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    PHOSPHAMIDON

    EXPLANATION

         Phosphamidon was evaluated for acceptable daily intake by the
    Joint Meetings in 1963, 1965, 1966, 1968, 1982, and 1985 (Annex 1,
    FAO/WHO, 1964, 1965a, 1967a, 1969a, 1983a, and 1986a). Toxicological
    monographs were published after the 1963 and 1965 Meetings (Annex 1,
    FAO/WHO, 1964, and 1965b), and monograph addenda were published after
    the 1966, 1968, and 1982 Joint Meetings (Annex 1, FAO/WHO, 1967b,
    1969b, and 1983b). An ADI was established at the 1966 Meeting on the
    basis of no-effect levels taken exclusively from data reported by
    Industrial Bio-Test Laboratories (IBT), which could not be validated.
    For this reason the 1982 Meeting made the ADI temporary and requested
    replacement studies. The required data were not available to the
    Meeting in 1985 and, because of the lack of support for maintaining
    the temporary ADI, the safety factor was doubled. The data have now
    been provided and are summarized and discussed in this monograph
    addendum.

    EVALUATION FOR ACCEPTABLE INTAKE

    BIOLOGICAL DATA

    Toxicological studies

    Special study on reproduction

    Rats

         Groups of 15 male and 30 female albino rats (CD-CRL, 7 weeks old)
    were fed diets containing 0, 5, 30, or 50 (80 for the first 2 weeks)
    ppm phosphamidon (technical, 92.1% pure) in a 2-generation (2
    litters/generation) study. Weanlings from the second litter were
    selected to become parents of the next generation.

         In the parental generations unthriftiness, hyperactivity, ocular
    and/or nasal discharge, and tremours were observed in animals of the
    50 and/or 30 ppm dose groups. There were no compound-related effects
    on mortality or food intake. Body weights were significantly reduced
    in F0 parental males at 50 ppm and in F1 parental males at 50 and
    30 ppm. F1 maternal body weights were slightly reduced at 50 ppm. In
    some cases F1 parental body weights were also decreased at 5 ppm,
    but this occurred in a non-dose-related manner. F0 and F1 parental
    absolute organ weights were significantly affected at 50 ppm. Relative
    brain and heart weights were significantly increased in F1 males at
    50 and 30 ppm. No treatment-related histopathological findings were
    observed in F0 or F1 parental animals. Reproductive performance,
    as expressed in indices for mating, fecundity, and male and female
    fertility, was decreased at 50 ppm.

         Mean litter size and pup survival were decreased in all
    generations (significantly for F2b litters and pups) at 50 ppm. Pup
    weights (at day 21) were decreased in F1a, F1b, F2a, and
    F2b pups at 50 ppm, and a tendency to lower pup weights was observed
    in F1a, F1b, and F2b pups at 30 ppm. Significantly-reduced
    absolute organ weights were observed in F1b and F2b offspring (in
    females only liver and kidney weights were reduced) at 50 ppm; F1b
    males receiving 30 ppm phosphamidon also had decreased liver, kidney,
    and testes weights. Relative brain weights of F1b males and females
    were increased in the 30 and 50 ppm dose groups and of F2b offspring
    at 50 ppm. The increase in relative brain weight reflects the
    decreased body weights of these animals. This was also true for heart
    and kidney weights in F2b weanlings. After macroscopic and
    microscopic examinations of F1b and F2b pups, no treatment-related
    findings were observed. Examination of craniofacial sections from
    F2a pups was performed because of the finding of hydrocephalus in
    the first teratogenicity experiment. On day 4 or day 21 postpartum no
    malformations or variations were noted.

         The NOEL in this study was 5 ppm (Holson, 1985a).

    Special studies on teratogenicity

    Rats

         Groups of 30 pregnant albino Sprague-Dawley rats were dosed by
    oral gavage with 0, 1, 2, or 4 mg phosphamidon (92.1% pure) in CMC/kg
    b.w./day from days 6 through 15 of gestation. All dams were sacrificed
    on day 20 of gestation and the fetuses were removed, weighed, and
    examined for sex and for external, visceral, skeletal, and head
    abnormalities.

         In the 2 and 4 mg/kg b.w./day groups increased incidences of oral
    and ocular discharge, hypoactivity, and tremours were observed. There
    was no mortality and none of the test animals delivered prematurely or
    aborted during the study. At 2 and 4 mg/kg b.w./day, mean body weight
    (actual and corrected for uterus weight) was decreased (significantly
    at 4 mg/kg b.w./day). The percentages of pregnant dams, number of
    corpora lutea, number of implantations, and number of pre-implantation
    losses were comparable among control and treated groups.

         Prenatal viability and death, mean fetal body weight, and sex
    ratios were not affected at any dose level. At 4 mg/kg b.w./day an
    increased incidence of fetuses with a body weight 30% less than the
    controls was noted, which was probably due to maternal toxicity. The
    incidence of external malformations was increased at 4 mg/kg b.w./day.
    Visceral and skeletal malformations were not observed. Hydrocephalus
    was observed in 2, 2, and 3 fetuses of the 1, 2, and 4 mg/kg b.w./day
    groups, respectively. Although the incidences were not statistically-
    significantly increased and no external observations of dome-shaped
    head were noted in any of the fetuses with suspected hydrocephalus,
    the finding of hydrocephalus was considered to be equivocal (Holson,
    1985b).

         In order to clarify the equivocal findings of hydrocephalus, a
    repeat study was initiated in which groups of 30 pregnant female
    albino Sprague-Dawley rats were dosed by oral gavage with 0, 0.5, 2,
    4, or 6 mg phosphamidon (92.1% pure) in CMC/kg b.w./day from days 6
    through 15 of gestation. All animals were killed on gestation day 20.
    Maternal gross lesions were observed and recorded as well as external,
    visceral, skeletal, and Bouin's head examinations on the removed
    fetuses.

         In the 2, 4, and 6 mg/kg b.w./day groups, increased incidences of
    salivation, ocular discharge (4 and 6 mg/kg b.w./day only), and
    tremours were observed. Twenty-four animals in the 6 mg/kg b.w./day
    group and 5 animals in the 4 mg/kg b.w./day group died during the
    dosing period. Pink pancreas and haemorrhages of the stomach were
    observed after necropsy and laparohysterectomy of animals in the 2
    highest dose groups.

         Statistical analysis was not carried out on maternal or prenatal
    data generated from the 6 mg/kg b.w./day group, due to the limited
    number of dams (less than 50%) surviving until scheduled death.

         The percentages of pregnant dams, number of corpora lutea, number
    of implantation sites, and number of pre-implantation losses were
    comparable among controls and all teated groups. Mean body weights
    (actual and corrected for uterine weight) of the dams were
    significantly reduced in the 2 and 4 mg/kg b.w./day dose groups. Mean
    fetal weight was significantly reduced at 4 mg phosphamidon/kg
    b.w./day. Significant differences were not observed between control
    and treated groups in prenatal viability, prenatal death, mean litter
    size of viable fetuses, or sex ratios. A range of variations was
    observed during skeletal, external, and Bouin's head examinations. In
    the 4 mg/kg b.w./day group, a significantly-increased combined
    incidence of either incompletely ossified sternebra 2, 5, and 6 or
    absent sternebra 2, 5, and 6 were noted. At the same dose level there
    was a significant increase in the incidence of fetuses having a body
    weight 30% less than the mean control. Both effects were probably
    secondary to the maternal toxicity observed in this dose group. No
    visceral or skeletal malformations were found, and there was no
    finding of hydrocephaly after evaluation of the head specimens of all
    fetuses. Fetotoxicity was not observed at 2 mg/kg b.w./day. Based on
    these data, the NOEL in this study was 0.5 mg phosphamidon/kg b.w./day
    for maternal toxicity. There was no evidence of any teratogenic effect
    in this study (Holson, 1985c).

    Rabbits

         Groups of 18 pregnant New Zealand white rabbits were dosed by
    oral gavage with 0, 1, 3, or 10 mg phosphamidon (91.8% pure) in CMC/kg
    b.w./day from day 6 to 18 of gestation. The dams were sacrificed on
    day 30 of gestation and removed fetuses were examined for external,
    skeletal, and visceral malformations. One dam in each dose group died,
    1 animal in each of the mid- and high-dose groups gave premature
    birth, and 1 animal in the 10 mg/kg b.w./day group aborted. At
    10 mg/kg b.w./day, mean body weights of the dams were significantly
    decreased. The number of pregnant dams, corpora lutea, implantations,
    and pre-implantation losses, as well as litter sizes, number of
    resorptions, prenatal viability, and fetal body weights were not
    affected by phosphamidon treatment. No treatment-related malformations
    were observed during external, visceral, or skeletal examinations. The
    NOEL in this study was 3 mg phosphamidon/kg b.w./day, based on
    maternal toxicity. Phosphamidon did not show teratogenic activity at
    the doses tested (Holson, 1985d).

    Special studies on mutagenicity

         For the results of mutagenicity studies with phosphamidon, see
    Table 1. Additionally, it was found that phosphamidon was mutagenic in
    several plant systems (Wuu & Grant, 1966; Reddy & Rao, 1969; Panda &
    Sharma, 1979; Srivastava & Sarma, 1979; Singh et al., 1979;
    Sharma et al., 1983).

    Special study on delayed neurotoxicity

         Twelve domestic hens, 12 months old and protected by atropine
    sulphate (10 mg/kg), received orally 30 mg phosphamidon (92.1%
    pure)/kg b.w. After an interval of 21 days, the same procedure was
    repeated. The dose of 30 mg/kg b.w. was chosen based upon the LD50
    of phosphamidon in laying hens ranging from 25 to 36 mg/kg b.w. A
    negative control group of 10 hens was treated with distilled water
    alone. A positive control group of 4 hens received a single oral dose
    of 1000 mg TOCP/kg b.w.

         No spontaneous mortality occurred, but 2, 2, and all 4 hens of
    the vehicle, dose, and positive control groups, respectively, were
    sacrificed before the end of the study, due to poor general condition.
    The animals of the TOCP group showed signs of severe ataxia. In the
    phosphamidon-treated animals, ataxia, hyper-irritability, trismus,
    ventral body position, and diarrhoea were observed, but after both
    applications (days 1 and 22), they recovered within 6 days. There were
    no indications of delayed neurotoxicity. In all hens of the positive
    control group, weight loss was observed, as well as progressive ataxia
    in the second week after administration. After neuro-pathological
    examination, no treatment-related changes were observed in the test
    group, whereas the positive control group developed neuropathy (Schoch
    & Krinke, 1985).

    Short-term study

    Dogs

         Groups of beagle dogs (8/sex/group) were orally administered in
    gelatine capsules 0, 0.05, 0.1, or 2.5 mg phosphamidon (91.8% pure)/kg
    b.w./day for 1 year. Interim sacrifice of 2 dogs/sex/group was carried
    out after 3 months of treatment. Two male and 2 female control dogs,
    and 1 male and 2 female dogs of the high-dose group, were sacrificed
    after a 4 week recovery period.

        Table 1.  Special studies on the mutagenicity of phosphamidon
                                                                                                                                              

    Test system                  Test object           Concentration           Purity                Results                  Reference
                                                       used                                 non-activated    activated
                                                                                                                                              

    In vitro
    Ames test                    S. typhimurium        25 - 2025 µg/plate      91.8%        negative         negative         Arni & Müller,
                                 strain:               TA98                                                                   1982
                                 TA100
                                 TA1535
                                 TA1537

    Mitotic gene conversion      S. cerevisiae         80 - 10,000             91.8%        negative         questionable     Arni & Müller,
      test                       strain D7             g/plate                                                                1983

    Back mutation test           S. cerevisiae         80 - 10,000             91.8%        negative         questionable     Arni & Müller,
                                 strain D7             g/plate                                                                1983

    Spot test reverse            E. coli               not given               not          negative         negative         Nagy et al., 1975
      mutation                   WP2                                           given

    Mouse lymphoma forward       mouse L5178Y          20.6 -33.0 nl/ml        91.8%        negative                          Beilstein &
      mutation assay             Tk+/- cells           65.0 - 1040 nl/ml       91.8%                         negative         Müller, 1983

    DNA repair test              human fibroblasts     2, 10, 50, & 250        91.8%                 negative                 Puri & Müller,
                                                       nl/ml                                                                  1983a

                                 rat hepatocytes       1, 5, 25 & 125 nl/ml    91.8%                 negative                 Puri & Müller,
                                                                                                                              1983b
                                                                                                                                              

    Table 1.  (cont'd).
                                                                                                                                              

    Test system                  Test object                Concentration              Purity             Results             Reference
                                                            used
                                                                                                                                              

    Chromosome aberration        human lymphocytes          1.9 - 61 µg/ml             not                positive            Georgian, 1975
      test                                                                             given

    In vivo

    Sister chromatid             Chinese hamster            oral, 1x 2.5, 5, &         91.8%              negative            Hool & Arni, 1983
      exchange test              bone marrow cells          10 mg/kg b.w.

    Nucleus anomaly test         Chinese hamster            oral, 2x (days 0) 2.5,     91.8%              questionable        Strasser et al.,
                                 bone marrow cells          5, & 10 mg/kg b.w.                                                1983

                                                            oral, 2x (days 0, 1)       91.8%              questionable        Strasser et al.,
                                                            3.5, 5.0, 7.1, &                                                  1983
                                                            10 mg/kg b.w.

                                 Chinese hamster bone       oral, 2x (days 0, 1)       92.1%              negative            Strasser et al.,
                                 marrow cells               1.67, 2.35, &                                                     1985
                                                            6.7 mg/kg

    Chromosome aberration        mouse spermatogonia        oral, 5x (days 0 - 4)      92.1%              negative            Strasser & Arni,
      test                                                  1.12 & 3.35 mg/kg                                                 1985

                                 mouse spermatocytes        oral, 5x (days 0, 2,       92.1%              negative            Strasser et al.,
                                                            3, 5, & 9) 2.2 &                                                  1986
                                                            6.7 mg/kg
                                                                                                                                              

    Table 1.  (cont'd).
                                                                                                                                              

    Test system                  Test object                Concentration              Purity             Results             Reference
                                                            used
                                                                                                                                              

    Micronucleus test            mouse bone marrow          oral, 2x (days 0, 1)       not                positive            Rani, 1980
                                                            5 mg/kg b.w.               given

    Host-mediated assay          S. typhimurium             i.p. 3x (days 0 - 2)       not                positive            Rani, 1980
                                 G-46, mouse                7.5 mg/kg b.w.             given

    Chromosome aberration        rat bone marrow            i.p. 0.07 - 9.56           not                positive            Georgian, 1975
      test                                                  mg/kg b.w.                 given

                                 mouse bone marrow          i.p. 0.07 - 9.56           not                positive            Georgian, 1975
                                                            mg/kg b.w.                 given
                                                                                                                                              
             One male dog in the 2.5 mg/kg b.w./day group had to be killed
    during week 24 due to poor general condition. In high-dosed dogs,
    vomiting was slightly increased. Mean body weight, food consumption,
    and food conversion were not adversely affected. Ophthalmoscopy and
    hearing tests showed no abnormal findings. Clinical analysis showed
    treatment-related effects on haematology and biochemical parameters.
    In high-dose males erythrocyte counts, haemoglobin concentrations, and
    haematocrits decreased significantly; alanine aminotransferase
    activity was increased, but at week 13 only. In males and females of
    the high-dose group, cholinesterase activity (measured by the Ellman
    method) was inhibited in plasma (20 - 30%), and erythrocytes
    (70 - 81%) at weeks 13 and 52; in the same group, brain cholinesterase
    was depressed (50%) at interim sacrifice and at the end of the
    administration period. During the 4 week recovery period, plasma and
    brain cholinesterase activities recovered completely, but inhibition
    in erythrocytes was still found (50%). Organ-weight ratios were not
    affected by phosphamidon treatment and no treatment-related effects
    were observed at macroscopic or microscopic examination. The NOEL was
    0.1 mg/kg b.w./day (Kobel et al., 1985).

    Long-term study

    Rats

         Groups of CD Sprague-Dawley (60 - 70/sex/group) rats were fed
    diets containing 0, 0.2, 0.8, 1, 30, or 80 ppm phosphamidon for 24
    months. The groups receiving 0.2 and 0.8 ppm phosphamidon were
    discontinued after 15 weeks.

         In the high-dose group, and to a lesser extent in the 30 ppm
    group, the incidences of crusty muzzle, irritability, foot-pad
    abnormalities, muscle tremours, yellow/brown-stained fur, and poor
    coat quality were significantly increased. Survival rates of rats in
    the treated groups were not significantly different from those of
    controls. Food consumption at 80 ppm was decreased initially, and
    increased in the majority of subsequent intervals, up to 1 year for
    males and up to 2 years for females. In males, growth was decreased at
    80 ppm throughout the study, and at 30 ppm during the first 3 months.
    Only a slight decrease in growth was observed in females at 80 ppm.
    Haemoglobin, haematocrit, and erythrocyte counts were decreased in
    males at 80 ppm and in females at 80 ppm after 18 and 24 months. A
    significant increase in Howell-Jolly bodies in the red blood cells was
    observed at final sacrifice in the 30 and 80 ppm male groups, and in
    the 80 ppm female group. Serum cholinesterase and brain cholinesterase
    activities were markedly inhibited in rats in the 30 and 80 ppm male
    and female groups. Erythrocyte cholinesterase activity was inhibited
    to a lesser extent at 80 ppm. Organ weights were not affected in a
    dose-related manner. In the 30 and 80 ppm dose groups, a variety of

    non-neoplastic alterations was observed. These alterations included
    ulcerative pododermatitis of the limbs, hyperkeratotic dermatitis of
    the tail, and inflammatory changes in the lung and liver. There were
    no differences in the incidence of neoplastic lesions between treated
    and control groups. The NOEL was 1 ppm phosphamidon in the diet
    (Mayhew & Wingard, 1986).

    COMMENTS

         Phosphamidon induced effects on litter size and pup viability at
    maternally-toxic dose levels in a rat-multigeneration study. In
    teratogenicity studies, fetotoxicity and maternal toxicity, but no
    teratogenic effects, were observed.

         A study with hens showed that phosphamidon did not induce delayed
    neurotoxicity.

         In a 1-year study in dogs, the main effect was inhibition of
    serum, erythrocyte, and brain cholinesterase activities at 2.5 mg/kg
    b.w./day. At 0.1 mg/kg b.w./day no effects were found. A long-term
    toxicity/carcinogenicity study in rats also revealed cholinesterase
    inhibition as the predominant effect. There was no increase in tumour
    incidence. In this study no effects were observed at 1 ppm.

         In mutagenicity studies, phosphamidon was negative in a number of
    in vitro test systems, except for 1 test on chromosome aberrations.
    Several in vivo tests on chromosome anomalies have been carried out
    in rodents. Reports submitted to WHO showed negative or questionable
    results, whereas literature data showed a positive effect.

         On the basis of the toxicological data and in view of the
    negative carcinogenicity study in rats, a full ADI was allocated.

    TOXICOLOGICAL EVALUATION

    LEVEL CAUSING NO TOXICOLOGICAL EFFECT

         Rat:      1 ppm, equivalent to 0.05 mg/kg b.w./day.
         Dog:      0.1 mg/kg b.w./day.

    ESTIMATE OF ACCEPTABLE DAILY INTAKE FOR MAN

         0 - 0.0005 mg/kg b.w.

    STUDIES WHICH WILL PROVIDE INFORMATION VALUABLE FOR THE CONTINUED
    EVALUATION OF THE COMPOUND

         Observations in man.

    REFERENCES

    Arni, P. & Müller, D. C 570 techn.: Salmonella/mammalian-microsome
    1982      mutagenicity test. Unpublished report dated 22 November 1982
              from Ciba-Geigy Ltd., Basle, Switzerland. Submitted to WHO
              by Ciba-Geigy Ltd., Basle, Switzerland.

    Arni, P. & Müller, D. C 570 techn.: Saccharomyces cerevisiae
    1983      D7/mammalian-microsome mutagenicity test in vitro.
              Unpublished report dated 29 September 1983 from Ciba-Geigy
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    Beilstein, P. & Müller, D. C 570 techn.: L5178Y TK+/- mouse lymphoma
    1983      mutagenicity test. Unpublished report dated 20 December 1983
              from Ciba-Geigy Ltd., Basle, Switzerland. Submitted to WHO
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    Georgian, L. The comparative cytogenetic effects of aldrin and
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    Holson, J.F. C 570 techn.: Two-generation reproduction study in albino
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    Holson, J.F. C 570 techn.: Teratology study in rats. Unpublished
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    Holson, J.F. C 570 techn.: Teratology study in rats. Unpublished
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    Holson, J.F. C 570 techn.: Teratology study (SEG II) in albino
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    Hool, G. & Arni, P. C 570 techn.: Sister Chromatid exchange study,
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    Kobel, W., Gretener, P. Zak, F., & Malinowski, W. C 570 techn.: One
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    See Also:
       Toxicological Abbreviations
       Phosphamidon (ICSC)
       Phosphamidon (PIM 454)
       Phosphamidon (FAO Meeting Report PL/1965/10/1)
       Phosphamidon (FAO/PL:CP/15)
       Phosphamidon (FAO/PL:1968/M/9/1)
       Phosphamidon (FAO/PL:1969/M/17/1)
       Phosphamidon (WHO Pesticide Residues Series 2)
       Phosphamidon (WHO Pesticide Residues Series 4)
       Phosphamidon (Pesticide residues in food: 1982 evaluations)