These compounds have not been previously evaluated by the Joint
    FAO/WHO Expert Committee on Food Additives. However, they were
    included in a toxicological monograph on aluminium published in 1977
    (see Annex I, Ref. 44). Additional data have become available. These
    data are summarized and discussed in the following monograph.

         The information included in the previous published monograph on
    aluminium has also been included.



    Special studies on teratogenicity and reproduction

         Groups each of 40 mice equally divided by sex were fed diets
    containing bread leavened with either yeast, or aluminium phosphate or
    alum. The presence of aluminium leavened bread in the diet resulted in
    a decreased number of offspring, as well as development of ovarian
    lesions (Schaeffer et al., 1928). In another study groups of mice were
    fed bread with yeast plus 4% physiological saline mixture or 13%
    saline mixture, or bread with alum phosphate baking powder (4.4% A1
    plus 4% saline mixture) or bread with alum phosphate powder (1.3% A1)
    for a period of 4 months. The presence of aluminium-treated bread
    resulted in a decreased number of offspring, as well as increased
    mortality of offspring during the first week of life. The ovaries of
    these animals contained a large number of atritic follicles, and were
    greatly reduced in size (Schaeffer et al., 1928).

         In another study, groups each of 24 rats were maintained on diets
    containing SAS powder (a mixture of sodium aluminium sulfate and
    calcium acid phosphate) at dietary levels equivalent to approximately
    0, 0.15, 1.8 or 0.44%.* Some of the test animals were bred for 7
    successive generations. The SAS had no effect on reproductive
    performance as measured by number of offspring, average birth weight,
    average weaning weight and number weaned. Histopathological
    examination of kidneys of rats that survived 21 months on the diet did
    not reveal any significant changes (Lymann & Scott, 1930).


    *    SAS baking powders contain ca. 20% sodium aluminium sulfate. Thus
         diet contained 400, 33 and 98 ppm (0.04, 0.0033 and 0.0098%)
         aluminium, respectively.

    Short-term studies


         Groups each of 40 mice equally divided by sex were fed diets
    containing bread leavened with aluminium (2.07 or 4.1 g Al/100 g
    bread) as aluminium phosphate baking powder for a period of 4 months.
    The groups fed bread leavened with aluminium salt developed serious
    lesions of the digestive tract (Schaeffer et al., 1928).


         Sodium aluminium phosphate (acidic) was administered to beagle
    dogs for 189 consecutive days (Katz et al., 1981) at dietary levels of
    0, 0.3, 1.0 or 3%. Each dose group consisted of 6 males and 6 females.
    The food intakes of all female test groups were sporadically lower
    than the control group, but no statistically significant differences
    in weekly mean body weights were evident between male or female test
    groups and their respective controls. There were no treatment-related
    effects seen in blood chemistry, haematology, urinalysis, or
    in ophthalmic and physical examinations. Gross necropsy and
    micropathological findings did not show any significant toxicological
    effects either. There was very mild renal tubular mineralization in
    both test and control groups with no significant difference in the
    frequency of occurrence or the degree of mineralization in the various


         Men were fed biscuits containing alum phosphate baking powder
    (ca. 8%) in addition to normal dietary items, and blood and urine
    samples were collected 2, 4, 6 and 8 hours after the meal.
    Aluminum was frequently found in the blood of control men (trace -
    0.1 mg/100 ml), and ingestion of the aluminium-rich diet caused
    occasional slight increase of levels of aluminium in the blood. Urine
    of man, before and after ingestion of the aluminium-rich diets, only
    contained small amounts of aluminium (less than 0.5 g excreted in 26
    hours) (Underhill et al., 1929).

         Aluminum antiacids may cause an inhibition of intestinal
    absorption of phosphorus and this may be followed by an increase in
    calcium loss. The effect is probably due to the binding of dietary
    phosphorus in the intestine by the aluminium. This effect was not
    observed when phosphorus-containing aluminium salts were used (Spencer
    & Lender, 1979).

         Patients with renal failure are at greater risk of aluminium
    overload, since administered aluminium is retained because of the
    functional impairment of the kidney (Alfrey et al., 1976). Dialysis
    encephalopathy has been associated with exposure of dialysis patients

    to excess aluminium (Schteeder, 1979). The possible relationship
    between increased brain aluminium and Alzheimer's disease has not been
    established (Crapper et al., 1976).


         Only minor amounts of orally administered aluminium salts are
    absorbed. However, patients with uraemia may absorb significant
    amounts of aluminium from orally administered aluminium compounds.
    Although high levels of aluminium in the diet have been reported to
    interfere with phosphate metabolism, presumably through the formation
    of insoluble aluminophosphate salts, this effect was not observed when
    phosphorus-containing aluminium salts were used. A recent study in
    dogs fed high levels of dietary sodium aluminium phosphate (up to 3%
    of the diet) failed to produce renal concretions that had been
    reported in earlier studies. There are no recent feeding studies in
    rodent species, although some of the earlier studies using aluminium
    phosphate baking powder have provided conflicting reports of a
    possible effect on reproduction.


    Level causing no toxicological effect

    Dog: 3% of the diet equivalent to 1250 mg/kg bw.

    Estimate of temporary acceptable daily intake for man

    0-6 mg/kg bw.


    Required by 1986

    (1) Absorption and metabolic studies preferably in man.

    (2) Short-term feeding study.

    (3) Multigeneration reproduction study.


    Alfrey, A. C., Le Gendre, G. R. & Kaehny, W. D. (1976) The dialysis
         encephalopathy syndrome. Possible aluminum intoxication. New
         England Journal of Medicine, 294, 184

    Crapper, D. R., Krishnan, S. S. & Quittkat, S. (1976) Aluminum,
         neurofilorillary degeneration and Alzheimer's disease, Brain,
         99, 67-80

    Katz, A. C. et al. (1981) A 6-month subchronic dietary toxicity study
         with Levain(R) (sodium aluminum phosphate, acidic) in beagle
         dogs, unpublished report by Stauffer Chemical Co., Farmington,
         Connecticut. Submitted to WHO by USFDA, 1982

    Lymann, J. F. & Scott, E. (1930) Effects of the ingestion of tartrate
         or sodium aluminum sulfate baking powder upon growth,
         reproduction and kidney structure in the rat, Amer. J. Hyg.,
         12, 271-282

    Schaeffer, G. et al. (1928) The dangers of certain mineral baking
         powders based on alum, when used for human nutrition, J. Hyg.,
         28, 92-99

    Schteeder, M. T. (1979) Dialysis encephalopathy, Arch. Intern. Med.,
         13, 510-511

    Spencer, H. & Lender, M. (1979) Adverse effects of aluminum-containing
         antiacids on mineral metabolism, Gastroenterology, 76,

    Underhill, F. P., Peterman, F. I. & Sperandeo (1929) Studies on the
         metabolism of aluminum. VII. A note on the toxic effects produced
         by subcutaneous injection of aluminum salts, Am. J. Physiol.,
         90, 76

    See Also:
       Toxicological Abbreviations