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    IMAZALIL

    EXPLANATION

         Imazalil was evaluated for acceptable daily intake by the Joint
    Meeting in 1977, and reviewed in 1980, 1984, and 1985 (Annex 1,
    FAO/WHO, 1978a, 1981a, 1985b, and 1986a). A toxicological monograph
    was published in 1977 (Annex 1, FAO/WHO, 1978b) and monograph addenda
    were published after each of the reviews (Annex 1, FAO/WHO, 1981b,
    1985c, and 1986c). The 1985 Joint Meeting was aware of several
    teratology studies that had not been submitted in full. Although 1 rat
    teratology study had been evaluated earlier, the 1985 Meeting wanted
    to review all the available teratology data, so it extended the
    temporary ADI pending the submission of these data. This monograph
    addendum summarizes these studies as well as other data on imazalil
    analogues that were submitted to the 1986 Joint Meeting for
    evaluation.

    EVALUATION FOR ACCEPTABLE INTAKE

    BIOLOGICAL DATA

    Toxicological studies

    Special studies on teratogenicity

    Mice

         Twenty-four female Cobs mice received orally 0, 2.5, 10, or 40 mg
    imazalil sulfate/kg b.w./day from days 6 through 16 of pregnancy. All
    animals were killed on day 19 of pregnancy. No effects were found on
    mortality, body weight, food consumption, pregnancy rate, number of
    live, dead, or resorbed fetuses, pup weight, or mean litter size.
    During gross observations, talipes valgus (club foot) was observed in
    all groups, the incidence not being significantly different in any
    dose group when compared to the control group. No additional
    abnormalities were seen after radiographic examinations and Lapras'
    sectioning technique (Marsboom et al., 1985).

    Rabbits

         Groups of 20 female New Zealand white rabbits received imazalil
    nitrate (purity 99.2%) in water by gavage at 0, 0.63, or 2.5 mg/kg
    b.w./day on days 6 to 18 of pregnancy. All surviving animals were
    killed on day 28 of pregnancy. Four females died during the test (3 in
    the control group and 1 in the 0.63 mg/kg b.w./day group). Body-weight
    gain of the dams was decreased in both dose groups, as well as average
    litter size, the percentages of live fetuses, and 24-hour survival
    rates. The percentages of resorbed fetuses increased with increasing
    dose. Retrospective statistical analysis showed that the effects on
    maternal body weight, litter size, and number of resorptions were not
    statistically significant. A small number of anomalies in all groups
    (hydrocephaly, fused ribs, and deformed legs) were considered to be
    non-dose related. Individual data were not available to the Meeting.
    In this study embryotoxic and maternally toxic effects were observed
    in both dose groups. Therefore, this study was repeated at lower
    dosages, as described in the next paragraph (Marsboom, 1974).

         Groups of 15 female New Zealand white rabbits received imazalil
    nitrate (purity 97.8%) in water by gavage at 0, 0.16, or 0.63 mg/kg
    b.w./day from days 6 to 18 of pregnancy. The surviving animals were
    killed on day 28 of pregnancy. Mortality (3 dams in the 0.16 mg/kg
    b.w./day group died during the study), body weight, and pregnancy rate
    were not significantly different among the groups. Mean litter size
    was normal in all groups, and no statistically-significant differences
    were seen with regard to the number of live, dead, or resorbed
    fetuses, birth weight, or 24-hour survival rate. Fetal skeletal
    examination and fetal sectioning revealed no compound-related
    abnormalities (Marsboom & Dirkx, 1981).

         Groups of 15 female New Zealand white rabbits received technical
    grade imazalil nitrate (purity 97.8%) in water by gavage at 0, 1.25,
    2.5, or 5 mg/kg b.w./day on days 6 - 18 of pregnancy. All animals were
    killed on day 28 of pregnancy. The dams were examined for mortality
    and body weight. The number of live, dead, and resorbed fetuses,
    litter size, survival rate, and pup weight were recorded and all live
    and dead fetuses were examined for gross pathology (fetal skeletal
    examination and fetal sectioning).

         One dam of the low-dose group and 1 of the high-dose group died
    during the study. Decreased body weight was observed in dams of the
    5 mg/kg b.w./day group. There were no differences with respect to the
    number of live, dead, or resorbed fetuses, litter size, number of
    implantations, or 24-hour survival rate. There was a slight decrease
    in pup weight at 5 mg/kg b.w./day. In 1 fetus of the high-dose group a
    split ninth thoracic vertebra on the right side, with each part having
    1 rib, was observed. Individual animal data were not available to the
    Meeting. The NOAEL for maternal toxic and embryotoxic effects was
    2.5 mg/kg b.w./day (Marsboom & Dirkx, 1985).

    Observations in humans

         Results of some clinical and non-clinical studies on the
    antifungal imidazoles miconazole, econazole, and ketonazole, which
    belong to the same chemical family as imazalil, were provided to the
    Joint Meeting. Clinical doses varied from 4 - 80 mg/kg b.w., and the
    routes of administration were dermal, inhalation, oral, or i.v.

         Occasional side effects of treatment of miconazole to patients
    were chills, dizziness, itching, skin rash, and diarrhoea. At high
    dose levels loss of appetite, nausea, and vomiting were seen. After
    prolonged treatment with miconazole in severely debilitated subjects
    and after oral treatment of 3 g/day for 9 weeks to normal volunteers,
    no adverse effects on renal, hepatic, or bone marrow functions were
    observed. Metabolism studies showed that the metabolic breakdown of
    miconazole was comparable in humans and rats (Brugmans et al., 1972;
    Symoens, 1977).

         Five days after oral administration of 500 mg (3H)-econazole to
    2 human subjects, the excretion of radioactivity was prolonged and
    incomplete (40% and 27% of the dose were found in the urine and
    faeces, respectively). Peak values in plasma of unchanged econazole
    and total radioactivity were reached 1.5 to 3 hours after adminis-
    tration, but the half-life of unchanged econazole (< 24 hours) in
    plasma was much shorter than that of the econazole metabolites. The
    main route of biotransformation of econazole in man involved multiple
    oxidation of the imidazole ring carbons followed by O-dealkylation and
    conjugation of the resulting alcohols, probably with glucuronic acid
    (Midgley et al., 1981).

         Kinetic studies with ketoconazole in man have shown that the drug
    is rapidly absorbed and widely distributed after oral administration.
    It is extensively metabolised by the liver to a series of inactive
    products, and is excreted mainly in the faeces. Plasma levels of
    ketonazole in man remained stable during chronic administration
    (Gascoigne et al., 1981).

    COMMENTS

         Additional teratogenicity studies in rabbits showed that in the
    first study there were maternally toxic and embryotoxic effects at
    both dose levels of 0.63 and 2.5 mg/kg b.w./day. However, these
    results could not be confirmed in 2 later studies. In the last one
    only minimal maternally toxic and embryotoxic effects occurred at
    5 mg/kg b.w./day and a NOAEL of 2.5 mg/kg b.w./day could be
    established. In an additional teratogenicity study in mice, no effects
    were observed at dosages up to 40 mg/kg b.w./day There were no
    indications of a teratogenic effect in any of the studies.

         Data on structurally-similar human antimycotic drugs indicated
    the improbability of adverse effects in man.

    TOXICOLOGICAL EVALUATION

    LEVEL CAUSING NO TOXICOLOGICAL EFFECT

         Rat:    100 ppm in the diet, equal to 5 mg/kg b.w./day
         Dog:    1.25 mg/kg b.w./day

    ESTIMATE OF ACCEPTABLE DAILY INTAKE FOR MAN

         0 - 0.01 mg/kg b.w.

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

         Observations in man.

    REFERENCES

    Brugmans, J., Van Cutsem, J., Heykants, J., Schuermans, V., &
    1972      Thienpont, D. Systemic antifungal potential, safety,
              biotransport and transformation of miconazole nitrate.
              Europ. J. Clin. Pharmacol. 5, 93 - 99.

    Gascoigne, E.W., Barton, G.J., Michaels, M., Meuldermans, W., &
    1981      Heykants, J. The kinetics of ketoconazole in animals and
              man. Clin. Res. Rev. 1, 177 - 187.

    Marsboom, R. Potential of oral R 18531 for embryotoxicity and
    1974      teratogenic effects in rabbits. Unpublished report No. 535
              from Janssen Research Laboratories. Submitted to WHO by
              Janssen Pharmaceutica N.V., Beerse, Belgium.

    Marsboom, R. & Dirkx, P. Imazalil: R 18531. Oral embryotoxicity and
    1981      teratogenicity study in New Zealand white rabbits
              (Segment II). Unpublished experiment No. 10816 from Janssen
              Research Laboratories. Submitted to WHO by Janssen
              Pharmaceutica N.V., Beerse, Belgium.

    Marsboom, R. & Dirkx, P. Imazalil: R 18531. Oral embryotoxicity and
    1985      teratogenicity study in New Zealand white rabbits
              (Segment II). Unpublished report No. 1482 from Janssen
              Research Laboratories. Submitted to WHO by Janssen
              Pharmaceutica N.V., Beerse, Belgium.

    Marsboom, R., Gillardin, J.M., & Sanz, G. R 27180 Imazalil.
    1985      Embryotoxicity and teratogenicity study in Cobs mice.
              Unpublished experiment No. 85-02 from Janssen Research
              Laboratories, submitted to WHO by Janssen Pharmaceutica
              N.V., Beerse, Belgium.

    Midgley, I., Biggs, S.R., Hawkins, D.R., Chasseaud, L.F., Darragh, A.,
    1981      Brodie, R.R., & Walmsley, L.M. The metabolic fate of
              (3H)econazole in man. Xenobiotica, 11, 595 - 608.

    Symoens, J. Clinical and experimental evidence on miconazole for the
    1977     treatment of systemic mycoses: A review. Proc. Roy. Soc.
             Med. 70, (Suppl. 1), 4 - 8.
    


    See Also:
       Toxicological Abbreviations
       Imazalil (ICSC)
       Imazalil (Pesticide residues in food: 1977 evaluations)
       Imazalil (Pesticide residues in food: 1980 evaluations)
       Imazalil (Pesticide residues in food: 1984 evaluations)
       Imazalil (Pesticide residues in food: 1984 evaluations)
       Imazalil (Pesticide residues in food: 1985 evaluations Part II Toxicology)
       Imazalil (Pesticide residues in food: 1991 evaluations Part II Toxicology)
       Imazalil (JMPR Evaluations 2000 Part II Toxicological)
       Imazalil (JMPR Evaluations 2001 Part II Toxicological)
       Imazalil (JMPR Evaluations 2005 Part II Toxicological)