WHO/FOOD ADD./69.35



    Issued jointly by FAO and WHO

    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 Geneva, 9-16 December,



    Geneva, 1969


    This pesticide was evaluated for acceptable daily intake by the Joint
    Meeting of the FAO Committee on Pesticides in Agriculture and the WHO
    Expert Committee on Pesticide Residues (FAO/WHO, 1965).

    Since that time information has become available on the identity of
    the technical material and its residues in food and their evaluation.
    Therefore the previously published monograph has been greatly expanded
    and is reproduced in its entirety below.


    Chemical names

         dimethyl phosphorothiolthionate

         OO-dimethyl phosphorodithioate (IUPAC).


         GuthionR, GusathionR, Bayer 17147.

    Structural formula


    Other information on identity and properties

    The pure material is a white, crystalline solid, M.P. 73-74C; soluble
    in water at 25C (1:30 000) and soluble in most organic solvents. The
    technical product is a brown waxy solid (M.P. 65-68C). It decomposes
    at elevated temperatures with the evolution of gas, and is rapidly
    hydrolyzed by cold alkali to form anthranilic acid and is subject to
    hydrolysis by acids. Suitable oxidizing agents convert it to the
    oxygen analogue.


    Biochemical aspects

    Azinphos-methyl is activated to gutoxon, a highly potent
    cholinesterase inhibitor which has a molar I50 in rat brain of 2.99 
    10-8 (Schrader, 1963). In vitro, the rate of degradation of gutoxon
    by liver microsomal enzymes is not altered by species, or sex
    variation in mammals (Johnsen and Dahm, 1966). Also the rate of in
    vitro metabolism by the liver is similar in mammals, birds, and fish
    (Murphy, 1966).

    In vitro studies showed that azinphos-methyl is a poor brain
    cholinesterase inhibitor in mammalian, avian, or piscine species but
    gutoxon is a potent inhibitor; avian brain cholinesterase inhibition
    being less than that in mammals, and fish brain cholinesterase being
    the most susceptible to inhibition. Species differences in sensitivity
    to gutoxon inhibition of brain cholinesterase are probably
    sufficiently large to modify the influence of variation in metabolic
    rates (Murphy et al., 1968).

    Acute toxicity

                           LD50 (mg/kg
    Animal        Route    body-weight)   Reference

    Mouse         Oral        8*          Sato, 1959

    Mouse         i.p.        8-10**      Murphy, 1966

    Rat           Oral        11-25       DuBois et al., 1955
                                          Gaines, 1960

    Rat           i.p.        5-11.6      DuBois et al., 1955

    Guinea-pig    Oral        80          DuBois et al., 1955

    Guinea-pig    i.p.        40          DuBois et al., 1955

    *  Given as azinphos-methyl emulsion.
    ** Given as a corn oil solution.

    Short-term studies


    Groups of 10 male rats were fed 0, 5, 10, 20, 50 or 100 ppm
    azinphos-methyl in the diet for nine weeks. At 50, and 100 ppm slight
    decrease in food intake, decrease in body-weight gain, and muscular
    spasms and trembling were observed. Whole blood cholinesterase
    activity was markedly decreased at 20, 50 and 100 ppm. At 5 and 10 ppm
    the maximum depression which occurred, was 20 per cent below the
    control values. (Huntingdon Research Centre, 1966.)

    The addition of azinphos-methyl to the diet of groups of 10 young male
    and 10 young female rats each, at levels of 2, 5 and 20 ppm did not
    markedly alter the growth-rate over 60 days. The body-weight of the
    male rats fed 20 ppm was about four per cent less than that of the
    controls. In the rats fed 2 and 5 ppm for 120 days, cholinesterase
    activity was unaffected, but at 20 ppm there was inhibition in the
    brain (10 per cent) and in serum and erythrocytes (about 30 

    per cent). After 120 days no appreciable changes in the gross and
    microscopic appearance of brain, heart, liver, spleen, adrenals,
    stomach, intestines, skeletal muscle and bone-marrow were found. There
    was no evidence of demyelination in the nervous system (Doull et al.,

    When weanling male rats were fed diets containing 50 and 100 ppm of
    azinphos-methyl for 16 weeks, approximately half of each group died.
    All animals receiving azinphos-methyl in the diet showed marked
    effects of cholinergic stimulation, including diarrhoea, salivation,
    lacrimation, muscular tremors and fasciculations. These symptoms were
    most marked during the first month on the diets. The rats fed 50 ppm
    of azinphos-methyl weighed about 10 per cent less, and the rats fed
    100 ppm, 18 per cent less than rats fed a normal diet. The
    cholinesterase activity of the serum, brain, erythrocytes and
    submaxillary glands of rats fed 50 and 100 ppm was markedly inhibited.
    The inhibition was most marked in the erythrocytes and brain and the
    animals did not fully recover from these effects during a three-week
    period on a normal diet. Both gross and microscopic examination failed
    to indicate any evidence of testicular atrophy due to the presence of
    the high levels of azinphos-methyl in the diet (Doull et al., 1957a).


    Groups of two dogs, one male and one female, given 5, 10, 20 and 50
    ppm of azinphos-methyl in their diet did not show any loss of weight
    nor any symptoms of azinphos-methyl poisoning during a 12-week period.
    At levels of 5, 10 and 20 ppm there was no significant decrease, but
    at 50 ppm there was a 25 per cent decrease in serum cholinesterase
    activity at the end of the 12-week period. The erythrocyte
    cholinesterase of the one male and one female dog began to be
    inhibited at the 10 ppm level (Doull et al., 1967b).

    Six groups of one male and one female dogs were fed 0, 20, 50, 100,
    200 or 400 ppm of azinphos-methyl in a dry diet, for 19 weeks. Whole
    blood cholinesterase depression was slight at 20 and 50 ppm, becoming
    apparent after four weeks on the diet; however, reactivation occurred
    by the sixth week at 20 ppm, and by the ninth week at 50 ppm. At the
    100 ppm level and above, cholinesterase activity was reduced by more
    than 50 per cent; reactivation was not apparent at 400 ppm, was
    doubtful at 200 ppm, and was slight at 100 ppm after 17 weeks. (Loser
    and Lorke, 1967.)

    Four groups of four male and four female dogs along with a control
    group, were fed azinphos-methyl in a dry diet for two years. At the
    lowest level the dogs were fed 5 ppm throughout the two-year period.
    At the second level they were fed 20 ppm for 36 weeks, followed by 50
    ppm for 15 months. At the third level the dogs received 50 ppm
    throughout the two-year period. At the top dose level they received 50
    ppm for 36 weeks, followed by 100 ppm for 21 weeks, 150 ppm for 27
    weeks and finally 300 ppm for 21 weeks. Mortality throughout was
    comparable to the controls. At 300 ppm, tremors, muscular weakness and

    abnormal quietness were noted, especially among the male animals.
    Weight loss occurred to a slight degree at this dose level. Food
    intake was slightly reduced in females at 150 and 300 ppm.
    Cholinesterase depression was not apparent during the first three
    months of the study. In the period three to nine months, red blood
    cell cholinesterase was slightly depressed at 20 ppm, and more
    markedly depressed at 50 ppm. In the second year of the study, plasma
    cholinesterase depression was apparent in dogs receiving 50 ppm and
    above. Red blood cell cholinesterase continued to be depressed at
    intermediate and high dose levels, and minimal depression was also
    seen at 5 ppm. Other parameters, including haematology, clinical
    chemistry, urinalysis, organ to body-weight ratios, and gross and
    histopathology were all comparable to controls. (Huntingdon Research
    Centre, 1966b.)

    Long-term studies


    Groups of 40 male and 40 female rats were fed 2.5, 5 and 20 ppm for
    two years and a top group was fed 50 ppm for 47 weeks and then 100
    ppm. Two control groups were also maintained. At 100 ppm, toxic
    symptoms in the form of salivation, diuresis, exophthalmos, loss of
    balance and co-ordination, muscular fasciculation, and minor tremors
    were observed in five females. Mortality, food intake, body-weight
    gain, food utilization, urinalysis, and haematology were comparable to
    controls. Depression of cholinesterase levels of red blood cells and
    plasma occurred at 20 ppm and above, and plasma cholinesterase
    depression was apparent up to 39 weeks at 5 ppm in the males. In the
    females, consistent depression of plasma and red blood cell
    cholinesterase was apparent only at the top dose. At 20 ppm plasma
    cholinesterase depression occurred up to and including 39 weeks. At 5
    ppm depression occurred at 10, 39 and 78 weeks. Red blood cell
    cholinesterase was depressed up to 65 weeks at 20 ppm, but only up to
    10 weeks at 5 ppm. Brain cholinesterase depression was significantly
    depressed at the top dose level only. Organ to body-weight ratios
    showed random variations, a possible increase with the liver occurring
    at the top dose level. There was no indication that tumour incidence
    was increased and it was concluded that azinphos-methyl was devoid of
    carcinogenic activity in the rat. Gross and histopathology showed no
    compound related effects. (Huntingdon Research Centre, 1966,)

    Special studies


    Mouse. Groups of six male and 24 female mice were fed 0, 5, 10, 25
    and 50 ppm in the diet over three generations. Initial exposure to the
    diet was for 30 days prior to the first mating of the Fo generation.
    Because of the high mortality (15 out of 24) among the females at 50
    ppm prior to mating, this dose level was eliminated after the first
    mating. Fertility and litter size were not affected in the 50 ppm

    group, but survival to weaning was significantly decreased. Up to and
    including 25 ppm no adverse effects were apparent as judged by
    fertility, gestation or lactation, litter size, or survival of
    offspring to 30 days. Gross and microscopic examination of F3b
    weanlings showed no compound related changes. (Root et al., 1965.)

    Rabbit. Three groups of 10 pregnant female rabbits were fed 0, 5 or
    25 ppm in the diet, from the eighth to the sixteenth day of pregnancy.
    Five rabbits in each group were sacrificed on the twenty-ninth day of
    pregnancy, the remainder being permitted to litter. No compound
    related effects occurred with respect to litter size, stillbirths, sex
    ratios, average foetal weights, incidence of immature foetuses, or
    survival to 30 days. (Doull et al., 1966.)


    Since the last evaluation by the FAO/WHO Joint Meeting (Rome, 15-22
    March 1965), results of reproduction studies in mice, short-term
    studies in dogs and long-term studies in rats have been provided. The
    studies performed appear satisfactory. Further work desirable includes
    studies on cholinesterase inhibition of plasma and erythrocytes in man
    and metabolic studies in man.


    Level causing no significant toxicological effects

         Rat: 2.5 ppm in the diet, equivalent to 0.125 mg/kg.

         Dog: About 5 ppm in the dry diet, equivalent to 0.125 mg/kg.

    Estimate of acceptable daily intake of azinphos-methyl for man

         0-0.0025 mg/kg body-weight.


    Use pattern

    Azinphos-methyl is used for the pre-harvest control of a wide spectrum
    of insects and mites attacking fruit, vegetable and forage crops.

    Residues resulting from supervised trials

    The following typical data are extracted from Chemagro internal
    reports of trials made at various field stations.

                   Rate of application      No. of       Pre-harvest      Residue
    Crop                 (kg/ha)          treatments    interval (days)   (ppm)
    Alfalfa             0.50                 1                5           0.4

    Apples              0.28-0.35            7                7           0.75

    Apricots            0.28-0.35            1               15           4.6
                                                             21           3.1

    Broccoli            0.56                 5               15           0.38

    Brussels            0.56                 1                7           0.6
    sprouts                                                  14           n.d.

    Cabbage             0.56                 3               15           n.d.

    Cherries            0.28-0.35            1                7           0.18-0.74
                                                             14           n.d.-0.23

    Clover              0.50                 1                5           0.4

    Grapes              0.28-0.35            1               15           0.6
                                                             22           0.4
                        0.28-0.35            2               16           5.1
                                                             23           3.7

    Grapefruit          1.12                 1               15           0.3-0.9

    Peaches             0.28-0.35            1               19           1.0
                                                             31           0.4

    Pears               0.28-0.35            1                8           0.3

    Peas                0.56                 3                7           n.d.

    Plums               0.28-0.56            1               14           n.d.-0.25

    Strawberries        1.12                 1                7           0.9-1.5
                                                             14           0.7

    Tomatoes            1.56                 1                7           0.09

    Plums               0.28-0.56            1               14           n.d.-0.25

    Strawberries        1.12                 1                7           0.9-1.5
                                                             14           0.7

    Tomatoes            1.56                 1                7           0.09
    n.d. = not detectable.
    Evidence of residues in food moving in commerce or at consumption

    No data available.

    Fate of residues

    In plants. Azinphos-methyl has not been shown to exhibit systemic
    action. No phosphorothiolate oxidation product could be found in or on
    sprayed cotton leaves (Tietz et al., 1957, 1960). Two unidentified
    phosphorus-containing metabolites, more lipophilic than the applied
    chemical, appeared and gave positive tests for anthranilic acid
    (Meagher et al., 1960). Further metabolites were recovered containing
    the radioactive phosphorus in phospholipids and as hydrolysis

    With lettuce, most of the chemical remained on the surface and no
    oxygen analogue was isolated (Magill et al., 1966). After 14 days, 95
    per cent of the extracted residue was azinphos-methyl with four
    components in the remaining five per cent Two were benzazimide and
    methyl benzazimide sulfide while the remaining two were not

    In animals. P32 and C14-labelled material administered orally to
    dairy cows did not result in azinphos-methyl or the P=0 derivative in
    the blood or milk (Everett et al., 1966). Excluded possible
    metabolites were anthranilic acid, benzazimide, hydroxymethyl
    benzazimide, mercaptomethyl benzazimide, N-methyl benzazimide, bis
    (N-methyl benzazimide) sulfide and the corresponding disulfide.
    However four unidentified components containing the benzazimide
    moiety, appeared, one of which accounted for 90 per cent of the total
    residue. They contribute a maximum of 0.017 ppm in the milk when
    feeding the animal at the rate of 0.2 mg/kg, equivalent to 2.8 ppm in
    the feed. At least two of the metabolites may be oxidation products of
    an intermediate metabolite, bis (N-methylbenzazimide) sulfide. Thus
    the residue in milk from feeding forage containing 2.8 ppm
    azinphos-methyl will be 0.008 ppm expressed as mercaptomethyl
    benzazimide while the residue in tissues will not exceed 0.1 ppm.

    The fluorometric method of Adams and Anderson (1966) is suitable for
    determining these metabolites.

    In storage and processing. Residues of azinphos-methyl were stable
    at frozen storage levels (-18 to -23C) in samples of fruit, fodder
    and vegetables (Chemagro, 1962). Washing oranges reduced the residues
    from 1.0 ppm to 0.7 ppm (whole fruit), from 2.7 to 1.9 ppm in the
    peel. While the juice and pulp were free of residues, the orange oil
    contained 30 ppm (Anderson et al., 1963). Simple washing reduces
    residues on the peel from 71 to 96 per cent, the greater amount with
    the fresher residue (Gunther et al., 1963). Field-sprayed snap beans
    bearing an initial residue of 1.09 ppm had a residue of 0.14 ppm after
    washing, blanching and freezing (Carlin et al., 1966). After canning
    the residue was reduced to 0.02 ppm. Soy-bean oil fortified with

    azinphos-methyl and deodorized according to commercial procedures had
    the residue reduced by 36 per cent (Thornton, 1967b). Sugar-cane
    containing 0.1 to 0.6 ppm showed no residues in the molasses or sugar
    when processed (FAO/WHO, 1965).

    Methods of residue analysis

    Colorimetric, gas chromatographic, fluorometric, infra-red and
    polarographic methods have been developed. One commonly used procedure
    is based on weak alkaline hydrolysis of the residue to liberate
    anthranilic acid which is then diazotized and coupled with
    N-(1-naphthyl)-ethylenediamine dihydrochloride and the resultant
    purple colour measured at 555 m (Meagher et al., 1960; MacDougall,
    1964; Cohen et al., 1966). Modifications have been made to shorten the
    procedure (Cox, 1964). Miles (1964) has done this by direct coupling
    of the benzotriazinyl-containing residue in an acetic-hydrochloric
    acid mixture and measuring the blue-violet colour at 556 m. Smart
    (1967) has modified the method by introducing an improved extraction

    Another colorimetric method involves the alkali cleavage and
    measurement of the dimethyl phosphorodithioate as the copper complex
    absorbance at 420 m. This measures the parent compound only and is
    similar to the infra-red measurement using the P=S stretching
    vibration at 654 cm-1 (15.25 microns) (Cohen et al., 1966),

    The sensitivity of the anthranilic acid colorimetric method can be
    increased to about 0.05 ppm by using 10 cm cells. The precision for
    recovery of azinphos-methyl from a number of crops indicates that in
    the range of 0.2 to 0.5 ppm the average deviation from the mean is
    approximately six per cent.

    A spectrophotofluorometric method is based on the measurement of the
    anthranilic acid released on alkaline hydrolysis by determining
    fluorometrically at an activating wavelength of 340 m and a
    fluorescence of 400 m (Adams and Anderson, 1966). It has a
    sensitivity of about 0.005 ppm for milk, 0.02 ppm for most animal
    tissues and 0.03 ppm for fat.

    More recently a gas chromatographic procedure has been developed for
    the determination of residues in soy-beans using the potassium
    chloride thermionic emission flame detector for phosphorus (Thornton,
    1967a). This method is sensitive to 0.005 ppm and distinguishes
    between azinphos-methyl and its P=O analogue.

    A method based on the measurement of the formaldehyde released on acid
    hydrolysis of the residue has been used (Giang and Schechter, 1958) as
    well as a polarographic analysis (Bates, 1962).

    National tolerances

                                             Tolerance     Pre-harvest
    Country                Crop                (ppm)      interval (days)

    Australia                                                   21

    Austria                                                     21

    Benelux            fruit, grapes            0.5

    Brazil             fruit, vegetables        2.0
                       cotton seed              0.5

    Canada             grapes                   0.5
                       fruits, vegetables       1-2.0

    Denmark                                                     21

    France                                                      15

    Germany            fruit, grapes,
    (Fed. Rep.)        vegetables               0.4             14

    Italy                                       0.4             20

    New Zealand        berry fruit,
                       leafy vegetables                         21
                       pip and stone
                       fruit, root
                       crops, tomatoes                          14

    Norway                                                      21

    Portugal                                                    21

    South Africa       citrus fruit             2.0             21
                       pome fruit                               14

    Switzerland        fruit, grapes            1.0             21

    United Kingdom                                              21

    United States      grapes                   5.0
     of America        fruit, vegetables        2.0
                       cereals, soy-beans,
                       nuts, peas,
                       cucumbers, melons
                       peppers and
                       potatoes                 "zero"



    Since the publication of the monographs resulting from the 1965 Joint
    Meeting, work has confirmed that the residue on plants is mainly
    present as the original compound, azinphos-methyl. In the five per
    cent of residue which is not accounted for as azinphos-methyl in
    lettuce 14 days after treatment, out of four metabolites present two
    were identified as benzazimide and methyl benzazimide.

    Investigations with dairy cows indicate that no residues of
    azinphos-methyl or the oxygen analogue will occur in milk from animals
    consuming fodder likely to contain residues. However, four
    non-phosphorus-containing metabolites, but still containing the
    benzazimide moiety, may be present, although they have not been
    precisely identified.

    Although colorimetric and gas-liquid chromatographic methods have been
    developed, none of these have been evaluated for regulatory or referee


    The following temporary tolerances (to be in effect until 1972) are
    to apply to raw agricultural products moving in commerce unless
    otherwise indicated. In the case of fruits and vegetables the
    tolerances should be applied as soon as practicable after harvest and
    in any event prior to actual retail to the public. In the case of
    commodities entering international trade, the tolerances should be
    applied by the importing country at the point of entry or as soon as
    practicable thereafter. Furthermore, the tolerances should not apply
    to the ethyl derivative nor to the oxygen analogue, the latter usually
    being insignificant.

    Temporary tolerances

         Apricots and grapes 4 ppm

         Other fruits        1 ppm

         Vegetables          0.5 ppm

    Further work or information

    Required before 30 June 1972

    1. Information on the nature of terminal residues in plants, animals
       and their products.

    2. Further data on residue levels in raw agricultural products moving
       in commerce.

    3. Data on disappearance of residues during storage and household
       cooking of vegetables.

    4. Data on the possible carry-over of residues into wine as a result
       of the treatment of grapes.

    5. Comparative evaluation of gas-liquid chromatographic and
       spectrophotometric methods for the determination of azinphos-methyl
       and its oxygen analogue for regulatory purposes.


    1. Studies on cholinesterase inhibition of plasm and erythrocytes in

    2. Metabolic studies in man.

    3. Identification and toxicology of metabolites, especially those
       having the benzazimide moiety, in milk.

    4. Collaborative studies to establish a referee method.


    Adams, J. M. and Anderson, C. A. (1966) Spectrophotofluorometric
    method for Guthion residues in milk and animal tissues. J. Agric. Food
    Chem., 14: 53-55

    Anderson, C. A., MacDougall, D., Kesterson, J. W., Hendrickson, R, and
    Brooks, R. F. (1963) The effect of processing on Guthion residues in
    oranges and orange products. J. Agric. Food Chem., 11: 422-424

    Bates, J. A. R. (1962) Polarographic determination of azinphos-methyl
    residues in certain crops. Analyst, 87: 786-790

    Carlin, A. F., Hibbs, E. T. and Dahm, P. A.  (1966) Insecticide
    residues and sensory evaluation of canned and frozen snap beans field
    sprayed with Guthion and DDT. Food Technol., 20: 80-83

    Chemagro. (1962) Effect of frozen storage on Guthion residues in  
    various crops. Report No. 8682

    Cohen, C. J., Betker, W. R., Wasleski, D. M. and Cavaghol, J. C.
    (1966) Analysis of Guthion insecticide, J. Agric. Food Chem., 14:

    Cox, W. S. (1964) Rapid determination of Guthion residues on crops.
    J.A.O.A.C., 47: 280-282

    Doull, J.,  Anido, P. and DuBois, K. P. (1957a) Effect of high dietary 
    levels of guthion on rats. University of Chicago. Unpublished report

    Doull, J., Anido, P. and DuBois, K. P. (1957b) Determination of the
    safe dietary level of guthion for dogs. University of Chicago.
    Unpublished report

    Doull, J., DiGiacomo, R. and Meskauskas, J. (1966) Short term breeding
    studies with guthion in rabbits. University of Chicago. Unpublished

    Doull, J., Rehfuss, P. A. and DuBois, K. P. (1956) The effects of
    diets  containing guthion (Bayer 17147) on rats. University of
    Chicago. Unpublished report

    DuBois, K. P., Thursh, D. R. and Murphy, S. D. (1955) The acute
    mammalian toxicity and mechanism of action of Bayer 17147. University
    of Chicago. Unpublished report

    DuBois, K. P., Thursh, D. R. and Murphy, S. D. (1957) Studies on the 
    toxicity and pharmacologic actions of the dimethoxy ester of
    benzotriazine dithiophosphoric acid (DBD guthion). J. Pharmacol.exp.
    Ther., 119: 208-218

    Everett, L. J., Anderson, C. A. and MacDougall, D. (1966) Nature and 
    extent of Guthion residues in milk and tissues resulting from treated
    forage. J. Agric. Food Chem. 14: 47-53

    FAO/WHO. (1965) Evaluation of the toxicity of pesticide residues in
    food. FAO Mtg. Rept. PL/1965/10/1; WHO/Food Add./27.65

    Gaines, T. B. (1960) The acute toxicity of pesticides to rats,
    Toxicol. appl. Pharmacol., 2: 88-99

    Giang, P. A. and Schechter, M. S. (1958) Colorimetric method for
    estimation of Guthion residues in cottonseeds and cottonseed oil. J.
    Agric. Food Chem., 6: 845-848

    Gunther, F. A., Carman, G. E., Blinn, R. C. and Barkley, J. H. (1963)
    Persistence of residues of Guthion on and in mature lemons and oranges
    and in laboratory processed citrus "pulp" cattle feed. J. Agric. Food
    Chem., 11: 424-427

    Huntingdon Research Centre. (1966a) Toxicity of gusathion during
    repeated administration to rats for two years. Unpublished report

    Huntingdon Research Centre. (1966b) Gusathion (Bayer 17147), Chronic
    oral toxicity studies in dogs.  Unpublished report

    Johnsen, R. E. and Dahm, P. A. (1966) Activation and degradation
    efficiencies of liver microsomes from eight vertebrate species, using
    organophosphates as substrates, J. Econ. Entomol., 59: 1437-1442

    Lser, E. and Lorke, D. (1967) Die Aktivitt der Cholinesterase bei
    Hunden nach Verabreichung von Gusathion mit dem Futter. Farbenfabriken
    Bayer. Unpublished report

    MacDougall, D. (1964) Guthion. In: G. Zweig, Analytical Methods for 
    Pesticides, Plant Growth Regulators and Food Additives, vol. II,
    Academic Press, New York-London

    Magill, L. J. and Everett, L. J. (1966) Guthion-C14 study on lettuce.
    Chemagro Report No. 18636

    Meagher, W. R., Adams, J. M., Anderson, C. A. and MacDougall, D.
    (1960) Colorimetric determination of Guthion residues in crops. 
    J. Agric. Food Chem., 8: 282-286

    Miles, J. R. W. (1964) A new colorimetric method for determination of 
    residues of Guthion and Ethyl Guthion and their oxygen analogs.
    J.A.O.A.C., 47: 882-885

    Murphy, S. D. (1966) Liver metabolism and toxicity of thiophosphate 
    insecticides in mammalian, avian and piscine species. Proc. Soc. exp.
    Biol. (N.Y.), 123: 392-398

    Murphy, S. D., Lauwerys, R. R. and Cheever, K. L. (1968) Comparative
    anticholinesterase action to organophosphorus insecticides in
    vertebrates. Toxicol. appl. Pharmacol., 12: 22-35

    Root, M., Vesselinovitch, D., Meskauskas, J, and Doull, J. (1965) 
    Effect of guthion in the diet on the reproduction and lactation of
    mice. University of Chicago. Unpublished report

    Sato, J. (1959) Studies on organic phosphorus. Gusathion and phosdrin.
    1. The toxicity of gusathion and phosdrin. Kumamoto med. J., 12:
    313-317 (Chem. Abstr., 54: 21473 (1960))

    Schrader, G. (1963) Gusathion in Die Entwicklung neuer insektizider
    Phosphosaure-Ester. Verlag Chemie, Weinheim., pp. 176-186

    Smart, N. A. (1967) A modification of Miles' method for determining
    azinphos-methyl residues in crops. Analyst, 92: 779-781

    Thornton, J. S. (1967a) Determination of Guthion M-E in soybeans by
    thermionic emission flame gas chromatography. Chemagro Report No.

    Thornton, J. S. (1967b) Effect of the oil deodorization process on 
    Guthion residues in soy bean oil (simulated). Chemagro Report No.

    Tietz, H., Metcalf, R. L. and Fukuto, T. R. (1957) Action of the 
    insecticide "Gusathion" on cotton plants, and the problem of residues
    in cottonseed. Hfchen-Briefe, 10: 279-289 (English edition)

    Tietz, H., Fukuto, T. R. and Metcalf, R. L. (1960) Untersuchungen mit 
    32P-markierten Verbindungen uber das Verhalten des Insektizids
    GusathionR bei Baumwollpflanzen und das damit verbundene
    Ruckstandsproblem bei Baumwollsamen. Verh. IV. Intern.
    Pflanzenschutz-Kongr. Hamburg 1957, Bd. 2, biol. bundesanstalt f.
    Land-und Forstwirtschaft, Braunschweig, S. 1645-1646

    See Also:
       Toxicological Abbreviations
       Azinphos-methyl (ICSC)
       Azinphos-Methyl (FAO Meeting Report PL/1965/10/1)
       Azinphos-methyl (WHO Pesticide Residues Series 2)
       Azinphos-methyl (WHO Pesticide Residues Series 3)
       Azinphos-methyl (WHO Pesticide Residues Series 4)
       Azinphos-methyl (Pesticide residues in food: 1991 evaluations Part II Toxicology)