IPCS INCHEM Home

    MALTOL

    Explanation

         This substance was evaluated for acceptable daily intake for man
    (ADI) by the Joint FAO/WHO Expert Committee on Food Additives in 1967
    and 1978 (see Annex, Refs. 14 and 48). Toxicological monographs were
    issued in 1968 and 1978 (see Annex, Refs. 15 and 50).

         Since the previous evaluation, additional data have become
    available and are summarized and discussed in the following monograph.
    The previously published monograph has been expanded and reproduced in
    its entirety below.

    BIOLOGICAL DATA

    BIOCHEMICAL ASPECTS

         No data available.

    TOXICOLOGICAL STUDIES

    Special studies on mutagenicity

         Maltol gave a positive response when tested for mutagenicity in
    the Ames plate assay system using Salmonella typhimurium strain
    TA-100. The mutagenic activity was not affected by the addition of a
    liver activation system. Maltol was not mutagenic to the TA-98 strain
    (Bjeldanes et al., 1979).

    Special studies on reproduction

    Rat

         A three-generation reproduction study was carried out on rats
    [Charles River Crl:COBS-CD(SD)BR(France)] using groups of 20 male and
    20 female rats for the production of each generation. Dosage levels of
    0, 100, 200 or 400 mg/kg of maltol was administered in the diet.
    During the course of the study on day 134 (F1 generation) all animals
    showed signs of sialodacryodenitis, a contagious disease of viral
    origin. No deaths occurred from this disease and signs regressed
    within 10 days.

         Criteria evaluated were body weight and food consumption of
    parents, fertility index, mating index, gestation index, survival
    index and sex ratio of each generation. At birth all offspring were
    examined for gross morphological abnormalities. Maltol had no effect
    on copulation rate, mating viability index, lactation index, 21-day
    survival index and sex ratios were within normal limits. Differences

    in growth rate of the pups appears to be related to the outbreak of
    sialodacryodenitis in the colony. No specific compound-related
    abnormalities or lesions were reported in the pups (King et al.,
    1978b).

    Acute toxicity
                                                                 

                             LD50
    Animal         Route  (mg/kg bw)        Reference
                                                                 

    Mouse          Oral       550    Dow Chemical Company, 1967

    Rat            Oral     1 410    Dow Chemical Company, 1967

    Guinea-pig     Oral     1 410    Dow Chemical Company, 1967
      (male)

    Rabbit         Oral     1 620    Dow Chemical Company, 1967
      (male)
                                                                 

    Short-term studies

    Mouse

         Charles River CD-1 mice in groups of 50 animals per sex per dose
    group were given 0, 100, 200 or 400 mg/kg maltol in the diet for up to
    six months. An interim sacrifice was conducted on half the animals in
    each group at three months and the liver, kidney and testes examined
    microscopically. A complete range of tissues was examined in the
    animals sacrificed at the end of the study. At the beginning of the
    study two animals in the 400 mg/kg group and one in the 100 mg/kg
    group died and another animal in the 100 mg/kg group was sacrificed in
    moribund condition. Body weight gain was lower in the high and mid
    dose males, but the effect was not statistically significant. No
    differences between dosed and control animals were reported with
    respect to gross or microscopic pathology organ weights, clinical
    signs or clinical chemistry (Marshall & Bouchard, 1980).

    Rat

         Groups of 15 males and 15 females were fed 0 and 1.0% maltol for
    six months without adverse effect on growth, survival, organ weights,
    haematology and microscopic appearance of major organs (Dow Chemical
    Company, 1967).

         Groups of Charles River rats, 25/sex, were fed diets containing
    0, 100, 200 or 400 mg/kg bw maltol in the diet for six months.

         No treatment-related effects were reported on mortality, gross or
    microscopic pathology or clinical signs. There were no statistically
    significant differences in body weight gain between dosed and control
    animals, although body weights were lower in the high dose female
    throughout the study. There were small but statistically significant
    increases in cholesterol and creatinine levels in the high dose males.
    Small statistically significant increases were also observed in the
    absolute and relative liver weights of the high dose males (Marshall &
    Bouchard, 1980).

    Dog

         Groups of four dogs, not necessarily distributed according to
    sex, were given maltol by capsule at levels of 0, 125, 250 and
    500 mg/kg/day, for 90 days.

         By day 41 dogs at the 500 mg/kg dose level had died. Signs of
    death suggested liver damage and red cell destruction, in addition to
    which emesis, ataxia and finally prostration were noted.

         Histological examination revealed pulmonary oedema, pericentral
    and midzonal hepatic necrosis, fatty degeneration of the myocardium,
    adrenal cortical and medullary necrosis and testicular degeneration.

         Elevated serum bilirubin was seen in the 500 mg/kg dose level
    group and at 30 days in the 250 mg/kg dose level group. Histologically
    the 250 mg/kg dose level group showed a moderate number of Kupffer
    cells containing haemosiderin and small amounts of intracellular
    bilirubin. At the 125 mg/kg level only a moderate number of
    haemosiderin-laden Kupffer cells were observed (Gralla et al., 1969).

         Beagle dogs in groups of 4/sex were given daily for three months
    0, 100, 200 or 300 mg/kg bw of maltol by capsule. No treatment-related
    effects were noted on gross or microscopic pathology, clinical
    chemistry, haematology or clinical signs. Compared to controls, the
    treated females exhibited lower body weights throughout the study. The
    high dose group had the lowest body weights (Marshall & Bouchard,
    1980).

    Long-term studies

    Mouse

         Groups each of 100 mice (Charles River CDI) equally divided by
    sex were maintained on diets containing maltol at levels of 0, 100,
    200 or 400 mg/kg for a period of 18 months.

         There were not significant differences in survival between test
    and control groups. The mean body weights of male mice in the
    400 mg/kg group were significantly lower than controls. Blood
    chemistry at sacrifice was within normal limits with the exception of
    plasma urea which was significantly elevated in males in the 400 mg/kg
    maltol group, and a dose-related increase in serum alkaline
    phosphatase in all female test groups. No dose-related haematological
    changes were observed. Ophthalmic observations at six, 12 and 18
    months showed no compound-related ocular lesions. At autopsy, the
    relative organ/body weight ratio was similar for test and control
    animals with the exception of the kidney and testes weights of males
    in the 400 mg/kg group, which were significantly lower than controls.
    Histological examination of tissues and organs did not show any
    compound-related lesions except for the testes. Focal testicular
    atrophy was observed in both control and test males, but was most
    severe in the 400 mg/kg group (King et al., 1978a).

    Rat

         A two-year study was carried out in the F1 generation of rats
    [Charles River Crl:COBS-CD(SD)BR(France)] derived from parents exposed
    to diets containing maltol at 0, 100, 200 or 400 mg/kg of diet. After
    weaning the rats (groups of 100 equally divided by sex) were
    maintained on the appropriate diets containing maltol. The rats were
    mated on days 189 and 245 respectively of the study to provide the
    F2a and F2b generations of a three-generation reproduction study.
    During the course of the study on days 134 and 418 respectively all
    animals showed signs of sialodacryodenitis, a contagious disease of
    viral origin. No deaths occurred from this disease and signs regressed
    within 10 days.

         There were not significant differences in survival between test
    and control animals. Ophthalmic examinations of the high and control
    groups performed at months 12, 18 and 24 showed no compound-related
    eye lesions. Blood chemistry and haematology at sacrifice showed that
    test and control animals were similar and within normal limits with
    the exception of significant increases in K+, Cl-, urea and
    bilirubin in the 400 mg/kg male and female groups, and urea and K+
    in the 200 mg/kg male group. The gross and microscopic examination of
    tissues and organs showed no compound-related lesions, nor was there
    any indication that maltol had an effect upon tumour incidence (King
    et al., 1978b).

    Comments

         In an 18-month study in the mouse at the highest dose tested
    (400 mg/kg bw), focal testicular atrophy was significantly greater
    than in controls. This effect has not been observed in the rat, and
    there were no compound-related effects in a three-generation

    reproduction study in the rat. A two-year feeding study in the rat
    showed some changes in serum clinical chemistry in the high dose
    groups. However, there were no gross or microscopic compound-related
    lesions.

         Elevated serum bilirubin and the occurrence of Kupffer cells
    containing haemasiderin was reported in dogs fed maltol at 250 and
    500 mg/kg/day for 30 days. However, this effect was not observed in
    another study in which dogs were dosed with maltol at levels up to
    300 mg/kg/day for a period of three months.

         Although maltol has been shown to be mutagenic in one strain of
    S. typhimurium (TA-100), there is no indication that maltol had an
    effect on tumour incidence in the two-year study in rats, and an
    18-month study in mice.

    EVALUATION

    Level causing no toxicological effect

    Rat: 100 mg/kg bw.

    Estimate of acceptable daily intake for man

    1 mg/kg bw.

    REFERENCES

    Bjeldanes, L. F. & Chew, H. (1979) Mutagenicity of 1,2-dicarbonyl
         compounds: maltol, kojic acid, diacetyl and related studies,
         Mutagenic Research, 67, 367-371

    Dow Chemical Company (1967) Unpublished report

    Gralla, E. J. et al. (1969) Toxicity studies with ethyl maltol,
         Toxicol. appl. Pharmacol., 15, 604-613

    King, T. O. et al. (1978) Three-generation and carcinogenicity study
         in rats. Unpublished data. Research Center, Pfizer, France
         Protocol 74107-Maltol

    King, T. O. et al. (1978a) 18-month mouse study with maltol.
         Unpublished data. Research Center, Pfizer, France Protocol 75-009

    Marshall, G. A. & Bouchard, E. F. (1980) Six-month oral toxicity study
         in rats. Unpublished data. Research Center, Pfizer, France
         Protocol 79031

    Marshall, G. A. & Bouchard, E. F. (1980) Six-month oral toxicity study
         in mice. Unpublished data. Research Center, Pfizer, France
         Protocol 79031

    Marshall, G. A. & Bouchard, E. F. (1980) Six-month oral toxicity study
         in dogs. Unpublished data. Research Center, Pfizer, France
         Protocol 79031
    


    See Also:
       Toxicological Abbreviations
       Maltol (FAO Nutrition Meetings Report Series 44a)
       Maltol (WHO Food Additives Series 13)
       MALTOL (JECFA Evaluation)