FAO/PL:1968/M/9/1 WHO/FOOD ADD./69.35 1968 EVALUATIONS OF SOME PESTICIDE RESIDUES IN FOOD THE MONOGRAPHS 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, 1968. FOOD AND AGRICULTURE ORGANIZATION OF THE UNITED NATIONS WORLD HEALTH ORGANIZATION Geneva, 1969 AZINPHOS-METHYL 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. IDENTITY Chemical names S-(3,4-dihydro-4-oxo-benzo[d]-[1,2,3]-triazin-3-ylmethyl) dimethyl phosphorothiolthionate S-(3,4-dihydro-4-oxo-benzo[d]-[1,2,3]-triazin-3-ylmethyl) OO-dimethyl phosphorodithioate (IUPAC). Synonyms GuthionR, GusathionR, Bayer 17147. Structural formulaOther information on identity and properties The pure material is a white, crystalline solid, M.P. 73-74°C; soluble in water at 25°C (1:30 000) and soluble in most organic solvents. The technical product is a brown waxy solid (M.P. 65-68°C). 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. EVALUATION FOR ACCEPTABLE DAILY INTAKE 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 Rat 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., 1956). 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). Dog 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 Rat 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 Reproduction 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.) Comments 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. TOXICOLOGICAL EVALUATION 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. RESIDUES IN FOOD AND THEIR EVALUATION 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 products. 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 identified. 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 -23°C) 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 mµ (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 mµ. Smart (1967) has modified the method by introducing an improved extraction procedure. Another colorimetric method involves the alkali cleavage and measurement of the dimethyl phosphorodithioate as the copper complex absorbance at 420 mµ. 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 mµ and a fluorescence of 400 mµ (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" RECOMMENDATION FOR TOLERANCES AND PRACTICAL RESIDUE LIMITS Appraisal 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 purposes. Recommendations 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. Desirable 1. Studies on cholinesterase inhibition of plasm and erythrocytes in man. 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. REFERENCES 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: 315-318 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 report 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 Löser, E. and Lorke, D. (1967) Die Aktivität 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. 20182 Thornton, J. S. (1967b) Effect of the oil deodorization process on Guthion residues in soy bean oil (simulated). Chemagro Report No. 20834 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. Höfchen-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)