PESTICIDE RESIDUES IN FOOD - 1979
Sponsored jointly by FAO and WHO
Joint meeting of the
FAO Panel of Experts on Pesticide Residues
in Food and the Environment
WHO Expert Group on Pesticide Residues
Geneva, 3-12 December 1979
2-methyl-2-(methylthio) propionaldehyde O-(methylcarbamoyl) oxime
TemikR, UC 21149, OMS 771
CH3 O H
' " '
CH3 - S - C - CH = N - O - C - N - CH3
Other Information on Identity and Properties
Molecular weight: 190.3
State: White, crystalline solid
Odor: Slight sulfurous odor
S.G.: 1.195 @ 25°C
B.P.: Decomposes above 100°C
V.P.: 0°C 1 × 10-5 mm Hg
25°C 1 × 10-4 mm Hg
50°C 7 × 10-4 mm Hg
75°C 4 × 10-3 mm Eg
Stability: Heat sensitive, relatively unstable chemical;
stable in acidic media; unstable, decomposes
rapidly in alkaline media.
Solubility: Percent Solubility at:
10°C 20°C 30°C 50°C
Water 0.4 0.6 0.9 1.4
Acetone 28 40 43 67
Benzene 9 24 49
Carbon tetrachloride 2 5 25
Chloroform 38 35 44 53
ketone 13 24 42
Toluene 10 10 12 33
Vapour Pressure of Aldicarb and Metabolites
V.P. (mm Hg) at:
Chemical 0°C 25°C 50°C 75°C
Aldicarb 1 x 10-5 1 x 10-4 7 x 10-4 4 x 10-3
Aldicarb Sulfoxide 1 x 10-5 7 x 10-5 5 x 10-4 2 x 10-3
Aldicarb Sulfone 8 x 10-6 9 x 10-5 6 x 10-4 3 x 10-3
Aldicarb in relatively non-volatile and the major toxic metabolites
are less volatile than aldicarb.
Purity of Technical Product
The Meeting noted that the technical product normally contains from
94.7 to 97.7% aldicarb and considered the likely impurities.
EVALUATION FOR ACCEPTABLE DAILY INTAKE
Absorption, Distribution and Excretion
Aldicarb is readily absorbed, distributed widely in the body and
excreted rapidly in mammals. Radiolabeled aldicarb (the 14C
radiolabel was present in one of three positions in the molecule,
S-methyl, tert-butyl or N-methyl) was administered orally to male
rats and residue were analyzed over a 14-day period. Excretion was
essentially complete within 4 days (greater than 95% of the
administered dose). The major concentrations of metabolites were
observed to have been excreted within 24 hours of dosing. Four days
following acute oral dosing residues were not detected in animal
tissues (Knaak et al., 1966). Following oral administration (0.4
mg/kg), aldicarb was rapidly eliminated predominantly in the urine
80%) and faeces (5%) within 24 hours. Low levels of radioactive
metabolite were noted in a variety of tissues in the first days after
treatment. Within four days there were essentially no residues which
could be suggestive of (selective) storage of residues in the body.
By the fifth day following acute treatment, tissues were free of
detectable residues (Andrawes, et al., 1967). Aldicarb sulfone, a
minor carbamate metabolite, was administered orally to rats and also
found to be rapidly absorbed and excreted in a manner similar to that
noted with aldicarb. Within 4 days from 90 to 95% of the orally
administered dose was excreted predominantly in urine. In two
analytical studies, performed at 7 or 11 days after treatment, tissue
residues were absent (Sullivan, 1968c; Andrawes 1977).
In dogs, the excretion pattern of aldicarb administered subacutely was
similar to that noted following acute administration in other species.
Aldicarb was administered to dogs at a dose of 0.75 mg/dog/day in the
diet for 20 days. On the 21st day, a single radiolabeled dose of
aldicarb was administered in the place of the non-radiolabeled
chemical. Dogs were thereafter maintained for an additional ten days
on a diet containing aldicarb. The daily excretion pattern was
examined in urine. Approximately 90% of the recovered urinary
radioactivity was observed to have been excreted within the first 24
hours of the administration time of the radio-labelled dose. Thus,
the elimination via the urine of aldicarb from dogs equilibrated for
up to three weeks showed an excretion pattern similar to that noted
with animals administered aldicarb in a single acute dosage (Sullivan,
1968a). A similar urinary excretion pattern was observed when
aldicarb sulfone (Sullivan, 1968b; Andrawes 1977) and aldicarb nitrile
(Sullivan and Carpenter, 1974) were orally or dietarily administered
to lactating dairy cows either alone or in combination with one or
more aldicarb metabolites. Following a single acute administration of
aldicarb, approximately 83% of the dosage was eliminated in the urines
within 24 hours. A minor quantity of residue was eliminated in the
faeces and small residues were observed in milk (less than 3% of the
administered dose was observed in milk over a 5-day interval) (Dorough
and Ivie, 1968). Increasing the number of days of treatment from one
to 14 did not change the magnitude or the elimination pattern of
aldicarb in milk or excretory products. Approximately 1% of the
administered dose was secreted in milk with 95% of the administered
dose eliminated by the other routes. Small levels of residues were
observed in tissues with the liver showing the major terminal residue.
Continuous exposure of cows to aldicarb in the diet did not
significantly alter its absorption and excretion patterns (Dorough, et
al., 1970). In an additional subchronic study a 1:1 mixture of
aldicarb sulfoxide and aldicarb sulfone was administered to cows to 32
to 46 days. Milk residues were found to be approximately 0.1% of the
administered aldicarb metabolites. In these studies there was no
apparent build-up of residues in milk or animal tissues from
continuous administration of aldicarb and/or its carbamate metabolites
Aldicarb and/or aldicarb sulfone administered as a single oral dose to
laying hens was rapidly excreted in the faeces. Minute quantities of
terminal residues were observed in eggs on the first day after
treatment but the residue level declined rapidly. Tissue residues
were maximal within 6 hours of treatment after which a rapid decline
was observed. Continuous administration of aldicarb for 21 days did
not change the pattern of rapid excretion or of terminal residues in
eggs or tissues (Hicks, et al., 1972).
The metabolic fate of aldicarb has been studied in a variety of
vertebrate and invertebrate species. Minor biotransformation
differences have been found to occur with respect to quantities of
individual metabolites. The basic metabolic profile of aldicarb in
all species examined appears to be the same and is shown in figure 1.
Aldicarb is rapidly oxidized to aldicarb sulfoxide, a relatively
stable metabolite. Aldicarb sulfoxide in slowly degraded by both
oxidative and hydrolytic mechanisms yielding the corresponding
aldicarb sulfone and sulfoxide oxime.
In rats, urinary metabolites include aldicarb sulfoxide (40%), the
sulfoxide oxime (30%) and a variety of more polar, relatively acidic,
metabolites. Aldicarb was noted in urine only in trace quantities
(Knaak, et al., 1966; Andrawes, et al., 1967). Results of in
vitro studies have shown that aldicarb was completely metabolized
rapidly through oxidative and/or hydrolytic mechanisms yielding the
same profile of metabolites noted in Figure 1. Further studies of the
metabolic fate of aldicarb sulfoxide and aldicarb sulfone have
confirmed the metabolic pattern of these components as shown in Figure
1 (Andrawes et al., 1967; Andrawes, 1977). Approximately one-half
of the administered dose of aldicarb sulfoxide was rapidly degraded
through cleavage of the ester carbonyl and eliminated as hydrolytic
products in the urine. Aldicarb sulfone was identified as a very
minor metabolite following administration of aldicarb sulfoxide. In
contrast to the rapid cleavage of the carbamate ester and urinary
elimination following aldicarb sulfoxide treatment, administration of
aldicarb sulfone to rats resulted in approximately 80% of the urinary
metabolites as the unchanged aldicarb sulfone. Conjugation mechanisms
for elimination of aldicarb from the body appeared to be minor
reactions possibly because of the polar nature of the metabolites
themselves. Studies using enzyme or acid hydrolysis of polar urinary
metabolites have resulted in the characterization of the aldicarb,
alcohol and aldehyde derivatives shown in Figure 1a. These represent
a very small portion of the degradation mechanism noted for aldicarb.
In dogs, the identification of a similar urinary metabolic pattern was
reported (Sullivan, 1968a). The major urinary metabolites were
aldicarb sulfoxide and sulfoxide oxime. Further characterizations of
the sulfone, sulfone oxime and nitrile were reported.
The metabolic fate of aldicarb in dairy animals was reported to be the
same as those metabolite species detected in urine with the principal
products being aldicarb sulfoxide, sulfoxide oxime and sulfoxide
nitrile (Dorough and Ivie, 1968).
Characterization of aldicarb metabolites in milk of cows fed for 14
consecutive days showed a slightly different metabolic profile than
animals receiving an acute single administration of aldicarb. In
animals treated for 14 days, the major milk metabolic component was
found to be aldicarb sulfone and its corresponding nitrile derivative.
Small quantities of aldicarb sulfoxide and larger quantities of the
sulfoxide oxime suggested that an increased level of oxidative and/or
hydrolytic metabolism would be expected following subacute, continuous
dietary administration as opposed to that pattern noted with the
single acute exposure (Dorough, et al., 1970). The metabolic fate
of aldicarb in hens (Hicks, et al., 1972), insects (Metcalf, et al.,
1966; Bull, et al., 1967) and plants (Metcalf, et al., 1966)
appears to follow the same pattern as noted in mammalian species with
oxidation of the sulfur atom predominating, yielding primarily
aldicarb sulfoxide and to a lesser extent, aldicarb sulfone which are
further degraded to the hydrolytic oximes and corresponding nitriles.
In rats, aldicarb nitrile was rapidly degraded to the sulfoxide
nitrile. This was identified as a major component in urine with the
sulfone nitrile and further degradation products also noted (Sullivan
and Carpenter, 1974).
Effects on Enzymes and Other Biochemical Parameters
As noted with other N-methylcarbamate esters aldicarb in an inhibitor
of cholinesterase activity (Chin & Sullivan, 1968). Aldicarb is a
readily reversible cholinesterase inhibitor and in vitro studies
have shown that cholinesterase inhibition, induced by aldicarb and its
oxidative metabolites (aldicarb sulfoxide and aldicarb sulfone) can be
readily reversed by simple dilution. Aldicarb sulfoxide in a more
active cholinesterase agent than aldicarb or the corresponding
sulfone. Aldicarb sulfoxide was 47 and 25 times more effective in
inhibiting cholinesterase than aldicarb and aldicarb sulfone
respectively with an insect-enzyme preparation and 23 and 60 times
more effective respectively when using a red blood cell preparation
obtained from cows (Bull, et al., 1967; Metcalf, et al., 1966).
Aldicarb sulfoxide and aldicarb sulfone were administered to rats in
the diet for periods of time varying from 1 to 56 days after which the
animals were sacrificed for plasma, erythrocyte and brain
cholinesterase determinations. Groups of 5 male and 5 female rats
were administered aldicarb sulfoxide in the diet at dosage levels of
0, 0.3 and 1.0 mg/kg/day and aldicarb sulfone was administered at
dietary levels of 0, 2.4 and 16.2 mg/kg/day. Animals were sacrificed
at 1, 3, 7, 14, 28 and 56 days for cholinesterase analyses. Plasma
and erythrocyte cholinesterase activity was measured at the first
three time intervals. At the last three time intervals, plasma,
erythrocyte and brain cholinesterase activity was examined. Over the
course of the of the growth was recorded routinely.
There was no mortality and growth, as evidenced by body weight, was
depressed at the highest dose levels with both the sulfoxide and
sulfone. Rats administered aldicarb sulfoxide at 1.0 mg/kg body
weight had a slight but significant cholinesterase depression during
the study. There were no effects noted at 0.3 mg/kg. Cholinesterase
depression was marked with the aldicarb sulfone consistently
throughout the study at the highest dose level, 16.2 mg/kg. Although
there were no clinical signs of poisoning and no deaths during the 56
days of treatment, plasma erythrocyte and brain cholinesterase were
consistently depressed below control values (Weil and Cox, 1975).
The acute toxicity of aldicarb and its metabolites has been studied in
a variety of mammalian species. A summary of acute toxicity data for
aldicarb in shown in Table 1 and for the metabolites, in Table 2.
Following acute oral administration to rats, aldicarb has been shown
to induce a strong muscarinic action at excretory, bronchial and
cardiac nerve sites. A nicotinic effect was also shown to occur at
myoneural junctions. The parasympathetic signs of poisoning were
readily reduced following atropine administration (Johnson and
Sullivan, 1968a). Administration of combinations of atropine and
2-PAM alone, or in combination, showed that while atropine was a more
effective antidote, 2-PAM was also active (Johnson and Sullivan,
1968b). While it has been shown that aldicarb elicits a strong
muscarinic action as well as nicotinic action at myoneural sites, the
control of signs of poisoning from both mechanisms appears to be
somewhat difficult to achieve. Atropine has been shown to be an
effective antidote to block the nicotinic effects but decamethonium,
commonly used to block the nicotinic effects, has been shown to be
somewhat ineffective. Additional studies to influence the nicotinic
action by such drugs as tubocurare also failed to completely eliminate
nicotinic activity. Further studies confirmed the therapeutic effects
of a variety of oximes (P2S and obidoxime) in reducing the acute toxic
signs of poisoning associated with aldicarb (Natoff and Reiff, 1973).
Signs of Poisoning
Aldicarb is an extremely toxic chemical by any route of
administration. Severe anticholinesterase signs of poisoning appear
almost immediately following poisoning. These signs of poisoning,
standard parasympathomimetic responses seen with other carbamates and
anti-cholinesterase organophosphate esters, include: tremors,
salivation, lacrimation, urination, diarrhea, convulsions, laboured
respiration, myosis, piloerection, ataxia, pinpoint pupils and death.
Table 1. Acute Toxicity - Aldicarb
Species Sex Route Vehicle1 LD50 Reference
Rat M Oral Corn oil 0.93 Striegel and Carpenter, 1962
M Oral Corn oil 0.67-1.23 Carpenter, 1963; Nycum and Carpenter, 1968b
F Oral Corn oil 0.62-1.07 Carpenter, 1963; Nycum and Carpenter, 1968b
F Oral Glycerol formal: 1.0 WHO, 1966
F ip Corn oil 0.71 Carpenter, 1963
M&F ip Corn oil 0.44 Carpenter, 1963
M ip PEG 0.37-0.44 Weil and Carpenter, 1970a
M ip Ethanol 0.57 Johnson and Carpenter, 1966b
M iv Water 0.47 Weil and Carpenter, 1970a
F Dermal DMP 3.2-7.0 (24 hr) WHO, 1966
M Dermal Dry 3952 (4 hr) Weil and Carpenter, 1970b
Dermal Water 38.1-44.9 (24 hr) Weil and Carpenter, 1968a
Mouse M Oral Corn oil 0.382 Weil and Carpenter, 1972b
M Oral Corn oil 0.50 Weil and Carpenter, 1972c
F Oral Cotton seed oil 1.5 Dorough, 1970
F ip Cotton seed oil 0.3 Dorough, 1970
Rabbit M Dermal PEG 5.0 Striegel and Carpenter, 1962
M&F Dermal Water 32-502 West and Carpenter, 1966b; Carpenter and Smyth 1966;
M Dermal Dry 141 - >200 Weil and Carpenter, 1968a
Chicken M Oral 9 West and Carpenter, 1965,
1 PEG = polyethylene glycol
DMP = dimethyl phthalate
2 Wettable powder formulation
Table 2. Acute Toxicity - Metabolites
Chemical Species Route1 (mg/kg) Reference
Aldicarb Rat Oral 0.84 West and Carpenter, 1966b
Aldicarb nitrile Rat Oral 570 West and Carpenter, 1966b
Aldicarb sulfoxide Rat (M) Oral (C.O.) 0.49-1.13 Weil and Carpenter, 1970a;
Nycum and Carpenter, 1968b
Aldicarb sulfone Rat (M) Oral (C.O.) 20-25 Weil and Carpenter, 1970a;
Nycum and Carpenter, 1968b
Aldicarb sulfoxide Rat (M) ip (Water) 0.47 Weil and Carpenter, 1970a
Aldicarb sulfone Rat (M) ip (PEG) 21.2 Weil and Carpenter, 1970a
Aldicarb sulfoxide Rat (M) iv (Water) 0.47 Weil and Carpenter, 1970a
Aldicarb sulfone Rat (M) iv (Water) 14.9 Weil and Carpenter, 1970a
Aldicarb sulfoxide Rabbit Dermal (Water) >20 mg/kg West and Carpenter, 1969b
Aldicarb suifone Rabbit Dermal (Water) >20 mg/kg West and Carpenter, 1969b
sulfinyl) propanol-1 Rat Oral 11,000 mg/kg Weil and Carpenter, 1969d
Hydroxymethyl aldicarb Rat Oral 42.9 Carpenter, 1969
Aldicarb sulfoxide oxime Rat (M) Oral 8060 Nycum and Carpenter, 1968a
Aldicarb sulfone oxime Rat (M) Oral 1590 Nycum and Carpenter, 1968a
Aldicarb sulfoxide nitrile Rat (M) Oral 4000 Nycum and Carpenter, 1968a
Aldicarb sulfone nitrile Rat (M) Oral 350 Nycum and Carpenter, 1968a
1 C.O. = corn oil
PEG = polyethylene glycol
Special Studies on Acute Toxicity
Administration of aldicarb to the conjunctival sac of rabbits did not
produce ocular irritation or corneal damage. Ocular irritation
studies were performed at doses that were lethal without indication of
ocular damage (Striegel and Carpenter, 1962).
There was no evidence of dermal irritation when aldicarb was applied
to the shaved, abraded backs of rabbits (Striegel and Carpenter,
1962). Penetration of aldicarb through the skin was observed to be
rapid, especially when the skin was moistened, simulating
perspiration. When dry, aldicarb did not penetrate the skin as
rapidly as evidenced by a substantial increase in toxicity when using
a wet versus the dry preparation (Carpenter and Smyth, 1965; Weil and
There was no indication of a sensitization reaction induced by
aldicarb. Male guinea pigs were administered aldicarb by multiple
subdermal applications (0.7 mg/kg body-weight) and re-administered
aldicarb three weeks later by a similar interderal administration.
There was no suggestion of sensitization in any of the animals tested
(Pozzani and Carpenter, 1968a).
Aldicarb is extremely toxic when administered by the inhalation route
(Striegel and Carpenter, 1962). Exposure of rats, mice and guinea
pigs to a dust formulation at a concentration of 200 mg/m3 for five
minutes resulted in the death of all animals. Exposure of female rats
to a dust formulation at concentrations of 6.7 mg/m3 for 15 minutes
was not lethal to any of the animals tested. When exposed for 30
minutes, 5 of 6 animals died. However, aldicarb is not volatile and
studies on the exposure of rats to aldicarb vapours emanating from
technical or granular formulations for 8 hours resulted in no
mortality (Pozzani and Carpenter, 1968b; Carpenter, 1963).
Groups of male rabbits (5 rabbits/group) were administered
aldicarb dermally for 15 days with a daily exposure of 6 hours per
day. Four groups of rabbits with abraded skin were administered
aldicarb at dose levels of 0, 5, 10 and 20 mg/kg/day. Water was added
periodically during the exposure time to the dressing containing the
aldicarb treatment, simulating a condition of excess perspiration.
One additional group was administered 20 mg/kg per day to intact,
unbraded skin with no water added to the dressing. The animals were
administered aldicarb 5 days per week with a 2-day interval of
non-treatment. One 3-day period of no treatment was reported, during
the third week of the study.
Those animals treated with aldicarb under a dry condition with
unabraded skin showed normal weight gains and no apparent effects as a
result of the treatment. During the interim where dermal treatment
was not applied, recovery of growth was extremely rapid, attesting to
the transient toxic nature of dermally-applied aldicarb. The
administration of aldicarb under conditions where the dressing was wet
and the skin abraded resulted in reduced body-weight reflecting rapid
absorption and an adverse effect at a dermal dosage of 5 mg/kg.
Plasma cholinesterase activity was inhibited at the two highest dose
levels. There were no adverse effects on haematology or clinical
chemical parameters or on gross weights of liver and kidney observed
at the conclusion of the study. Microscopic examination of several
major tissues showed no pathological events to attributable to
aldicarb (Carpenter and Smyth, 1966).
In a similar study, application of 10 mg/kg aldicarb and above
when administered to abraded rat skin in the presence of water, again
severely depressed body-weight. The 5 mg/kg dosage also depressed
body weight, but to a lesser extent. No deaths were noted over the 14
day interval. When administered dry, aldicarb at 20 mg/kg (the
highest dose level) was without effect (Weil and Carpenter, 1968a).
Special Study on Behaviour
The effects of acute administration of aldicarb and aldicarb
sulfoxide on avoidance behaviour in rats, was compared to a variety of
other carbamate esters. Rats were trained and evaluated for their
ability to avoid electrical shock in standard avoidance behaviour
tests. Aldicarb and aldicarb sulfoxide were administered by
intraperitoneal injection and the rats were evaluated for their
ability to avoid shocks over a 6-hour period following administration.
The effects of aldicarb and its sulfoxide were compared with 3 other
carbamate esters. The lowest behaviourally effective dose was found
to be 0.266 mg/kg body weight which, when compared to the acute IP
LD50 value, was noted to have a smaller ratio of behaviour effects to
acute LD50 than any of the other carbamates tested. These data
suggest that the level of aldicarb needed to produce measurable
avoidance in greater (closer to a fatal dose and less likely to be
achieved at the suggested use level) than the chemicals to which it
was compared. Additionally, the activity over the 6 hour period was
seen to rapidly decline again attesting to the transient nature of the
cholinesterase inhibition (Johnson and Carpenter, 1966b).
Special Studies on Potentiation
Aldicarb was administered orally to male rats alone and in combination
with a series of 8 organophosphate esters or 1 carbamate ester, all
anticholinesterase agents, to examine the potential interactive or
additive effect. Results of the study, using proportions of the acute
lethal dose of each material alone and in combination with aldicarb,
showed a simple additive effect with all materials tested. Aldicarb
was not found to potentiate the acute oral toxicity of other
anticholinesterase agents (West and Carpenter, 1966a).
Further studies were reported on the potential interaction of aldicarb
with alpha-naphthol, aldicarb sulfoxide with aldicarb sulfone and
aldicarb sulfone with parathion administered orally and aldicarb with
alpha-naphthol or with carbaryl administered by the interperitoneal
route. In no case were any interactions greater than the predicted
additive effects (Weil and Carpenter, 1970a).
Special Studies on Reproduction
Groups of rats (8 male and 16 female rats per group) were administered
aldicarb in the diet at concentrations of 0, 0.05 and 0.1 mg/kg body
weight in their diet for approximately 90 days and mated to initiate a
3 generation reproduction study. The offspring from the first
generation were mated to produce the second generation in the one
litter per generation reproduction study. In addition to the
reproduction indices (fertility, gestation, viability and lactation)
the F3 generation was maintained for an additional period and tissues
from these animals were histologically examined at either weaning or
at 90 days of age.
In all animal groups, the reproduction indices from the
aldicarb-tested animals were statistically similar to the mean values
of the control groups. Body weights of both male and female pups at
weaning were statistically similar to control values as were results
of gross and microscopic examinations of tissues and organs in the F3
weanling and 90-old animals. In all three generations, with all
criteria examined, there were no effects of aldicarb on reproduction
at a dosage level of 0.1 mg/kg body weight (Weil and Carpenter, 1964).
Groups of rats (10 male and 20 female per group) were administered
aldicarb in the diet at dosage levels of 0, 0.2, 0.3 and 0.7 mg/kg
body weight for 100 days and mated to initiate an additional 3
generation (1 litter per generation) reproduction study. A larger
group was used for the F2 generation (15 male and 25 female rate) as
male pups of this generation were maintained on aldicarb-diets for 148
days and subjected to a (modified) dominant lethal (mutagenesis)
bioassay where they were mated with groups of untreated virgin females
for a period of 10 weeks. Each female in the group was mated with 2
treated males and allowed to maintain pregnancy until day 12 when they
were sacrificed and examined.
There was some mortality over the course of the study which was
associated with lung infection and not as a result of aldicarb in the
diet. A significant difference from control values was noted in the
second generation pups with respect to body weight at the highest dose
level fed. At this dose level, body weights of both male and female
were lower than the control values. Overall, there were no effects on
any of the reproduction indices (fertility, gestation, viability or
lactation). Gross and microscopic examinations of the parents and
pups of the high level and control groups showed no effects
attributable to aldicarb.
The dietary dominant lethal mutagenesis bioassay showed no statistical
differences between the aldicarb-treated rats and controls with
respect to early or late fetal death or any other parameter examined
(Weil and Carpenter, 1974a).
Special Studies on Teratogenicity
Using a test protocol where both the reproductive and teratologic
potential of aldicarb was evaluated, groups of pregnant rats were
administered aldicarb in the diet at dosage levels of 0, 0.04, 0.2 and
1.0 mg/kg body weight. Five or six females from each of the dietary
groups were assigned to one of three treatment groups: (1) aldicarb
administered in the diet throughout pregnancy or until pups were
weaned; (2) aldicarb administered in the diet from day 0 to day 7 of
gestation; (3) aldicarb administered in the diet from day 5 to day 15
of gestation. Five or six females from each group were sacrificed and
examined on day 20 of pregnancy and a similar number of females were
allowed to bear, nurse and wean the pups.
Qualitative data were recorded with respect to fertility, gestation,
viability and lactation, the indices of a standard reproduction study.
There were neither gross manifestations of teratogenesis in any of the
pups carried by females administered aldicarb at dosage levels of up
to 1 mg/kg body weight nor was there apparent interference with the
reproductive process by any of the dosing regimens used in this study.
The administration of aldicarb at dosage levels up to and including
1.0 mg/kg body weight had no apparent effect on the growth of pregnant
females during the course of the study. There were no anomalies
observed in the animals sacrificed just prior to term nor in the
animals undergoing natural birth and allowed to be maintained until
weaning. Aldicarb, at levels of 1 mg/kg body weight, administered to
rats during sensitive stages of gestation, did not induce a
teratogenic effect (Weil and Carpenter, 1966a).
Special Studies for Mutagenesis
Rat-Dominant Lethal Study
Groups of virgin female rats (15 rats per group) were mated with male
rats that had been administered aldicarb (in the diet at dose levels
of 0, 0.2, 0.3 or 0.7 mg/kg body weight) prenatally through gestation,
through weaning and thereafter for up to 148 days of age. The males,
part of a 3-generation reproduction study were mated with virgin
untreated females at weekly intervals for a total of 10 consecutive
weeks. At the initiation of the dominant lethal study, the males were
fed control diets (having been exposed to aldicarb prenatally and for
148 days prior to mating). Each female was mated with 2 treated males
and allowed to develop for 12 days of gestation.
At 12 days of gestation each female was sacrificed and examined for
pregnancy, implantation sites and for viable fetuses. Data from all
of the ten mating periods, at all of the dosage levels, were compared
to control values. There were no significant differences with respect
to any of the parameters of mating, pregnancy and fetal deaths at any
dose levels in the study. In this slightly modified dominant lethal
mutagenic study, aldicarb did not induce adverse or mutagenic effects
in males as evidenced by sperm abnormalities (Weil and Carpenter,
Special Study on Carcinogenicity
Groups of C3H/HeJ male mice were administered aldicarb, dissolved in
acetone, dermally 3 times a week for 28 months. Aldicarb was
administered by applying a brush full of an acetone solution to the
shaved back of the mice. Aldicarb was administered for the first two
weeks at the rate of 3 times a week using a 0.25% solution in acetone.
After two weeks this was reduced to a twice-weekly application. This
dosing regimen was maintained for two months and further reduced
thereafter to a concentration of 0.125% which was maintained for the
remainder of the study.
While there was some aldicarb-induced mortality noted over the course
of the study, this mortality was not substantially different from that
noted with control applications. There were no substantial
differences with respect to the incidence or onset of tumors. Two
growths, a hemangioma and a thymoma, were noted in the animals
administered aldicarb. Neither of these internal growths was
accompanied by cutaneous papillomas or carcinomas and were considered
to be spontaneous growths unrelated to treatment. Aldicarb,
administered dermally to this sensitive species, did not induce any
incidence of malignancy (Weil and Carpenter, 1966b).
Special Studies on Delayed Neurotoxicity
Groups of 6 adult chickens were administered aldicarb as a single oral
dose of 4.5 mg/kg body weight or as daily oral doses of 0, 2.25 or 4.5
mg/kg body weight for 30 days. A positive control, treated with 100
mg of TOCP, was used to produce typical delayed neurotoxic signs of
While there was some weight loss, which was correlated with the dose
of aldicarb administered, the only neurological effects attributable
to aldicarb were acute signs of poisoning noted in the first two or
three days of treatment. Neither ataxia nor hind limb paralysis were
noted over the course of the study. Aldicarb does not induce a
delayed neurotoxic syndrome similar to that induced by certain
organophosphate esters (Johnson and Carpenter, 1966a).
Short Term Studies
Groups of rats (5 male and 5 female rats per group, 6-week old rats)
were fed aldicarb in the diet for 7 days at dosage levels of 0, 4, 8
and 16 mg/kg body weight. Animals were observed for acute signs of
toxicity and were weighed three times during the course of the week's
Mortality was noted predominantly at the highest dose level, at which
all males and 2 of 5 females died. One of 5 males also died at the 8
mg/kg dose level. There were substantial body weight changes noted at
all dose levels. In males, kidney weight was significantly reduced at
8 mg/kg and liver weight was depressed at the 4 and 8 mg/kg dose
levels. In females, both liver and kidney weight was significantly
depressed at all dose levels in the study (Weil and Carpenter, 1970c).
Groups of young rats (5 male and 5 female rats per group, 7 weeks of
age) were fed aldicarb in the diet at dose levels of 0, 0.8, 1.6 and
3.2 mg/kg body weight for 7 days. Animals were weighed three times
during the week and observed for clinical signs of toxicity. At the
conclusion of the study, animals were sacrificed and brain, red blood
cell and plasma cholinesterase activity was measured.
Growth was depressed during the one week study at dosage levels of 1.6
mg/kg and above. There was no apparent mortality in the study
attributable to aldicarb. Slight effects were noted on both liver and
kidney weight. In males, liver weight and liver to body weight ratios
were depressed in all treatment groups. In females, liver weight was
affected only at the highest dose level, but the liver to body weight
ratio was reduced at 1.6 mg/kg and above. Kidney weight was reduced
in males at all dose levels and in females only at the highest dose
Cholinesterase depression, measured on day after the conclusion of
feeding, was normal at the highest dose level tested with the
exception of plasma cholinesterase which was slightly reduced at the
highest level (Weil and Carpenter, 1969b).
Groups of rats (5 male and 5 female rats per group) were fed diets
containing aldicarb, at dosage levels of 0, 0.4, 0.8, 1.6 and 3.2
mg/kg body weight, or aldicarb sulfoxide, at dosage levels of 0, 0.4
and 0.8 mg/kg body weight, or aldicarb sulfone, at dosage levels of 0,
0.4, 1.0, 2.5, 5.0 and 20.0 mg/kg body weight, for 7 days. With
aldicarb (as with its two major carbamate metabolites) there was a
significant growth (body weight) depression at the highest dose level.
There were no effects noted with respect to gross liver or kidney
weight at the conclusion of the study. Erythrocyte and plasma
cholinesterase activity was depressed by aldicarb at the highest dose
level; with aldicarb sulfoxide, erythrocyte-cholinesterase activity
was also depressed at the highest dose level; with aldicarb sulfone,
plasma and erythrocyte cholinesterase activity was also depressed at
the two highest dose levels, while brain cholinesterase was inhibited,
in both males and females only at the highest dose level (20 mg/kg).
The erythrocyte cholinesterase appeared to be the most sensitive
parameter with all three materials tested. A no-effect level based on
erythrocyte-cholinesterase depression or decreased body weight over
the 7-day interval was suggested to be: aldicarb - 0.8 mg/kg; aldicarb
sulfoxide - 0.4 mg/kg; and aldicarb sulfone - 2.5 mg/kg (Nycum and
Groups of rats (5 male and 5 female rats per group, 7 weeks of age)
were fed dietary levels of aldicarb (0.3 mg/kg body weight), aldicarb
sulfoxide (0.4, 0.8 and 1.6 mg/kg body weight), aldicarb sulfone (0.6,
5.0 and 20 mg/kg body weight), a 1:1 mixture of aldicarb sulfoxide and
aldicarb sulfone (1.2 mg/kg body weight) or a control diet. Animals
were weighed three times during the course of the study and were
examined daily for clinical signs of toxic reaction. At the end of
the seven days of feeding, animals were placed on control diets for
one day after which they were sacrificed for cholinesterase
determination and for examination for liver and kidney toxicity.
A second one-week feeding trial was performed to compare the data with
other strains of rats. Aldicarb sulfoxide was fed to groups of 5 male
rats at dosage levels of 0, 0.4, 0.8 or 1.6 mg/kg body weight.
Aldicarb sulfone was also fed to male rats at dosage levels of 0, 5.0
or 20 mg/kg body weight.
In the initial study, aldicarb did not affect growth in males but did
reduce female growth substantially (during the course of the one week
study. Aldicarb sulfoxide substantially reduced growth at 0.8 mg/kg
and above in males and females. Aldicarb sulfone reduced growth at 5
mg/kg and above in males and at 0.6 mg/kg and above (all dose levels
in females). The combination of the sulfoxide and sulfone reduced
growth only in females and only at the least measurement interval.
In males, aldicarb did not appear to affect liver or kidney weight
while in females there was a slight but significant decrease in liver
weight at the conclusion of the study. Aldicarb sulfoxide reduced
both liver and kidney weight in males and females at the highest dose
level. Aldicarb sulfone in both males and females reduced kidney and
liver weight over the course of the study at the highest dose level
tested. The 1:1 combination of the sulfoxide and sulfone in males and
females had no adverse affect on liver and kidney.
As might be expected with the protocol followed in the study,
cholinesterase depression was not observed in either plasma,
erythrocyte or brain at the conclusion of the study.
The second trial using both the same and a different strain of rats
was performed in an effort to explain a slight but non-significant
inhibition of erythrocyte cholinesterase activity measured in the
initial study. Over the course of this study, there were no effects
noted on erythrocyte cholinesterase activity. With aldicarb
sulfoxide, growth was slightly reduced at the two highest dose levels
(0.8 and 1.6 mg/kg) in both strains and at 5 mg/kg body weight and
above with aldicarb sulfone. Liver and kidney weight were unaffected
by aldicarb sulfoxide but were slightly reduced with aldicarb sulfone
at the highest dose level (Weil and Carpenter, 1970d).
Groups of rats (15 male and 15 female rats/group) were fed aldicarb
sulfoxide in the diet at dose levels of 0, 0.125, 0.25, 0.5 and 1.0
mg/kg body weight for 6 months. Animals were sacrificed at 3 months
and at the conclusion of the study for cholinesterase determinations
and for gross and microscopic examination of liver and kidney. There
was no mortality noted during the course of the study, although
growth, especially in males, at 0.25 mg/kg and above was reduced. In
females growth was depressed only at the highest dose level.
Cholinesterase activity was substantially reduced at the three highest
dose levels, especially in plasma and erythrocytes of males. In
females, erythrocyte and plasma cholinesterase depression was noted at
the two highest dose levels. Gross examination of liver and kidney
revealed no abnormalities attributable to aldicarb.
In an attempt to resolve the question of cholinesterase depression and
rapid recovery, groups of rats (5 male and 5 female rats per group)
were administered aldicarb sulfoxide for one week or one week plus one
day of control diets at a dietary level of 1 mg/kg body weight. When
the study was concluded (within one week), animals were sacrificed at
0 and 24 hours after the dietary feeding interval (the 24 hour animals
were fed control diets). Cholinesterase depression was noted at the 0
hour sacrifice in erythrocyte and plasma preparations. Administration
of a control diet for one day (24 hour sacrifice) completely reversed
the cholinesterase depression noted when animals were sacrificed
without any recovery interval.
Groups of 5 male and 5 female rats were also fed aldicarb sulfoxide in
the diet at dosage levels of 0, 0.0625, 0.125, 0.25, 0.50 and 1.0
mg/kg body weight for 3 and 6 months after which some of the animals
were sacrificed immediately and others were placed on a control diet
for 24 hours prior to sacrifice and cholinesterase analyses.
Cholinesterase activity in the brain was unaffected by aldicarb
sulfoxide. Plasma and erythrocyte cholinesterase was substantially
reduced at the 0 hour sacrifice in both males and females. Males were
slightly more sensitive with depression being noted at 0.25 mg/kg and
above, while with females depression was noted at 0.5 mg/kg and above.
There was no cholinesterase depression noted in any of the animals
treated for either 3 months or 6 months when the animals were allowed
to recover from cholinesterase depression for a one-day recovery
interval. Depression of cholinesterase activity, of as much as 89% of
control values, was completely reversed within one day on a control
diet. A no-effect level of 0.125 mg/kg body weight was observed (Weil
and Carpenter, 1968b).
In a series of studies similar to those reported with aldicarb
sulfoxide, groups of rats (15 male and 15 female rats per group) were
administered aldicarb sulfone in the diet at dosage levels of 0, 0.2,
0.6, 1.8, 5.4 and 15.2 mg/kg body weight for 6 months. Animals were
sacrificed at 3 and 6 months for examination of liver and kidney
abnormalities and for evaluation of cholinesterase activity.
Cholinesterase determinations were made at the end of 3 and 6 month
intervals with rats fed continuously until sacrifice for analysis.
Additional rat studies using 5 male and 5 female rats per group were
performed for one week or for 3 months on diets containing aldicarb
sulfone at dose levels comparable to the levels reported above. In
these studies, animals were either sacrificed at the end of the
feeding regimen or were allowed to consume a control diet for 24 hours
prior to sacrifice and determination of cholinesterase activity.
There was no mortality over the course of the study. A transient but
significant growth depression was noted at the highest level in the
6-month feeding study. There were no effects noted with respect to
diet consumption or on gross and microscopic examinations of liver and
kidney. Plasma, erythrocyte and brain cholinesterase were
significantly depressed at 5.4 mg/kg dose level and above.
Erythrocyte cholinesterase depression was also noted at 1.8 mg/kg.
There was no cholinesterase depression noted at 0.6 mg/kg in any of
the tissues examined. In the study to evaluate recovery of
cholinesterase activity, aldicarb sulfone was fed for 7 days at a
dosage of 5.4 mg/kg body weight. At the conclusion of dosing,
significant depression of cholinesterase (plasma, erythrocyte and
brain) was noted. When animals were allowed to equilibrate for 1 day
on control diets, all depressed cholinesterase values returned to
normal. A similar study was run for 3 months and 3 months and 1 day
at dietary levels of 0, 0.2, 0.6, 1.2, 1.8, 5.4 and 16.2 mg/kg. The
data showed that extensive cholinesterase depression, noted at the
conclusion of the feeding trial was completely recovered within one
day of feeding control diets. In this 3-month trial there was a
substantial depression of plasma cholinesterase activity at 1.8 mg/kg
erythrocyte activity at 5.4 mg/kg and brain activity at 16.2 mg/kg.
At 1.2 mg/kg cholinesterase was not substantially depressed (Weil and
Groups of rats (the number of males and females per group was not
stated) were administered aldicarb oxime in the diet at dose levels of
0, 31.25, 62.5, 125, 250, 500 and 1000 mg/kg body weight for 7 days.
There was no mortality over the course of the study. Growth was
slightly reduced at the initiation of the study at dose levels of 125
mg/kg and above, but at the end of one week only the two highest dose
levels appeared to show a retardation in growth. Gross changes were
noted in both liver and kidney at the two highest dose levels in both
males and females. A dietary dosage level without substantial effect
appeared to range between 62.5 and 250 mg/kg body weight over the
course of this short term trial (Weil and Carpenter, 1974b).
Groups of rats (5 male and 5 female rats per group, 6 weeks of age)
were fed the hydrolytic metabolite of aldicarb
(2-methyl-2-(methylsulfinyl)propanol-1) in the diet for 7 days at
dosage levels of 0, 500 and 1000 mg/kg body weight.
Growth was depressed at both dosage levels fed to males but only at
the highest dosage level in females. In females, while growth was
depressed within one day of treatment, the animals appeared to recover
during the rest of the week. There was no apparent effect on major
organs, although, in females at the high dosage level, kidney weight
was slightly depressed. Cholinesterase was not measured (Weil and
Groups of mice (5 males and 5 females per group) were fed aldicarb in
the diet at dosage levels of 0, 0.1, 0.3, 0.6 and 1.2 mg/kg body
weight for 7 days. Mortality was noted in both males and females at
the high dose level. Growth was not affected over the course of the
study. Liver and kidney weight were also unaffected. In this one
week study, an actual dosage level of aldicarb, based on food
consumption data varying from 0.65 mg/kg body weight for females to
0.75 mg/kg body weight for males was without substantial acute effects
(Weil and Carpenter, 1970f).
Groups of mice (3 male and 5 female mice per group) were fed a mixture
of aldicarb and aldicarb sulfone (1:1) in the diet at dosage levels of
0, 2, 6, 18, and 36 mg/kg body weight for 7 days. Growth was measured
three times during the course of the study, and animals were observed
daily for any signs of abnormality.
No mortality was noted at any dosage level. Severe cholinergic signs
of poisoning were observed at the high dose level in males.
Depression of growth, observed at the two highest dose levels, was
statistically significant in both males and females. Reduced body
weights were, however, observed in all animals on the study at all
dosage levels. Kidney weight was depressed at the highest dose level
within one week in both males and females. No effects on the kidney
were noted at dose levels of 18 mg/kg and below. Liver weight was
reduced substantially at dosage levels of 6 mg/kg and above in both
males and females. Significant liver reduction was observed at the
two highest dose levels in males and at the highest dose level in
females (Weil and Carpenter, 1970e).
Groups of beagle dogs (2 male and 2 female dogs per group) were fed
dietary levels of aldicarb at dosage levels of 0, 0.2, 0.3 and 0.7
mg/kg body weight for 7 days. Dogs were weighed three times during
the week and observed daily for clinical signs of poisoning. At the
end of 7 days of feeding, 24 hours after being placed on control
diets, the dogs were sacrificed for cholinesterase examinations and
for gross examinations of kidney and liver.
There was no mortality over the course of the one-week study. Plasma,
erythrocyte and brain cholinesterase activity, measured one day after
conclusion of the dietary treatment, was normal. Gross liver and
kidney weight and organ-to-body weight ratios were unaffected by
aldicarb in the diet (Weil and Carpenter, 1973).
Groups of beagle dogs (4 male and 4 female dogs per group) were fed
aldicarb in the diet for five days per week at dosage levels of 0,
0.2, 0.3 and 0.7 mg/kg body weight for 99-100 days. Clinical
chemistry (including plasma and erythrocyte cholinesterase) and
haematology parameters were examined prior to the initiation of
feeding and at two intervals during the course of the study. At the
conclusion of the study, a final clinical chemistry and haematology
evaluation and gross and microscopic examinations of tissues and
organs were performed. At the conclusion of the study, brain
cholinesterase activity was also measured.
There was no mortality over the course of the study. Growth was
comparable within all dosage groups. At the conclusion of the study,
organ weight and organ-to-body weight ratios were slightly affected
only at the highest level of aldicarb. A slightly decreased testes
weight was observed in all treated groups with a significant effect
noted only at the highest level. A slight increase in adrenal weight
was also noted at this level. There were no effects in females on any
of the tissues and organs examined. Microscopic analysis did not
suggest any abnormalities including tissues where gross changes had
been seen to occur. Cholinesterase values, as well as other clinical
chemistry and haematology parameters were unaffected by the presence
of aldicarb in the diet. As the animals had been removed from
aldicarb exposure for 24 to 48 hours prior to cholinesterase analyses,
and considering the reversibility of inhibition, this parameter was
not useful in this study in defining an effect of aldicarb. A
no-effect level in the study is 0.3 mg/kg body weight (Weil and
Groups of dogs (3 male and 3 female dogs/group) were fed aldicarb
sulfoxide in the diet at dosage levels of 0, 0.0625, 0.125, 0.25 and
0.5 mg/kg body weight five days per week for three months. There was
no mortality over the course of the study. Slight body weight changes
were noted in many of the dogs at the highest dose level within the
first week of treatment and thereafter the body weight changes were
similar to, but lower than, control values. No effects on
haematologic and blood chemistry were observed. Cholinesterase
depression measured 24-48 hours after the final exposure was not
observed in plasma, erythrocytes or brain of any of the animals at the
conclusion of the study. Gross and microscopic examination of tissues
and organs did not show any adverse effect attributable to the
presence of aldicarb. A no-effect level based on somatic effects is
0.25 mg/kg body weight (Weil and Carpenter 1968b).
Groups of dogs (3 male and 3 female dogs per group) were fed aldicarb
sulfone in the diet at dosage levels of 0, 0.2, 0.6, 1.8 and 5.4 mg/kg
five days per week for 90 days. Prior to the study and at 1, 2 and
3-month intervals, plasma and erythrocyte cholinesterase were
examined. In addition, at the beginning and end of the study, blood
chemistry and haematologic values were examined. At the conclusion of
the study, gross and microscopic examination of a variety of tissues
and organs was performed.
There was no mortality over the course of the study. Slight body
weight depression was noted at the highest dose level, although the
body weight was not statistically lower than control levels. There
were no effects noted with respect to biochemical and haematologic
parameters and gross and microscopic examination of tissues and organs
revealed no effects attributable to the presence of aldicarb sulfone
in the diet. Cholinesterase depression was not noted over the course
of the study. Based upon available information, a no-effect level of
5.4 mg/kg for dogs was observed (Weil and Carpenter, 1968). In all of
the three previous dog studies, cholinesterase activity is not a
significant parameter to be considered in a toxicological evaluation
because the animals were not administered aldicarb continuously, but
were removed from dietary treatment for 1-2 days before the enzyme
activity was measured.
Groups of rats (20 male and 20 female rats per group) were fed
aldicarb in the diet for 2 years at dosage levels of 0, 0.005, 0.025,
0.05 and 0.1 mg/kg body weight. Additional groups of 16 of each sex
were maintained for serial sacrifices at 6 and 12 months.
There was no mortality over the course of the study attributable to
the presence of aldicarb in the diet. Growth was normal at all dosage
levels, as was consumption of food, and behavioural characteristics.
Results of gross examination of liver and kidney weight at 6 months
and at one year did not differ from control values. Haematologic
values, including cholinesterase analyses, were normal. (Haematologic
data included red blood cell or haematocrit determinations in the
highest dosage level and control groups.) Blood and brain
cholinesterase activity, measured at 6 and 12 months, were normal.
Microscopic examination of tissues and organs for histopathologic
occurrences and neoplasms showed the incidence of lesions to be
similar in aldicarb-treated and in control groups. An apparent
no-effect level in the study is 0.1 mg/kg body weight (2 ppm) in the
diet (Weil and Carpenter, 1965).
Groups of rats (20 male and 20 female rats per group) were fed
aldicarb in the diet at dosage levels of 0 and 0.3 mg/kg body weight.
In addition, groups of rats were fed aldicarb sulfoxide (0.3 and 0.6
mg/kg body weight).
There was no significant mortality observed over the course of the
study with any of the individual chemicals or the mixture of sulfoxide
and sulfone. In the initial phases of the study, there was a slightly
higher mortality noted in the high dosage level of aldicarb sulfoxide
and in the group receiving the combined aldicarb sulfoxide and
aldicarb sulfone. A slight increase in mortality was also noted at
the latter part of the study with aldicarb sulfoxide. Growth was
slightly depressed at the high dose level of the sulfoxide:sulfone
mixture, primarily in males. There were no apparent effects on growth
with respect to the aldicarb, aldicarb sulfoxide or aldicarb sulfone
administered alone. Hemocrit values observed at various intervals
over the course of the study did not differ from controls.
Cholinesterase determinations were made periodically over the course
of the study (6, 12 and 24 months). Plasma, erythrocyte and brain
cholinesterase were examined only at a 24-hour interval after animals
were removed from test diets. There was a slight depression of plasma
cholinesterase noted in males administered the high dose level of the
combination aldicarb sulfoxide and sulfone at the 24-month interval.
A repeat of the data within the final week of the study showed slight
depression in all chemical groups with respect to plasma
cholinesterase. There were no effects noted at any interval with
respect to red blood cell or brain cholinesterase. The plasma
cholinesterase depression noted at the 24-month interval was limited
to male rats.
An evaluation of the incidence of tumors suggested that there was no
statistical difference between treated and control groups. Gross and
microscopic examination of tissues and organs at various periods over
the two-year test interval showed that these sporadically distributed
lesions were not considered to be indicative of damage induced by
aldicarb, its major metabolites, or the combination of the sulfoxides
and sulfone (Weil and Carpenter, 1972a).
Groups of rats (50 male and 50 female F344 rats per group, 25 of each
sex were used as controls) were administered aldicarb in the diet at
dosage levels of 0, 2 and 6 ppm for 103 weeks. A preliminary dietary
study used 10 male and 10 female rats fed dietary levels of aldicarb
(0, 5, 10, 20, 40, 80, 160 and 320 ppm) for 13 weeks. Microscopic
examinations performed on male and female rats of the 0 and 80 ppm
dosage levels at the conclusion of the preliminary trial showed no
significant somatic effects.
In the long-term carcinogenicity study, there was no mortality noted
attributable to aldicarb in the diet. A variety of benign and
malignant tumors occurring at different sites in both control and
aldicarb treated rats were not unusual for this strain of rat and were
evaluated to be independent of the administration of aldicarb. Gross
and microscopic examination of tissues, organs and all gross lesions
was performed and it was concluded that aldicarb was not carcinogenic
for the F344 strain of rat of either sex (NIH, 1979).
Groups of beagle dogs (3 male and 3 female dogs per group) were fed
aldicarb in the diet at dose levels of 0, 0.025, 0.05 and 0.1 mg/kg
body weight for 2 years. Aldicarb was administered in a moistened
diet and the concentration was adjusted monthly to correspond to the
mean body weight and diet consumed. The dogs, 8 to 20 months of age
at the initiation of the study, were administered aldicarb in the diet
5 days per week for the two-year test interval.
There was no mortality over the course of the study and growth and
food consumption data were comparable to control values. Haematology
parameters and clinical chemistry values evaluated at five intervals
over the course of the study were normal. Plasma and erythrocyte
cholinesterase, evaluated over the course of the study, did not differ
from control values. At the conclusion of the study brain
cholinesterase, while somewhat lower at the high dosage level, was
not statistically different from controls. Gross and microscopic
examination of tissues and organs showed no lesions which could be
attributable to the presence of aldicarb in the diet at dosage levels
up to and including 0.1 mg/kg/day (Weil and Carpenter, 1966c).
Groups of male mice (50 male and 50 female B6C3F1 mice per group, 25
of each sex were used as controls) were administered aldicarb in the
diet at dosage levels of 0, 2 and 6 ppm for 103 weeks in a
carcinogenicity bioassay. A preliminary dietary study used 10 male
and 10 female mice fed dietary levels of aldicarb (0, 0.5, 1.0, 2.5,
5.0, 10, 20 and 40 ppm) for 13 weeks. Microscopic examinations,
performed on male and female mice of the 0, 20 and 40 ppm dose levels
at the conclusion of the preliminary trial showed no significant
In the long-term carcinogenicity study there was no mortality noted
attributable to aldicarb in the diet. A variety of benign and
malignant tumors occurring at different sites in both control and
aldicarb-treated mice were not unusual for this strain of mice and
were evaluated to be independent of the administration of aldicarb.
Gross and microscopic examination of tissues, organs and all gross
lesions was performed and it was concluded that aldicarb was not
carcinogenic for the B63F1 strain of mice of either sex (NIH, 1979).
Groups of mice (44 male and 44 female CD-1 mice per group) were fed
aldicarb in the diet at dosage levels of 0, 0.1, 0.2, 0.4 and 0.7
mg/kg body weight for 18 mouths (539 days or 77 weeks or 17.8 months
of actual dosing). Gross and microscopic examinations were performed
on all surviving animals and on those mice that died during the course
of the study.
Mortality was evident in males at the two highest dosage levels and in
females at the three highest dosage levels during the first two and
one-half months of the study. Following this period, aldicarb was
mixed with the diet in a different manner which appeared to eliminate
its acutely toxic effects. (In the early parts of the study, aldicarb
was mixed in a dry fashion using a finely ground aldicarb preparation.
At the 2.5 month interval, aldicarb was dissolved in acetone and the
acetone-aldicarb solution was dispersed in the diet at a more uniform
rate. It was assumed that consumption of small crystalline particles
of aldicarb may have led to the high mortality during the initial
phases of the study.) At the high dosage level in males there was a
statistically significant increase in hepatomas found predominantly in
the survivors at the termination of the study and an increase in
lymphoid neoplasias which occurred in the mice that died. None of the
male mice surviving at the end of the study were found to have
lymphoid neoplasias. There were no significant increases in any other
types of tumors at dosage levels of 0.4 mg/kg and below (Weil and
Groups of 50 male CD-1 mice were fed aldicarb in the diet at dosage
levels of 0, 0.1, 0.3 and 0.7 mg/kg body weight in an effort to verify
the results of the previous mouse carcinogenicity bioassay. A group
of 150 mice were used as concurrent controls with a mouse being
sacrificed for each treated animal that died during the course of the
study. Diets were prepared by dissolving aldicarb in acetone and
mixing the solution with the diet. The aldicarb was the same sample
as used in the previous study and the duration of the study was
approximately the same as in the previous trial.
There was no mortality observed in the study an a result of aldicarb
in the diet. At the end of 18 months cumulative mortality at all
dosage levels was the same as noted in controls. There was no effect
of aldicarb on growth in any of the groups.
An examination of the animals that died during the course of the study
and those that were sacrificed at the end of 18 months was made and
the data compared with control values. There was no significant
association between aldicarb in the diet and the formation of tumors,
particularly with respect to the incidence of hepatomas, lung
adenomas, and lymphoid neoplasias. The data were evaluated with
respect to the mice that died, those that survived the test and the
total of all animals. It was concluded that the administration of
aldicarb at levels up to and including 0.7 mg/kg body weight for
approximately 18 months did not result in a higher than normal
incidence of tumors and the inclusion of aldicarb in the diet of CD-1
mice did not result in an increased incidence of carcinogenic response
(Weil and Carpenter, 1974d).
Observations in Humans
Groups of 4 adult male volunteers were administered aldicarb orally in
aqueous solution at dosage levels of 0.025, 0.05 and 0.1 mg/kg body
weight. Clinical signs of poisoning were recorded and whole blood
cholinesterase activity was measured up to six hours after
administration of the sample. Total urine voided was collected and
aldicarb-excretion patterns for the initial eight hours after dosing
were evaluated. In addition, spot samples were taken at 12 and 24
Acute signs of poisoning, typical of anticholinesterase agents, were
observed at the high dose level within one hour after administration
of aldicarb. There were no signs of poisoning observed at the 0.05
mg/kg body weight dose level. Cholinesterase depression was observed
in all volunteers predominantly within 1-2 hours after treatment.
Within the first six hours of treatment almost all cholinesterase
depression and clinical signs of poisoning were diminished.
Examination of urinary excretion patterns showed that approximately
10% of the administered dose was excreted as carbamates (toxic
residues) within the first eight-hour interval. Cholinesterase
analyses confirmed the same rapid inhibition and recovery pattern with
man as had been observed in experimental animals (Haines, 1971).
In another study, two additional subjects were administered aldicarb
in water solution at dosage levels of 0.05 and 0.26 mg/kg body weight.
Acute signs of poisoning were recorded at the higher dose level and
atropine was administered to aid recovery. No signs of poisoning were
recorded with the lower dose level. Urinary excretion of carbamate
residues within 24 hours accounted for approximately 10% of the
administered dose (Cope and Romine, 1973).
A series of human exposure episodes was reported occurring as a result
of a variety of field and glasshouse conditions in an effort to assess
the potential for human harm from exposure under actual occupational
conditions. In several instances, slight blood cholinesterase
depression attested to the actual exposure situation. Exposure data,
as indicated by cholinesterase depression or urinary excretion,
suggested that there was no change in the general health of workers
exposed under any of the working conditions. Although there were
acute clinical signs of poisoning there was no indication that the
workers exposed were harmed once removed from exposure situation
(Williams, 1966; Burrows, et al., 1970; Wakefield, et al., 1973;
Shrivastava, 1975; Pandey, 1977).
From 1966 to 1979, 133 cases of apparent overexposure to aldicarb
formulations were reported (Abdalla, 1977; 1979). Of these cases, 40
were confirmed aldicarb poisoning episodes where clinical diagnosis
and/or urinalysis for aldicarb and its metabolites were performed.
There have been no confirmed deaths resulting from (predominantly
occupational) overexposure, and, as has been the case with other
carbamate insecticides, the acute signs of toxicity are rapidly
dissipated, although atropine therapy and hospitalization have been
useful therapeutic regimens.
California, which has one of the best pesticide reporting systems for
accidental overexposure, reported that in 1974, 75 & 76 a total of 10,
14 and 13 cases of human illnesses were reported respectively for the
three years (Peoples, et al., 1977). In these incidents, people
were directly exposed to aldicarb and illness was brought on by
dermal, inhalation and in one instance, ocular exposure. While most
illnesses resulted from aldicarb exposure in loading or applying the
formulated pesticide, some illness has been reported from the handling
of plants and soils treated with aldicarb (Abdalla, 1977; 1979).
Aldicarb is an N-methyl carbamate ester of an aliphatic oxime
currently used as an insecticide in agriculture. Aldicarb has been,
and is currently formulated as, a granular preparation for use as a
soil treatment having systematic activity in plants against a variety
of insect, mite and nematode pests. Aldicarb in extremely toxic with
an extremely low LD50 value in a wide variety of mammalian species.
The onset of acute signs of poisoning appears to be due to reversible
cholinesterase inhibition resulting in parasympathomimetic signs of
poisoning. The acute signs of poisoning are alleviated rapidly
usually without treatment, and frequently within hours, but always
within 1-2 days of exposure.
Aldicarb is rapidly absorbed, widely distributed in the body and
rapidly excreted. Bioaccumulation does not appear to be a factor with
aldicarb. Aldicarb metabolism has been widely studied in a variety of
organisms and appears to be similar in all species examined. Aldicarb
is rapidly metabolized through oxidation of the sulfur atom to produce
a toxic, relatively stable metabolite, aldicarb sulfoxide. Aldicarb
sulfoxide in slowly converted by hydrolytic and/or oxidative
mechanisms to aldicarb sulfone and related oxime and other degradation
A wide variety of special studies have been performed to evaluate the
toxicological hazard associated with the use of aldicarb. Aldicarb
does not affect reproduction, is not teratogenic or carcinogenic in
mammals and there is no evidence of a delayed neurotoxic potential.
Cholinesterase depression is the most significant parameter of
exposure that can be evaluated with respect to the toxicology of
aldicarb. Considerable attention was paid to the analytical
methodology used to develop cholinesterase depression data.
Short-term and long-term dietary studies were conducted with aldicarb
and aldicarb metabolites both alone and in combination, and no-effect
levels were noted. In some of these studies, there was a
discontinuation of feeding of aldicarb or its metabolites for short
periods prior to the evaluation of cholinesterase activity. This
practice served to point to the rapid reversibility of cholinesterase
depression, although in the toxicological evaluation, continuous
exposure prior to analysis of cholinesterase activity was thought to
be very important.
Erythrocyte and plasma cholinesterase were the most sensitive
parameters of exposure. In a short-term study in rats with aldicarb
sulfoxide, cholinesterase depression served as the basis for
evaluating a dietary no-effect level. Cholinesterase depression in
plasma and erythrocytes, measured through the use of an acceptable
analytical procedure, was not observed at 0.125 mg/kg body weight.
Studies on dogs have been performed with aldicarb, aldicarb sulfoxide
and sulfone for various time intervals up to and including two years.
Cholinesterase depression was not noted in the dog studies because of
interrupted treatment. An appropriate short-term cholinesterase study
in dogs would be desirable to allow further evaluations to be made.
Currently, standardized tests for mutagenicity have not been reported,
although a dominant lethal assay in mice suggested no potential for
mutagenic events. Microbial mutagenicity tests were considered to be
Human volunteer studies show that man reacts in a similar manner to
experimental animals. Data on the rapid onset and diminution of signs
of poisoning and depression and recovery of cholinesterase activity
parallel those observed in animal bioassays.
As the slope of the acute toxicity curve is so steep, an additional
margin of safety reflected the high acute toxicity of aldicarb. The
rapid reversibility of cholinesterase depression, the lack of
long-term pathological events and the lack of effects in a wide
variety of toxicological parameters were all reassuring in estimating
an acceptable daily intake for man.
Level Causing No Toxicological Effects
Rat: 2.5 ppm in the diet, equivalent to 0.125 mg/kg body weight
Dog: 0.25 mg/kg body weight
Estimate of Acceptable Daily Intake for Man
0-0.001 mg/kg body weight
RESIDUES IN FOOD AND THEIR EVALUATION
Aldicarb is employed as a systemic pesticide to control insect, mite
and nematode pests in plants. Technical aldicarb is so extremely
toxic to man that it has never been commercially available in
conventional wettable powder, emulsifiable or solution form. The
inventor and sole manufacturer, Union Carbide Corporation, markets
aldicarb only as granular products containing 5 to 15 percent active
ingredient. This formulation allows the product to be handled and
applied with minimal hazard to man.
The granular products employ ground corn cobs, gypsum, or ground
charcoal as substrates. Granular particle size range is 16 to 60
mesh, or about 0.25 to 1.5 mm diameter. Technical aldicarb is
produced in acetone or methylene chloride solution, impregnated into
granules and the solvent in removed by evaporation. One percent of
water-soluble resin is added as a bonding agent to hold the aldicarb
on the granule. Various antistatic or colouring agents may be added
in small amounts. The finished granular products are clean,
free-flowing, and stable in storage for at least two years. Aldicarb
is marketed worldwide in waterproof dispensers, bags or cartons
containing 1.5 or 10 kg of granular product.
The pesticide is most commonly applied by mechanical tractor-mounted
applicators which deliver the granules 2.5 to 5 cm beneath the soil
surface. For field crops like cotton, sugar beets, and potatoes,
granules are applied in the seed furrow, adjacent to the seed, or
alongside the row after crop emergence. In some cases, surface
application followed by immediate rototilling to incorporate the
granules into the soil is recommended. In glasshouse usage for
treating commercially grown ornamental plants, smaller hand-held
applicators spread the granules over beds, benches, or pots and the
aldicarb is watered into the soil.
Rate of use range from one to three kg/ha for row crops. As much as 5
kg ai/ha may be used in potatoes against the golden nematode. Citrus
and some ornamentals require higher rates, up to 11 kg ai/ha.
Usually, only one application is made per crop either at planting or
within six weeks after emergence. In bananas, 2.5 to 3 g ai/mat/6 mos
is applied. Aldicarb is also used as a seedling treatment for coconut
and cacao. For most food crops, a 90-120 day pre-harvest interval is
required for residues to be reduced below acceptable levels. There
are no post-harvest uses.
Aldicarb is used on numerous crops in many countries. Registered
usages include potatoes, coffee, sugar beets, cotton, soybeans, dry
beans, bananas, oranges, sugarcane, peanuts, sweet potatoes, pecans
and ornamentals. In 1979, Temik 15G was tke major product used in the
USA for aphids, golden nematode, and Colorado potato beetle on
potatoes; for early season insects and nematodes on cotton; and for
aphids, maggots, and nematodes on sugar beets. The USA consumes 70%
of world production; Pan America, 15%; Europe, 10%; and other areas,
RESIDUES RESULTING FROM SUPERVISED TRIALS
Extensive data provided by the manufacturer on residues of aldicarb
and its toxic metabolites are the basis for the following discussions.
During 1966 through 1968 with aldicarb applied at planting time, as
sidedress treatment, and a combination of the two treatments, 75% of
244 samples showed no residues above the sensitivity of the method;
90% less than 0.07 mg/kg and 1% more than 0.1 mg/kg. Aldicarb itself
was not detected in any sample, but the sulfone formed the main
portion of the residue.
Residue data was collected in the United States for nine consecutive
crop years (1964 through 1972). There was a total of 342 samples from
21 states in the USA, representing all the potato growing areas.
Samples were also collected from Quebec and Ontario.
Growth dilution is the important factor as regards residues in tubers.
In the period from 70 to 90 days after planting, the tuber is growing
rapidly with much increase in bulk. The uptake of new pesticide
apparently cannot match the dilution by new tissue, and there is a
rapid decrease in residue concentration. From 90-110 days, residues
are still increasing at a slowing rate, an average decrease of about
40 percent, and after 110 days, the tuber residue changes very little.
Aldicarb itself has not been found as a residue in potato tubers. The
toxic tuber residue consists entirely of aldicarb sulfoxide and
aldicarb sulfone. At harvest, a ratio of 78 percent aldicarb
sulfoxide and 22 percent aldicarb sulfone has been found.
There was considerable variation in tuber residue even for those
seemingly grown under identical cultural practices and climatic
conditions, pointing to the need to rely on the determined values
rather than general assumptions. Samples collected from Maine, USA
for potatoes treated at the rate of 0.5 to 1.5 kg in-furrow ranged
from 0.01 to 0.5 mg/kg after 107 days. Of the 248 samples from
recommended at-planting treatments, only two show residues which might
exceed one mg/kg at harvest assuming a pre-harvest interval of 90
days. Sidedressing after an application at planting time did not add
significantly to tuber residues.
In South Africa measurements of residues in potatoes, at periods
ranging from 90 to 180 days after treatment in eight sites and at the
registered application rate of 7.5 kg ai/ha, show that the recommended
120 days PHI could accommodate the national limit of 1 mg/kg. (As the
PHI is normally extended up to 150-170 days, the evidence indicates
that this figure would not generally be exceeded.) In New Zealand
single pre-planting applications at 10 kg ai/ha gave ca. 0.1 mg/kg
aldicarb at harvest 118 days later (New Zealand, 1979).
In the Netherlands, trials in several localities with aldicarb applied
90-160 days before harvest at the 5 kg ai/ha application rate gave
levels mainly in the 0.06 - 0.5 mg/kg range. Only one sample out of
52 had residues in the 0.6 - 1 mg/kg range. At the normally
recommended application rate of 3 kg ai/ha, the maximum residues
occurred in the 0.06 - 0.1 mg/kg range.
Aldicarb is generally applied at 1 to 2 lbs ai/A in-furrow at
planting. In the samples of harvest peanuts from at-planting
treatments of up to 4 lbs. ai/A, the range of residues were as
Residue Range in Whole Nuts (mg/kg) No. Samples in Range %
>0.2 0 -
0.1 - 0.2 1 2
0.05 - 0.1 5 11
0.01 - 0.05 20 43.5
<0.01 20 43.5
Whole nut residues were concentrated primarily in the hull and peanut
kernels generally contained less than 0.02 mg/kg aldicarb.
Analysis of over 200 samples of oranges treated at rates of 2.3 to 22
kg ai/ha showed that the maximum residues in ripe oranges was 0.2
mg/kg. Residues are higher in immature green fruit than in ripe fruit
and residues in peel are higher than in edible pulp, averaging about
4:1 peel-pulp in both green and ripe fruits. The maximum residue
found in ripe orange pulp was 0.1 mg/kg in a Valencia, 30 days after a
treatment of 11 kg ai/ha. The peel residue was 0.5 mg/kg, resulting
in a calculated whole fruit residue of 0.2 mg/kg. Fruits becoming
ripe six to seven months after the ripe fruit cited above continued to
show whole fruit residues of 0.1 - 0.2 mg/kg.
When aldicarb was applied to the soil around orange trees at rates of
0.09, 0.45, and 2.26 g ai/929 cm2, analysis of the orange peel and
pulp at approximately 100 days after treatment did not detect the
presence of aldicarb. The aldicarb sulfoxide residues in the peel
from the three treatments were 0.06, 1.4, and 12.8 mg/kg, while the
residues in the pulp were 0.03, 0.4, and 2.6 mg/kg. The aldicarb
sulfoxide residues in the peel from the three treatments were 0.06,
1.4, and 12.8 mg/kg, while the residues in the pulp were 0.01, 0.1 and
Iwata et al. (1977) detected 0.03 - 0.05 mg/kg residues in orange
pulp 28 days after treatment with 22 kg ai/ha, but not at 11 kg ai/ha.
Samples were obtained from Ecuador, Peru, Philippines and Costa Rica.
The maximum residue found in whole bananas treated either at or near
the recommended rate of three g ai/mat (i.e. ca. m2) is 0.2 mg/kg.
The data are summarized in Table 3. Measurements in Ecuador, Peru,
the Philippines and S. Africa of residues in fruit at known periods
after application show that peak levels are reached in 40 to 100 days.
This is illustrated in Table 4 (S. Africa). The variation in time
after treatment when peak residues occur is probably a combined effect
of differences in moisture, plant size, soils, temperature and growth
dilution. Apparently, residues in harvest fruit are not additive nor
accumulative from multiple treatments at six months intervals.
Analysis of the pulp and peel showed that there is no significant
difference in residues and that the whole fruit data could represent
the edible pulp residues as well. There is also no discernible
difference in the residue content of the top, middle and bottom hands
on the stem. The first application resulted in residues in some
samples slightly higher than the proposed MRL; but the Meeting viewed
the more extensive residues data from Ecuador, Peru, Philippines and
Costa Rica, the traditional banana suppliers of the world, as being
more indicative of the residues situation.
About 75 dry beans seed samples have been analyzed. Aldicarb was
applied at a maximum treatment rate of 22 kg ai/ha in-furrow at
planting time. The maximum residue found at normal harvest was 0.07
mg/kg after application of the highest rate tested, 3.3 kg ai/ha at
planting. At normal rates, the maximum residues was 0.02 mg/kg. The
type of application at planting did not influence residues at harvest.
Each sample was a composite of green ripe fruit from bottom, middle
and top of bunch.
Bean (Dry) forage
The highest residue found in dry bean forage was 2.8 mg/kg in a sample
of straw after an at-planting application of 3.3 kg ai/ha. Harvest
residues in other samples from this application, timing and use rate
ranged from 0.2 to 1.2 mg/kg.
Residues in green forage may approach 30 mg/kg at recommended use
rates, but decline as the plants mature, lose some of their leaves and
become dry toward harvest. Dry bean straw, green forage, and hay are
restricted from use by directions to the label.
Aldicarb was applied at 0.8 to 3.3 kg ai/ha at planting. Forty-eight
soybean seed samples and 44 forage samples were collected. No
detectable residues (0.02 mg/kg) were found in any soybean seed at
harvest, regardless of the application rate or type of application.
Low level aldicarb residues were found in some immature seeds but
these residues quickly diminished as the seed matured to become
non-detectable at harvest. The highest residue found in any soybean
seed was 0.15 mg/kg in very immature seed 58 days before threshing.
Three weeks later (still 36 days before normal harvest) the residues
diminished to non-detectable (0.02 mg/kg) and remained so at harvest).
Table 3. Maximum Residues of Aldicarb (mg/kg) in Bananas Collected
from Different Countries
Location 21 3 4 6 7-8
Ecuador 0.04 0.09 0.1
Peru - 0.2 0.2 - 0.6
1973 - 0.1 - - -
1975 0.05 0.09 - - 0.8
Costa Rica - - 0.3 - -
1 Application to the nearest gram.
(mat similar or equal to sq.m)
Table 4. Aldicarb Residues in Bananas at Different Periods after
Application (South Africa)
Residues of Aldicarb (mg/kg)
Days After First Treatment Treatment 6 Months Later
Application A-3g ai/m2 A-6g ai/m2 B-3g ai/m2 B-6g
15 0.04 0.05 0.04 0.2
30 0.2 0.4 0.03 0.04
45 0.3 0.7 0.06 0.1
60 0.4 0.7 0.1 0.2
90 0.4 0.6 0.2 0.2
120 0.4 0.5 0.3 0.05
180 0.1 0.4 0.2 0.4
Soybean forage and straw
At-harvest residues in soybean straw are generally quite low and do
not exceed 0.1 mg/kg. Aldicarb residues in green soybean forage may
exceed 5 mg/kg at the proposed treatment rates two months before
harvest and younger plants would contain even higher residues. Use of
soybean forage or hay as animal feed is not recommended.
Soybean oil and meal
Soybean seeds do not contain detectable residues (<0.01 mg/kg) when
treated up to two to three times the recommended rates; higher rates
are generally phytotoxic to soybeans. Just the same, soybeans from
fields treated at 1× and 2× the recommendations were composited and
fractionated by procedures closely paralleling the commercial solvent
extraction process to yield oil and meal. No residues were found in
either the oil or meal components. The procedure applied would have
detected residues at 0.005 mg/kg in soybean oil and 0.01 mg/kg in the
Only 6 of the 47 samples of green coffee analyzed show analytically
significant residues at a method sensitivity of 0.02 mg/kg. These
samples include exaggerated treatment rates (up to 2×) as well as
multiple treatments (1-3) and preharvest intervals from 15 days to 274
days. Aldicarb residues seem to preferentially concentrate in the
hulls of the dry coffee berry as shown below:
Hulls 0.01 mg/kg
Parchment 0.05 mg/kg
Green coffee 0.04 mg/kg
The higher residue level in hulls is logical since more water is lost
from the pulpy hull on drying than from either the parchment or seeds.
From the results of supervised trials undertaken in Finland, it was
noted that quite high residues could be found after application of
aldicarb to strawberries (Finland, 1979). It was also noted that use
on this crop has not been recommended.
Applications of 5.5 kg ai/ha at planting time into the furrows and to
ratoon canes resulted in residues shown in Table 5 (South Africa,
1979). Aldicarb appears to be concentrated in the leaves.
Table 5. Residues of Aldicarb in Sugarcane following application of
5.5 kg ai/ha at Planting Time (An extract from results received from
Treatment Application intervals (days)
18 25 32 46 60 75
(Residues in mg/kg)
I. Plant cane
Site A. T1 18.3 5.7 5.1 4.3(L) 0.9 0 6(L)
21 5.5 5.1 4.0(L) 1.0 0:6(L)
Site A. T3 12.8 4.0 4.7 3.9(L) 1.1 0.8(L)
11.1 3.4 3.9 3.6(L) 1.2 0.8(L)
II. Ratoon cane
Site A. 15 29 54 91
5.1 12.3 4.7 0.01
5.4 11.6 4.5 0.01
Site B. 7 13 20 28
7.3 2.1 0.4 0.2
7.5 2.0 0.5 0.2
L = leaves
S = stalk
It is seen below that aldicarb is concentrated on the sugarbeet tops
(Denmark, 1979). Low level residues occurred 135 and 180 days after
application at dosage rates of 0.7 and 1.4 kg ai/ha. The numbers
refer to mg/kg aldicarb sulfone.
135 days 180 days
root top root top
0.7 kg ai/ha 0.007 1.0 n.d. 0.05
0.007 1.0 n.d. 0.08
1.5 kg ai/ha 0.009 1.4 n.d. 0.2
0.02 2.9 n.d. 0.3
Residue trials in the Netherlands showed residues less than the 0.05
mg/kg limit of detection after application of 1.5 kg ai/ha as row
treatment, 150-168 days after application (Netherlands, 1979).
FATE OF RESIDUES
The common metabolic pathway for aldicarb in plants, animals, insects
and soils is shown in Figure 2. The consistency of aldicarb
metabolism in plants has been illustrated with cotton, potatoes,
spearmint, lettuce, sugarbeets, peanuts and tobacco. Following soil
treatment, aldicarb is readily absorbed by the plant with subsequent
translocation. Within the plant, the initial step is thioether
oxidation to aldicarb sulfoxide. This biochemical conversion occurs
rapidly since no parent aldicarb is found in the plant after a few
weeks. Aldicarb sulfoxide is subsequently metabolized primarily by
hydrolysis to yield the sulfoxide oxime. It also produces aldicarb
sulfone through slow thioether oxidation. Both the sulfoxide and the
sulfone suffer extensive degradation through hydrolysis elimination,
oxidation, reduction and conjugation reactions. Such products include
the oximes and the resulting alcohols and their glycoside conjugates,
the amides, the nitriles and the carbonic acids. Essentially, these
are of no toxicological significance. There has been no evidence of
conjugated carbamate metabolites in plants resulting from aldicarb
treatment. Consequently, the only significant terminal carbamate
containing residues in plants following aldicarb treatment are the
aldicarb sulfoxide and aldicarb sulfone, and depending on the
harvesting time, a minor residue of parent aldicarb.
There is essentially no retention of aldicarb and its carbamate
metabolites in tissues, milk and eggs. Residues can be detected in
milk only when cows were fed with exaggerated dosages. At residue
levels normally resulting from aldicarb usage, no residues can be
detected in milk. Excretion is mainly through the urine. In laying
hens, excretion of aldicarb sulfoxide and sulfone is rapid for both
single oral and continuous feeding for up to 10 days. About 75
percent of the doses are in the faeces by 24 hours and a large portion
of the metabolites are water-soluble materials. Only minute
quantities of the toxic carbamate compounds were observed.
A positive correlation exists between temperature and moisture and the
rate of loss of aldicarb in soils. Aldicarb is very susceptible to
alkaline hydrolysis and is presumably unstable at higher soil pH.
Upward movement is observed with most soils with aldicarb apparently
leaving the soil surface entrained with water vapour. Only in pure
sand is downward movement readily achieved through water action so
that aldicarb does not pose a hazard through ground water
Aldicarb is degraded by micro-organisms and the catalytic action of
clays and other inorganic soil constituents. No hazard from carryover
residues is expected. Bacteria or fungi do not appear to be
susceptible to the toxic action of aldicarb and the compound could
even serve as a carbon source for some micro-organisms.
(see Biochemical Aspects).
Metcalf et al. (1966) demonstrated that aldicarb was completely
oxidized to aldicarb sulfoxide in cotton foliage within four to nine
days. Further hydrolysis yielded the sulfoxide oxime, and oxidation
of the aldicarb sulfoxide to aldicarb sulfone occurred. Coppedge et
al. (1967) confirmed these findings, and identified the sulfoxide
nitrile as a definite metabolite in cotton. Once formed, aldicarb
sulfone is not reduced to provide a secondary source of aldicarb
sulfoxide, nor could evidence of oxidative N-demethylation be found.
The total radioactivity in the cotton plant in reduced with time
through volatilization and dilution by plant growth.
Field-grown cotton was treated with radioactive aldicarb by in-furrow
at planting and by side-dressed applications (Andrawes and Bagley,
1968c). The residues were identified, quantitated, and the rates of
decline determined. The metabolic pattern of aldicarb in vivo was
in agreement with that described by earlier investigators. A second
field study employed petiole injection and obtained similar results
(Bull, 1968). A complete distribution of radioactivity in the cotton
plant was described and the residue in the maturing fruit was
characterized. After four weeks no toxic residues were present in the
Bartley, et al. (1970) showed that sulfoxide oxime in further
transformed to a mixture of water-soluble products. These consist
primarily of sugar conjugates of sulfoxide alcohol, as well as smaller
quantities of sulfoxide and sulfone acids and sulfone amide. There is
no evidence for the presence of N-methylol or N-demethyl derivatives
as sugar conjugates.
After gaining entrance into the potato plant, aldicarb residues move
primarily by xylem transport with highest concentrations appearing in
the foliage. Stem injection studies have shown that only limited
quantities of aldicarb and its metabolites move downward into the
tuber. The toxic carbamate residues appearing in the tuber do not
persist, but are actively degraded to non toxic water-soluble products
similar to those formed in the foliage (Andrawes and Bagley, 1968b;
Andrawes et al., 1971b).
Systemic movement and concomitant metabolism of aldicarb resulted in a
preferential accumulation of the residues in peanut foliage
(Andrawes,l972). A small fraction of the observed radioactivity was
found in the fruits. Translocation of residues to the forming fruit
is facilitated by the polar nature of the metabolic products present
in the maturing plants. These water-soluble metabolites were the
predominant component of the terminal residues in the foliage and
constituted 90 to 95 percent of the recovered radioactivity in the
Aldicarb sulfoxide, aldicarb sulfone, and the non-toxic water soluble
metabolites constituted the major portion of the residual C14
materials in sugar beets (Andrawes et al., 1970). Most of the
absorbed radioactivity was found in the foliar portion of the plant
throughout the growing season. At maturity (140 days after treatment)
total C14 residues were 27.2 mg/kg in the foliage and 2.5 mg/kg in
the roots. The corresponding values for total toxic residues was 11.0
mg/kg in the foliage and 0.6 mg/kg in the roots.
The chemical changes that occur in soil are essentially the same as
for plants, animals and insects. Series of parallel experiments have
been performed under the same environmental conditions with single
factors varied to assess the roles in controlling the persistence of
aldicarb in the soil. These factors include soil types, moisture, pH,
and temperature (Coppedge, et al., 1967; Bull, 1968; Romine et
al., 1968; Bull et al., 1970; Quraishi, 1972; Supak, 1972; Gawaad
et al., 1971).
A positive correlation exists between temperature moisture and rate
loss from soil. Changes in pH in the 6 to 8 range do not appear to
adversely affect aldicarb although the compound in is very susceptible
to alkaline hydrolysis so that it is anticipated that it would be
unstable in high soil pH.
Under greenhouse and field conditions, aldicarb and its breakdown
products leave the soil with unexpected rapidity; a half-life of seven
days was observed (Bull et al., 1968). This emission is definitely
linked to the degree of soil moisture and consists primarily of an
upward movement. This phenomenon has been studied in an elaborate
series of percolation experiments with different soil types in
assorted sizes of columns (Bull et al., 1968; Romine et al., 1968)
and under field conditions (Bull, 1968; Bull et al., 1968). Only in
pure sand is downward movement readily achieved through water action.
Aldicarb and related compounds probably leave the soil entrained with
water vapour as little movement has been noted in dry soils.
The dissipation of aldicarb in the soil is sufficiently rapid and
complete that recommended rates will offer no hazard of contamination
of subsequent crops in a treated area (Andrawes and Bagley, 1968;
Andrawes et al., 1971a; Quraishi, 1972). Predictably, discing or
other soil manipulations will serve to disperse and dilute aldicarb
that has been placed in-furrow. Tomatoes transplanted into fields 90
days after a 3.3 kg/ha application of radioactive aldicarb showed no
detectable radioactivity when analyzed seven days later. Bioassays of
volunteer potato plants taken from fields treated the previous year
with 6.6 kg/ha active ingredient were completely non-toxic to the
highly sensitive Colorado potato beetle (Clarkson, 1968).
Extensive laboratory screening tests in which high concentrations of
aldicarb and its metabolites were incorporated into various nutrient
media and then inoculated with bacteria or fungi suggest that the
pesticide has no toxic effect on microorganisms (Spurr and Chancey,
1968; Spurr and Sousa, 1974; Anderson, 1971). Gawaad et al., (1972)
also found no effect on the nodulation rate of Rhizobium phaseoli
and R. trifolii in broad beans and Egyptian clover. Soil
enrichment experiments even demonstrated that aldicarb could serve as
a carbon source for certain microbes (Spurr and Chancey, 1968).
Aldicarb was however very toxic to oribatid mites while it was less
toxic than several other materials to earthworms, enchytraeids,
predatory mites and collembola (Heungens, 1970).
Since aldicarb does not readily move downward through different soil
types by leaching action except in sandy soil, resultant contamination
of ground water from surface-treated fields is unlikely. Clarkson et
al. (1968a) treated a graded 0.2 ha with 4.5 kg of aldicarb. They
did not find any significant movement of the pesticide during the
30-day test period and over 20 cm of rainfall. On the other hand,
Gawaad et al. (1971) showed that aldicarb had leaching rates of
47.12, 42.3 and 56.14 percent from sand, loam and sandy clay loam
soils respectively. Lateral movement of aldicarb is low (Woodham et
Kearby et al. (1970) in a study of the distribution and persistence
of residues in a Pennsylvania tree farm soil, wherein aldicarb was
applied at 0.23 and 0.45 kg trees, found no apparent chemical residues
in soil samples taken at depths of 15 and 30 cm, 36 and 63 days after
treatment. The half-lives of aldicarb and its major metabolites were
estimated to be 15 days.
The disappearance of aldicarb was determined over a 30-day period in
distilled water at pH 6, 7 and 8, and in pond water and lake water,
the latter two in the presence and absence of their respective bottom
material (Moorefield, 1974). The initial concentration of aldicarb in
all samples was 0.5 mg/kg. There was little or no degradation of
aldicarb carbamates in the distilled water, or in the pond and lake
water in the absence of bottom material. In the pond water with about
5% mud (percent by weight, dry basis) present, the aldicarb carbamate
residue degraded to a concentration of 0.02 mg/kg in 20 days, the
half-life being about 5 days. After 20 days, the bottom mud contained
less than 0.01 mg/kg aldicarb carbamates. In lake water in the
presence of bottom silt, aldicarb carbamates degraded to a
concentration of 0.03 mg/kg in 25 days; half-life is about 6 days.
Moorefield (1974) further reported on a field study in which a farm
pond was treated with aldicarb at an initial concentration of 3 mg/kg.
Samples of water and bottom and were taken periodically. Aldicarb
carbamate residues in the pond water declined to 1.1 mg/kg after 2
weeks; 0.26 mg/kg after 4 weeks; 0.06 mg/kg (the limit of sensitivity
of the method) after 6 weeks. The half-life was about 7 to 10 days.
The maximum concentration of aldicarb carbamate residues in the bottom
mud was 0.09 mg/kg at 4 weeks. The dissipation of aldicarb carbamate
residues on this farm pond was rapid and complete, without residue
buildup in pond sediment.
Quraishi (1972) studied the persistence of aldicarb in water collected
from fields. Treatment at 100 mg/kg of aldicarb resulted in residues
of aldicarb and metabolites at 0.4 mg/kg after 11 months.
In storage and processing
Processed cotton meal from seed treated at 0.1 mg/kg contained only a
fraction of the residue present in the whole seed and no detectable
residues (<0.003 mg/kg) were found in refined cottonseed oil.
The processing of potatoes into potato chips, potato flakes and the
process of baking, boiling, making into french fries, hash browning
and canning of potatoes was investigated for their effect on residues
in raw tubers. In the case of potato chips, 95 percent of the residue
in raw tubers is lost during the manufacturing. However, since up to
5 lbs. of tubers are required to produce kg × kg of chips, the
concentrative effect results in chips having an apparent loss of only
69 percent. The maximum residues found in potato chips was 0.2 mg/kg
and resulted from tubers having 0.45 mg/kg residues. The rest shows
residue of 0.1 mg/kg or less. In potato flakes, the maximum residues
found from harvest tubers treated at recommended rates was 0.12 mg/kg.
Aldicarb residues destroyed in the other processes were: baking, 65
percent; boiling, 60 percent; french frying, 36 percent; hash
browning, 72 percent; canning, 65 percent. This in an average
destruction of about 60 percent of the raw tuber residue for these
commonly used cooking procedures.
Smelt et al. (1975) found in five samples of peeled potatoes and
peelings that the contents in the peelings were on the average 11%
higher than in the peeled potatoes. Hence, peeling does not lead to a
significant decrease of the residue. On boiling with 2% NaCl solution
for 20-24 minutes 42-52% lower residues were observed than before
cooking. Only about 2.5 -8.1% of the initial residue was found in the
water drained off potatoes. Storage of potatoes at 20°C for two
months also resulted in 42-55% lower residues.
Fractionation of peanuts containing 0.01 to 0.04 mg/kg residues on the
whole dry nuts (equivalent to 0.002 to 0.02 mg/kg residues in the
kernel) resulted in peanut oil with no detectable residues (<0.003
mg/kg), whether the oil was recovered by the screwpress or solvent
extraction procedure. The peanut meal contains about the same level
of residues as the kernels.
In a simulated commercial processing operation for using roots of
treated sugar beet, the residue was <0.005 mg/kg in all fractions
except the diffusion juice which had a maximum of 0.02 mg/kg. When
diffusion juice was fortified with lime water under conditions
simulating plant processing, <0.005 mg/kg residue remained at the
exaggerated fortification level of 13.0 mg/kg. No detectable residues
were found in fortified beet pulp after simulating plant drying
conditions. Therefore, there in no reasonable expectation of
detectable residues in sugar, molasses or beet pulp.
Aldicarb-treated oranges were processed as in a commercial operation
and the different fractions were analyzed for residues. It is seen in
Table 6 that the residues in the whole fresh fruit can be concentrated
in the dried citrus pulp by a factor of 1.75%. The portion of the wet
peel residues which do not survive the dried citrus pulp process are
believed to be destroyed by the liming process prior to screw pressing
and during the application of heat in the pulp drier. Orange juice
residues are equal to fresh pulp residues. Concentrated orange juice
(concentrated about 3×) shows residues greater then fresh juice and
reconstitution prior to consumption would generate the original juice
residue. The other by-products of commercial processing which were
investigated, molasses oil, press liquor and oil water layer contain
only low level residues, not exceeding 0.04 mg/kg.
Table 6. Effect of Commercial Processing on Aldicarb Residues in
Aldicarb Residues, mg/kg
First Fractionation Second Fractionation
Orange Fraction UCC1 UCR UCC UCR
Whole fruit 0.22 - 0.07 0.1
Wet pulp 0.1 0.1 - -
Wet peel 0.6 0.4 0.08 0.09
Dried citrus pulp 0.4 0.4 0.04 0.07
Dilute juice 0.1 0.2 0.06 0.09
Conc. juice - - 0.2 0.3
Press liquor - - 0.02 0.02
Molasses 0.04 0.04 0.04 0.02
Oil 0.02 0.02 0.03 0.02
1 Analyzed by UCC = Union Carbide Corp., UCR = University of
2 The orange pulp is 75% by weight of the whole fruit and the wet
peel 25%. The calculated whole fruit residue from the pulp and wet
peal analysis in 0.24 mg/kg [(0.1 × 0.8) + (0.6 × 0.2) = 0.2]. Whole
fruit containing 0.2 mg/kg aldicarb residues resulted in 0.4 mg/kg in
the dried citrus pulp or a 1.75-fold concentration.
Dry beans (cooking)
Cooking as usually done in homes reduces dry beans residues by 85%
after 1 hour and over 90 percent after 3 hours. Apparently, the
residues are diluted by water absorption and resultant weight gain of
the seed or diffuse from the dry seed into the water during the
soaking process. This is reflected in 0.5 mg/kg residues in the dry
seed becoming 0.2 mg/kg in the soaked seeds. Most of the residues are
then destroyed during cooking at 100°c.
EVIDENCE OF RESIDUES IN FOOD IN COMMERCE OR AT
Aldicarb in generally not yet included in pesticide monitoring
programmes. Therefore no data were available to the Meeting.
METHODS OF RESIDUE ANALYSIS
The most widely-used procedure is that wherein aldicarb and aldicarb
sulfoxide are converted to the sulfone by hydrogen peroxide-acetic
acid oxidation and quantitated by GLC (Maitlen et al., 1968, 1969,
1970). The method is simple and rapid.
Generally, aldicarb residues are extracted from the crop by blending
the sample in a mixed solvent consisting of 75 percent acetone and 25
percent water. The aldicarb residues are oxidized to aldicarb sulfone
by addition of peracetic acid to the extracting solvent. After
clean-up on a Florisil column, the residues are determined with a
flame photometric detector and reported as aldicarb. Alternatively,
the metabolites may be separated by Florisil column chromatography
prior to oxidation. Detection limits of 0.007 to 0.01 mg/kg have been
obtained in apples alfalfa, bananas, beans, coffee, cucumbers,
oranges, potatoes, soybeans and sugar beets.
NATIONAL MRLs REPORTED TO THE MEETING
The following were reported:
Country Crop Limit
USA cattle (meat, fat, meat by-products) 0.01
citrus pulp, dried 0.6
cottonseed hulls 0.3
goats, hogs, horses, sheep (meat,fat,
meat by-products) 0.01
peanut hulls 0.5
sugar beets 0.05
sugar beet tops 1.0
sweet potatoes, sugar cane 0.02
Argentina cottonseed 0.1
sweet potatoes 0.02
Brazil cottonseed 0.1
Panama potatoes 1.0
Mexico cottonseed 0.1
National MRLs, Continued...
Country Crop Limit
Netherlands onions, bulb 0.1
sugar beets 0.02
other products of plant origin 0.01*
of Germany strawberries 0.05
sugar beets 0.05
(DDR) onions, bulb 0.1
Switzerland corn 0.02
sugar beets 0.05
Hungary sugar beets 0.05
South Africa potatoes 0.1
Aldicarb is a very toxic systemic pesticide for the control of
insects, mites and nematodes. It is sold only an the granular
material containing 5 to 15 percent active ingredient. Among the
crops for which aldicarb in registered are bananas, citrus, cotton,
coffee, potatoes, peanuts, sugar beets, sugarcane, sweet potatoes, dry
beans and soybeans. Application rate is generally from 1 to 3 kg/ha.
For most food crops the use pattern involves a 90 day pre-harvest
interval. There is a common metabolic pathway in plants, animals,
insects and soils. The initial step in the rapid thioether oxidation
to the sulfoxide followed by a slower conversion to sulfone. Both the
sulfoxide and sulfone undergo extensive degradation; the primary
metabolic step is hydrolysis to the corresponding oximes. Aldicarb,
aldicarb sulfone and aldicarb sulfoxide are the toxicologically
important residues, but aldicarb itself is seldom detected at harvest.
Feeding studies with dairy cows at 0.12, 0.6 and 1.2 ppm for 14 days
showed no apparent harmful effects. There were also no changes in
blood cholinesterase levels, milk production, quantity of excretory
* At or about the limit of detection.
products, or food consumption. About 90 percent of the applied dose
was excreted in the urine. At feeding levels above that normally
encountered as a result of field treatment, no toxic carbamate
residues could be detected in milk.
Considerable residue data for potatoes, cottonseed, sugar beets,
peanuts, coffee and bananas were reviewed. Residue levels were
normally low following the long pre-harvest intervals prescribed.
Processing further reduced the residue levels either due to dilution
or to thermal degradation.
The most widely-used analytical procedure requires the conversion of
aldicarb and the sulfoxide to the sulfone and then quantitation by gas
chromatography with a flame photometric detector in the sulfur mode.
Residues are expressed as aldicarb. Alternatively, the three
carbonate materials can be separated by column chromatography prior to
oxidation. For a variety of crops limits of determination ranged from
0.007 to 0.01 mg/kg.
The following levels are recommended as MRLs which need not be
exceeded when aldicarb is used according to good agricultural
practice. They refer to aldicarb, aldicarb sulfoxide, and aldicarb
sulfone determined as aldicarb sulfone and expressed as aldicarb.
Limit on which recommendations
Commodity mg/kg are based
bananas 0.5 1
beans, dry 0.1 2
citrus fruits 0.2 90
cottonseed 0.1 90
meat 0.01* -
milk 0.002* -
peanuts 0.05* 90
soybeans 0.02* 3
sugar beets 0.05* 90
sugar beet tops 120
coffee beans (green) 0.1 2
1 No PHI because of continuous harvesting
2 At planting time only.
* at or about the limit of determination
1. Studies on cholinesterase activity in dogs associated with
short-term continuous dietary exposure.
2. Examination of the mutagenic potential of aldicarb using
short-term microbial bioassays.
3. Data on use patterns and resultant residues in important crops in
countries other than USA.
Abdallah, N.A. Alleged Overexposure Cases Reported from Use of Temik
Formulations - 1966 to 1976. (1977) Unpublished report from Union
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UCC Project Report 9218. May 24 (1968a), Unpublished.
Degradation of 2-methyl-2-(methylthio)
propionaldehyde-O-(methylcarbamoyl) oxime (Temik) in potato foliage.
UCC Project Report 10495, Nov. 11 (1968b), Unpublished.
Metabolism of C14 Temik in cotton plants under field conditions.
UCC Project Report 10492, Nov. 13 (1968c), Unpublished.
Degradation and carry-over properties of 2-methyl-2-(methylthio)
propionaldehyde O-(methyl-carbamoyl) oxime (Temik) in soil. UCC
Report 104949, Nov. 19 (1968d), Unpublished.
Andrawes, N.R., Bagley, W.P. and Herrett, R.A. Metabolism of Temik
aldicarb pesticide (2-methyl-2-(methylthio)-propionaldehyde
O-(methyl-carbamoyl) oxime in sugar beets. UCC Project Report 12694
May 1 (1970), Unpublished.
Fate and carryover properties of Temik aldicarb pesticides. J. Agr.
Food Chem. 19(4), 727-730
Metabolism of 2-methyl-2-(methylthio) propionaldehyde
O-(methylcarbamoyl) Oxime in potato plants. J. Agr. Food Chem. 19, 731
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pesticide in peanut plants under field conditions. UCC Project Report
17613, Sept. 14 (1972), Unpublished.
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Rat. 1977 Unpublished report from Union Carbide Corporation.
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J. Agr. Food Chem. 18, 454
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with special reference to chemical changes, movement and volatization.
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with Several of its Analogues. (1963) Unpublished report from Mellon
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Miscellaneous Toxicity Studies. (1969) Unpublished report from
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Carpenter, C.P. and Smyth, H.F. A 4-hour Test for Evaluation of
Comparative Skin Penetration Hazard. (1965) Unpublished report from
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Temik 10G (10.5% Granular Formulation of Compound 21149). 15-Day
Dermal Applications to Rabbits. (1966) Unpublished Report from Mellon
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Chin, G.H. and Sullivan, L.J. Some Biochemical Considerations of
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presented to the 156th ACS National Meeting, submitted by UCC.
Clarkson, V.A. The persistence of Temik in an agricultural soil as
indicated by field and laboratory bioassay. UCC Project Report 10490,
Nov. 11 (1968), Unpublished.
Clarkson, V.A. Rowe, B.K.and Romine, R.R. Field evaluation of the
persistence and movement of Temik and its carbonate metabolites in
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Dorough, H.W., Davis, R.B. and Ivie, G.W. Fate of Temik-Carbon-14 in
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Gawaad, A.A.A., Ali, E.S.N.M. and Shazli, A.Y. Leaching of some
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Heungers, A. The Influence of some pesticides in the soil fauna in
Azalea culture. Ueded, Fac. Landbonwivet. Ryksuniv, Gent, 35(2),
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Temik (Technical Grade Compound 21149). Comparative Behavioural
effect in Rats. (1966b) Unpublished report from Mellon Institute
submitted by UCC.
Johnson, H.E., and Sullivan, L.J. Studies on an Effective Therapy for
Overdoses of Temik, Temik Sulfoxide, and Temik Sulfone in the Rat.
(1968a) Unpublished report from Mellon Institute submitted by UCC.
Temik (UC 21149) Antidotal Therapy in Rats Following Administration of
Multiple Lethal Doses. (1968b) Unpublished report from Mellon
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2-Methyl-2-(methylthio) propionaldehyde O-(methylcarbamoyl) oxime in
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Maitlen, J.C., McDonough, L.M., Dean, F., Butt, B.A., and Landis B.J.
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performance in apples and pears, U.S.D.A. ARS-33-135. March, 1970.
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South Africa. Data submitted to the 1979 JMPR
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micro-organisms and their importance to ecological relationships in
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the Dog and their Metabolic Profile as Revealed by Silica Gel
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Urinary Metabolic Profiles as Determined by Silica Gel
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Two Year Feeding of Compound 21149 in the Diet of Rats. (1965)
Insecticide Temik. Teratogenic Potential in Rats. (1966a)
Results of Long-Term Tests for Mouse Skin Carcinogenicity of Three
Process Residues, One Epoxide and Three Compounds. (1966b)
Two Year Feeding of Compound 21149 in the Diet of Dogs. (1966c)
Temik 10G-V (10.3% Granular Formulation of Compound 21149). Acute
and 14-Day Dermal Applications to Rabbits. (1968a)
Temik Sulfoxide. Results of Feeding in the Diet of Rats for Six
Months and Dogs for Three Months. (1968b)
Temik Sulfone. Results of Feeding in the Diet of Rats for Six Months
and Dogs for Three Months. (1968c)
Temik Sulfoxide and Temik Sulfone Single Rabbit Skin Penetration
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Rats for One Week. (1969b)
2-Methyl-2-(Methysulfinyl) Propanol-1. Results of Feeding in the
Dicta of Rats for One Week. (1969c)
Temik and Other Materials. Miscellaneous Single Dose Peroral and
Peroral and Parenteral LD50 Assays and Some Joint Action Studies.
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Temik (T) Temik Sulfoxide (TSO), Temik Sulfone (TS02), 1:1
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1:1 Temik: Temik Sulfone. Results of Feeding in the Diet of Mice for
7 Days. (1970e)
Temik. Results of Feeding in the Diet of Mice for 7 Days. (1970f)
Aldicarb (A), Aldicarb Sulfoxide (ASO), Aldicarb Sulfone (ASO2) and
a 1:1 Mixture of ASO:ASO2. Two Year Feeding in the Diet of Rats.
Miscellaneous Toxicity Studies. (1972b)
Aldicarb. 18 Month Feeding in Diet of Mice. (1972c)
Aldicarb. Seven-Day Inclusion in Diet of Dogs. (1973)
Aldicarb. Inclusion in the Diet of Rats for Three Generations and a
Dominant Lethal Mutagenesis Test. (1974a)
Aldicarb Oxime (All). Results of Feeding in the Diet of Rats for 7
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and 20047A for White Leghorn Cockerels. (1965)
Temik (Compound 21149, Technical). Joint Action with Selected
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Miscellaneous Acute Toxicity Data. (1966b)
WHO Insecticide Evaluation and Testing Programme, Stage I, Mammalian
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