Sponsored jointly by FAO and WHO


    Joint meeting of the
    FAO Panel of Experts on Pesticide Residues
    in Food and the Environment
    and the
    WHO Expert Group on Pesticide Residues
    Geneva, 3-12 December 1979



    Owing to insufficiency of data the 1978 Meeting was only able to
    undertake a preliminary review of information concerning this
    compound.  Toxicological and residue data, made available to the
    current meeting, are reviewed and summarized in this monograph


    Chemical Name:      4-dimethylamino-3-methylphenyl N- 
    methylcarbamate     4-dimethylamino-m-tolyl N-methylcarbamate

    Synonyms:           Matacil (R), Bayer 44,646, A 353, Matacil (R)

    Chemical Structure:


    Empirical Formula:  C11H16N2O2

    Other Information on Identity and Properties:

    Description:        White, crystalline solid
    M.P.                93-94°C
    V.P.                Non-volatile
    Solubility:         Slightly soluble in water; moderately soluble
    in aromatic         solvents; soluble in polar organic solvents
    Stability:          Unstable in alkaline media.

    FIGURE 1

    The half-life for the hydrolysis of aminocarb in pH 9.3 buffer was
    reported to be 4 hours.  On glass surfaces under fluorescent light at
    25°C the rate of loss was approximately linear for the first few hours
    with a half-life of 1.6 hours.  In the period of 4 to 12 hours, after
    application, there was a decrease in slope, indicative of conversion
    to less volatile products on exposure to air and light (Abdel-Wahab
    et al., 1966).



    Absorption, Distribution, Excretion and Biotransformation

    Miniature swine (Sus scrofa, 1 male and 1 female) received a
    single oral dose of 0.5 mg/kg body weight 14C labelled aminocarb. 
    The compound was rapidly absorbed.  The 14C peak value in blood was
    reached within one hour.  Excretion via the faeces did not exceed 2
    percent, while 96% was excreted in the urine within 48 hours.
    Elimination was rapid with approximately 75 percent observed in urine
    within 6-24 hours.

    The major urinary metabolites consisted of
    conjugated-4-dimethylamino-, 4-methylamino-, and 4-
    amino-3-methyl-phenol.  Additionally, slight amounts (1-4%) of
    aminocarb, its 4-formylamino-3-methyl phenol, and demethylation
    products were observed.  The same animals received 0.26 mg/kg body
    weight of 14C-labelled aminocarb for five days and were sacrificed 45
    minutes after the last dose.  More than 90% of the daily dose was
    excreted in the urine and with less than 2% in the faeces.  Remarkable
    amounts of 14C occurred in the kidney (0.7 ppm, expressed as
    aminocarb) and liver (0.2 ppm) with conjugated
    4-dimethyl-amino-3-methyl-phenol characterized as the main metabolite.
    A similar amount of unidentified metabolite(s) was also observed.
    Additionally, slight amounts (1-5%) of aminocarb, its demethylation
    products, the formylamino derivative, and conjugated phenol-analogues
    were determined.  Slight quantities of 14C (0.02-0.09 ppm) were found
    in other tissues (skin, brain, heart, muscles, and fat) with higher
    values noted in the skin and fat (Shaw, 1978).


    Quail were fed 0, 10 and 50 ppm of 14C ring labelled aminocarb.  The
    14C content of liver, breast muscle, and mesenteric fat continuously
    increased during the 14 days of treatment followed by continuous
    elimination during a 14-day withdrawal period (Lamb, et al., 1976).

    In channel catfish (Ictalurus punctatus) exposed to 10 ppb 14C
    ring-labelled aminocarb, accumulation reached an equilibrium level
    after one day.  Elimination was rapid.  A 50% reduction of residues
    was noted in one day following a 28-day exposure.  14C was equally
    distributed in the edible and non-edible parts of the fish (Lamb and
    Roney, 1976).

    A group of 9 male albino rats received a single dose of 25 mg/kg
    aminocarb by gavage.  The cholinesterase activity in the erythrocytes
    was reduced by 50% after 1,3 and 5 hours.  Recovery was rapid, being
    complete within 24 hours (Kimmerle, 1961).

    Special Studies on Cholinesterase Inhibition


    Groups of male and female (Sprague-Dawley) rats (3 animals/group)
    received oral doses of 0, 0.5, 2.0 and 8.0 mg/kg aminocarb by gavage
    once a week for three weeks.  Reduced cholinesterase activity was
    noted at the highest dose (8.0 mg/kg) 1 and 3 hours after treatment
    (approximately 10 to 20% in plasma and 30 to 40% in erythrocytes).  In
    the 2 mg/kg group, reduced erythrocyte cholinesterase activity was
    observed after one hour.  Twenty-four hours after dosing, all
    inhibitory effects had disappeared in the blood.  There was no
    inhibition of brain cholinesterase activity noted in this study
    (Nelson, 1978b).

    A group of male albino rats which received 5 mg aminocarb/kg by gavage
    for four weeks showed a 20-30% inhibition of erythrocyte
    cholinesterase activity.  There were no clinical signs of poisoning
    associated with this dose level.

    Groups of young adult female Sprague-Dawley rats (5 animals/group)
    were administered aminocarb by intraperitoneal injection at daily dose
    levels of 0, 2, 4, 8 and 10 mg/kg for 60 days.  At dosage levels above
    2 mg/kg, a decrease in body weight was noted.  The animals
    administered 4 and 8 mg/kg developed acute signs of poisoning which
    persisted for one or two hours after dosing.  All animals at the
    highest dose level and one animal of the 8 mg/kg level failed to
    survive the 60-day trial.  One day after the last dose, cholinesterase
    activity of brain, submaxillary gland and serum was measured and
    inhibition data are represented in the following table:

                                      % of inhibition at:
                                  2 mg/kg   4mg/kg    8mg/kg

         Brain                    0         0         0
         Submaxillary gland       11        24        34
         Serum                    29        44        53

    (Dubois and Kinoshita, 1762).


    Special Studies or Reproduction

    Four groups of 10 male and 20 female (Sprague Dawley) rats were fed
    aminocarb in the diet at doses of 0, 100, 200 and 800 ppm.  Treatment
    started when the parents were approximately 75 days old and was
    continued through a standard three generation reproduction study.  All

    generations showed a light hypersensitivity at 800 ppm.  With the
    exception of females of the F1b generation, retarded weight gain was
    noted in all rats at 800 ppm.  Weight gain was also retarded in the
    females of the F0 and in males of the F1 and F2 generation at 200
    ppm.  Food consumption at the two higher dose levels was depressed in
    a dose dependent manner.  At birth, a reduced litter size and weight
    was noted in the first mating of the F0, F1 and F2 generations at
    800 ppm.  At weaning, a reduced litter weight and mean pup weight for
    all generations was seen at 800 ppm.  At 200 ppm, a reduced pup weight
    was observed at the first mating of the F0 generation.  No
    abnormalities were found as a result of aminocarb in the diet.  The
    young animals from the second litter of the third generation of rats
    treated with 800 ppm did not show significant alteration in tissue
    morphology associated with treatment.  A no-effect level in this study
    was 100 ppm (Palmer and Fletcher, 1966).

    Special Studies on Neurotoxicity

    In 20 hens over 9 months of age, which were orally administered
    aminocarb (74 mg/kg) on day 0 and day 30, no signs of delayed
    neurotoxicity were noted over the observation period of 30 days or in
    the 30-day observation period following the second dosing.
    Histopathologically, no alterations were observed in the nervous
    tissue (Kruckenberg, 1978a).

    In groups of 18-20 month old hens (3 animals/group) which were fed 0,
    250, 500, 1000 and 2000 ppm aminocarb in the diet for 30 days and
    thereafter observed for another four weeks, no delayed neurotoxic
    effects were found.  At doses of 500, 1000, and 2000 ppm, mortality
    was observed as 2, 6 and 7 animals, respectively, died.  At all dose
    levels, blood cholinesterase was significantly inhibited and body
    weight was reduced (Kimmerle, 1965a).

    Acute Toxicity

    Table 1.  Acute-Toxicity of Aminocarb

                       Route of          LD50
    Species      Sex   administration    (mg/kg)   Reference

    Mouse        M     IP                8         Dubois & Raymund, 1962a
    Mouse        F     IP                9         Dubois & Raymund, 1962a
    Mouse        F     IP                4.7       Abdel-Wahab & Casida,
    Mouse        F     Dermal            31        "             "
    Mouse        F     1 hr exposure
                       2 um size)        4 mg/L    Dilley & Doull, 1962
    Rat          M&F   Oral              30        Dubois & Raymund, 1962a
    Rat          F     Oral              22-27     Nelson, 1978a
    Rat          M     Oral              ca.50     Kimmerle, 1961

    Table 1.  Continued...

                       Route of          LD50
    Species      Sex   administration    (mg/kg)   Reference

    Rat          M     IP                13        Dubois & Raymund, 1962a
    Rat          M     IP                21        Kimmerle, 1961
    Rat          F     IP                13.5      Dubois & Raymund, 1962a
    Rat          F     Dermal            275       "         "
    Rat          M     Dermal            <1000     Kimmerle, 1961
    Rat          F     Inhalation
                       (1 hr exposure)   6 mg/L    Dilley & Doull, 1962
    Rat          M&F   Inhalation
                       (4 hr exposure)   0.2 mg/L  Kimmerle, 1961; 1966
    Guinea pig   M     Oral              60        Dubois de Raymund,1962a
    Guinea pig   M     IP                30        "          "
    Chicken      F     Oral              74        Kruckenberg, 1978b
    Chicken      F     Oral              75        Dubois, 1962
    Chicken      F     Oral              50-100    Kimmerle, 1965b
    Chicken      F     IP                25-50     Kimmerle, 1965b

    In an acute inhalation toxicity test, groups of rats (20 males/group)
    were exposed using a dynamic flow chamber into which aerosols at
    concentrations of 0.1 and 1 mg/L aminocarb were continuously dispersed
    for four hours.  All animals at 1 mg/L and 4/20 animals at 0.1 mg/L
    died within eight hours after exposure (Kimmerle, 1961; 1966).

    In a subacute inhalation toxicity test with 20 male albino rats using
    a dynamic flow chamber into which an aerosol with a concentration of
    0.04 mg/L was dispersed eight hours per day for five consecutive days,
    no specific signs of poisoning were observed.  One animal died four
    days after the end of the test (Kimmerle, 1961).

    Signs of poisoning

    Acutely toxic doses of aminocarb produce cholinergic effects typical
    of cholinesterase inhibitors.  The signs of poisoning appeared rapidly
    after oral or intraperitoneal administration and were similar in all
    species examined.  After lethal doses, death occurred within two
    hours, and usually within the first 30 minutes.  After sublethal
    doses, the symptoms subsided rapidly and apparent complete recovery
    was usually noted within three hours (Dubois and Raymund, 1962a).

    Special Studies on Potentiation

    Potentiation of the acute toxicity of aminocarb was absent in female
    (Sprague Dawley) rats when aminocarb was given by intraperitoneal
    injection alone and in combination with 15 other anticholinesterase
    insecticides (Dubois and Raymund, 1962b).

    Short-Term Studies


    In a cat which received 5 mg/kg aminocarb by gavage for ten
    consecutive days, salivation, loss of appetite, and weight loss was
    observed.  Signs of cholinesterase inhibition were noted after two
    days in 2 cats which received doses of 10 mg/kg; these animals died
    after 4 days of treatment (Kimmerle, 1961).

    Quail and Duck

    Aminocarb and four of its major metabolites (THS 1013, THS 1003, THS
    0995 and THS 1029) were fed to 15-day old bobwhite quail and 12-day
    old mallard ducks at a dose of 1000 ppm for a period of 5 days.
    Except for a reduction in feed consumption and reduced weight gain of
    the mallard ducks, no toxic signs were observed (Lamb and Jones,


    Groups of weanling (Sprague Dawley) rats (12 male and 12 female
    rats/group) were fed 0, 5, 10 and 50 ppm aminocarb in the diet for 16
    weeks.  No effects on cholinesterase activity, growth, food
    consumption, gross organ weight, or on histological examination of
    tissues and organs were found in this study.  A similar study was
    started with dietary levels of 0, 100 and 200 ppm.  As these levels
    also failed to induce a significant inhibition of cholinesterase in
    the first 3 weeks, the dietary levels were increased to 400 and 800
    ppm, and were maintained for a further 19 weeks.  The duration of this
    study was 22 weeks.  Over the course of the study, many of the animals
    appeared to be hyperexcited and irritable.  At the end of the study, a
    decrease in growth rate was noted in males (14%) and females (13%) fed
    800 ppm and in males (13%) and females (10%) fed 400 ppm.
    Cholinesterase activity was measured on five animals/sex/group.  Data
    at the conclusion of the study revealed an inhibition in the serum of
    males (16%) and females (42%) fed 800 ppm, and in the serum of females
    (31%) fed 400 ppm.  No inhibition was found in the brain, submaxillary
    glands and erythrocytes.  No effects were observed with respect to
    organ weights and histopathological examination of tissues and organs
    (Root, et al., 1963).

        Table 2. Acute Toxicity of Aminocarb Metabolites

    Compound                                Species    Sex   Route      (mg/kg)            Reference

    4-(N'formyl-N'-methylamino-             Mouse      F     IP         21                 Abdel-Wahab & Casida, 1967
    3-methylphenyl-N-methylcarbamate        Mouse      F     Dermal     >500               "             "

    phenyl-N-methylcarbamate                Mouse      F     IP         3.0                "             "
                                            Mouse      F     Dermal     52                 "             "
                                            Rat        F     Oral       27.8(22.9-33.7)    Kimmerle, 1974

    4-formylamino-3-methylPhenyl-           Mouse      F     IP         13                 Abdel-Wahab & Casida, 1967
                                            Mouse      F     Dermal     500                "             "
    4-amino-3-methylphenyl-N-               Mouse      F     IP         1.6                "             "
    methylcarbamate                         Mouse      F     Dermal     17                 "             "
                                            Rat        F     Oral       18.3(16.2-20.7)    Kimmerle, 1974

    4-(N'-methoxy-N'-methylamino)-          Rat        F     Oral       102.8(88.5-119.4)  Kimmerle, 1974

    4-methoxyamino-3-methylphenyl-          Rat        F     oral       40.1(33.7-47.5)    Kimmerle, 1974


    Groups of two male and two female beagle dogs were fed 0, 200, 400 and
    800 ppm aminocarb in the diet for 12 weeks.  At the end of this
    feeding period, the dogs were returned to the control diet for an
    additional 4-week period.  Weight loss was observed in the animals of
    the 800 ppm and 400 ppm groups.  Signs of poisoning (e.g. vomiting,
    retching, ataxia and incoordination) were dose-related and were found
    in all dose groups, especially in the female animals.  Signs of
    poisoning were particularly prevalent during and just after
    consumption of the aminocarb diet and were minimal or absent during
    the remaining part of the day.  There were no signs of poisoning noted
    in the 4-week recovery period.  Blood samples, taken prior to feeding
    when symptoms were minimal or absent showed no inhibition of the
    cholinesterase activity, of the serum or erythrocytes (Doull and Root,

    Groups of beagle dogs (4 male and 4 female dogs/group) were orally
    dosed by gavage at dosage levels of 0, 2, 4 and 10 mg/kg/day (0, 1, 2
    and 5 mg/kg twice a day) for two years.  After 12 weeks, one dog in
    the highest dose group died.  Moderately severe signs of poisoning,
    (e.g., general excitability, salivation, pupil constriction and fine
    visible trembling of muscles) were seen in all dogs in the high dose
    group.  Less severe signs of poisoning were noted in dogs at 4 and 2
    mg/kg/day.  The highest dose group showed a slight reduction in body
    weight and a reduced rate of growth.  No inhibition of cholinesterase
    activity in serum and erythrocytes was noted, nor were changes in
    hematology and blood chemistry found, except with the one dog that
    died.  Brain cholinesterase activity was not measured.  Samples for
    serum and erythrocyte cholinesterase were taken prior to daily dosing
    in the first 20 months of the study and in the last 4 months of the
    study, within 45 minutes of dosing.

    At the conclusion of the study, adrenal weight, as a percentage of
    body weight only, was increased in the high dose level group.  Other
    organ and organ weight ratios were within normal limits.
    Histopathologically, macrophages containing lipofucsin materials were
    seen throughout the liver of all groups, possibly more frequently in
    the high dose animals.  In the other tissues, no compound-related
    effects were seen histologically (Noel, et al., 1966).

    Long-Term Studies


    Groups of weanling Sprague-Dawley rats (24 males and 24 females/group)
    were fed 0, 100, 200, 400 and 800 ppm aminocarb in the diet for 20
    months.  Growth was reduced in males and females at 800 ppm, and to a
    lesser extent, at all lower dose levels.  The median survival time and
    food consumption were not affected by aminocarb.  Final examinations
    of 5 animals/sex/group did not reveal significant effects on
    cholinesterase activity in the brain, serum, and erythrocytes, whereas
    a slight inhibition (approximately 20%) was noted in the submaxillary

    glands of males and females at 800 ppm.  The relative weight of the
    heart was slightly increased in all dose groups and in microscopic
    examination showed cardiac lesions in both males and females at 800
    ppm and in males at 400 ppm.  Reduced spermato-genesis was observed in
    some animals of the two highest dose groups.  Liver changes were also
    noted at dose levels of 200 ppm and above (Doull, et al., 1967).


    Aminocarb, an N-methyl carbamate ester, is rapidly absorbed and
    metabolized by demethylation and/or hydroxylation or ester hydrolysis.
    Those metabolites containing an intact carbamate ester structure show
    acute toxicity similar to or greater than the parent compound.

    Aminocarb and its metabolites are rapidly excreted and there is no
    evidence of accumulation.  In acute toxicity studies, aminocarb was
    not potentiated by other cholinesterase inhibitors, nor did it induce
    a delayed neurotoxic response in hens.

    In several short- and long-term studies in the rat, aminocarb induced
    a reversible cholinesterase inhibition.  In a 2-year dog study,
    clinical symptoms of poisoning were seen in all dose levels tested.

    In a 3-generation study with rats, no effects were observed at dose
    levels of 100 ppm or below.

    The meeting concluded that the short- and long-term rat studies were
    not carried out in accordance with currently acceptable protocols.  As
    there was growth depression and an increased relative weight of the
    heart at all dose levels tested in the long-term rat study, a
    no-effect level in the rat could not be determined.  An acceptable
    daily intake for man was not allocated.  The meeting recommended that
    aminocarb be re-examined when the ongoing long-term study in rodents
    becomes available.



    Aminocarb has been used mainly for the control of lepidopterous
    defoliators of Canadian forests where it has been found notably
    effective against the spruce budworm, Choristoneura fumiferana
    (Clemens).  About 3.7 million hectares of Canadian forest have been
    treated by aircraft at an average dosage of 0.07 kg ai/ha.  167 g/l
    oil-soluble concentrate is used.

    Aminocarb is also effective for the control of lepidopterous larvae
    and other biting insects in cotton, tomatoes, tobacco and fruit crops,
    but usage in these crops appears to be low.  For these purposes, 50
    and 75% wettable formulations are used.  In New Zealand, the
    insecticide was, but is no longer used widely against the coddling
    moth, leaf roller and mealy bug.  It is applied at 0.75-1.12 kg ai/100
    L.  In stone fruit and citrus, it is effective against the leaf

    roller, mealy bug and scales, where it is applied at 75-94 g ai/100 L.
    Aminocarb is also effective against caterpillars in vegetables and is
    applied at 0.75-1.5 kg ai/ha (New Zealand, 1978).


    Very few residue data on food crops are available because of the
    limited usage of aminocarb in these crops.  The manufacturer provided
    the data available for apples and pears.

    Studies carried out in Australia with apples involved the application
    of aminocarb at 0.075, 0.1 and 0.125% solutions, equivalent to 3/4, 1,
    and 1 1/4 lbs./100 gals, respectively, to give a spray coverage of
    13-18 L/tree.  The recommended preharvest interval of three days
    justify a limit of 4 mg/kg (Table 3).  The data for pears (Table 4)
    also adequately support a 4 mg/kg limit at the three days preharvest

    Table 3.  Aminocarb Residues in Apples

    Application rates          Residue levels (mg/kg)
    (% Solution)                  Period in days
                         3         10        17        24
    0.075                2.8       1.3       1.6       0.6
    0.1                  2.2       1.0       1.6       1.4
    0.125                2.6       1.4       1.8       1.0

    Table 4.  Aminocarb Residues in Pears

                                   Residue levels (mg/kg)
    Application rate                   Period in days
    (% solution)        0         7         13        15        21

    (23-27 L/tree)
    0.1                 1         0.8       n.d.      -         ND
    0.1                 3.0       1.0       0.4       -         0.4
    0.1                 1.3       -         -         n.d.      0.4

    (23-27 L/tree)
    0.1                 1.4       -         -         n.d.      0.4

    (23-27 L/tree
    0.125               1.9       -         -         0.4       0.4

    (23-27 L/tree)
    0.075               1.4       -         -         n.d.      n.d.


    General Comments

    Most of the data on aminocarb were generated in connection with its
    use in the control of forest pests.  Aminocarb was degraded rapidly in
    soil, water, plants, animals and by ultraviolet irradiation (Chemagro,
    1976).  The major route of breakdown in the presence of light or on
    surfaces was oxidation of the dimethylamino portion of the molecule to
    produce traces of 4-(formamidomethylamino)-, 4-(formamidoamino)- and
    4-amino-3-methylphenol.  These products are not detected in animals or
    within plant tissues.  In plants, hydroxylation followed by
    conjugation is the main degradation pathway.  In soil, N-demethylation
    is predominant.  In swine, conjugates of aminocarb phenol and the
    methylamino analogue of aminocarb phenol were the major metabolites
    found in males and females respectively.  The principal tissue
    constituent was conjugated aminocarb phenol.

    Under normal use conditions, aminocarb was found at about 0.01 mg/kg
    in soil and water, and about 2 mg/kg on foliage.  Half-lives under
    normal use conditions ranged from less than one day in soil to about
    six days on spruce foliage.  Maguire (1973) reviewed the chemistry of
    aminocarb and the effect on the environment has been summarized
    (Chemagro, 1976, 1979).  The metabolism of aminocarb in different
    substrates is shown in Figure 1.

    In animals

    (See Biochemical Aspects).  In an ascorbic acid system which simulates
    biological oxidation processes, Balba and Saha (1974) found at least
    12 products formed from aminocarb.  At least 10 of these products
    contained either one or both the N-14CH3 groups.  The ascorbic acid
    system caused demethylation, hydroxylation of the aromatic ring,
    oxidation of the -NHCH3, group to -NHCH20N, and cleavage of the
    carbamate to the phenol.  The 4-methylamino derivative was the major
    degradation product.

    In Plants

    Abdel-Wahab et al., (1966) found that aminocarb was degraded with
    the carbamate moiety intact when the carbamate was applied to glass or
    silica gel surfaces or the leaves of growing bean plants, or injected
    into the stems of bean plants.  The methylcarbamate derivatives formed
    included the 4-methylamino, 4-amino, 4-methylformamido, and
    4-formamido analogues.  The C14-carbonyl activity was found in the
    unextractable portion six days after injection into bean plants.  The
    water-soluble metabolites formed following injection into the bean
    plants result in part from hydroxylation of the carbamate on the
    N-methyl group, on the ring, or on a ring substituent, followed by
    conjugation of the hydroxylated carbamates, mainly as glycosides (Kuhr
    and Casida, 1967).  These glycosides were quite persistent.

    Dorough (1964) determined the stability of aminocarb applied as a leaf
    surface treatment to cotton, garden snap beans, broccoli and tomatoes.
    The metabolic fates of directly injected and surface-applied
    carbonyl-C14 aminocarb appeared to be the same.  The original
    carbamate was converted into water-soluble metabolites which were
    probably conjugates.  Conversion was almost quantitative and the
    metabolites were persistent.  Leaf surface residues appear to be
    degraded via hydrolysis at the carbamate group before or during
    penetration.  Penetration of aminocarb through the leaf surface of
    beans and cotton was about eight percent after eight hours, although
    50% of the residues was already lost from the surface (Dorough, 1979).
    On the other hand, broccoli plants did not contain any internal
    residues.  Aminocarb was metabolized to persistent water-soluble
    metabolites in these plants.

    The fate and persistence of aminocarb in spruce foliage was
    investigated by Sundaram and Hopewell (1977a) using a simulated spray
    at the rate of 3.4 L/ha containing 57 g ai.  The initial concentration
    in foliage was about 10 mg/kg and dropped to less than 0.2 mg/kg
    within 47 days.  The half-life was six days.  Aminocarb was found to
    be labile and was dissipated rapidly under normal weathering

    In a similar study, Nagel et al. (1978) was not able to detect
    volatilization of radioactivity with ring -1-C14 aminocarb. 
    Aminocarb residues declined from an initial level of 6.7 mg/kg to 3.3
    mg/kg in 28 days.  They attributed the decline to growth dilution. 
    The methylamino analogue was the only identified metabolite.  Although
    several unidentified metabolites were detected, no single component
    contributed more than 10% of the total radioactivity.

    The actual situations where aminocarb was applied serially at 70 g
    ai/ha, the concentration in spruce foliage at 0.6 days was 0.7 mg/kg,
    increased to a maximum of 2.2 mg/kg after four days and thereafter
    decreases exponentially with a half-life of 5.6 days (Sundaram et
    al., 1976).  No residues could be detected after 64 days, presumably
    owing to physical factors.

    The penetration, translocation and fate of C14 aminocarb in spruce
    trees was also investigated using trunk implantation (TIT), foliar
    painting (FP), and basal bark painting (BBP) (Sundaram and Hopewell
    1977b).  Aminocarb appears to be weakly systemic.  The aminocarb
    absorbed after trunk implantation was gradually lost after 64 days,
    probably owing to hydroxylation to water-soluble metabolites, some of
    which were incorporated into the cellular structure of the foliage.
    The major route of translocation was from the old to the
    newly-developing foliage.  In the case of foliar painting, basal bark
    painting techniques, the mechanism of dissipation appeared to be
    physical rather than biochemical.

    In soil

    In a comparative study of the persistence of aminocarb in silt loam
    and sandy loam soil, Murphy et al, (1975) using
    carbonyl-C14-aminocarb, found that breakdown was slower and more
    soil-bound radioactivity was detected in the latter.  In silt loam,
    less than 15 percent of the applied insecticide was still present 24
    hours after application.  Microbial activity was essential for rapid
    metabolism and C14102 was the principal product.  Some of the
    liberated C14102 was assimilated into the normal, insoluble soil
    constituents.  Minor (1978) also found that the insecticide was
    degraded through removal of the carbamate portion by hydrolysis
    followed by soil binding.

    Aminocarb could be readily absorbed from aqueous solutions by loam
    soil (Atwell, 1978).  Although it is ranked as intermediate in soil
    mobility using the soil thin layer system (Thornton et al, 1976)
    leaching studies with sandy loam soil columns showed aminocarb to be
    essentially retained in the upper 2.5 cm of soil.  Less than 0.1% of
    the radiolabel used was found in the leaching water after passing
    through the soil column.

    When aminocarb was applied to sandy loam soil at 1 mg/kg, the
    half-life was less than 24 hours (Minor, 1978).  The only identified
    compounds were aminocarb and its N-demethylated analogue.  Within 24
    hours, 75% of the radioactivity was bound.  Microbial activity was
    necessary for degradation.  In a pond water/soil study, aminocarb had
    a half-life of 3.5 days and the metabolites identified were the
    N-demethylated analogues and the phenolic hydrolysis product of
    aminocarb.  Formation of soil-bound residues was observed.

    Sundaram and Hopewell (1977a) found that with simulated aerial
    application, the initial residue in soil was 7 mg/kg.  The half-life
    was two days and residues could no longer be detected after 27 days.

    In Water

    In buffered solutions, aminocarb stability increased as the
    temperature and pH decreased.  At pH 4, its half-life was >127 days,
    at pH 7, it varied between five and eleven days, while at pH 9, it was
    <1 day (Tessier et al., 1978).  Murphy et al. (1975) observed a
    half-life of 28.5 days at pH 7 and 28.5 days in pond water under
    normal environmental conditions.  The principal metabolite appeared to
    be the phenol although the methylamino and formylamino analogues were
    also observed. (Tessier et al., 1978; Murphy et al., 1975; Minor,

    Forest aerial application at 70 g ai/ha resulted in 2.1 and 1.9 mg/kg
    residues in pond and stream water respectively (Sundaram et al.,
    1976).  Half-lives were 4.4 and 8.7 days, respectively, in the above
    substrates.  Residues were below the 0.1 mg/kg limits of analytical
    sensitivity within 32 days.

    In a pilot study, application of the insecticide at 2.4 lb ai/acre
    resulted in residues ranging from <0.1 to 0.2 mg/kg 48 hours after
    application.  These levels were generally higher than found after 24
    hours (Chemagro, 1976).


    Irradiation of aminocarb in aerated and degassed ethanol and
    cyclohexane at >300 pm gave the phenol as the major product (Addison
    et al., 1974).  Trace quantities of other products were also
    observed.  On the other hand, Abdel-Wahab and Casida (1967) found that
    in bean foliage, photolysis involved extensive oxidation of the
    dimethylamino moiety but not of other groups.  There was a stepwise
    demethylation of the dimethylamino moiety and one of the methyl
    radicals was oxidized to the formamido group.  The same result was
    obtained earlier by Abdel-Wahab et al (1967).  Aminocarb was not
    readily decomposed when exposed as spots on the thin layer plates in
    the dark, in fluorescent light or in long-wavelength UV light.  Short
    wavelength UV-light or sunlight resulted in considerable degradation.
    Crosby et al. (1965) observed at least two compounds with
    acetylcholinesterase inhibitory effects of many decomposition products
    upon exposure to sunlight and ultraviolet radiation.

    In aqueous buffer at pH 4.9, aminocarb had a half-life of 10 days when
    irradiated with a mercury lamp.  The methylamino analogue and two
    unknown products amounting to 10% and 12% of the total radioactivity,
    were detected in the solution after 30 days exposure.  In an
    acetone-sensitized solution, the half-life was reduced to 1.5 days
    (Mulkey et al., 1978).

    When ring -C14 aminocarb applied to a soil surface was subjected to
    light from a high intensity mercury lamp, the calculated half-life was
    4.6 hours (Augenstein, 1978).  Approximately 33% of the applied
    radioactivity was volatilized and 50% was bound to the soil during 192
    hours of exposure to the light.  The methylamino, methylformylamino,
    formylamino and amino analogues of aminocarb as well as the
    formylamino analogue of the phenol were detected.  Unidentified
    products accounted for <10% of the applied radioactivity.


    In New Zealand, six samples of apples in 1971 showed residues ranging
    from 0.06 to 2.1 mg/kg with a mean of 0.86 mg/kg.


    The analysis of carbamate insecticides by the popular GLC technique
    has been an on-going problem for two reasons: 1) the thermal
    instability of some compounds and 2) the lack of a sensitive detector
    for the underivatized material.  Several GLC derivatization procedures
    using the sensitive electron capture detector have been tried.  For
    aminocarb, Sundaram et al. (1976) initially tried forming the
    N-hepta-fluorobutyryl derivative.  The procedure had an unsatisfactory
    minimum detection limit (MDL) of 0.5 mg/kg in foliar extracts because
    of impurities with retention times similar to aminocarb.  Stanley and
    Delphia (1978) subsequently used the 2,4-dinitrophenyl ether
    derivatization technique of Holden (1973) and obtained a MDL of <0.01
    mg/kg for spruce needles, soil and fish and <0.001 mg/kg for water.

    GLC analysis of aminocarb as the intact molecule detected by such
    nitrogen-"specific" detectors as the alkali flame ionization (AFID)
    and the Hall microelectrolytic conductivity detectors appear
    promising.  The direct GLC procedures generally require only minimum
    cleanup because they are less subject to sample interferences.  Bayer
    (1975) used the AFID to detect 0.1 mg/kg aminocarb on plant materials
    and 0.02 mg/kg in water.  Sundaram and Hopewell (1977) using the Hall
    detector, found an MDL of 0.2 mg/kg for spruce foliage and soil.  In
    water, Sundaram et al. (1978) achieved an MDL of 1 × 10-4 mg/kg for
    both aminocarb and its phenol.

    High-pressure liquid chromatography (HPLC) has been applied by
    Laurence (1977) to the detection of aminocarb in cabbage, corn, potato
    and wheat.  A UV detector was used at 254 nm.  As little as 0.8 ng of
    insecticide can be detected in the above crops.

    Olson (1964) described a colorimetric procedure for residue
    determination in soil, after the reaction of the phenol with
    4-aminoantipyrine.  The procedure can detect as little as 0.1 mg/kg
    aminocarb and recovery was 90% for soils.  It is also applicable to

    In effect, the determination of the intact carbamate offers
    possibilities as a regulatory method, especially with improvements in
    the detection limits of the nitrogen specific detectors.  The Hall
    detector is particularly useful.  If greater sensitivity is needed,
    the 2,4-dinitrophenyl ether derivative can be used.  Adoption of HPLC
    for regulatory purpose would have to await further improvements in the
    detection system and widespread use of the technique.  The
    4-aminoantipyrine procedure can be used for spectrophotometry.


    According to the information supplied to the meeting, only the
    following countries have established limits for aminocarb in food:

                                               Limit     Preharvest
    Country           Commodity             established   Interval
                                              (mg/kg)      (days)

    Australia     apples, pears                  4            3
                  cottonseed                     1
                  vegetables, fruit
                  (except apples, pears)         1

    Germany       pome fruit                     1


    Aminocarb is mainly used for the control of lepidopterous defoliators
    in conifer forests where it is applied by air.  There is only limited
    usage in other crops.  For aerial application, a 1.4 lb ai/US gal.
    oil-soluble concentrate formulation is used.  For general usage, 50
    and 75% wettable powder formulations are available.

    In view of the limited usage in food crops, very few residue trials
    have been done to establish MRLs.  Data on apples and pears adequately
    support MRLs of 5 and 2 mg/kg, respectively.

    Aminocarb is degraded rapidly in soil, water, plants, animals and when
    exposed to short-wave ultraviolet radiation.  In plants, metabolism
    involves hydroxylation of the molecule at the carbamate on the
    1,1-methyl group, on the ring, or on a ring substituent, followed by
    conjugation of the hydroxylated carbamates mainly as glycosides.
    Conjugates of aminocarb phenol and the methylamino analogue of
    aminocarb phenol were the major metabolites in swine.  The principal
    tissues constituent was conjugated aminocarb phenol.  In soil,
    N-demethylation predominate.  Under normal use conditions, half-lives
    of aminocarb ranged from less than one day in soil to about six days
    on spruce foliage.  Detection by gas chromatography as the intact
    carbamate or detection as the 2,4-dinitrophenyl ether derivative
    appear adequate as regulatory methods; the latter can detect as low as
    0.01 mg/kg aminocarb in spruce needles, soil and fish and 0.001
    aminocarb in water.


    Since the main use of aminocarb is in forest pest control, the
    likelihood of its occurrence in food items for international trade is
    generally low.  However, the setting of MRLs are considered necessary
    in some cases.  In the absence of an ADI, the following guideline
    levels are recorded for aminocarb:

    Commodity                 GL

    apples                     5
    pears                      2


    If the usage of aminocarb in food items should increase, additional
    information should be provided.


    Abdel-Wahab, A.M., Kuhr, R.J. and Casida, J.E. - Fate of
    C14-carbonyl-labelled aryl methylcarbamate insecticide chemicals in
    and on bean plants.  J. Agr. Food Chem. 14., 290-298.

    Abdel-Waheb, A.M. and Casida, J.E. - Photo-oxidation of Two
    4-Dimethylaminoaryl methylcarbamate Insecticides (Zectram and Matacil)
    on Bean Foliage and of Alkylaminophenyl Methylcarbamates on Silica Gel
    Chromatoplates.  J. Agr. Food Chem. 15: 479-487.

    Addison, J.B., Silk, P.J. and Unger, I. - The photochemical reactions
    of carbamates II. The solution photo chemistry of Matacil
    (4-dimethylamino m-tolyl-N-methyl (carbamate) and Landrin
    (3,4,5-trimethylphenyl-N-methyl carbamate). Bull. Environmental
    Contam. Toxicol. 11, 250-255.

    Atwell, S.M. Soil absorption and desorption of C14-Natacil. Chemagro
    Report No. 55424 July 12 (1973), Unpublished.

    Augenstein, L.L., McPhaul, L. and Wargo, J.P., Jr. - Photodegradation
    of 14C Matacil on a soil surface. Cemagro Report No. 50446, October
    20 (1973), Unpublished.

    Balba, M.M. and Saha, J.G. - Degradation of Matacil by the ascorbic
    acid oxidation system. Bull. Environ. Contam. Toxicol. 11, 193-200.

    Bayer, A.G.  Gas Chromatographische bestimmung von
    aminocarbruckstanden in boden und wasser. Oct. 28 (1975), Unpublished.

    Bayer, A. G.  Data submitted to the 1979 JMPR

    Chemagro. Matacil - The effect on the environment. Chemagro Report,
    April 17 (1976), Unpublished.

    Coburn, J.A., Ripley, B.D. and Chau, A.S.Y. - Analysis of Pesticide
    residues by chemical derivatization. II. N-methylcarbamates in natural
    water and soils. J. Assoc. Off. Anal. Chem. 59, 188-196.

    Crosby, D.G., Leitis, E and. Winterlin, W. L. - Photodecomposition of
    carbamate insecticides. J. Agr. Food Chem. 13, 204-207.

    Dilley, J. and Doull, J. - The Acute Inhalation Toxicity of Bayer
    44646 to Rats and Mice. (1962) Unpublished report from the University
    of Chicago, submitted by Bayer, AG.

    Dorough, H.W.  Fate of Bayer 44646 in several plant species. Progress
    Report, Texas A & M University, Sept. 1 (1964), Unpublished.

      Fate of Matacil in several plant species. Progress Report, Texas A &
    M University, July (1970), Unpublished.

    Dorough, H.W. and Thorstenson, J.H. - Analysis of carbamate
    insecticides and metabolites J. Chromatogr. Sci. 13, 212-224.

    Doull, J. and Root, M. - Subacute Oral Toxicity of Bayer 44646 in Male
    and Female Dogs.  (1963) Unpublished report from the University of
    Chicago, submitted by Bayer AG.

    Doull, J., Root, M. and Keskauskas, J. - Chronic Oral Toxicity of
    Bayer 44646 to Rat. (Addendum: Hibbs, C., and Nelson, D.L. Microscopic
    Findings in Tissues of Male and Female Rats Fed Bayer 44646 for Two
    years). (1967) Unpublished report from the University of Chicago,
    submitted by Bayer AG.

    Dubois, K.P.  The Acute Oral Toxicity of Bayer 44646 to Chickens.
    (1962) Unpublished report from the University of Chicago, submitted by
    Bayer AG.

    Dubois, K.P. and Raymund, A.B. - Acute Toxicity of Bayer 44646 to
    Mammals.  (1962a) Unpublished report, from the University of Chicago,
    submitted by Bayer AG.

      The Acute Toxicity of Bayer 44646 in Combination with other
    Anticholinesterase Insecticides.  (1962b) Unpublished report, from the
    University of Chicago, submitted by Bayer AG.

    Dubois, K.P. and Kinoshita, F. - The Subacute Parenteral Toxicity of
    Bayer 44646 to Female Rats. (1962) Unpublished report, from the
    University of Chicago, submitted by Bayer AG.

    Holden, E.R.  Gas Chromatographic determination of residues of
    methylcarbamate insecticides in crops as their 2,4-dinitrophenyl ether
    derivatives. J. Assoc. Off. Anal. Chem. 56, 713-717.

    Kimmerle, G., Wirkstoff Dr. Heib A. 363 (E 44646). (1961) Unpublished
    report from Bayer AG, Tox. Gew. Hyg. Labor, submitted by Bayer AG.

    Neurotoxische Untersuchungen mit A 363-Wirkstoff. (1965a) Unpublished
    report from the Institut für Toxikologie, submitted by Bayer AG.

      Wirkstoff A 363 als Formulierung F1 604/149 Acute
    Neurotoxizitätsprüfung bei Hühnern. (1965b) Unpublished report from
    the Institut für Toxikologie, submitted by Bayer AG.

      Matacil-Wirkstoff. (1966) Unpublished report from the Institut für
    Toxikologie, submitted by Bayer AG.

    3-methyl-4-monomethyl-aminophenyl-N-monomethyl-carbamat, und
    3-methyl-4-aminophenyl-N monomethylcarbamat. Akate Akute Toxizität bei
    Ratten.  (1974) Unpublished report from the Institut Für Toxikologie,
    submitted by Bayer AG.

    Kuhr, R.J. and Casida, J.E. - Persistent glycosides of metabolites of
    methylcarbamate insecticide chemicals formed by hydroxylation in bean
    plants. J. Agr. Food Chem. 15, 814-824.

    Kruckenberg, S.M. - Delayed Neurotoxicity Study of Matacil in Hens.
    (1978a) Unpublished report from Kansas State University, by Bayer AG.

      Acute Oral Toxicity of Matacil in Chickens. (1978b) Unpublished
    report from Kansas State University, submitted by Bayer AG.

    Lamb, D. W. and Jones, R.E. - Dietary Toxicity of Matacil Technical
    and 4-Matacil Metabolites to Bobwhite Quail and Mallard Ducks. (1975)
    Unpublished report from Chemagro Agr. Div., Mobay Chemical Corp.,
    submitted by Bayer AG.

    Lamb, D.W. and Roney, D.J. - Accumulation and Persistence of Residues
    in Channel Catfish exposed to Matacil-14C. (1976) Unpublished report
    from Mobay Chemical Corp., submitted by Bayer AG.

    Lamb, D.W. et al.  Accumulation and Elimination of Residues in
    Bobwhite Quail Exposed to Matacil-14C. (1976) Unpublished report from
    Mobay Chemical Corp., submitted by Bayer AG.

    Lawrence, J.F.  Direct analysis of some carbamate pesticides in food
    by high pressure liquid chromatography. J. Agr. Food Chem. 25,

    Maguire, R.J.  Aminocarb: A review of its chemistry. Manuscript
    submitted for publication by the Canadian Forestry Service. (1978).

    Minor, R.G.  Metabolism of Matacil in soil and in an aquatic
    environment. Chemagro Report No. 50427, October 15, 1978, Unpublished.

    Mobay, Matacil - the effect on the environment, Addition no. 1 to
    Chemagro Report 1976, January 14 (Unpublished).

    Mulkey, N.S., McPhaul, L., Augenstein, L.L. and Wargo, J.P. Jr.
    Photodegradation of 14C Matacil in aqueous solution.  Chemagro report
    No. 50447, October 18 (1978), Unpublished.

    Murphy, J.J., Jacobs, K. and Minor, R.G. - Stability of Matacil in
    aqueous systems. Chemagro Report No. 43450. January 20 (1975a),

    Murphy, J.J., Minor, R.G., Jacobs, K. and Shaif II, H.R. - Persistence
    of Matacil in soil.  Chemagro Report No. 43444, January 31 (1975b),

    Nagel, C.D., Tessier, J.F., McPhaul, L., Augenstein, L.L. and Wargo,
    Jr. J.P. - Spruce foliage metabolism study with 14C Matacil. Chemagro
    report No. 50445, October 16 (1978), Unpublished.

    Nelson, D.L. - Acute Oral Toxicity of Matacil Technical and Matacil
    Analytical Grade to Female Rats.  (1973a) Unpublished report from
    Chemagro Agr. Div., Mobay Chemical Corp., submitted by Bayer AG.

      Acute Rat Cholinesterase No-effect Study with Matacil Technical.
    (1978b) Unpublished report from the Chemagro Agr. Div., Mobay Chemical
    Corp., Submitted by Bayer AG.

    New Zealand  Report of the Codex Contact Point. (1978).

    Noel, R.B., Mawdesley-Thomas, L.E. Chesterman, H., Clarke, E., and
    Street, A.E. Bayer 44646 Chronic Oral Toxicity Study in Dogs. Final
    Report.  (1966) Unpublished report from the Huntingdon Research Centre
    submitted by Bayer AG.

    Obrist, J.J. - Leaching characteristics of aged Matacil soil residues.
    Chemagro report No. 65857, April 28 (1978), Unpublished.

    Palmer, K.A. and Fletcher, M.A. - Effect of Bayer 44646 Upon
    Reproduction of Multiple Rat Generations. Addendurn Histopathology.
    (1966) Unpublished report from the Huntingdon Research Centre
    submitted by Bayer AG.

    Root, M., Cowan, J. and Doull, J. - Subacute Oral Toxicity of Bayer
    44646 to Male and Female Rats. (1963) Unpublished report from the
    University of Chicago, submitted by Bayer AG.

    Shaw, H. R. - Metabolism of Matacil in Swine. (1978) Unpublished
    report from Mobay Chemical Corp., submitted by Bayer AG.

    Silk, P.J., Semeluk, G.P. and Unger, I. - The photoreactions of
    carbamate in insecticides. Phytoparasitica, 4, 51-63.

    Stanley, C.W. and Delphia, L.M. - Gas-liquid chromatographic method
    for detecting residues of Matacil in spruce needles, fish, soil and
    water. Chemagro Report No. 66512, Sept. 15 (1978), Unpublished.

    Sundaram, K.M.S. and Hopewell, W.W. - Fate and persistence of
    aminocarb in conifer foliage and forest soil after simulated aerial
    spray application. Canada Forest Pest Management Institute Report No.
    FPM-x-6), October (1977a), Unpublished.

      Penetration, translocation and fate of C-14 aminocarb in spruce
    trees. Canadian Forestry Service Report CC-x-140 February (1977b),

    Sundaram, K.M.S., Volpe, Y. Smith G.G. and Duffy J.R. - A preliminary
    study on the persistence and distribution of Matacil in a forest
    environment. Canadian Forestry Service Report No. CC-X-116, January
    (1976), Unpublished.

    Sundaram, K.M.S., and Hindle, R. - Isolation and analysis of aminocarb
    and its phenol from environmental waters. Canadian Forest Pest
    Management Institute report. FPM-X-18 June (1978), Unpublished.

    Tessier, J.F., Mulkey, W.S., Augenstein, L.L. and Wargo jr, J.P. -
    14C Matacil buffer hydrolysis study. Chemagro Report No. 50444,
    October 5 (1978), Unpublished.

    Thornton, J.S., Hurley, J.B. and Obrist, J.J. -Soil thin-layer
    mobility of twenty four pesticide chemicals. (Chemagro Report No.
    57016, Dec. 15 (1976), Unpublished.

    See Also:
       Toxicological Abbreviations
       Aminocarb (ICSC)
       Aminocarb (Pesticide residues in food: 1978 evaluations)