WHO/Food Add./68.30



    The content of this document is the result of the deliberations of the
    Joint Meeting of the FAO Working Party of Experts and the WHO Expert
    Committee on Pesticide Residues, which met in Rome, 4 - 11 December,
    1967. (FAO/WHO, 1968)

    Rome, 1968



    Chemical names

    0,0-dimethyl S-(N-methylcarbamoylmethyl) phosphorodithioate;
    S-methylcarbamoylmethyl 0,0-dimethyl phosphorodithioate; 0,0-dimethyl
    S-alpha-mercapto-N-methylacetamido dithiophosphate; N-monoethylamide
    of 0,0-dimethyldithiophosphoryl acetic acid; methyl
    dimethyldithiophosphoryl acetamide.


    Rogor, Fortion MM

    Empirical formula


    Structural formula

    (CH3O)2 -  P - S -CH2-CO - NHCH3

    Other relevant chemical properties

    Technical dimethoate - 93.3 per cent


    Biochemical aspects

    Dimethoate is a cholinesterase inhibitor. The molar concentration of
    the pure compound necessary to produce 50 per cent cholinesterase
    inhibition in the rat brain in vitro (I50) is 8.5  10-3. It
    decomposes to give products which are more toxic than the original
    substance (Casida & Sanderson, 1963).

    Various studies (O'Brien, 1959; O'Brien, 1961); Sanderson & Edson,
    1964) carried out with dimethoate labelled with 32P have shown that
    there is rapid absorption from the digestive tract. The radioactivity
    is concentrated in the liver, bile, kidneys and urine. There is no
    accumulation in the fat depots. Elimination is rapid in the rat and in
    man, 76-90 per cent of the radioactivity being found in the urine
    after 24 hours. In the guinea-pig, 25-40 per cent of the radioactivity
    is recovered in the faeces. Four dimethoate metabolites with
    anticholinesterase activity (molar I50's in 30 minutes at 37 in rat
    brain; 4.7  10-6; 1.1  10-5; approximately 0.2  10-5 and
    approximately 0.1  10-5) have been identified in the rat and in man.
    One of them seems to be a product resulting from thiono-oxidation,
    leading to the formation of the oxygen homologue of dimethoate and

    followed by hydrolysis with production of a thiocarboxyl derivative
    which constitutes the chief metabolite of dimethoate in mammals.

    In vitro studies on human liver enzymes indicated that dimethoate
    could inhibit the non-specific esterases to a greater degree than
    acetylesterase (Ecobichon & Kalow, 1963).

    For further information see In animals.

    Acute toxicity                                  Dimethoate
    Animal                Route                 (mg/kg body-weight)                Reference

                                          Pure      Laboratory     Technical

    Mouse, female         Oral             60            -           60           Sanderson &
                                                                                  Edson, 1964

    Rat, male             Oral           500-600      280-350      180-325             "

    Rat, female           Oral           570-680      300-356      240-336             "

    Rat, male        Intraperitoneal        -         175-325         -                "

    Rat, female      Intraperitoneal        -           350           -                "

    Rat, male          Intravenous          -           450           -                "

    Hamster, male         Oral              -           200           -                "

    Guinea-pig            Oral             550          600        350-400             "

    Rabbit                Oral             500          450        approx. 300         "

    Hen                   Oral              50           40        approx. 30          "

    The rat oral LD50's (mg/kg body weight) of desmethyl oxy-carboxy
    dimethoate and oxycarboxy dimethoate have been determined to be <600
    and <800 respectively whereas the hen oral LD50 of oxygen analog of
    dimethoate has been determined to be 100 (Levinskas and Shaffer,

    Acute oral toxicity of dimethoate was not potentiated by any of 17
    other insecticides (Sanderson & Edson, 1964).

    Short-term studies

    Mouse. A three generation reproduction study was conducted at
    dietary levels of 0, 5, 15 and 50 ppm of dimethoate, with two litters
    produced per generation. Second litter animals were used for composing
    succeeding generations. No effect of the compound was seen in
    fertility, lactation or survival of the pups to weaning, gross 
    appearance of all pups produced, weights of major organs of F2b
    animals and gross and microscopic appearance of tissues of the F3b
    animals, autopsied at 21 days of age (Ribelin et al., 1965).

    Rat. Groups of 10 male rats were fed diets containing 1, 5, 25 and
    125 ppm of dimethoate for 15 weeks. At the highest concentration, a
    slight fall in the rate of gain of weight was observed as well as mild
    symptoms of poisoning (slight muscular fibrillation). In the group fed
    25 ppm and higher concentrations, a significant fall in the
    cholinesterase activity of the plasma and erythrocytes was observed,
    while in the animals fed 5 ppm a fall of 20 per cent in cholinesterase
    activity was found. At 1 ppm there was no effect on the cholinesterase
    activity of the plasma, erythrocytes or brain (Edson & Noakes, 1960).

    Young rats in groups of 20 fed diets containing 2, 8 and 32 ppm of
    dimethoate for 90 days and other groups of 20 rats fed 50, 100 and 200
    ppm for 35 days showed no haematological abnormalities, nor any
    significant histopathological changes. Regarding the cholinesterase
    activity of the plasma and the erythrocytes, the highest dose which
    did not give a significant inhibition was 32 ppm of dimethoate (West
    et al., 1961).

    Groups of 20 male rats were maintained for 6-12 months on diets
    containing various concentrations of laboratory grade dimethoate. At
    800 ppm severe intoxication developed within a few days; the chemical
    was withdrawn after a week and complete recovery occurred in 10-14
    days. No toxic effects were seen at 50 ppm or below. Marked inhibition
    of erythrocyte cholinesterase activity occurred at 50 ppm but at 10
    ppm and below neither erythrocyte nor plasma cholinesterase showed
    significant inhibition throughout the test. At the end of the
    experiment there were no gross or microscopic changes in any group
    attributable to dimethoate. The maximum no-effect level in these
    experiments corresponded to 0.5-0.8 mg/kg body-weight per day.

    In the same experiment, further groups of 20 weanling male rats were
    treated for 5-1/2 months at dose levels of 5, 10 and 20 ppm of
    dimethoate. The maximum no-effect level in these experiments was 5 ppm
    corresponding to 0.3-0.6 mg/kg body-weight per day.

    A further test with the commercial liquid formulation of dimethoate on
    similar groups of male and female rats lasted 12 weeks. The maximum
    no-effect level in these experiments was again 5 ppm corresponding to
    0.4-0.6 mg/kg body-weight per day (Sanderson & Edson, 1964).

    Groups of 10-15 males and 10-15 females were fed 0, 330, 1000 and 3000
    ppm of oxy-carboxy dimethoate for 33 days. At 3000 ppm, rate of weight
    gain, food consumption and food utilization were affected in both
    sexes, and kidney weight ratios were slightly elevated in the males.
    Erythrocytic cholinesterase activity was inhibited in relation to dose
    in both sexes at 1000 and 3000 ppm, and slightly inhibited in the
    females at 330 ppm. Brain cholinesterase activity was significantly
    affected in the 3000 ppm females. Plasma cholinesterase was unaffected
    at all levels. No effect was seen on mortality, behaviour and gross
    and microscopic appearance of major organs (Levinskas & Sheffer,

    Initial groups of 25 males and 25 females were fed 0, 0.2, 0.4, 0.8
    and 1.6 ppm at the oxygen analog of dimethoate for 28 days. Animals
    from each group were selected for determination of cholinesterase
    activities at 3, 7, 14 and 28 days. At 8 ppm, there was a marked
    effect on erythrocyte, plasma (except in the females) and brain
    cholinesterase activities. At 1.6 ppm, erythrocyte cholinesterase
    activity was affected in both sexes and brain cholinesterase activity
    in the females at 28 days. No distinct effect on cholinesterase was
    found at lower levels. No effect at any level was found on food
    intake, rate of weight gain, and gross and microscopic appearance of
    major organs (Fogleman et al., 1965).

    Guinea-pig. Groups of guinea-pigs were fed for 3 weeks on lettuce
    and brassica leaves that had been treated with dimethoate and
    contained residues of up to 189 ppm. No toxic effects were seen, and
    the cholinesterase inhibition observed was in agreement with that in
    parallel groups given daily oral doses of the same quantity of
    laboratory grade dimethoate (Sanderson & Edson, 1964).

    Chicken. In laying hens, dimethoate given over a period of 59 weeks
    at a concentration of 30 ppm daily in the drinking-water caused
    inhibition of plasma cholinesterase and some reduction in appetite,
    but no egg abnormalities (Sherman, et al., 1963).

    Groups of 6 hens were fed 0, 65, 130 and 260 ppm of dimethoate for 4
    weeks. There was no effect on mortality, but hens at the high level
    were unable to maintain their original weights. Groups of 6 hens
    received 0 and 130 ppm of dimethoate and 2000 and 4000 ppm of
    tri-o-cresyl phosphate for 4 weeks. At the termination of the study,
    samples of brain, thoracic cord and sciatic nerve were examined for
    effects on axons and myelin sheaths. Tri-o-cresyl phosphate was found
    to produce a demonstrable general myelin loss, but dimethoate had no
    effect on either sheaths or axons. (Levinskas and Shaffer, 1965).

    Groups of 6 hens were fed 0, 60, 120 and 240 ppm of oxygen analog of
    dimethoate for 4 weeks. At the termination of the study, samples of
    brain, thoracic cord and sciatic nerve were examined for effects on
    axons and myelin sheaths. No effect was found on nerve tissue or on
    survival, but it was noted that the test birds were generally unable
    to maintain body weight satisfactorily (Levinskas and Shaffer, 1965).

    Dog. Three groups each of 4 dogs, 2 males and 2 females, were fed
    diets containing 2, 10 and 50 ppm for 13 weeks. No significant harmful
    effect was noted. The cholinesterase activity of the erythrocytes was
    only slightly decreased at the highest concentration of 50 ppm while
    that of the plasma was unaffected at any of the concentrations
    employed (West et al., 1961).

    Man. Twenty subjects ingested 2.5 mg of dimethoate in aqueous
    solution, corresponding to about 0.04 mg/kg body-weight daily for 4
    weeks. No toxic effect was observed, nor any significant change in the
    blood cholinesterase activity. The same results were found in 2
    subjects who ingested daily during 21 days, 9 mg (0.13 mg/kg) and 18
    mg (0.26 mg/kg body-weight) dimethoate respectively (Sanderson and
    Edson, 1964).

    Thirty-six male and female volunteers were given daily oral doses of
    dimethoate of 5, 15, 30, 45 and 60 mg for periods of 14 to 57 days.
    There was no effect on the blood cholinesterase levels with intakes of
    5 and 15 mg daily, but there was at 30 mg and above (Edson et al.,

    Long-term studies

    No data available.


    The findings now available from man provide a satisfactory basis for
    assessment. The reproduction studies now completed in the mouse meet
    the needs of the request previously made for such experiments in the


    Level causing no significant toxicological effect

         Man               0.2 mg/kg body-weight/day.

    Estimate of acceptable daily intake for man

         0.02 mg/kg body-weight.



    Pre-harvest treatments

    Dimethoate is a systemic insecticide used on a number of fruit and
    vegetable crops to combat aphids, leafhoppers, leafminers, lygus bugs, 

    pear psylla, various mites (except rust mites), olive flies, various
    citrus pests and fruit eating larvae. Typical maximum recommended
    usages are presented in the following Table I.


       Crop               Dosage, lbs             Pre-harvest
                             actual              period, days

    apples - pears        0.5 lbs/100 gal             28

    beans                 0.25 - 0.5 lbs/A             0*

    peas                  0.2 lbs/A                    0

    brassica              0.25 - 0.5 lbs/A             7

    cabbage               0.25 - 0.5 lbs/A             3

    leafy vegetable       0.25 lbs/A                  14

    *  Cattle should not be allowed to graze on vines

    Dimethoate is also used on alfalfa, wheat, safflower and pea forage
    against aphids, leafhoppers, lygus bugs, grasshoppers and thrips with
    applications of 0.25 - 0.5 lb/100 gal and a pre-grazing and
    pre-harvest period of 21 - 28 days.

    Post-harvest treatments

    No post harvest use of dimethoate is known.

    Other uses

    Dimethoate is used in formulations on a large number of ornamental
    plants, shrubs and trees. It has been recommended for control of
    houseflies and maggots and is used for this purpose around the home,
    barn, and commercial establishments with a caution to avoid
    contamination of human and animal food supplies.


    Numerous supervised field trials have been made on a large number of
    crops under varying cultural and climatic conditions with different
    rates of application and harvest times. Much of this data has been
    submitted to the U.S. Food and Drug Administration in the form of
    petitions. Table II summarizes data representative of residues found
    when the maximum recommended dosage of pesticide (see Table I) was

        TABLE II

       Crop                 Typical initial   Pre-harvest    Residue at end    Estimated
                            residues, ppm     period, days   of pre-harvest    half-life
                                                               period, ppm.      days


    Apples                    4.0 - 6.0           28            1.0 - 1.5         15

    Pears                     1.0 - 2.0           28                  0.4         10

    Cole crops

    Cauliflower               5.0 - 6.0            7            0.6 - 0.9          3

    Broccoli                  9.0 - 23.0           7                  2.0          2

    Cabbage                   3.0 - 8.0            3                  2.0        1-4

    Head lettuce              5.0                  7                  1.2          4

    Leafy vegetables

    Spinach                   4.0 - 12.0          14              0 - 0.3        2-3

    Kale                      5.0                 14                  0.1          1

    Turnip and
    greens                    7.0 - 9.0           14                  0.3          2

    Leaf lettuce              0.2 - 0.9           14            0.1 - 0.3          4

    Collards                  1.0 - 10.0          14            0.1 - 0.5          3

    Endive                    2.0 - 3.0           14                  0.1          2

    TABLE II (cont'd)

       Crop                 Typical initial   Pre-harvest    Residue at end    Estimated
                            residues, ppm     period, days   of pre-harvest    half-life
                                                               period, ppm.      days

    Escarole and
     chard                    1.0 - 2.0           14                  0.1          3

    (fruit and pod only)

    Snap beans                1.5                  0                  1.5          4

    Green beans               0.5 - 1.0            0            0.5 - 1.0          7

    Lima beans                0.4                  0                  0.4          1

    Peas                      1.0                  0                  1.0          7

    Other vegetables

    Peppers                   0.1 - 0.3            0            0.1 - 0.3          7

    Tomatoes                  0.2 - 0.8            7                  0.2          4


       Crop                 Dosage         Typical        Pre-harvest    Residue at and     Estimated
                          lbs actual       initial          period       of pre-harvest     half-life
                          per 100 gal    residues ppm        days          period, ppm        days

    Peaches                0.25 lb         3.0-7.0            14             1.0-1.5            7

    Apricots               0.12 lb         8.0-10.0           14            <1.0              5-7

    Cherries               0.2 lb          2.0-12.0           14             1.0-1.5          3-5

    Grapes                 0.5 lb          7.0-10.0           28            <1.0                8

    Strawberries           0.4 lb                              7             0.3

    Grapefruit             0.8 lb          2.0                90             1.2              120

    Oranges (peeled)       0.8 lb         <1.0                90            <0.5              100

    Lemons                 1.0 lb                             21             0.1

    Tangerines             0.5 lb                             48             0.1

    Artichokes             0.25-4.0 lb                         7             1.1

    Brussels sprouts       1.5 lb                             12             1.1

    Potatoes               0.4-1.0 lb                       10-126           0.1

    Sugar beats            0.4-2.0 lb                       48-100          <0.1-0.2

    Wheat                  0.3 lb                             58             0.2

    Corn                   0.5-1.0 lb                         21             0.1

    TABLE III (cont'd)


       Crop                 Dosage         Typical        Pre-harvest    Residue at and     Estimated
                          lbs actual       initial          period       of pre-harvest     half-life
                          per 100 gal    residues ppm        days          period, ppm        days
    Olives (eating)        0.16 lb         2.0-4.0            30             0.6               12

    Olive oil              0.5 lb          2.0-3.0            14            <1.0               10

   A number of studies made throughout the world are also reported in a
    review by de Pietri-Tonelli et al., (1965). Table III summarizes the
    results of these studies on crops not listed in Table II.


    General considerations

    Extensive studies have been made on the metabolism of dimethoate in
    both plants and mammals. The major route in mammals appears to be
    through the thiocarboxy derivative to the corresponding dimethyl
    esters of phosphoric, thiophosphoric or dithiophosphoric acids. A side
    pathway may also occur through the thiodesmethyl carboxy derivative.
    The oxygen analog of dimethoate forms in animals and although this
    route may be considered minor with respect to the principle route, it
    is an important one to consider because of the toxicity of the oxygen
    analog. Evidence indicates that in plants the formation of the oxygen
    analog is a major route. However, various investigators are not in
    agreement regarding the quantitative measure of the material degraded
    by this oxidation route, nor are they in agreement on the other
    pathways of metabolism involving hydrolysis and demethylation which
    occur to a substantial degree. See Figure I for the proposed schemes.

    In soils

    The fate of dimethoate in soils is pertinent to this presentation
    since the compound is systemic from soils; that is, it is absorbed by
    plants from the soil and transported to the aerial part of the plant
    in sufficient quantity to make the whole plant insecticidal to certain

    The persistency of dimethoate in sandy loam soil was determined by
    Bohn (1964). The biological half-life was found to be 4 days under
    drought conditions and shortened to 2-1/2 days with moderate rainfall.

    Parker and Dewey (1965) applied a dosage 5 times that used by Bohn to
    gravelly silt loam. Bioassay with vinegar flies showed a rapid decline
    of dimethoate in the first few days with 40 per cent remaining on the
    5th day. The rate of dissipation then slowed down considerably with
    approximately 20 per cent remaining after 54 days.

    In plants

    Santi and de Pietri-Tonelli (1959b) showed the systemic nature of
    dimethoate. Application of the insecticide and its oxygen analog to
    roots, stems and leaves of bean plants resulted in translocation to
    other parts of the plant. Foliar spray on trees resulted in residues
    in the fruit. Both compounds penetrate from the outside to the inside
    of the fruit and kill fruit-eating larvae. They showed that
    transformation to the oxygen analog occurs in broad bean plants after
    root absorption of the insecticide and in cherries picked from sprayed


    Dauterman et al. (1960) studied the metabolism of dimethoate-32P on
    the surface and inside cotton, corn, pea and potato leaves following
    foliar application. Substantial quantities of oxygen analog were found
    in all samples. Although the quantity decreased with time, there was a
    proportionate increase in the oxygen analog relative to dimethoate.
    Internally this is attributed to enzymatic oxidation; however, since
    this same oxidation results on non-biological surfaces exposed to the
    atmosphere, non-enzymatic oxidation may occur on the leaf surface.

    Based on the quantities of water-soluble metabolites on the surface
    and inside leaves, Dauterman postulates that different mechanisms of
    degradation occur. There also appears to be a marked difference in
    crop species. Plant-surface water-soluble metabolites were primarily
    the oxycarboxy derivative; whereas the desmethyl derivatives were the
    major internal metabolites. Pea plants did not follow the pattern of
    cotton, corn and potato plants, but had about 50 per cent residue of
    phosphoric acid both on the surface and inside leaves. No
    dithiophosphoric acids or thiocarboxy derivative were found in any
    samples. Apparently oxidation occurs more rapidly than hydrolysis.

    Hacskaylo and Bull (1963) found that metabolism of dimethoate in
    excised cotton leaves resembles the pathway proposed for mammals and
    is different from that occurring from foliar treatments. They found
    the level of oxygen analog fairly constant and always less than 6 per
    cent of the total metabolites found.

    Recently Lucier (1967) studied the metabolism of 32P and 14C-carbonyl
    labeled dimethoate in bean plants using four modes of application:
    foliar treatment, stem injection, root absorption and excised leaves.
    Conversion of dimethoate to the oxygen analog was the major route of
    degradation and was directly correlated with the ease of translocation
    of dimethoate to the leaf tissue. Thus the amount of oxygen analog was
    greatest for the excised leaves and less for the foliar application.
    In root absorption studies, the oxygen analog content was 4-1/2 times
    the amount of dimethoate and represented 10 per cent of the
    administered dose 10 days after application. The major hydrolysis
    products were the thiocarboxy derivative, dimethyl phosphorothioate
    and dimethyl phosphorodithioate. Only trace quantities of the
    thiodesmethyl carboxy compound were found.

    A new compound, des-N-methyl dimethoate was detected in trace
    quantities in all samples. Foliar application gave rise to large
    quantities of two unknown metabolites which were postulated to be the
    N-hydroxy methyl derivatives of dimethoate and its oxygen analog.
    These unknowns are rapidly degraded and not detectable after four

    Chillwell and Beecham (1960) found that climatic conditions had no
    substantial effect on residue level of dimethoate if similar
    applications were made on crops at the same growth stage. Recent
    preliminary investigations by Watts and Storherr (1967) show that
    residues on field-sprayed kale may contain five times as much oxygen
    analog as the parent compound 14 days after treatment.

    The oxygen analog seems to be the only metabolite of toxicological
    importance. Therefore, its residue level in food products must be
    considered. Data submitted to the U.S. Food and Drug Administration
    and data reported in the literature by Santi* (1961), Santi and
    Giacomelli (1962) and Dauterman et al. (1960) indicate that the amount
    of oxygen analog is generally not above 10-20 per cent of the total
    toxic residue. Results in olives are an exception where the oxygen
    analog was found as high as 67 per cent of the total residue after 30

    In animals

    Early studies by Roberts at al (1958) and Kaplanis et al (1959)
    revealed that dimethoate was absorbed rapidly into the blood of cattle
    and was converted to a metabolite several times more toxic than the
    parent compound as determined by enzymatic analysis and bioassay. This
    compound and many of the major urinary metabolites were not
    identified. Santi and de Pietri-Tonelli (1959a) showed that dimethoate
    converted chemically and in vitro by incubation in rat liver slices
    to the oxygen analog. An unusually high rate of degradation of
    dimethoate in sheep liver to the thiocarboxy derivative was found by
    Uchida et al, (1964). This was attributed to amidase activity.
    Sanderson and Edson (1964) found that dimethoate behaved as a typical
    indirect anticholinesterase agent by conversion in the liver to at
    least four short lived metabolites whose hydrolysis products are
    rapidly excreted mainly in the urine.

    Oral administration of dimethoate-32P at dosages of 100 mg/kg to rats
    and 10 to 40 mg/kg to lactating cows led Dauterman and co-workers
    (1959) to conclude that the metabolic pathway was similar for both
    species, and that dimethoate was attacked hydrolytically at five sites
    on the molecule. Only small quantities of labelled material were found
    in the feces. Dimethoate was rapidly absorbed into the blood and
    rapidly excreted in the urine with 75 per cent of the administered
    dose eliminated within 24 hours primarily as the thiocarboxy
    derivative. As the quantity of the thiocarboxy derivative and
    dimethylthiophosphoric acid decreased, the level of dimethylphosphoric
    acid increased and appeared relatively stable since conversion to
    simpler phosphoric acids was very slow. When the desmethyl derivative
    was fed to rats, recovery of better the 85 per cent of unchanged
    chemical in the urine occurred suggesting that this is not the major
    metabolic route in animals.

    Analysis of blood samples indicated that a maximum of chloroform
    solubles was reached at two hours with 1.5 ppm dimethoate equivalents
    present in cows which were, treated with 10 g/kg. The level of
    cholinesterase was severely depressed for the animal treated at 
    40 mg/kg but no depression occurred at the lower feeding level.

    * As quoted by de Pietri-Tonelli et al (1965)

    A composite sample representing total milk secreted over a 288 hour
    period showed that 0.0068 per cent of the administered dose was
    eliminated in this manner. The amount of chloroform solubles decreased
    rapidly with less than 0.02 ppm dimethoate equivalents present after
    48 hours from the oral dose of 10 mg/kg and 0.04 ppm from the 40 mg/kg

    Chloroform solubles in the fat were less than 0.1 ppm after eight
    hours. The only significant quantity of residue in bovine tissues was
    found in the liver with a maximum of 0.23 ppm of chloroform solubles
    at the lower feeding level.

    Chamberlain et al. (1961) investigated the metabolism of dimethoate
    by intramuscular administration and oral feeding of sheep at 10 and 40
    mg/kg. He too found that only a small per cent of the labeled dose was
    excreted in the faeces and that over 80 per cent of the radioactive
    material was eliminated in the urine by 72 hours with the thiocarboxy
    derivative being the major component. As the thiocarboxy content
    decreased there was an increase in dimethyl phosphoric acid and an
    unknown which he tentatively identified as the desmethyl carboxy
    derivative and suggested that it formed from the thiocarboxy compound.
    Trace quantities of dimethoate and its oxygen analog were present in
    all sheep urine samples.

    Analysis of the blood samples showed that the amount of
    organo-solubles decreased very rapidly with less than 0.1 per cent
    remaining after 12 hours. Ninety per cent of the organosoluble residue
    vas dimethoate or its oxygen analog. The proportion of oxygen analog
    to dimethoate increased as the quantity of dimethoate decreased.

    In storage and processing

    No commercial use of dimethoate for storage products is known. Rowland
    (1966) studied the metabolism in stored wheat and sorghum grains
    fortified at 2 and 10 parts per million. Trace amounts of dimethoate
    and its oxygen analog were found after 4 and 7 days' storage. No
    active anti-cholinesterase components were found at subsequent
    samplings. No hydrolytic products of the oxygen analog were found, but
    significant quantities of dimethoate hydrolysis products were detected
    by paper chromatography. These included the thiocarboxy derivative,
    the thiodesmethyl and thiodesmethyl carboxy derivative, and the
    dimethyl esters of thio and dithiophosphoric acid.


    The major metabolic pathway in plants indicates that the oxygen analog
    of dimethoate is a significant metabolite. A minor pathway in animals
    yields the same compound. Any adequate method for residue analysis
    must take this compound into account.

    Most of the data presented in Table II was obtained from one of two
    methods of analysis.

    The first method of Waldron (1962) (adapted for apples from a method
    described by George (1962) for dimethoate in alfalfa) determines only
    the parent compound, dimethoate. The pesticide is extracted with
    methylene chloride, followed by alkaline hydrolysis, and colorimetric
    determination of the resultant methylamine by reaction with
    1-chloro-2,4-dinitrobenzene. Numerous tests were made to show that the
    method in specific for dimethoate and that some 28 commonly used
    pesticides do not interfere.

    Steller and Curry developed a method incorporating a thin layer
    chromatographic isolation of dimethoate and its oxygen analog and a
    total phosphorous determination of the separate fractions measuring a
    molybdenum blue complex. This method is specific for dimethoate and
    its oxygen analog. Although recoveries were lower than for the Waldron
    method, they were consistent and the authors claim a sensitivity of
    0.06 ppm.

    The data in Table II were obtained by a variety of methods. Chillwell
    and Beecham (1960) macerated plant tissues with water acidified with
    acetic acid and extracted the aqueous phase with chloroform.
    Microdistillation was used to purify the extracted insecticide and
    phosphorous was determined colorimetrically after an acid digestion.
    Santi and de Pietri-Tonelli (1959), referred to by de Pietri-Tonelli
    et al (1965), used a chloroform extraction with isolation by paper
    chromatography and determination of phosphorous with a molybdic
    reagent and 2, 6-dibromo-N-chloro-p-quinoneimine and subsequent
    spraying with propylene glycol.

    Van Middlem and Waites (1964) compared a dinitrochlorobenzene
    colorimetric procedure with an electron capture gas chromatography
    procedure for dimethoate. Recoveries were 71 per cent for the
    colorimetric procedure and about 85 per cent for the gas
    chromatography procedure. Correcting for recoveries the results of the
    two procedures were in agreement. In both procedures methylene
    chloride was used to extract the pesticide. The organic phase was
    further cleaned with activated carbon and the aqueous phase was passed
    through a polyethylene-coated alumina column prior to colorimetric
    determination. For the gas chromatographic analysis benzene was added
    to the extract before evaporation of the methylene chloride. These
    investigators reported that the oxygen analog is infinitely more
    soluble in water than in organic solvents. Unlike dimethoate which has
    a partition coefficient of 20 for chloroform and water, the oxygen
    analog coefficient is only 0.7.

    Watts and Storherr (1967) found a much higher ratio of oxygen analog
    in residues using an ethyl acetate extraction with a nuchar carbon
    cleanup and a gas chromatography thermionic detection.

    Since the oxygen analog in so highly water-soluble and favors the
    aqueous phase in many partitioning systems, care must be exercised in
    choosing any method of analysis to ensure that the more polar oxygen
    analog is not lost. It is difficult to evaluate fully the quantitative

    data published on metabolism without knowledge of the exact conditions
    of the experiments. It is hoped that improved methodology will assist
    in clarifying some apparent anomalies.


    Country                        Tolerances, ppm    Product

    United States of America       2                  apples, pears

                                   2                  18 vegetables

    Canada                         2                  apples, pears

    Benelux                        0.5                fruits and

    Federal Republic of
    Germany                        0.5                fruits and

    Australia                      2.0


    Temporary tolerances until 3 December 1970

    When dimethoate is utilized in accordance with good agricultural
    practice to protect food products, when necessary against insect
    infestation, the treated product may have residues as high as those
    shown below (total of dimethoate and oxygen analog):

              Tree fruits (including citrus)          2 ppm

              Vegetables (excluding tomatoes and      2 ppm

              Tomatoes and peppers                    1 ppm

    By no means will all samples of fruits and vegetables contain this
    amount of residue; in fact, only a small, yet unknown portion of each
    product in these categories is likely to be treated. There are some
    data available on the disappearance of this compound during storage of
    treated wheat. The nature of this disappearance simulates that which
    occurs in living plants. The compound is systemic; it can be assumed
    that residues will not be reduced materially during washing and

    Since the compound is not recommended, generally, for use on a large
    variety of food products, it is recommended that the above levels be

    adopted on a temporary basis until further data are made available on
    losses during cooking and data are acquired from total diet studies.

    The proposed temporary tolerance is for a combination of dimethoate
    and its oxygen analog.


    Further work required before 30 June 1970

    1.   Studies on the fate of the compound during processing and
         preparation for consumption.

    2.   Amount of residue appearing in total diet studies.

    Further work desirable

    Worldwide use data.


    Casida, J.E. and Sanderson, D.M. (1962) Nature, 189, 507.

    Casida, J.E. and Sanderson, D.M. (1963) J. Agr. Food Chem., 2, 91.

    Ecobichon, D.J. and Kalow, W. (1963) Canad. J. Biochem., 41, 1537

    Edson, E.F. and Noakes, D.N. (1960) Toxicol. appl. Pharmacol., 2,

    Edson, E.F., Jones, K.H. and Watson, W.A. (1967) Brit. med. J., ii,

    Fogleman, R.W., Levinskas, G.J. and Shaffer, C.B. (1965) Unpublished
    reports submitted by American Cyanamid Company.

    Levinskas, G.J. and Shaffer, C.B. (1965) Unpublished reports submitted
    by American Cyanamid Company.

    O'Brien, R.D. (1959) Nature, 183, 121

    O'Brien, R.D. (1961) Biochem. J., 79, 229

    Ribelin, W.B., Levinskas, G.J. and Shaffer, C.B. (1965) Unpublisbed
    reports submitted by American Cyanamid Company

    Sanderson, D.M. and Edson, E.F. (1964) Brit. J. industr. Med., 21,

    Sherman, M., Ross, E., Sanchet, F.F. and Chang, M.T.Y. (1963) 
    J. econ. Ent., 56, 10

    West, B., Vidone, L.B. and Shaffer, C.B. (1961) Toxicol. appl.
    Pharmacol., 3, 210


    American Cyanamid Co. (1962-7) Pesticide petitions submitted to the
    U.S. Food and Drug Administration.

    Bohn, W.R. (1964) The disappearance of dimethoate from soil. J. Econ.
    Ent. 57: 798-9. 

    Chamberlain, W.R., Gatterdam, P.E., and Hopkins, D.E. (1961) The
    metabolism of p32-labelled dimethoate in sheep. J. Econ. Ent. 54 (4)
    : 733-40.

    Chillwell, E.D. and Beecham, P.T. (1960) Residues of 0,0-dimethyl
    S-(N-methyl-carbamoyl-methyl) Phosphorothiolothionate (dimethoate) in
    sprayed crops. J. Sci. Fd. Agric. 11 (7) : 400-7.

    Dauterman, W.C., Casida, J.E., Knaak, J.B. and Kowalczyk, T. J. (1959)
    Agr. Food Chem. 7 (3) : 188-93.

    Dauterman, W.C., Biado, G.B., Casida, J.E. and O'Brien, R.D. J. Agr.
    Food Chem. 1960 8 (2) a 115-19.

    de Pietri-Tonelli, F. and Barontini, A. (1959) Analisi per via
    biologica dei residue di Rogor in campioni di carciofi ed indivia.
    Internal report of Montecatini.

    de Pietri-Tonelli, P., Bazzi, B. and Santi, R. (1965) Rogor
    (dimethoate) residues in food crops. Residue Reviews. Vol 11. New
    York : Springer-Verlag.

    George, D.A., Walker, K.C., Giang, P.A. and Murphy, R.T. (1962)
    Colorimetric method for the determination of dimethoate residues.
    Presented 142nd Meeting Amer. Chem. Soc. 9 -14 September 1962.

    Hacskaylo, J. and Bull D.L. (1963) Metabolism of dimethoate in cotton
    leaves. J. Agr. Food Chem. 11 (6) : 464-6.

    Kaplanis, J.N., Robbins, W.E., Darrow, D.E. et al. (1959) The
    metabolism of dimethoate in cattle. J. Econ. Entomol. 52 (6) :

    Lucier, G.W. (1967) Thesis entitled : Metabolism of dimethoate in bean
    plants in relation to its mode of application. Dept. of Entomol.
    University of Maryland, College Park, Md.

    Parker, B.L. and Dewey J.E. (1965) Decline of phorate and dimethoate
    residues in treated soils based on toxicity to Drosophila
    melanogaster. J. Econ. Ent. 58: 106-11.

    Roberts, R.H., Radeleff, R.D. and Kaplanis, J.N. (1958) Bioassay of
    the blood from cattle treated with Am. Cyanamid 12,880. J. Econ.
    Entomol. 51 (6): 861-4.

    Rowlands, D.G. (1966) The in vitro and in vivo metabolism of
    dimethoate by stored wheat and sorghum grains. J. Sci. Fd. Agric.
    17: 90-3.

    Sanderson, D.M. and Edson, E.F. (1964) Toxicological properties of the
    organophosphorus insecticide dimethoate. Brit. J. Ind. Med. 21, 52.

    Santi, R. (1961) Ricerche sulla penetrazione e sul destino metabolico
    del Rogor-P32 nelle ciliege e nelle pesche. Internal report of

    Santi, R. and de Pietri-Tonelli, P. (1959a) Research on the mechanism
    of action of N-monomethyl-0,0-dimethyl dithiophosphorylacetamide. Is.
    Ric. Agr. Soc. Montecatini, Milano, Italy. 2 : 3-28.

    Santi, R. and de Pietri-Tonelli, P. (1959b) Mode of action and
    biological properties of the S-(Methylcarbanyl) methyl
    0,0-dimethyldithiophosphate. Nature 183 : 398-9.

    Santi, R. and Giacomelli, R. (1962) Metabolic fate of P32-labeled
    dimethoate in olive fruits and some toxicological implications. 
    J. Agr. Food Chem. 10 (3) : 257-61.

    Steller, W.A. and Curry, A.N. (1964) Measurement of residues of Cygon
    insecticide and its oxygen analog by total phosphorus determination
    after isolation by thin-layer chromatography. J.A.0.A.C. 47 (4) :

    Uchida, T., Dauterman, W.C. and O'Brien, R.D. (1964) The metabolism of
    dimethoate by vertebrate tissues. J. Agr. Food Chem. 12 (1) : 48-52.

    Van Middelem, C.H. and Waites, R.E. (1964) Gas chromatographic and
    colorimetric measurement of dimethoate residues. J. Agr. Food Chem.
    12 (2) : 178-182.

    Waldron, A.C. (1962) Colorimetric method for the determination of
    dimethoate residues in plant tissues. Unpublished but in dimethoate
    petition submitted to U.S. Food and Drug Administration by American
    Cyanamid Co.

    Watts, R. and Storherr, R. (1967) Personal communication. U.S. Food
    and Drug. Administration.

    See Also:
       Toxicological Abbreviations
       Dimethoate (EHC 90, 1989)
       Dimethoate (HSG 20, 1988)
       Dimethoate (ICSC)
       Dimethoate (FAO Meeting Report PL/1965/10/1)
       Dimethoate (FAO/PL:CP/15)
       Dimethoate (JMPR Evaluations 2003 Part II Toxicological)
       Dimethoate (AGP:1970/M/12/1)
       Dimethoate (Pesticide residues in food: 1983 evaluations)
       Dimethoate (Pesticide residues in food: 1984 evaluations)
       Dimethoate (Pesticide residues in food: 1984 evaluations)
       Dimethoate (Pesticide residues in food: 1987 evaluations Part II Toxicology)
       Dimethoate (Pesticide residues in food: 1996 evaluations Part II Toxicological)