INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY
ENVIRONMENTAL HEALTH CRITERIA 121
ALDICARB
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
Geneva, 1991
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coordination of laboratory testing and epidemiological studies, and
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chemicals.
WHO Library Cataloguing in Publication Data
Aldicarb.
(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)
ISSN 0250-863X
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CONTENTS
ENVIRONMENTAL HEALTH CRITERIA FOR ALDICARB
1. SUMMARY
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
METHODS
2.1. Identity
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
3.2.1.1World production figures
3.2.1.2Manufacturing processes
4. ENVIRONMENTAL TRANSPORT, DISTRIBUTION, AND TRANSFORMATION
4.1. Transport and distribution between media
4.1.1. Air
4.1.2. Water and soil
4.1.3. Vegetation and wildlife
4.2. Biotransformation
4.3. Interaction with other physical, chemical or biological
factors
4.3.1. Soil microorganisms
5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE
5.1. Environmental levels
5.1.1. Air
5.1.2. Water
5.1.3. Food and feed
5.2. General population exposure
5.3. Occupational exposure during manufacture, formulation
or use
6. KINETICS AND METABOLISM
6.1. Absorption
6.2. Distribution
6.3. Metabolic transformation
6.4. Elimination and excretion in expired air, faeces, and
urine
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
7.7. Carcinogenicity
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;
epidemiological studies
9. EFFECTS ON OTHER ORGANISMS IN THE LABORATORY AND FIELD
9.1. Microorganisms
9.2. Aquatic organisms
9.3. Terrestrial organisms
9.4. Population and ecosystem effects
10. EVALUATION OF HUMAN HEALTH RISKS AND EFFECTS ON THE
ENVIRONMENT
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. Conclusions
11.1.1. General population
11.1.2. Occupational exposure
11.1.3. Environmental effects
11.2. Recommendations
12. FURTHER RESEARCH
13. PREVIOUS EVALUATIONS BY INTERNATIONAL BODIES
REFERENCES
RESUME
EVALUATION DES RISQUES POUR LA SANTE HUMAINE ET DES EFFETS
SUR L'ENVIRONNEMENT
CONCLUSIONS ET RECOMMENDATIONS
RECHERCHES A EFFECTUER
RESUMEN
EVALUACION DE LOS RIESGOS PARA LA SALUD HUMANA Y DE LOS
EFFECTOS EN EL MEDIO AMBIENTE
CONCLUSIONES Y RECOMENDACIONES
OTRAS INVESTIGACIONES
WHO TASK GROUP ON ENVIRONMENTAL HEALTH CRITERIA FOR ALDICARB
Members
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
(Joint Rapporteur)
Dr S. Dobson, Institute of Terrestrial Ecology, Monks Wood
Experimental Station, Abbots Ripton, Huntingdon, United Kingdom
(Vice Chairman)
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,
Ahmedabad, India
Dr H. P. Misra, University Center for Toxicology, Virginia
Polytechnic Institute and State University, Blacksburg, Virginia,
USA
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,
Ontario, Canada
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,
Belgium
Dr J. M. Charles, International Group of National
Associations of Manufacturers of Agrochemical Products (GIFAP),
Brussels, Belgium
Secretariat
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
(Joint Rapporteur)
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
7985850).
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.
ABBREVIATIONS
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
UV ultraviolet
1. SUMMARY
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
hydrolytic reactions.
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
fate.
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
market-basket survey.
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
field.
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
atropine.
2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, AND ANALYTICAL METHODS
2.1 Identity
Common name: Aldicarb
Chemical structure:
CH3 O
' "
CH3S - C - CH = N - OCNHCH3
'
CH3
Molecular formula: C7H14N2O2S
Synonyms and Aldicarb (English); Aldicarbe (French);
common trade Carbanolate; ENT 27 093; 2-methyl-2-
names: (methylthio)propanal
O-[(methylamino)-carbonyl]oxime (C.A.);
2-methyl-2-(methylthio)propionaldehyde
O-methyl-carbamoyloxime (IUPAC);
NCI-CO8640; OMS-771; Propanal,
2-methyl-2-(methylthio)-,
O-((methylamino)carbonyl)oxime; Temic;
Temik; Temik G; Temik M; Temik LD; Sentry;
Temik 5G; Temik 10G; Temik 15G; Temik 150G;
Union Carbide UC 21 149.
CAS registry
number 116-06-3
RTECS no. UE2275000.
2.2 Physical and chemical properties
Some physical and chemical properties of aldicarb are given in
Table 1.
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
(AOAC, 1990).
Table 1. Some physical and chemical properties of aldicarba
Relative molecular mass: 190.3
Form: colourless crystals (odourless or slight
sulfurous smell)
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)
propionitrile; 2-methyl-2-(2-methyl-
thiopropylenaminoxy) propinaldehyde
O- (methylcarbamoyl) oxime;
2-methyl-2-(methylthio) propionaldehyde
oxime
Log octanol/water partition 1.359
coefficient
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
aldicarb/litre.
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
compound.
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
manufacturer.
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).
3.2.1.1 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.
3.2.1.2 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
significant.
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
detail.
4.1.1 Air
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
50-500 weeks.
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
(days) (days)
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
the application.
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
Plough-layer soil
sterilized 2.5 (2.3-2.6) 10 (7-16)
unsterilized 1.0 (0.9-1.1) 44 (39-50)
Soil water
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.
pH measurements
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
or sulfone.
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
Harrellsville, NC
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
Livingston, CA
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
Clay
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
Sand
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
Loam
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
Muck
aldicarb T
sulfoxide 0.1
sulfone 0
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
same.
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
and fruit.
4.2 Biotransformation
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
5.1.1 Air
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.
5.1.2 Water
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
metabolites.
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
USA population).
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
6.1 Absorption
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).
6.2 Distribution
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
contents
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
contents
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 &
Ivie, 1968).
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
P-450-dependent oxygenation.
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
faeces.
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,
1990b).
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
intraperitoneal route.
Table 9. Acute toxicity of aldicarb and its formulation products
Compound Route of Vehicle Species LD50 Reference
adminis (mg/kg body
tration weight)a
Technical oral rat 0.93 Martin & Worthing
aldicarb (1977)
oral peanut oil rat M: 0.8 Gaines (1969)
F: 0.65
oral corn oil rat M: 0.09 Carpenter & Smyth
(1965)
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)
F: 2.5
skin not specified rabbit 5.0 Weiden et al. (1965)
skin propylene glycol rabbit 5.0 Striegel & Carpenter
(5%) (1962)
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
(1965)
Table 9 cont'd. Acute toxicity of aldicarb and its formulation products
Compound Route of ad- Vehicle Species LD50 Reference
ministration (mg/kg body
weight)a
dermal none rat 850 Weil (1973)
dermal water (50%) rabbit 32 West & Carpenter
(1966)
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
rats only.
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
tested.
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
sensitizing properties.
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.,
1983).
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 &
Carpenter, 1968).
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,
respectively.
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