potatoes. Bull. environ. Contam.
Toxicol., 32: 274-281.
CAMBON, C., DECLUME, C., & DERACHE, R. (1979) Effect of the
insecticidal carbamate derivatives (carbofuran, primicarb, aldicarb)
in the activity of acetylcholinesterase in tissues from pregnant rats
and fetuses. Toxicol. appl. Pharmacol., 49: 203-208.
CAMBON, C., DECLUME, C., & DERACHE, R. (1980) Foetal and maternal rat
brain acetylcholinesterase: Isoenzymes changes following insecticidal
carbamate derivatives poisoning. Arch. Toxicol., 45: 257-262.
CARPENTER, C.P. & SMYTH, H.F. (1965) Recapitulation of pharmacodynamic
and acute toxicity studies on Temik (Unpublished Mellon Institute
Report No. 28- 78).
CARPENTER, C.P. & SMYTH, H.F. (1966) Temik 10G. 15-Day dermal
applications to rabbits (Unpublished Mellon Institute Report No.
CDC (CENTERS FOR DISEASE CONTROL) (1979) Epidemiologic notes and
reports: Suspected carbamate intoxications - Nebraska. Morb. Mortal.
wkly Rep., 28: 133-134.
CHAPUT, D. (1988) Simplified multiresidue method for liquid
chromatographic determination of N-methyl carbamate insecticides in
fruit and vegetables J. Assoc. Off. Anal. Chem., 71(3): 542-546.
CID, M.G. & MATOS, E. (1984) Induction of sister-chromatid exchanges
in cultered human lymphocytes by aldicarb, a carbamate pesticide.
Mutat. Res., 138: 175-179.
CID, M.G. & MATOS, E. (1987) Chromosomal aberrations in cultured human
lymphocytes treated with aldicarb, a carbamate pesticide. Mutat. Res.,
CID, M.G., LORIA, D., & MATOS, E. (1988) Nitroso-aldicarb induces
sister-chromatid exchanges in human lymphocytes in vitro. Mutat. Res.,
CIMINO, M.C., GALLOWAY, S.M., & IVETT, J.L. (1984) Mutagenesis
evaluation of aldicarb technical 93.43% in the mouse bone marrow
cytogenetic assay (Study conducted for Union Carbide Corporation,
submitted to WHO).
CLARKSON, V.A. (1968a) Field evaluations of the toxic hazard of
misapplied Temik formulations to Bobwhite quail and chickens (Study
conducted for Union Carbide Corporation, submitted to WHO).
CLARKSON, V.A. (1968b) Toxicity of Temik, Temik sulfoxide and Temik
sulfone to Bluegill sunfish (Study conducted for Union Carbide
Corporation, submitted to WHO).
CLARKSON, V.A. & ROWE, B.K. (1970) Field evaluations of the toxic
hazard of Temik formulations 10G, 10GV, 10GC and 10GV134 to Bobwhite
quail (Study conducted for Union Carbide Corporation, submitted to
CLARKSON, V.A., ROWE, B.K., & HENSLEY, W.H. (1968) Field evaluation of
the toxic hazard of Temik to Bobwhite quail (Unpublished Union Carbide
Corporation study, submitted to WHO).
CLARKSON, V.A., ROWE, B.K., & HENSLEY, W.H. (1969) Report on
additional field tests with Temik 10G aldicarb pesticide on the
potential hazard to Bobwhite quail (Study conducted for Union Carbide
Corporation, submitted to WHO).
COHEN, S.Z., EIDEN, C., & LORBER, M.B. (1986) Monitoring groundwater
for pesticides. In: Garner, W.Y., ed. Evaluation of pesticides in
groundwater, Washington, DC, American Chemical Society, pp. 170-196
(ACS Symposium Series 315).
COPE, R.W. & ROMINE, R.R. (1973) Temik 10G aldicarb pesticide: Results
of aldicarb ingestion and exposure studies with humans and results of
monitoring human exposure in working environments (Unpublished Union
Carbide study, Project No. 111A13, 116A16, File No. 18269).
COPPEDGE, J.R., LINDQUIST, D.A., BULL, D.L., & DOROUGH, H.W. (1967)
Fate of 2-methyl-2-(methylthio)propionaldehyde
O-(methylcarbamoyl)oxime (Temik) in cotton plants and soil. J. agric.
food Chem., 15: 902-910.
COPPEDGE, J.R., BULL, D.L., & RIDGWAY, R.L. (1977) Movement and
persistence of aldicarb in certain soils. Arch. environ. Contam.
Toxicol., 5: 129-141.
COWAN, C.B., Jr, RIDGWAY, R.L., DAVIS, J.W., WALKER, J.K., WATKINS,
W.C., Jr, & DUDLEY, R.F. (1966) Systemic insecticides for control of
cotton insects. J. econ. Entomol., 59: 958.
DAVIS, J.W., WATKINS, W.C., Jr, COWAN, C.B., Jr, RIDGWAY, R.L., &
LINDQUIST, D.A. (1966) Control of several cotton pests with systemic
insecticides. J. econ. Entomol., 59: 159.
DEAN, T.N., SELVAN, R.S., MISRA, H.P., NAGARKATTI, M., & NAGARKATTI,
P.S. (1990) Aldicarb treatment inhibits the stimulatory activity of
macrophages without affecting the T-cell responses in the syngeneic
mixed lymphocyte reaction. Int. J. Immunopharmacol., 12: 337-348.
DE HAAN, F.A.M. (1988) Effects of agricultural practices on the
physical, chemical and biological properties of soils: Part III.
Chemical degradation of soil as the results of the use of mineral
fertilizers and pesticides: Aspects of soil quality evaluation. Neth.
J. agric. Sci., 36: 211-235.
DEPASS, L.R., WEAVER, E.V., & MIRRO, E.J. (1985) Aldicarb sulfoxide/
aldicarb sulfone mixture in drinking water of rats: Effects on growth
and acetylcholinesterase activity. J. Toxicol. environ. Health, 16:
DOROUGH, H.W. & IVIE, G.W. (1968) Temik-S35 metabolism in a lactating
cow. J. agric. food Chem., 16: 460-464.
DOROUGH, H.W., DAVIS, R.B., & IVIE, G.W. (1970) Fate of
Temik-carbon-14 in lactating cows during a 14-day feeding period. J.
agric. food Chem., 18: 135- 142.
DOULL, J., KLAASSEN, C.D., & AMDUR, M.O., ed. (1980) Casarett &
Doull's toxicology: the basic science of poisons, 2nd ed., New York,
MacMillan Publishing Co., pp. 374-379.
DUNKEL, V.C., ZEIGER, E., BRUSICK, D., MCCOY, E., MCGREGOR, D.,
MORTEIMANS, K., ROSENKRANZ, S., & SIMMON, V.F. (1985) Reproducibility
of microbial mutagenicity assays: II. Testing of carcinogens and
noncarcino-gens in S. typhimurium and E. coli. Environ. Mutagen.,
ELESPURU, R.K. & LIJINSKY, W. (1973) The formation of carcinogenic
nitroso compounds from nitrite and some types of agricultural
chemicals. Food Cosmet. Toxicol., 11: 807-817.
ERCEGOVICH, C.D. & RASHID, K.A. (1973) Mutagenesis induced in mutant
strains of Salmonella typhimurium by pesticides. Abstracts of papers,
Washington, DC, American Chemical Society, p. 43.
FAO/WHO (1980) Pesticide residues in food. 1979 Report of the Joint
Meeting of the FAO Panel of Experts on Pesticide Residues in Food and
the Environment and the WHO Expert Group on Pesticide Residues, Rome,
Food and Agriculture Organization of the United Nations (Plant
Production and Protection Paper 20).
FAO/WHO (1983) Pesticide residues in food. 1982 Report of the Joint
Meeting of the FAO Panel of Experts on Pesticide Residues in Food and
the Environment, and the WHO Expert Group on Pesticide Residues, Rome,
Food and Agriculture Organization of the United Nations (FAO Plant
Production and Protection Paper 46).
FARAGE-ELAWAR, M. (1988) Toxicity of aldicarb in young chicks.
Neurotoxicol. Teratol., 10: 549-554.
FARAGE-ELAWAR, M., EHRICH, M.F., & MISRA, H.P. (1988) Effects of
multiple oral doses of two carbamate insecticides on esterae levels in
young and adult chickens. Pestic. Biochem. Physiol., 32: 262-268.
FATHULLA, R.N., JONES, F.A., HARKIN, J.M., & CHESTERS, G. (1988)
Distribution and persistence of aldicarb residues in the
sand-and-gravel aquifer of central Wisconsin. 1. Relationship between
aldicarb residue concentration and groundwater chemistry. Adv.
environ. Modelling, 13: 59-84.
FELDMAN, R.J. & MAIBACH, H.I. (1970) Pesticide percutaneous
penetration in man. J. invest. Dermatol., 54: 435.
FIORE, M.C., ANDERSON, H.A., HONG, R., GOLUBJATNIKOV, R., SEISER,
J.E., NORDSTROM, D., HANRAHAN, L., & BELLUCK, D. (1986) Chronic
exposure to aldicarb-contaminated ground water and human immune
function. Environ. Res., 41: 633-645.
FORAN, J.A., GERMUSKA, P.J., & DELFINO, J.J. (1985) Acute toxicity of
aldicarb, aldicarb sulfoxide and aldicarb sulfone to daphnia laevis.
Bull. environ. Contam. Toxicol., 35: 546-550.
GAINES, T.B. (1969) Acute toxicity of pesticides. Toxicol. appl.
Pharmacol., 14: 515-534.
GALOUX, M., VAN DAMME, J.C., BARNES, A., & POTVIN, J. (1979) GLC
determination of aldicarb sulfoxide and aldicarb in soils and water
using a Hall electrolytic conductivity detector. Chem. Abstr., 91: 164
GIVEN, C.J. & DIERBERG, F.E. (1985) Effect of pH on the rate of
aldicarb hydrolysis. Bull. environ. Contam. Toxicol., 34: 627-633.
GODEK, E.G., NAISMITH, R.W., & MATTHEWS, R.J. (1984) Rat hepatocyte
primary culture/DNA repair test (Study conducted for Union Carbide
Corporation, submitted to WHO).
GOES, E.H., SAVAGE, E.P., GIBBONS, G., AARONSON, M., FORD, S.A., &
WHEELER, H.W. (1980) Suspected foodborne carbamate pesticide
intoxications associated with ingestion of hydroponic cucumbers. Am.
J. Epidemiol., 111: 254- 259.
GOLDMAN, L.R., SMITH, D.F., NEUTRA, R.R., SAUNDERS, L.D., POND, E.M.,
STRATTON, J., WALLER, K., JACKSON, R.J., & KIZER, K.W. (1990a)
Pesticide food poisoning from contaminated watermelons in California,
1985. Arch. environ. Health, 45(4): 229-236.
GOLDMAN, L.R., BELLER, M., & JACKSON, R.J. (1990b) Aldicarb food
poisonings in California, 1985-1988: Toxicity estimates for humans.
Arch. environ. Health, 45(3): 141-147.
GONZALEZ, D.A. & WEAVER, D.J. (1986) Monitoring concentrations of
aldicarb and its breakdown products in irrigation water runoff and
soil from agricultural fields in Kern Country 1985, Sacramento,
California Department of Food and Agriculture, Environmental
Monitoring and Pesticide Management, pp. 1-9 (Unpublished report).
GREEN, M.A., HEUMANN, M.A., WEHR, H.M., FOSTER, L.T., WILLIAMS, P.,
Jr, POLDER, J.A., MORGAN, C.L., WAGNER, S.H., WANKE, L.A., & WITT,
J.M. (1987) An outbreak of watermelon-borne pesticide toxicity. Am. J.
public Health, 77: 1431-1434.
GRIFFITH, J. & DUNCAN, R.C. (1985) Grower reported pesticide
poisonings among Florida citrus fieldworkers. J. environ. Sci. Health,
HAINES, R.G. (1971) Ingestion of aldicarb by human volunteers: A
controlled study of the effect of aldicarb on man, Terryton, NY, Union
Carbide Corporation (Unpublished report with addendum).
HAJJAR, N.P. & HODGSON, E. (1982) Sulfoxidation of
thioether-containing pesticides by the
flavin-adenine-dinucleotide-dependent monooxygenase of pig liver
microsomes. Biochem. Pharmacol., 31: 745-752.
HAMADA, N.N. (1988) One-year chronic oral toxicity study in beagle
dogs with aldicarb technical (Study conducted for Rhône-Poulenc AG
Company, submitted to WHO).
HANSEN, J.L. & SPIEGEL, M.H. (1983) Hydrolysis studies of aldicarb,
aldicarb sulfoxide and aldicarb sulfone. Environ. Toxicol. Chem., 2:
HAQUE, A. & EBING, W. (1983) [Toxicity determination of pesticides to
earthworms in the soil.] Z. Pflanzenkr. Pflanzenschutz, 90: 395-408
(Abstract) (in German).
HAYES, W.J. (1982) Pesticides studied in man, Baltimore, Maryland,
Williams & Wilkins Publishers, pp. 447-462.
HEGG, R.O., SHELLY, W.H., JONE, R.L., & ROMINE, R.R. (1988) Movement
and degradation of aldicarb residues in South Carolina loamy sand
soil. Agric. Ecosyst. Environ., 20: 303-315.
HICKS, B.W., DOROUGH, H.W., & MEHENDALE, H.M. (1972) Metabolism of
aldicarb pesticide in laying hens. J. agric. food Chem., 20: 151-156.
HIEBSCH, S. (1988) The occurence of 35 pesticides in Canadian drinking
water and surface water, Ottawa, Canada, Environmental Health
Directorate, Department of National Health and Welfare.
HILL, E.F. & CAMARDESE, M.B. (1981) Subacute toxicity testing with
young birds: Response in relation to age and interest variability in
LC50 estimates. In: Lamb, D.W. & Kenaga, E.E., ed. Proceedings of
the Conference on Avian and Mammalian Toxicology, Philadelphia,
American Society for Testing and Material, pp. 41-65 (Abstract) (STP
HILL, E.F. & CAMARDESE, M.B. (1986) Lethal dietary toxicities of
environmental contaminants and pesticides to Coturnix, Washington, DC,
US Department of Interior, Fish and Wildlife Service, 23 pp (Technical
Report No. 2).
HILL, E.F., HEALTH, R.G., SPANN, J.W., & WILLIAM, J.D. (1975) Lethal
dietary toxicities of environmental pollutants to birds, Washington,
DC, US Department of Interior, Fish and Wildlife Service, 8 pp
(Special Report No. 191).
HIRSCH, G.H., MORI, B.T., MORGAN, G.B., BENNETT, P.R., & WILLIAMS,
B.C. (1987) Report of illness caused by aldicarb-contaminated
cucumbers. Food Addit. Contam., 5: 155-160.
HOPKINS, A.R. & TAFT, H.M. (1965) Control of certain cotton pests with
a new systemic insecticide, UC-21149. J. econ. Entomol., 58: 746-749.
HUDSON, R.H., TUCKER, R.K., & HAEGELE, M.A. (1984) Handbook of
toxicity of pesticides to wildlife, Washington, DC, US Department of
Interior, Fish and Wildlife Service (Resource Publication No. 153).
IRDC (INTERNATIONAL RESEARCH & DEVELOPMENT CORPORATION) (1983)
Teratology study in rabbits, Institute, West Virginia, Union Carbide
IRPTC (1989) IRPTC data profile on aldicarb, Geneva, International
Register of Potentially Toxic Chemicals, United Nations Environment
Programme (Report No. OR 2134).
IWATA, Y., WESTLAKE, W.E., BARKLEY, J.H., CARMAN, G.E., & GUNTHER,
F.A. (1977) Aldicarb residues in oranges, citrus by-products, orange
leaves and soil after an aldicarb soil application in an orange grove.
J. agric. food Chem., 25: 933.
JACKSON, R.J., STRATTON, J.W., GOLDMAN, L.R., SMITH, D.F., POND, E.M.,
EPSTEIN, D., NEUTRA, R.R., KELTER, A., & KIZER, K.W. (1986) Aldicarb
food poisoning from contaminated melons - California. Morb. Mortal.
wkly Rep., 35: 255-257.
JONES, A.S. (1976) Metabolism of aldicarb by five soil fungi. J.
agric. food Chem., 24: 115-177.
JONES, R.L. (1986) Field, laboratory and modelling studies on the
degradation and transport of aldicarb residues in soil and
groundwater. In: Garner, W.Y., ed. Evaluation of pesticides in
groundwater, Washington, DC, American Chemical Society, pp. 197-218
(ACS Symposium Series 315).
JONES, R.L. (1987) Central California studies on the degradation and
movement of aldicarb residues. J. Contam. Hydrol., 1: 287-298.
JONES, R.L., ROURKE, R.V., & HANSEN, J.L. (1986) Effect of application
methods on movement and degradation of aldicarb residues in Maine
potato fields. Environ. Toxicol. Chem., 5: 167-173.
JONES, R.L., HORNSBY, A.G., RAO, P.S., & ANDERSON, M.P. (1987a)
Movement and degradation of aldicarb residues in the saturated zone
under citrus groves on the Florida ridge. J. Contam. Hydrol., 1:
JONES, R.L., KIRKLAND, S.D., & CHANCEY, E.L. (1987b) Measurement of
the environmental fate of aldicarb residues in a Nebraska sand Hills
soil. Appl. agric. Res., 2: 177-182.
KNAAK, J.B., TALLANT, M.J., & SULLIVAN L.J. (1966a) The metabolism of
2-methyl-2-(methylthio)propionaldehyde O-(methylcarbamoyl)oxime in the
rat. J. agric. food Chem., 14: 573-578.
KNAAK, J.B., TALLANT, M.J., BARTLEY, W.J., & SULLIVAN, L.J. (1966b)
Metabolism of carbaryl in the rat, guinea pig and man. J. agric. food
Chem., 13(6): 537-543.
KRAUSE, R.T. (1979) Resolution, sensitivity and selectivity of an HPLC
post-column fluorometric labelling technique for determination of
carbamate insecticides. J. Chromatogr., 185(1): 615-624.
KRAUSE, R.T. (1980) Resolution, sensitivity and selectivity of
HPLC-post column fluorometric labelling technique for determination of
carbamate insecticides Chem. Abstr., 92: 141601.
KRAUSE, R.T. (1985a) Liquid chromatographic determination of N-
methylcarbamate insecticides and metabolites in crops. I.
Collaborative study. J. Assoc. Off. Anal. Chem., 68(4): 726-733.
KRAUSE, R.T. (1985b) Liquid chromatographic determination of N-
methylcarbamate insecticides and metabolites in crops. II. Analytical
characteristics and residue findings. J. Assoc. Off. Anal. Chem.,
68(4): 734- 741.
KUHR, R.J. & DOROUGH, H.W. (1976) Carbamate insecticides: Chemistry,
biochemistry, and toxicology, Cleveland, Ohio, CRC Press, Inc., pp.
2-6, 103- 112, 187-190, 211-213, 219-229.
KUSESKE, D.W., FUNK, B.R., & SCHULTZ, J.T. (1974) Effects and
persistence of Baygon (propoxur) and Temik (aldicarb) insecticides in
soil. Plant Soil, 41: 255-269.
LAFRANCE, P., AIT-SSI, L., BANTON, O., CAMPBELL, P.G.C., & VILLENEUVE,
J.P. (1988) Sorption of the pesticide aldicarb by soil: Its mobility
through a saturated medium in the presence of dissolved organic
matter. Water Pollut. Res. J. Can., 23(2): 253-269.
LANDAU, M. & TUCKER, J.W. (1984) Acute toxicity of EDB and Aldicarb to
young of two estuarine fish species. Bull. environ. Contam. Toxicol.,
LASKI, R.R. & VANNELLI, J.J. (1984) Survey of potatoes grown in New
York state for aldicarb residues. Bull. environ. Contam. Toxicol., 32:
LEE, M.H. & RANSDELL, J.F. (1984) A farmworker death due to pesticide
toxicity: a case report. J. Toxicol. environ. Health, 14: 239-246.
LEMLEY, A.T. & ZHONG, W.Z. (1983) Kinetics of aqueous base and acid
hydrolysis of aldicarb, aldicarb sulfoxide and aldicarb sulfone. J.
environ. Sci. Health, B18: 189-206.
LEMLEY, A.T., WAGNET, R.T., & ZHONG, W.Z. (1988) Sorption and
degradation of aldicarb and its oxidation products in a soil-water
flow system as a function of pH and temperature. J. environ. Qual.,
LIGHTFOOT, E.N. & THORNE, P.S. (1987) Laboratory studies on mechanisms
for the degradation of aldicarb, aldicarb sulfoxide and aldicarb
sulfone Environ. Toxicol. Chem., 6: 337-394.
LIJINSKY, W. & SCHMAHL, D. (1978) Carcinogenicity of N-nitroso
derivatives of N-methylcarbamate insecticides in rats. Ecotoxicol.
environ. Saf., 2: 413-419.
LORBER, M.N., COHEN, S.Z., NOVEN, S.E., & DEBUCHANANNE, G.D. (1989)
Focus: A national evaluation of the leaching potential of aldicarb:
Part I - An integrated assessment methodology. Groundwater monit.
Rep., Fall 1989: 109- 125.
LORBER, M., COHEN, S. & DEBUCHANNE (1990) Focus: A national evaluation
of the leaching potential of aldicarb: Part II - An evaluation of
groundwater monitoring data. Groundwater monit. Rep., Winter 1990:
MAIBACH, H.I., FELDMAN, R.J., MILBY, T.H., & SERAT, W.F. (1971)
Regional variation in percutaneous penetration in man. Arch. environ.
Health, 23: 208- 211.
MAITLEN, J.C. & POWELL, D.M. (1982) Persistence of aldicarb in soil
relative to the carry-over of residues into crops. J. agric. food
Chem., 30: 589-592.
MAITLEN, J.C., MCDONOUGH, L.M., DEAN, F., BUTT, B.A., & LANDIS, B.J.
(1970) Aldicarb residues in apples, pears, sugarbeets and cottonseed,
performance in apples and pears, Washington, DC, US Department of
Agriculture, Agricultural Research Service (Report AR5-33-135).
MARSHALL, E. (1985) The rise and decline of Temik. Science, 229:
MARSHALL, T.C. & DOROUGH, H.W. (1979) Biliary excretion of carbamate
insecticides in the rat. Pestic. Biochem. Physiol., 11: 56-63.
MARTIN, A.D., NORMAN, G., STANLEY, P.I., & WESTLAKE, G.E. (1981) Use
of reactivation techniques for the differential diagnosis of
organophosphorus and carbamate pesticide poisoning in birds. Bull.
environ. Contam. Toxicol., 26: 775-780.
MARTIN, G., MAGRUDER, L., PATRICK, K., VAIL, M., SCHUETTE, W., KELLER,
R., MUIRHEAD, K., HORAN, P., & GRAINICK, H. (1985) Normal human blood
density gradient lymphocytes subset analysis. 1. An interlaboratory
flow cytometric comparison of 85 normal adults. Am. J. Hematol., 20:
MARTIN, H. & WORTHING, C.R., ed. (1977) Pesticide manual, Croydon,
British Crop Protection Council, p. 6.
MAYER, F.L. (1987) Acute toxicity handbook of chemicals to estuarine
organisms, Gulf Breeze, Florida, US Environmental Protection Agency,
Environmental Research Laboratory, 14 pp (Unpublished report).
MAYER, F.L. & ELLERSIECK, M.R. (1986) Manual of acute toxicity:
interpretation and data base for 410 chemicals and 66 species of
freshwater animals, Washington, DC, US Department of Interior, Fish
and Wildlife Service, 9 pp (Report No. 160).
METCALF, R.L., FUKUTO, T.R., COLLINS, C., BORCK, K., BURK, J.,
REYNOLDS, H.T., & OSMAN, M.F. (1966) Metabolism of
2-methyl-2-(methylthio)-propianaldehyde O-(methylcarbamoyl)oxime in
plant and insect. J. agric. food Chem., 14: 579-584.
MILLER, W.L., DAVIDSON, J.M., FORAN, J.A., MOYE, H.A., & SPANGLER,
D.P. (1985) Peer Review Committee Report - The Florida Temik study:
Groundwater monitoring, Las Vegas, NV, US Environmental Protection
Agency (Final report) (EMSL/ORD).
MITCHELL, A., RUDD, C.J., & CASPARY, W.J. (1988) Evaluation of L5178Y
mouse lymphoma cell mutagenesis assay: intralaboratory results for
sixty-three coded chemicals tested at SRI International Environ. mol.
Mutagen., 12: 37-102.
MOYE, H.A. (1975) Esters of sulfonic acids as derivatives for the gas
chromatographic analysis of carbamate pesticides. J. agric. food
Chem., 23(3): 415-418.
MOYE, H.A. & MILES, C.J. (1988) Aldicarb contamination of groundwater
Rev. environ. Contam. Toxicol., 105: 99-146.
MOYE, H.A., SCHERER, S.J., & ST. JOHN, P.A. (1977) Dynamic fluorogenic
labeling of pesticides for HPLC: Detection of N-methyl carbamates with
o-phthaladehyde. Anal. Lett., 10(3): 1049-1073.
MUSZKAT, L. & AHARONSON, N. (1983) GC/CI/MS analysis of aldicarb,
butocar-boxim and their metabolites. J. chromatogr. Sci., 21: 411-414.
MYERS, R.C., WEIL, C.S., & FRANK, F.R. (1982) Temik 5G (Corn Cob
Grits). Percutaneous toxicity and skin irritancy study, Export,
Pennsylvania, Union Carbide Bushy Run Research Center, 12 pp
(Unpublished Project Report No. 45-88, submitted to WHO by
MYERS, R.C., DEPASS, L.R., & FRANK, F.R. (1983) Temik 5G (Corn Cob
Grit). Acute peroral toxicity and eye irritancy study, Export,
Pennsylvania, Union Carbide Bushy Run Research Center, 10pp
(Unpublished Project Report No. 46-100, submitted to WHO by
MYHR, B.C. & CASPARY, W.J. (1988) Evaluation of the L5178Y mouse
lymphoma cell mutagenesis assay: Intralaboratory results for
sixty-three coded chemicals tested at Litton Bionetics, Inc. Environ.
mol. Mutagen., 12: 103-194.
NAS (1986) Drinking water and health, Washington, DC, National Academy
of Sciences, Vol. 6, pp. 13-19.
NCI (1979) Bioassay of aldicarb for possible carcinogencity, Bethesda,
Maryland, National Cancer Institute (Report NCI-CG-TR-136).
NYCUM, J.S. & CARPENTER, C. (1970) Summary with respect to guideline
PR70-15 (Unpublished Mellon Institute Report No. 31-48).
OLSON, L.J., ERICKSON, B.J., HINSDILL, R.D., WYMAN, J.A., PORTER,
W.P., BINNING, L.K., BIDGOOD, R.C., & NORDHEIM, E.V. (1987) Aldicarb
immunomodulation in mice: An inverse dose-response to parts per
billion levels in drinking water. Arch. environ. Contam. Toxicol., 16:
OONNITHAN, E.S. & CASIDA, J.E. (1967) Oxidation of methyl- and
dimethyl-carbamate insecticide chemicals by microsomal enzymes and
anticholinesterase activity of the metabolites. J. agric. food Chem.,
OU, L.-T., THOMAS, J.E., EDVARDSSON, K.S.V., RAO, P.S.C., & WHEELER,
W.B. (1986) Aerobic and anaerobic degradation of aldicarb in
asceptically collected soils. J. environ. Qual., 15: 356-363.
PACENKA, S., PORTER, K.S., JONES, R.L., ZECHARIAS, Y.B., & HUGHES,
H.B.F. (1987) Changing aldicarb residue levels in soil and
groundwater, Eastern Long Island, New York, J. environ. Hydrol., 2:
PANT, S.C. & KUMAR, S. (1981) Toxicity of Temik for a freshwater
teleost, wBarbus conchoniusHamilton. Experientia (Basel), 37:
PAYNE, L.K., STANSBUR, H.A., & WEIDEN, M.H.J. (1966). Synthesis and
insecticidal properties of some cholinergic trisubstituted acetaldehye
O-(methylcarbamoyl)oximes. J. agric. food Chem., 14: 356-365.
PEOPLES, S.A., MADDY, K.T., & SMITH, C.R. (1978) Occupational exposure
to Temik (aldicarb) as reported by California physicians for
1974-1976. Vet. hum. Toxicol., 20(5): 321- 324.
PETERSON, B. & GREGORIO, C.A. (1988) Aldicarb acute dietary exposure
analysis (Unpublished report prepared for Rhône-Poulenc Co.).
PICKERING, D.J. & GILLIAM, W.T. (1982) Toxicity of aldicarb and
fonofos to the early-life stage of the fathead minnow. Arch. environ.
Contam. Toxicol., 11: 699-702.
POZZANI, U.C. & CARPENTER, C.P. (1968) Sensitizing potential in guinea
pigs as determined by a modified Lansteiner test (Unpublished Mellon
Institute Report No. 31-143).
PRIDDLE, M.W., JACKSON, R.E., & MUTCH, J.P. (1989) Contamination of
the sandstone aquifer of Prince Edward Island, Canada, by aldicarb and
nitrogen residues Groundwater monit. Rep., Fall 1989: 134-140.
PROCTOR, N.H., MOSCIONI, A.D., & CASIDA, J.E. (1976) Chicken embryo
NAD levels lowered by teratogenic organophosphorus and methylcarbamate
insecticides. Biochem. Pharmacol., 25: 757-762.
QUARLES, J.M., SEGA, M.W., SCHENLEY, C.K., & LIJINSKY, W. (1979)
Transformation of hamster fetal cells by nitrosated pesticides in a
transplacental assay. Cancer Res., 39: 4525-4533.
QURAISHI, M.S. (1972) Edaphic and water relationships of aldicarb and
its metabolites. Can. Entomol., 104: 1191-1196.
RAMASAMY, P. (1976) Carbamate insecticide poisoning. Med. J. Malaysia,
RASHID, K.A. & MUMMA, R.O. (1986) Screening pesticides for their
ability to damage bacterial DNA. J. environ. Sci. Health, B21(4):
REDING, R. (1987) Chromatographic monitoring methods for organic
contaminants under the Safe Drinking Water Act. J. chromatogr. Sci.,
RICHEY, F.A., BARTLEY, W.J., & SHEETS, K.P. (1977) Laboratory studies
on the degradation of the pesticide aldicarb in soils. J. agric. food
Chem., 25: 47- 51.
RIDGWAY, R.L., JACKSON, C.G., PATANA, R.L., LINDQUIST, D.A., REEVES,
B.G., & BARIOLA, L.A. (1966) Systemic insecticides for control of
Lygus hesperus Knight on cotton. J. econ. Entomol., 59: 1017.
RIVA, M. & CARISANO, A. (1969) Compact dual-channel flame ionization
and thermionic detector for high-specificity chromatographic analysis.
J. Chromatogr., 42: 464.
ROTHSCHILD, E.R., MANSER, R.J., & ANDERSON, M.P. (1982) Investigation
of aldicarb in ground water in selected areas of the central sand
plain of Wisconsin. Groundwater, 20: 437-445.
RYAN, A.J. (1971) The metabolism of pesticidal carbamates. CRC crit.
Rev. Toxicol., 1: 33-54.
SAKAI, K. & MATSUMURA, F. (1968) Esterases of mouse brain active in
hydrolysing organophosphate and carbamate insecticides. J. agric. food
Chem., 16(5): 803-807.
SAKAI, K. & MATSUMURA, F. (1971) Degradation of certain
organophosphate and carbamate insecticides by human brain esterases.
Toxicol. appl. Pharmacol., 19(4): 660-666.
SCHAFER, E.W., Jr & BOWLES, W.A., Jr (1985) Acute oral toxicity and
repellency of 933 chemicals to house and deer mice. Arch. environ.
Contam. Toxicol., 14: 119-129.
SCHLINKE, J.C. (1970) Toxicologic effects of five soil nematocides in
chickens. J. Am. Vet. Med. Assoc., 31: 119-121.
SEILER, J.P. (1977) Nitrosation win vitrow by sodium nitrate, and
mutagenicity of nitrogenous pesticides Mutat. Res., 48: 225-236.
SELVAN, R.S., DEAN, T.N., MISRA, H.P., NAGARKATTI, P.S., & NAGARKATTI,
M. (1989) Aldicarb suppresses macrophage but not natural killer (NK)
cell-mediated cytotoxicity of tumor cells. Bull. environ. Contam.
Toxicol., 43: 676-682.
SEXTON, W.F. (1966) Report on aldicarb. EPA Pesticide Petition No.
9F0798, Section C., submitted to US Environmental Protection Agency,
SHARAF, A.A., TEMTAMY, S.A., DEHONDT, H.A., BELAH, M.H., & KASSAM,
E.A. (1982) Effect of aldicarb (Temik), a carbamate insecticide, on
chromosomes of the laboratory rat. Egypt. J. Genet. Cytol., 11(2):
SHIRAZI, M.A., ERICKSON, B.J., HINSDILL, R.D., & WYMANN, J.A. (1990)
Analysis of risk from exposure to aldicarb using immune response of
nonuniform population of mice. Arch. environ. Contam. Toxicol., 19:
SINGH, O. & AGARWAL, R.A. (1981) Toxicity of certain pesticides to two
economic species of snails in northern India. J. econ. Entomol., 74:
SPARACINO, C.M., PELLIZARRI, E.D., COOK, C.E., & WALL, M.W. (1973)
Reexamination of the GC determination of ý-d-propoxyphene. J.
Chromatogr., 77(2): 413-418.
SPIERENBURG, TH.J., ZOUN, P.E.F., DOORENBOS, F.W., & WANNINGEN, H.
(1985) [A case of aldicarb intoxication in cattle.] Tijdschr.
Diergeneeskd., 110: 555-558 (in Dutch with English abstract).
SPURR, H.W., Jr & SOUSA, A.A. (1966) Pathogenicidal activity of a new
carbamoyloxime insecticide. Plant Dis. Rep., 50: 424-425.
SPURR, H.W., Jr & SOUSA, A.A. (1967) Effects of aldicarb as a systemic
fungicide. Chem. Abstr., 67: 10927 (116136m).
SPURR, H.W., Jr & SOUSA, A.A. (1974) Potential interactions of
aldicarb and its metabolites on nontarget organisms in the
environment. J. environ. Qual., 3: 130-133.
SRI (1984) Chemical economics handbook, Menlo Park, California,
Stanford Research Institute, Chemical Information Service.
STANKOWSKI, L.F., NAISMITH, R.W., & MATTHEWS, R.J. (1985) Mammalian
cell forward gene mutation assay (Study conducted for Union Carbide
Corporation, submitted to WHO).
STRIEGEL, J.A. & CARPENTER, C.P. (1962) Range finding tests on
Compound 21149 (Unpublished Mellon Institute Report No. 25-53).
SUPAK, J.R., SWOBODA, A.R., & DIXON, J.B. (1977) Volatilization and
degradation losses of aldicarb from soils. J. environ. Qual., 6:
TAKUSAGAWA, F. & JACOBSON, R.A. (1977) Crystal and molecular structure
of carbamate insecticides. 2. Aldicarb. J. agric. food Chem., 25:
THOMAS, P.T., & RATAJCZAK, H.V. (1988) Assessment of carbamate
pesticide immunotoxicity. Toxicol. ind. Health, 4(3): 381-390.
THOMAS, P.T., RATAJCZAK, H.V., EISENBERG, W.C., FUREDZ MACHACEK, M.,
KETELS, K.V., & BARBERA, P.W. (1987) Evaluation of host resistance and
immunity in mice exposed to the carbamate pesticide aldicarb. Fundam.
appl. Toxicol., 9: 82-89.
THOMAS, P.T., RATAJEZAK, H., DEMETRAL, D., HAGEN, K., & BARON, R.
(1990) Aldicarb immunotoxicity: Functional analysis of cell- mediated
immunity and quantitation of lymphocyte subpopulations. Fundam. appl.
Toxicol., 15: 221-230.
TING, K.C. & KHO, P.K. (1986) High performance liquid chromatographic
method for the determination of aldicarb sulfoxide in watermelon.
Bull. environ. Contam. Toxicol., 37: 192-198.
TING, K.C., KHO, P.K., MUSSELMAN, A.S., ROOT, G.A., & TICHELAR, G.R.
(1984) High performance liquid chromatographic method for
determination of six N-methylcarbamates in vegetables and fruits.
Bull. environ. Contam. Toxicol., 33: 538-547.
TRUTTER, J.A. (1989a) Acute oral toxicity study in cynomolgus monkeys
of aldicarb sulfoxide/sulfone residues in watermelons (Unpublished
Union Carbide Corporation study, submitted to WHO).
TRUTTER, J.A. (1989b) Acute oral toxicity study in cynomolgus monkeys
of aldicarb sulfoxide/sulfone residues in bananas (Unpublished Union
Carbide Corporation study, submitted to WHO).
TYL, R.W. & NEEPER-BRADLEY, T.L. (1988) Developmental toxicity
evaluation of aldicarb administered by gavage to CD rats (Study
conducted for Rhône-Poulenc Co., submitted to WHO).
UNION CARBIDE (1983) Temik aldicarb pesticide: A scientific assessment
(Unpublished study submitted by Union Carbide to US EPA).
US EPA (1984) Method 531. Measurement of N-methylcarbamoyloximes and
N-methylcarbamates in drinking water by direct aqueous injection HPLC
with post column derivatization, Cincinnati, Ohio, US Environmental
Protection Agency, Environmental Monitoring and Support Laboratory.
US EPA (1985) Risk assessment of potential Temik contamination of
drinking water in Florida, Cincinnati, Ohio, US Environmental
Protection Agency, Environmental Criteria and Assessment Office.
US EPA (1986) Reference dose for aldicarb, Cincinnati, Ohio, US
Environmental Protection Agency, Environmental Criteria and Assessment
Office (Prepared for US EPA, Office of Solid Waste, Washington).
US EPA (1988a) Aldicarb special review technical support document.
Washington, DC, US Environmental Protection Agency, Office of
Pesticides and Toxic Substances.
US EPA (1988b) Pesticides in groundwater. Data base 1988 interim
report, Washington, DC, US Environmental Protection Agency, Office of
Pesticide Programs, Environmental Fate and Groundwater Branch.
US EPA (1989) Protection of environment. Aldicarb tolerance for
residues. Fed. Reg., 40: 324 180.269.
VARMA, A.O., ZAKI, M., & STERMAN, A.B. (1983) Results of a preliminary
survey, Stony Brook, New York, State University of New York, School of
WEIDEN, M.H.J., MOOREFIELD, H.H., & PAYNE, L.K. (1965)
O-(methyl-carbomyl)-oximes: A class of carbamate insecticides -
Acarides. J. econ. Entomol., 58: 154-155.
WEIL, C.S. (1968) EPA Pesticide Petition No. 9F0798 (Unpublished
Mellon Institute Report No. 31-48).
WEIL, C.S. (1973) Miscellaneous toxicity studies (Unpublished Mellon
Institute Report No. 35-41).
WEIL, C.S. & CARPENTER, C.P. (1963) Results of three months of
inclusion of Compound 21149 in the diet of rats (Unpublished Mellon
Institute Report No. 26-47, Section C).
WEIL, C.S. & CARPENTER, C.P. (1964) Results of a three-generation
reproduction study on rats fed Compound 21149 in their diet
(Unpublished Mellon Institute Report No. 27-158).
WEIL, C.S. & CARPENTER, C.P. (1965) Two-year feeding of Compound 21149
in the diet of rats (Unpublished Mellon Institute Report No. 28-123).
WEIL, C.S. & CARPENTER, C.P. (1966) Two-year feeding of Compound 21149
in the diet of dogs (Unpublished Mellon Institute Report No. 29-5).
WEIL, C.S. & CARPENTER, C.P. (1968a) Temik 10G. Acute and fourteen-day
dermal applications to rabbits (Unpublished Mellon Institute Report
WEIL, C.S. & CARPENTER, C.P. (1968b) Temik sulfoxide. Results of
feeding in the diet of rats for six months and dogs for three months
(Unpublished Mellon Institute Report No. 31-141).
WEIL, C.S. & CARPENTER, C.P. (1968c) Temik sulfone. Results of feeding
in the diet of rats for six months and dogs for three months
(Unpublished Mellon Institute Report No. 31-142).
WEIL, C.S. & CARPENTER, C.P. (1970) Temik and other materials.
Miscellaneous single dose peroral and parenteral LD50 assays and
some joint action studies (Mellon Institute Report No. 33-7. Amendment
to EPA Pesticide Petition No. 9F0798).
WEIL, C.S. & CARPENTER, C.P. (1972) Aldicarb (A), aldicarb sulfoxide
(ASO), aldicarb sulfone (ASO2) and a 1:1 mixture of ASO:ASO2. Two-year
feeding in the diet of rats (Unpublished Mellon Institute Report No.
WEIL, C.S. & CARPENTER, C.P. (1974a) Aldicarb. Inclusion in the diet
of rats for three generations and a dominant lethal mutagenesis test
(Unpublished Mellon Institute Report 37-90).
WEIL, C.S. & CARPENTER, C.P. (1974b). Aldicarb. 18-Month feeding in
the diet of mice, Study II (Unpublished Mellon Institute Report
WEST, J.S. & CARPENTER, C.P. (1965) The single dose peroral toxicity
of Compounds 20299, 21149, 19786 and 20047A for white leghorn
cockerels (Unpublished Mellon Institute Report No. 28-30).
WEST, J.S. & CARPENTER, C.P. (1966) Miscellaneous acute toxicity data
(Unpublished Mellon Institute Report No. 28-140).
WHO (1986) Environmental Health Criteria 64: Carbamate pesticides: a
general introduction, Geneva, World Health Organization, 137 pp.
WHO (1990a) Environmental Health Criteria 104: Principles for the
toxicological assessment of pesticide residues in food, Geneva, World
Health Organization, 117 pp.
WHO (1990b) The WHO recommended classification of pesticides by hazard
and guidelines to classification 1990-1991. Geneva, World Health
Organization (Document WHO/PCS/90.1).
WILKINSON, C.F., BABISH, J.G., LEMLEY, A.T., & SODERLUND, D.M. (1983)
A toxicological evaluation of aldicarb and its metabolites in relation
to the potential human health impact of aldicarb residues in Long
Island ground water, Ithaca, New York, Cornell University, Committee
from the Institute for Comparative and Environmental Toxicology
WOODHAM, D.W., EDWARDS, R.R., REEVES, R.G., & SCHUTZMANN, R.L. (1973a)
Total toxic aldicarb residues in soil, cotton seed, and cotton lint
following a soil treatment with the insecticide on the Texas High
Plains. J. agric. food Chem., 21: 303-307.
WOODHAM, D.W., REEVES, R.G., & EDWARDS, R.R. (1973b) Total toxic
aldicarb residues in weeds, grasses, and wildlife from the Texas High
Plains following a soil treatment with insecticide. J. agric. food
Chem., 21: 604-607.
WOODSIDE, M.D., WEIL, C.S., & COX, E.F. (1977) Inclusion in the diet
of rats for three generations (aldicarb sulfone), dominant lethal
mutagenesis and teratology studies (Unpublished Mellon Institute
Report No. 419, submitted to WHO by Union Carbide Corporation).
WORTHING, C.R. & WALKER, S.B. (1987) The pesticide manual: a world
compendium, 8th ed., London, British Crop Protection Council.
WRIGHT, L.H., JACKSON, M.D., & LEWIS, R.G. (1982) Determination of
aldicarb residues in water by combined high performance liquid
chromatography/mass spectrometry. Bull. environ. Contam. Toxicol., 28:
WYMAN, J.A., JONES, R.L., JOSE, M., CURWEN, D., & HANSEN, J.L. (1987)
Environmental fate studies of aldicarb and aldoxycarb applications to
Wisconsin potatoes. J. Contam. Hydrol., 2: 61-72.
1. Identité, propriétés et méthodes d'analyse
L'aldicarbe est un ester carbamique. Il se présente sous la forme
d'un solide cristallin blanc, modérément soluble dans l'eau, sensible
à l'oxydation et à l'hydrolyse.
Plusieurs méthodes d'analyse sont utilisables, notamment la
chromatographie en couche mince, la chromatographie en phase gazeuse
(capture d'électrons, ionisation de flamme, etc.) et la
chromatographie en phase liquide. Actuellement la méthode de choix
pour le dosage de l'aldicarbe et de ses principaux produits de
décomposition est la chromatographie en phase liquide à haute
performance avec formation de dérivés après passage sur colonne et
détection par fluorescence.
2. Usages, sources et niveaux d'exposition
L'aldicarbe est un pesticide endothérapique que l'on applique
dans le sol pour détruire certains insectes, acariens et nématodes.
Les récoltes concernées sont très diverses: bananes, coton, café,
maïs, oignons, agrumes, haricots (secs), noix de pécan, pommes de
terre, arachide, soja, betteraves sucrières, canne à sucre, patates
douces, sorgho, tabac ainsi que les plantes ornementales et les
pépinières. L'exposition de la population générale à l'aldicarbe et à
ses métabolites toxiques (le sulfoxyde et la sulfone) intervient
principalement par l'intermédiaire des aliments. C'est ainsi que
l'ingestion de produits alimentaires contaminés a entraîné des cas
d'intoxication par l'aldicarbe ou ses métabolites toxiques (sulfoxyde
En raison de la forte toxicité aiguë de l'aldicarbe, l'inhalation
et le contact cutané avec cette substance, dans des conditions
d'exposition professionnelle, peuvent être dangereuses pour les
travailleurs en l'absence de mesures de prévention. On dénombre
quelques cas d'exposition accidentelle de travailleurs qui
s'expliquent par des erreurs de manipulation ou l'absence de mesures
L'aldicarbe s'oxyde rapidement en sulfoxyde, le taux de
conversion étant de 48% en l'espace de sept jours après application
sur certains types de sol. L'oxydation en sulfone est beaucoup plus
lente. L'hydrolyse du groupement ester carbamique, qui inactive le
pesticide, dépend du pH, la demi-vie dans l'eau distillée allant de
quelques minutes à pH > 12 à 560 jours à pH 6,0. Dans le sol de
surface, la demi-vie varie d'environ 0,5 à trois mois et dans la zone
saturée, de 0,4 à 36 mois. L'aldicarbe s'hydrolyse un peu plus
lentement que le sulfoxyde ou la sulfone. L'étude en laboratoire de la
décomposition biotique et abiotique de l'aldicarbe a fourni des
résultats très variables qui ont donné lieu à des extrapolations
radicalement différentes sur la base d'observations en situation
réelle. En ce qui concerne les produits de dégradation de l'aldicarbe,
ce sont les données obtenues sur le terrain qui permettent les
hypothèses les plus fiables quant à la destinée de ce pesticide.
Les terrains sablonneux à faible teneur en matières organiques
permettent un lessivage maximal, en particulier lorsque la nappe
phréatique est haute. Des nappes de drainage et des puits de faible
profondeur ont été contaminés par du sulfoxyde et de la sulfone
d'aldicarbe; les concentrations étaient généralement comprises entre
1 et 50 µg/litre, avec une fois une teneur d'environ 500 µg/litre.
L'aldicarbe étant un pesticide endothérapique, il peut laisser
des résidus dans les aliments. On a fait état de résidus dépassant 1
mg/kg dans des pommes de terre crues. Aux Etats-Unis d'Amérique, où la
limite de tolérance pour les pommes de terre est de 1 mg/kg, on a
signalé des teneurs en résidus allant jusqu'à 0,82 mg/kg à la suite
d'essais contrôlés sur le terrain aux doses d'emploi recommandées par
le fabriquant. Les données obtenues ont permis de fixer le 95ème
percentile à 0,43 mg/kg, cette valeur atteignant 0,0677 mg/kg dans les
pommes de terre crues lors d'une enquête basée sur le panier de la
3. Cinétique et métabolisme
L'aldicarbe est bien résorbé au niveau des voies digestives et
dans une moindre mesure, au niveau de la peau. Présent sous la forme
de poussière, il pourrait être très facilement absorbé dans les voies
respiratoires. Il se distribue dans l'ensemble des tissus et notamment
dans ceux du foetus de rat en développement. Il subit ensuite une
transformation métabolique en sulfoxyde et en sulfone, qui sont tous
deux toxiques, puis une détoxification par hydrolyse en oximes et en
nitriles. L'excrétion de l'aldicarbe et de ses métabolites s'effectue
rapidement, principalement par la voie urinaire. Il est également
excrété en faible proportion dans la bile et subit donc un recyclage
entérohépatique. L'aldicarbe ne s'accumule pas dans l'organisme par
suite d'une exposition de longue durée. In vitro , l'inhibition de
la cholinestérase par l'aldicarbe est spontanément réversible, avec
une demi-vie de 30 à 40 minutes.
4. Etudes sur les animaux d'expérience
L'aldicarbe est un puissant inhibiteur de cholinestérases et
présente une forte toxicité aiguë. Si l'animal ne meurt pas, les
effets cholinergiques disparaissent spontanément et complètement en
six heures. Rien n'indique que l'aldicarbe soit tératogène, mutagène,
cancérogène ou immunotoxique.
Des oiseaux et de petits mammifères sont morts après ingestion de
granulés d'aldicarbe qui n'étaient pas complètement incorporés au sol
conformément aux recommandations d'emploi. Au laboratoire, l'aldicarbe
se révèle doté d'une forte toxicité aiguë pour les organismes
aquatiques. Rien n'indique toutefois que ces effets se produiraient
sur le terrain.
5. Effets sur l'homme
L'inhibition de l'acétylcholinestérase au niveau de la synapse
nerveuse et de la plaque motrice est le seul effet qui ait été dûment
observé chez l'homme et il est analogue à celui qu'exercent les
organophosphorés. L'enzyme carbamylée est instable et elle se réactive
spontanément assez vite par comparaison avec l'enzyme phosphorylée.
Lorsqu'elle n'est pas mortelle, l'intoxication est rapidement
réversible chez l'homme. La réactivation est facilitée par
EVALUATION DES RISQUES POUR LA SANTE HUMAINE ET EFFETS SUR
1. Evaluation des risques pour la santé humaine
L'aldicarbe est un pesticide extrêmement dangereux. Pour l'homme,
les risques découlent principalement d'erreurs de manipulation et de
la non-utilisation de matériel protecteur au cours de la fabrication,
de la formulation et de l'épandage. L'aldicarbe peut contaminer les
denrées alimentaires et l'eau de boisson. Les effets d'une
surexposition sont aigus mais réversibles. Les effets cholinergiques
peuvent être graves, incapacitants et nécessiter une hospitalisation,
mais ils sont rarement mortels.
1.1 Niveaux d'exposition
1.1.1 Population générale
Les principales sources d'exposition de la population générale
sont les denrées alimentaires et l'eau.
Il existe aux Etats-Unis un certain nombre de données qui
permettent d'estimer l'apport alimentaire journalier d'aldicarbe (voir
section 5.2). De nombreuses données montrent que les résidus présents
dans la plupart des produits après récolte sont généralement peu
abondants et ne dépassent pas en tout cas les limites maximales de
résidus, dans la mesure où l'aldicarbe est utilisé conformément aux
bonnes pratiques agricoles pendant les périodes recommandées avant la
récolte. Toutefois, même dans ce dernier cas, on trouve des
concentrations dans les pommes de terre pouvant aller jusqu'à 1 mg/kg
et parfois plus.
On a découvert de fortes concentrations d'aldicarbe dans
certaines cultures vivrières traitées illégalement avec ce produit. Un
cas d'intoxication s'est produit après consommation de concombres
obtenus par culture hydroponique, à des concentrations de 6,6 à 10,7
mg d'aldicarbe par kg. Deux autres cas d'intoxication ont été signalés
aux Etats-Unis par suite de la consommation de pastèques contaminées,
la teneur en aldicarbe allant de < 0,01 à 6,3 mg/kg. Toutefois il
n'est pas certain que ces valeurs correspondent à l'exposition réelle.
Il y a eu des cas de contamination des eaux souterraines par de
l'aldicarbe. Dans certaines régions du Canada, environ 12% des puits
contrôlés en contiennent plus de 9 µg/litre. Sur 7802 puits soumis à
des prélèvements dans l'Etat de New York aux Etats-Unis, dans un
secteur où l'on épandait de l'aldicarbe sur des pommes de terre, 5745
(73,6%) ne présentaient aucun résidu décelable, 1032 (13,3%) en
contenaient des traces et 1025 (13,1%) présentaient une teneur
supérieure à 7µg/litre.
Aux Etats-Unis, on a constaté à la suite d'une enquête portant
sur l'eau de 15 000 puits privés, que celle-ci contenait entre 1 et 50
µg/litre d'aldicarbe dans environ un tiers des cas. Occasionnellement,
on a relevé lors de forages de contrôle, des concentrations de 500
mg/litre dans les eaux souterraines.
1.1.2 Exposition professionnelle
Lorsqu'on effectue des épandages à des fins agricoles, on peut
réduire les concentrations atmosphériques d'aldicarbe en utilisant le
produit sous forme de granulés. Toutefois certaines opérations, comme
le chargement, demeurent dangereuses si des mesures de protection
individuelle suffisantes ne sont pas prises. Un jeune ouvrier qui
travaillait au chargement d'une formulation d'aldicarbe est décédé par
suite d'une surexposition à ce produit qui avait conduit une
concentration tissulaire de 0,275 mg/kg. La principale voie
d'exposition professionnelle est la voie cutanée, en particulier
lorsque les ouvriers ne respectent pas les précautions d'emploi et
omettent d'utiliser un équipement protecteur.
1.2 Effets toxiques
Les effets ou manifestations toxiques de l'aldicarbe et de ses
métabolites (sulfoxyde et sulfone) proviennent de leur action
inhibitrice sur l'acétylcholinestérase. Cette inhibition est
réversible. Les symptômes, qui dépendent de l'ampleur et de la gravité
de l'exposition, sont les suivants: maux de tête, sensation
vertigineuse, anxiété, sueur profuse, salivation, lacrymation,
hypersécrétions bronchiques, vomissements, diarrhées, coliques,
fibrillation musculaire et myosis. Rien n'indique que le produit soit
cancérogène, mutagène, tératogène ou immunotoxique.
Chez l'homme, l'administration par voie orale d'une seule dose de
0,025 mg d'aldicarbe par kg de poids corporel a produit une inhibition
sensible de l'activité cholinestérasique du sang total, qui est
toutefois restée asymptomatique. A la dose de 0,10 mg/kg de poids
corporel, sont apparus des symptômes cholinergiques et à celle de 0,26
mg/kg une intoxication aiguë nécessitant un traitement.
1.3 Evaluation du risque
Les risques découlant de l'utilisation d'une substance chimique
extrêmement dangereuse ne peuvent s'évaluer qu'en fonction des
différents types d'exposition, ainsi que des mesures de sécurité qu'on
peut mettre en oeuvre et du degré de certitude qu'on a de leur
Ce sont les personnes qui fabriquent, formulent et utilisent
l'aldicarbe qui sont de loin les plus exposées au risque. La
fabrication s'effectue en vase clos. L'emploi de l'aldicarbe sous
forme de granulés réduit la formation de poussière et le risque
d'exposition professionnelle. Quelques accidents se sont produits lors
des opérations de formulation et d'épandage mais dans chaque cas il y
avait eu, à une ou plusieurs reprises, violation indiscutable des
règles de sécurité (voir section 8.2.1). Toutefois, même utilisé en
granulés, l'aldicarbe peut être dangereux pour les ouvriers chargés de
l'épandage s'ils n'observent pas les précautions recommandées.
Des résidus d'aldicarbe peuvent être présents dans les denrées
alimentaires par suite de l'application en toute légalité de ce
produit sur des récoltes pour lesquelles on en a autorisé l'emploi,
ainsi d'ailleurs qu'en raison d'une utilisation illicite ou
défectueuse de ce produit. Rien ne permet de penser que la population
générale courre un risque dû à la présence d'aldicarbe dans les
produits alimentaires lorsque cette substance est appliquée aux doses
recommandées et selon les techniques actuelles. Toutefois il existe un
risque non négligeable si l'on répand de l'aldicarbe sur des cultures
pour lesquelles il n'est pas autorisé ainsi que le montrent un certain
nombre de cas d'intoxication. D'ailleurs, on a établi des limites et
des tolérances pour les taux d'application sur le sol dans les cas où
l'emploi d'aldicarbe est autorisé afin de protéger la population dans
son ensemble. Ces mesures ont été couronnées de succès puisqu'on ne
signale pas de cas d'effets nocifs dus à une exposition à l'aldicarbe
par suite de la consommation de denrées traitées correctement au moyen
de ce produit. Des enquêtes sur le panier de la ménagère ont fourni
des données limitées qui montrent que l'exposition à l'aldicarbe ne
dépasse probablement pas aux Etats-Unis 1 µg/kg de poids corporel et
par jour. Cette valeur est très inférieure à la dose journalière
admissible (DJA), fixée lors de la Réunion conjointe FAO/OMS sur les
résidus de pesticides (FAO/OMS, 1983).
On n'a pas retrouvé d'aldicarbe dans l'eau d'adduction provenant
de nappes profondes ou d'eau de surface et il n'y a donc pas lieu de
craindre un risque d'intoxication par l'aldicarbe qui aurait cette
origine. On a signalé des cas de contamination d'eau souterraine par
de l'aldicarbe, en général à des doses de 1 à 50 µg/litre aux
Etats-Unis, avec parfois des teneurs allant jusqu'à 500 µg par litre.
Toutefois, la plupart des puits qui ont été contrôlés dans les zones
contaminées ne contenaient tout au plus que des traces d'aldicarbe ou
de ses métabolites. Les restrictions imposées à l'utilisation de
l'aldicarbe sur les sols sableux ont permis de réduire la
contamination des eaux souterraines.
Si l'on admet que la consommation d'eau est en moyenne de 2
litres par jour pour un poids corporel moyen de 60 kg, on peut en
déduire que l'exposition des personnes qui consommeraient de l'eau
provenant de puits peu profonds contaminés par de l'aldicarbe à des
teneurs allant de 1 à 50 µg/litre, serait de 0,033 à 1,7 µg/kg de
métabolites par jour. Un puits dont l'eau serait contaminée à la dose
de 500 µg/litre entraînerait une exposition de 17 µg/kg de poids
corporel et par jour. La meilleure étude relative au risque de
contamination par consommation d'eau de boisson a été effectuée sur
des rats qui recevaient de l'aldicarbe sous forme de sulfoxyde et de
sulfone dans leur eau de boisson. La dose sans effet observable sur
l'acétylcholinestérase mesurée dans cette étude était de 480 µg/kg de
poids corporel et par jour. On voit donc que l'exposition qui
résulterait de la consommation d'eau de source contaminée se situe
bien endessous de cette valeur.
2. Evaluation des effets sur l'environnement
Lorsque les granulés d'aldicarbe sont convenablement enfouis dans
le sol jusqu'à une profondeur de 5 cm, comme le recommande le
fabricant, le danger est minime pour les oiseaux et les petits
mammifères. Aux doses d'emploi recommandées, l'aldicarbe peut être
mortel pour certains invertébrés terricoles non visés comme les
lombrics. Jusqu'à 600 oiseaux chanteurs ont été détruits par suite
d'applications défectueuses d'aldicarbe sur le sol; en effet les
oiseaux peuvent mourir après ingestion d'un seul granulé. Les petits
mammifères courent un risque analogue en cas d'épandage d'aldicarbe à
la surface du sol.
Rien n'indique que des organismes aquatiques aient été détruits
par suite d'intoxications à l'aldicarbe malgré la très forte toxicité
potentielle de ce produit. L'aldicarbe pourrait contaminer les fossés
de drainage lorsqu'on l'applique dans des secteurs où il y a risque de
pluies torrentielles périodiques et par voie de conséquence,
possibilité de ruissellement et d'entraînement des particules du sol.
Toutefois il est peu probable que des poissons et des invertébrés
aquatiques soient détruits de cette manière.
CONCLUSIONS ET RECOMMANDATIONS POUR LA PROTECTION DE LA SANTE HUMAINE
ET DE L'ENVIRONNEMENT
1.1 Population générale
L'aldicarbe est un pesticide hautement toxique.
A l'occasion d'intoxications accidentelles et lors d'une étude
contrôlée en laboratoire, on a observé des symptômes de type
cholinergique parmi lesquels: malaise général, vision trouble,
faiblesse musculaire dans les bras et les jambes, crampes
épigrastriques, sueur profuse, nausées, vomissements, pupilles
contractées aréactives, sensation vertigineuse, dyspnée, respiration
de Kussmaul, diarrhée et fibrillation musculaire. Ces symptômes ont
disparu spontanément en l'espace de six heures. La dose orale la plus
forte sans effet observable mesurée lors d'une étude sur l'homme se
situait à 0,05 mg/kg de poids corporel. Toutefois, on a tout de même
observé à cette dose une inhibition passagère mais sensible de la
cholinestérase du sang total.
Le mécanisme essentiel de l'intoxication par l'aldicarbe consiste
en une inhibition de l'acétylcholinestérase. On admet que les
carbamates insecticides abolissent la capacité de
l'acétylcholinestérase à dégrader l'acétylcholine, qui joue le rôle de
médiateur chimique au niveau de la synapse et de la plaque motrice. On
observe le même mode d'action chez les organismes visés ou non visés.
Rien n'indique que l'aldicarbe soit cancérogène, mutagène, tératogène
1.2 Exposition professionnelle
On connaît des cas d'intoxication professionnelle par suite de
négligences dans l'observation des mesures de sécurité.
1.3 Effets sur l'environnement
L'aldicarbe ne représente aucune menace pour les divers
organismes qui peuplent l'environnement. Il peut cependant y avoir des
cas de mortalité individuelle d'oiseaux ou de petits mammifères
lorsque les granulés ne sont pas convenablement enfouis dans le sol.
Les organismes aquatiques ne courent aucun risque.
2. Recommandations en vue de la protection de la santé humaine et de
a) La manipulation et l'épandage de l'aldicarbe doivent être confiés
à des personnes convenablement formées.
b) L'utilisation d'aldicarbe à des fins agricoles doit être limitée
aux cas où il n'existe pas de produits de remplacement moins
c) La fabrication de l'aldicarbe comporte des risques d'exposition
à des substances chimiques toxiques. Les systèmes de sécurité
doivent empêcher toute fuite ou décharge accidentelle.
d) Pour réduire au minimum ou éliminer l'exposition des vertébrés à
l'aldicarbe, il faut que les granulés soient bien enfouis dans le
sol jusqu'à une profondeur de 5 cm, ainsi que le recommande le
RECHERCHES A EFFECTUER
a) Des études pharmacocinétiques - comportant notamment une étude de
la fixation du produit après application cutanée - sont
nécessaires pour permettre une modélisation pharmacocinétique
fondée sur des données physiologiques.
b) Dans un cas d'intoxication résultant de la consommation de menthe
contenant de l'aldicarbe, on a observé des effets à une dose
anormalement faible. L'étude de la menthe traitée par l'aldicarbe
pourrait révéler l'existence d'un métabolite encore inconnu
susceptible d'expliquer ce phénomène.
c) Les études concernant les effets immunologiques ne sont pas
concluantes. Des travaux supplémentaires sont nécessaires pour
approfondir la nature des effets exercés sur le système
d) Une étude de reproduction sur le rat est nécessaire pour voir
s'il y a lieu de craindre une sensibilité du foetus. Une étude de
ce genre est en cours.
1. Identidad, propiedades y métodos analíticos
El aldicarb es un éster de carbamato. Se trata de un sólido
cristalino blanco, moderadamente hidrosoluble y susceptible de
oxidación y de reacciones hidrolíticas.
Existen varios métodos analíticos, entre los que se cuentan la
cromatografía en capa fina, la cromatografía de gases (captura
electrónica, ionización de llama, etc.), y la cromatografía en fase
líquida. Actualmente, el método preferido de análisis del aldicarb y
de sus principales productos de descomposición es la cromatografía en
fase líquida de elevado rendimiento con derivación postcolumnar y
detectores de fluorescencia.
2. Usos, fuentes y niveles de exposición
El aldicarb es un plaguicida sistémico que se aplica al suelo
para combatir ciertos insectos, ácaros y nematodos. Este tipo de
aplicación se hace en una gran variedad de cultivos, como la banana,
el algodón, el café, el maíz, la cebolla, los cítricos, las legumbres
(secas), la pacana, la papa, el cacahuete, la soja, la remolacha
azucarera, la caña de azúcar, la batata camote, y el sorgo, así como
en plantas ornamentales y en viveros de árboles. La exposición de la
población general al aldicarb y sus metabolitos tóxicos (el sulfóxido
y la sulfona) tiene lugar principalmente por vía alimentaria. La
ingestión de alimentos contaminados ha ocasionado casos de
intoxicación por aldicarb y sus metabolitos tóxicos (el sulfóxido y la
Dada la elevada toxicidad aguda del aldicarb, tanto la inhalación
como el contacto cutáneo en condiciones de exposición profesional
pueden resultar peligrosos para los trabajadores si las medidas
preventivas son insuficientes. Se han producido algunos incidentes de
exposición accidental de trabajadores debidos al uso inadecuado o a la
ausencia de medidas de protección.
El aldicarb se oxida con relativa rapidez para dar el sulfóxido;
a los 7 días de la aplicación a ciertos tipos de suelo se produce la
conversión del 48% del compuesto original en sulfóxido. La oxidación
sulfona es mucho más lenta. La hidrólisis del grupo éster del
carbamato, que inactiva al plaguicida, depende del pH; la semivida en
agua destilada varía entre algunos minutos en un pH > 12 y 560 días
en un pH de 6,0. Las semividas en los suelos de superficie son de
aproximadamente 0,5 a 3 meses y en la zona saturada de 0,4 a 36 meses.
El aldicarb se hidroliza un poco más despacio que el sulfóxido o la
sulfona. La medida en el laboratorio de la degradación biótica y
abiótica del aldicarb ha producido resultados sumamente variables y ha
llevado a extrapolaciones que difieren radicalmente de las
observaciones sobre el terreno. Los
datos obtenidos en el terreno sobre los productos de la degradación
del aldicarb proporcionan estimaciones más fiables de su evolución
Los suelos arenosos con bajo contenido de materia orgánica son
los que más favorecen la lixiviación, en particular allí donde el
nivel freático es alto. Algunos acuíferos de drenaje y pozos locales
poco profundos se han contaminado con sulfóxido y sulfona de aldicarb;
en general, los niveles han variado entre 1 y 50 µg por litro, aunque
en una ocasión se registró un nivel de aproximadamente 500 µg/litro.
Como el aldicarb tiene acción sistémica en las plantas, pueden
aparecer residuos en los alimentos. Se han notificado niveles de
residuos superiores a 1 mg/kg en papas crudas. En los EE.UU., donde el
límite de tolerancia para las papas es de 1 mg/kg, se han comunicado
niveles de residuos de hasta 0,82 mg/kg en ensayos controlados sobre
el terreno con los regímenes de aplicación recomendados por el
fabricante. A partir de los datos obtenidos en los ensayos sobre el
terreno se ha calculado un nivel máximo del 95° percentilo de 0,43
mg/kg; en una encuesta sobre la cesta de la compra se han determinado
niveles máximos del 95° percentilo de hasta 0,0677 mg/kg en papas
3. Cinética y metabolismo
El aldicarb es absorbido con facilidad a partir del tracto
gastrointestinal y, en menor medida, a través de la piel. Se
absorbería fácilmente en el tracto respiratorio si hubiera polvo. Se
distribuye a todos los tejidos, inclusive los del feto de rata en
desarrollo. Se transforma metabólicamente en el sulfóxido y la sulfona
(los cuales son tóxicos), y es detoxificado por hidrólisis dando
oximas y nitrilos. La excreción del aldicarb y de sus metabolitos es
rápida y se produce principalmente por la orina. Una pequeña parte
puede ser objeto de eliminación por vía biliar y, en consecuencia, de
reciclaje enterohepático. El aldicarb no se acumula en el organismo
como resultado de la exposición a largo plazo. La inhibición in vitro
de la actividad de la colinesterasa por el aldicarb es
espontáneamente reversible; la semivida es de 30-40 minutos.
4. Estudios en animales de experimentación
El aldicarb es un potente inhibidor de las colinesterasas y tiene
una elevada toxicidad aguda. Sus efectos colinérgicos revierten de
modo espontáneo y completo al cabo de 6 horas a menos que entretanto
sobrevenga la muerte. No se dispone de pruebas bastantes que indiquen
que el aldicarb sea teratogénico, mutagénico, carcinogénico o
Se han producido muertes de aves y pequeños mamíferos por la
ingestión de gránulos de aldicarb no incorporados plenamente al suelo
como se recomienda. En pruebas de laboratorio, el aldicarb ha
demostrado ser sumamente tóxico para los organismos acuáticos. Nada
indica, no obstante, que esos efectos se produzcan sobre el terreno.
5. Efectos en el ser humano
La inhibición de la acetilcolinesterasa en la sinapsis nerviosa
y la unión neuromuscular es el único efecto reconocido del aldicarb en
el hombre y se asemeja a la acción de los organofosfatos. La enzima
carbamiolada es inestable y la reactivación espontánea es
relativamente rápida en comparación con la de una enzima fosforilada.
La intoxicación no mortal en el hombre es rápidamente reversible. La
recuperación se acelera mediante la administración de atropina.
EVALUACION DE LOS RIESGOS PARA LA SALUD HUMANA Y DE LOS EFECTOS EN EL
1. Evaluación de los riesgos para la salud humana
El aldicarb es un plaguicida sumamente peligroso. El riesgo para
la salud humana se debe principalmente a su uso incorrecto y a la no
utilización de equipo de protección durante su fabricación,
elaboración y aplicación. El aldicarb puede contaminar los alimentos
y el agua de bebida. Los efectos de la exposición excesiva son agudos
y reversibles. Aunque los efectos colinérgicos pueden ser graves y
discapacitantes y exigen la hospitalización de la persona afectada, en
muy raros casos han sido mortales.
1.1 Niveles de exposición
1.1.1 Población general
Las principales fuentes posibles de exposición para la población
general son los alimentos y el agua.
En los EE.UU. se dispone de algunos datos para calcular la
ingesta diaria de aldicarb (véase la sección 5.2). Muchos datos
demuestran que, en la mayoría de los cultivos cosechados, los residuos
suelen aparecer en pequeñas cantidades y no sobrepasan los límites
máximos para residuos cuando la sustancia se usa siguiendo prácticas
agrícolas correctas y se respetan los periodos de precosecha
recomendados. No obstante, incluso en ese caso, se han encontrado en
las papas niveles de hasta 1 mg/kg, y en ocasiones superiores.
En algunos cultivos tratados ilegalmente con aldicarb se han
descubierto niveles elevados de esa sustancia. Se produjo un caso de
intoxicación tras el consumo de pepinos cultivados hidropónicamente
con niveles de 6,6-10,7 mg de aldicarb/kg. En los EE.UU. se
notificaron dos casos de intoxicación por sandías contaminadas en las
que los niveles de aldicarb se encontraban entre < 0,01 y 6,3 mg/kg.
No obstante, no puede asegurarse que este margen refleje la verdadera
Se ha producido algún caso de contaminación de aguas subterráneas
con aldicarb. Alrededor del 12% de los pozos examinados en algunas
regiones del Canadá excedieron los 9 µg/litro. De 7802 pozos
muestreados en el Estado de Nueva York (EE.UU.), en una zona en la que
se tratan las papas con aldicarb, 5745 (73,6%) no tenían residuos
detectables, 1032 (13,3%) tenían cantidades mínimas y 1025 (13,1%)
tenían concentraciones superiores a 7 µg/litro.
En una encuesta a escala nacional de 15 000 pozos privados en los
Estados Unidos de América se observaron niveles de aldicarb en el agua
de 1 a 50 µg/litro en aproximadamente un tercio de las muestras
positivas. En perforaciones experimentales se han comunicado niveles
ocasionales de 500 µg/litro en aguas subterráneas.
1.1.2 Exposición profesional
Las concentraciones de aldicarb en la atmósfera durante la
aplicación agrícola quedan reducidas al mínimo por la forma granular
del producto. No obstante, algunas operaciones, como el proceso de
carga, pueden ser peli-grosas si no se adoptan las medidas apropiada
de protección individual. La exposición excesiva al aldicarb, que
ocasionó un nivel tisular de 0,275 mg/kg, contribuyó a la muerte de un
joven obrero que cargaba preparaciones de aldicarb. La principal vía
de exposición profesional es a través de la piel, especialmente cuando
los trabajadores no adoptan las precauciones recomendadas ni usan
equipo de protección.
1.2 Efectos tóxicos
Los efectos o manifestaciones de la toxicidad del aldicarb y sus
metabolitos (sulfóxido y sulfonas) se deben a su acción inhibitoria de
la acetilcolinesterasa. La inhibición de la colinesterasa es
reversible. Entre los signos y síntomas clínicos, según la magnitud y
la gravedad de la exposición, figuran: dolor de cabeza, mareo,
ansiedad, transpiración excesiva, salivación, secreción de lagrimas,
aumento de las secreciones bronquiales, vómitos, diarrea, calambres
abdominales, fasciculaciones musculares y pupilas contraídas. No
existen pruebas importantes de carcinogenicidad, mutagenicidad,
teratogenicidad o inmunotoxicidad.
En sujetos humanos, la administración única por vía oral de 0,025
mg de aldicarb/kg de peso corporal produjo una inhibición
significativa de la actividad de la colinesterasa en sangre entera,
aunque sin síntomas. Con dosis de 0,10 mg/kg de peso corporal se
produjeron signos y síntomas colinérgicos y con una dosis de 0,26
mg/kg de peso corporal se produjo una intoxicación aguda que exigió
1.3 Evaluación del riesgo
Los riesgos que representa una sustancia química sumamente
peligrosa sólo pueden evaluarse en función de los distintos tipos de
exposición y sólo en función de las medidas de seguridad disponibles
y el grado de certeza de que se usan.
Con diferencia, el grupo más expuesto al riesgo del aldicarb está
formado por los que lo fabrican, lo elaboran y lo usan. El aldicarb se
fabrica en un sistema cerrado. El uso del aldicarb en forma granular
reduce la formación de polvo y el riesgo de exposición profesional. Se
han producido algunos accidentes asociados a la elaboración y el uso,
pero en todos los casos se debieron a una o varias transgresiones
claras de las normas de seguridad (véase la sección 8.2.1). No
obstante, aunque el aldicarb se usa en forma granular, puede
representar un riesgo para las personas que lo aplican si no se
adoptan todas las precauciones recomendadas.
Las fuentes de residuos de aldicarb en los alimentos comprenden
la aplicación de acuerdo con la ley a los suelos en los que se
cultivan cosechas para las que se ha aprobado el uso de aldicarb, y no
sólo el uso ilícito o indebido de esa sustancia. No hay pruebas de que
la salud de la población general corra riesgos debidos al aldicarb
presente en los alimentos en los niveles de aplicación recomendados y
con las técnicas actuales. No obstante, existe un riesgo importante
cuando el aldicarb se usa en cultivos no aprobados, como lo indican
los informes de varios casos de intoxicación. Por otro lado, se han
establecido regímenes de aplicación en el suelo y límites de
tolerancia para los residuos de aldicarb en los usos aprobados de la
sustancia a fin de proteger a la población general. El éxito de estas
medidas viene indicado por la observación de que no se han notificado
efectos adversos para la salud que puedan atribuirse a la exposición
al aldicarb a partir de productos básicos en los que la sustancia se
usó debidamente. Los limitados datos obtenidos en la encuesta sobre la
cesta de la compra sugieren que la exposición al aldicarb
probablemente no excederá 1 µg/kg de peso corporal al día en los
EE.UU. Esto se encuentra muy por debajo de la ingesta diaria admisible
(IDA), establecida en la Reunión Conjunta FAO/OMS sobre Residuos de
Plaguicidas (FAO/WHO, 1983).
No se ha encontrado aldicarb en los canales públicos de agua
procedentes de acuíferos profundos o aguas de superficie, por lo que
no se prevé riesgo alguno debido al aldicarb en las aguas de esa
procedencia. Se han comunicado casos de contaminación por aldicarb en
aguas subterráneas, generalmente con niveles de 1-50 µg/litro en los
EE.UU. y con casos excepcionales de hasta 500 µg por litro. No
obstante, la mayoría de los pozos muestreados en zonas contaminadas
tienen cantidades indetectables o indicios de aldicarb o sus
metabolitos. La restricción del uso de la sustancia en suelos arenosos
ha reducido la contaminación de las aguas subterráneas.
Suponiendo un consumo diario medio de agua de 2 litros y un peso
corporal medio de 60 kg, las personas que consumen agua de pozos poco
profundos contaminados localmente que contienen entre 1 y 50 µg/litro
estarian sometidas a una exposición a los metabolitos de aldicarb de
entre 0,033 y 1,7 µg/kg de peso corporal al día. Un pozo de agua
contaminada con aldicarb a un nivel de 500 µg por litro daria lugar
a una exposición de 17 µg/kg de peso corporal al día. El estudio
más apropiado que se conoce para la evaluación del riesgo en el agua
de bebida es un estudio en el que se administraron sulfóxido y sulfona
de aldicarb a ratas en el agua de bebida. En ese estudio, el nivel de
no observación de efectos en la inhibición de la acetilcolinesterasa
fue de 480 µg/kg de peso corporal al día. La exposición estimada por
consumo de agua subterránea contaminada está, por lo tanto, muy por
debajo de ese nivel.
2. Evaluación de los efectos en el medio ambiente
La plena incorporación de los gránulos de aldicarb al suelo a una
profundidad de 5 cm, tal y como recomienda el fabricante, representa
un riesgo mínimo para las aves y los pequeños mamíferos. Los
invertebrados del suelo que no se pretende destruir con la sustancia,
como las lombrices, pueden morir cuando se usa el aldicarb de
acuerdocon los regímenes de aplicación recomendados. Se han comunicado
casos de hasta 600 muertes de aves canoras debidas a la aplicación
indebida de los gránulos en la superficie del suelo, ya que los
pájaros pueden morir por la ingestión de un solo gránulo. La
aplicación superficial del aldicarb expone a los pequeños mamíferos a
un riesgo similar.
No se tienen pruebas de que hayan muerto organismos acuáticos por
intoxicación con aldicarb a pesar de su toxicidad potencial
relativamente elevada. El aldicarb puede contaminar las zanjas de
drenaje cuando se usa en zonas de lluvias torrenciales periódicas, que
provocan una intensa escorrentía del agua y el suelo de la superficie.
No obstante, es poco probable que con ello mueran peces o
CONCLUSIONES Y RECOMENDACIONES PARA LA PROTECCION DE LA SALUD DEL
HOMBRE Y DEL MEDIO AMBIENTE
1.1 Población general
El aldicarb es un plaguicida sumamente tóxico.
La intoxicación accidental y un estudio controlado en el
laboratorio dieron lugar a síntomas colinérgicos entre los que
figuraron los siguientes: malestar, visión borrosa, debilidad muscular
en los brazos y las piernas, calambres epigástricos dolorosos,
transpiración excesiva, náuseas, vómitos, pupilas contraídas no
reactivas, mareos, disnea, hambre de aire, diarrea y fasciculación
muscular. Los síntomas desaparecieron espontáneamente al cabo de seis
horas. La dosis oral más elevada que produjo síntomas no observables
en un estudio en el ser humano fue de 0,05 mg/kg de peso corporal,
aunque se produjo una significativa inhibición transitoria de la
colinesterasa de sangre entera con ese nivel.
El mecanismo primario de la toxicidad del aldicarb es la
inhibición de la acetilcolinesterasa. Comúnmente se acepta que los
insecticidas con carbamato interfieren con la capacidad de la
acetilcolinesterasa de degradar el transmisor químico acetilcolina en
las uniones sinápticas y neuromusculares. El mismo mecanismo de acción
se manifiesta en los organismos que se prentende combatir y en los
demás. No hay pruebas sustanciales de carcinogenicidad, mutagenicidad,
teratogenicidad o inmunotoxicidad.
1.2 Exposición profesional
Se han producido casos de intoxicación y envenenamiento debidos
a la exposición profesional por no adoptarse las precauciones
1.3 Efectos en el medio ambiente
El aldicarb no ejerce efecto alguno en los organismos del medio
ambiente en el nivel de población. Pueden producirse casos de muerte
de aves y pequeños mamíferos aislados cuando los gránulos no se
incorporan plenamente al suelo. Los organismos acuáticos no están
expuestos al riesgo del aldicarb.
2. Recomendaciones para la protección de la salud humana y del medio
a) La manipulación y la aplicación del aldicarb debe ser llevada a
cabo por personal adiestrado.
b) El uso del aldicarb en la agricultura debe limitarse a aquellos
casos en los que no se disponga de sustitutos menos peligrosos.
c) La fabricación del aldicarb es un proceso peligroso que entraña
el posible riesgo de exposición a sustancias químicas tóxicas.
Los sistemas de seguridad deben ser suficientes para impedir los
derrames y vertidos.
d) Para reducir al mínimo o eliminar la exposición de los
vertebrados terrestres al aldicarb, los gránulos deben quedar
plenamente incorporados al suelo a una profundidad de 5 cm, tal
y como recomienda el fabricante.
a) Se necesitan más estudios farmacocinéticos, inclusive estudios
de asimilación tras la aplicación por vía cutánea, que permitan
la formulación de modelos farma-cocinéticos de base fisiológica.
b) En un caso de intoxicación debida al consumo de menta que
contenía aldicarb se observaron efectos con una dosis
aparentemente muy reducida. El estudio de la menta tratada puede
revelar la existencia de un metabolito desconocido o de otros
factores que hayan intervenido en ese caso de intoxicación.
c) Los estudios sobre los efectos inmunológicos del aldicarb no han
dado resultados concluyentes. Es necesario hacer nuevos estudios
para examinar más a fondo los efectos del aldicarb en el sistema
d) Es preciso llevar a cabo un estudio de reproducción en la rata
para investigar aspectos relacionados con la susceptibilidad
fetal. Hay un estudio de ese tipo en marcha.