SODIUM ALUMINIUM PHOSPHATE (ACIDIC AND BASIC)
Explanation
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.
BIOLOGICAL DATA
TOXICOLOGICAL STUDIES
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
Mice
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).
Dog
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
groups.
OBSERVATIONS IN MAN
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 µg 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).
Comments
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.
EVALUATION
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.
FURTHER WORK OR INFORMATION
Required by 1986
(1) Absorption and metabolic studies preferably in man.
(2) Short-term feeding study.
(3) Multigeneration reproduction study.
REFERENCES
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,
603-606
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