FAO Nutrition Meetings Report Series 
    No. 46A WHO/FOOD ADD/70.36

    The content of this document is the result of the deliberations of the
    Joint FAO/WHO Expert Committee on Food Additives which met in Rome,
    27 May - 4 June 19691

    Food and Agriculture Organization of the United Nations

    World Health Organization

    1 Thirteenth report of the Joint FAO/WHO Expert Committee on Food
    Additives, FAO Nutrition Meetings Report Series, in press;
    Wld Hlth Org. techn.  Rep. Ser., in press.


    (includes: silica aerogel, hydrated silica, silicic acid, dehydrated
    silica gel, Kaolin, Talc and magnesium trisilicate)

    Silica, silicic acid and the (calcium, magnesium and aluminum salts
    occur ubiquitously in the environment and some have been used for many
    years medically. Food contains various amounts of SiO2, for example:
    potatoes 10.1, milk 2.1, drinking water 7.1, mineralwater 22.5, beer
    131 gamma SiO2 per g or cm3 (Bauman 1960).

    Biological Data

    Biochemical aspects

    Very small amounts of silica are normally present in all body tissues
    but there is no evidence that they play any physiological role.

    Silicic acid is a normal constituent of the union, where it is found
    as early as a few days after birth. The amount excreted in the urine,
    which varies considerably according to the diet, is in the order of
    10-30 mg per day (Thomas 1965). The silica content of human tissue
    varies from 10-200 mg/100 g dry weight (spleen 15 mg, lung 140 mg)
    (Unilever Research Laboratory 1964). The normal level of silicic acid
    in human blood is below 1 µg SiO2/cm3; the concentration in the
    corpuscles is practically the same as that in the plasma. Silicic acid
    is present in plasma in a molybdate reactive form and is not bound to
    protein or any other substance of high molecular weight. Ingested
    monomeric silicic acid rapidly penetrates the intestinal wall and
    becomes distributed throughout the whole extracellular fluid. It
    enters the blood corpuscles at a slower rate (Baumann 1960).

    Silica dust was administered intragestrically to rabbits and dogs
    leading to a rise in urinary silica output without significant
    variation in blood silica levels. Considerable absorption took place
    with peak excretion in dogs occurring between four to eight hours
    after administration. There appears to be little retention in any
    organ of the body even if animals ingest large amounts of silicates in
    their food. Intragastric five per cent. silicic acid administered to
    dogs leads to considerable absorption and urinary excretion, peak
    excretion occurring between three to eight hours after dosing. I.V.
    infusion of neutralized sodium silicate (1 mg/ml) in dogs leads to
    rapid urinary elimination of about 50 per cent. of the dose (King et
    al., 1933).

    In experiments with two volunteers, it was shown that, after ingestion
    of 50 mg of monomeric silicic acid in 50 cm3 liquid, the renal
    excretion of SiO2 per time unit was not related to the quantity of
    urine excreted in the same time unit. Maximum excretion appeared after
    one to two hours. Even at high concentrations up to more than 700µg
    SiO2/cm3 urine, the silicic acid was still present in a molybdate

    reactive form. Silicic acid polymerizes above 100-150 gamma
    SiO2/cm3. The speed of polymerization is dependent on ph and
    concentration. The experiment was designed so as to exclude damage to
    the urinary tract through precipitation of proteins by polymeric
    silicic acid formed by polymerization of monomeric silicic acid at
    high concentrations. If the urine at concentration. in the order of
    700 gamma SiO2/cm3 was taken at longer intervals, such as two
    hours, the concentration of monomeric silicic acid as below the total
    SiO2 concentration, thus suggesting that some polymerization had
    taken place, There was no indication of storage breakdown of
    reabsorption (Baumann 1960).

    Administration of 5 g of the siliceous materials listed below in 20 ml
    of milk by stomach tube to cats showed the following urinary excretion
    within 120 hours; silicic acid (fresh) 43.3, calcium silicate 37.2,
    magnesium trisilicate 34.1, silicic acid (moist) 29.0, SiO2 (quarz)
    (air sediment very fine) 20.8, magnesium silicates (talc) 9.2,
    diatomaceous earth 8.8 and calcium silica aluminate hydrate (kaolin)
    7.6 mg SiO2. From this it can be observed that free silica is
    attacked to a variable extent depending on its physical and chemical
    condition. Several silicates are apparently unattacked, as non-treated
    animals excreted an average of 8.6 mg in 120 hours. Some complex
    silicates appear to suffer partial decomposition by the hydrochloric
    acid of the stomach, with partial solution of same of the products in
    the intestine (King et al. 1938).

    Oral administration of a single dose of 2.5 g of amorphous polymeric
    silicon dioxide (99.8 per cent. SiO2 content of the water free
    compound) to 12 volunteers caused a slight but statistically
    insignificant increase in the silicon dioxide level of the urine
    (Langendorf et al., 1966).

    "Quarz water" (water in which silicic acid had been dissolved as a
    result of contact with quarz powder) given to rats over a prolonged
    period as the only source of liquid intake did not show any SiO2
    storage in tissues (Klösterkotter 1956).

    In vitro investigations on slices of tissue showed that monomeric
    silicic acid penetrated liver and kidney cells easily, whereas spleen
    and muscle cells were more or less impenetrable (Kirsch 1960).

    Ten gamma mononmeric SiO2/cm3 was shown in vitro to damage the
    enzymes of isolated mitochondria in rat liver (Hanger et al., 1963).

    Acute toxicity

    Animal    Route           LD50          Reference
                        (mg/kg body-weight)

    Rat       Oral             3.16         Elsea, 1958a

    The oral LD5 in mice of finely ground silicic acid is > 5 g/kg body
    weight (Kimmerle 1968).

    Rabbits receiving 3 mg of silicon in their conjunctival sac showed
    mild irritation for 48 hours (Elsea 1958a).

    A single dose of 50 mg of monomeric silicic acid in 50 cm3 liquid was
    tolerated by two volunteers. Higher doses should be taken either with
    more liquid or at intervals of about 20 mins. in order to avoid
    polymerization of silicic acid in the urine (Baumann 1960). A single
    dose of 2.5 g of amorphous polymeric silicon dioxide to volunteers did
    not significantly raise the SiO2 excretion in the urine thus
    suggesting poor absorption of the compound (Langendorf 1966).

    The probable lethal dose of silica (oral) for man is over 15 g/kg body
    weight. The probable oral lethal dose of magnesium trisilicate for man
    is over 15 g/kg body weight. There is same doubt as to whether large
    doses cause laxation. The probable oral dose for man of sodium
    silicate lies lower at between 0.5 and 5 g/kg and may well be due to
    its alkalinity (Unilever Research Laboratories 1964). Data on
    inhalation toxicity of silica and silicates are not relevant to
    consideration of toxic hazard by the oral route.

    Short-term studies

    Rat. Oral administration of 50 mg amorphous silica to rats for three
    months did not cause any toxic effects but no experimental details are
    available (Malten et al., 1964). Micronized silica gel was fed to four
    groups of ten male rats each in their diet at 0 per cent., 0.2 per
    cent., 1.0 per cent. and 2.5 per cent. levels for 28 days. No adverse
    effects on mortality or abnormal gross autopsy findings were
    discovered. Body weight gain was significantly reduced at the 2.5 per
    cent. level and nearly significantly at the 1.0 per cent. level. No
    other parameters were examined (W. R. Grace & Co., 1958).

    Fifteen male and 15 female rats received daily 50 mg of amorphous
    polymeric silicone dioxide (99.8 SiO2 content of water free
    compound) by stomach tube for three months. There was no adverse
    effect an body weight gain and mortality. Pathology of organs not
    enumerated showed no abnormalities in comparison with the controls
    (Kuschinsky 1955).

    Groups of 15 male and 15 female rats were fed diets containing silica
    at concentrations of 0.0, 1.0, 3.0 and 5.0 per cent. for 90 days. A
    fifth positive control group received a diet containing 3.0 per cent.
    cosmetic talc. No evidence of systemic toxicity caused by silica was
    found in terms of survival, body weights and food consumption. No
    appreciable deposition of silicon dioxide was seen in the kidney,
    livers, spleen, blood and urine in the animals fed at the five per
    cent. level. No gross or microscopic pathology attributable to silicon
    were seen (Elsea 1958b).

    The same compound was fed to 20 male and 20 female rats at a
    concentration of 500 mg/kg body weight per day for six months. The
    same number of animals served as the control. After four and a half
    months five females were mated. No adverse effects were noted on
    mortality, body weight gain, haematology (haemoglobin, erthrocyte- and
    leucocyte-count) and reproductive performance. Histopathology of
    stomach, intestines, pancreas, liver and kidney of the test group
    showed no significant difference to that of the control group. Litter
    size, birth weight and morphological development of the offspring as
    well as weight gain were normal (Leuschner 1963).

    In a similar experiment (see Leuschner 1963) the same results were
    obtained when feeding a hydrophobic preparation of amorphous polymeric
    SiO2 in which some of the silanol groups on the surface reacted with
    dimethyl-dichlorosilane (98.5 per cent. SiO2 content of water free
    compound) (Leuschner 1965).

    The compound (see Leuschner 1965) was also fed to groups of five male
    and five female rats at levels of 0, 500, 1000, 2000 mg/kg body weight
    for five weeks. The highest level was raised after 14 days to 4000,
    after 28 days to 8000 and after 42 days to 16 000 mg/kg body weight.
    When the level was raised to 16 g/kg, all animals lost weight and four
    animals died. Seven days after the level had been raised to 8000
    mg/kg, the animals did not gain weight normally. At 1000 mg/kg two
    rats out of 10 showed slight changes in the liver epithelia. At higher
    levels atrophy of the liver epithelia, regression of the basophilic
    structure and glycogen content were observed. Histopathology of other
    organs (not enumerated) including the kidney of the animals at all
    levels showed no significant changes compared with the controls
    (Leuschner 1964).

    Rabbit. The dermal effects of silica was tested on groups consisting
    of two male and two female rabbits at levels of five and 10 g/kg/day.
    A negative control group received methyl cellulose solution (0.5 per
    cent. w/w) and a positive control group received 10 g/kg/day of
    cosmetic talc. Applications were made five days/week for three weeks.
    No evidence of systemic toxicity caused by silica was found in terms
    of body weight, behaviour, silicon content of blood, urine, spleen,
    liver and kidney. No gross or microscopic pathology was seen in the
    major organs examined or in the skin (Elsea 1958c).

    Man. 60-100 g daily for three to four weeks of 12 per cent.
    amorphous silicic acid administered orally to patients suffering from
    gastritis or enteritis were tolerated without adverse effects. Only
    one thousandth of the substance administered was excreted in the urine
    (Sarre 1953).

    Long-term studies

    None available.


    The available data on orally administered silica and silicates,
    including flumed silicate dioxide, appear to substantiate the
    biological inertness of these compounds. Any silicate absorbed is
    excreted by the kidneys without evidence of toxic emulation in the
    body. Methods for estimating silica in body tissues have been greatly
    improved in recent years making some of the earlier data somewhat less
    valuable. A number of short-term studies in two species are available.
    This information taken together with human clinical experience and the
    ubiquitous occurrence of these compounds in the environment does not
    point to any significant toxic effects when these substances are used
    as food additives.


    Not limited except for good manufacturing practice.


    Baumann, H. (1960) Hoppe-Seylers Z. physiol. Cbemie., 320, 11

    Elsea, J.R. (1958a) Unpublished report, January 8, from Hazleton
    Laboratories, Inc.

    Elsea, J. R. (1958b) Unpublished report, July 11, from Hazleton
    Laboratories, Inc.

    Elsea, J.R. (1958c) Unpublished report, May 6, from Hazleton
    Laboratories, Inc.

    Hanger, R., Kirsch, K. & Standinger, Hj. (1963)
    Beitr.Silikose-Forsch.S-Bd Grundfragen Silikoseforsch Bd. 5, 69

    Keller, J. G. (1958) Unpublished report to W. R. Grace & Co.

    Kimmerle (1968) unpublished report submitted by Bayer

    King, E. J. Stantial, H. & Dolan, M. (1933) Biochem. J., 27, 1002

    King, E. J. &, McGeorge, M. (1938) Biochem. J., 32, 426

    Kirsch, K. (1960) Beitr. Silikose-Forsch. S-Bd. Grundfragen der
    Silikoseforsch., 4, 33

    Klosterkötter (1956) Diskussionsbemerkung,  Beitr. Silikose-Forsch.
    S-Bd. Grundfragen Silikoseforsch. Bd., 2, 348

    Kuschinsky, G. (1955) Unpublished summary report submitted by Degussa

    Langendorf, H. von & Lang, K. (1966) Zeitschrift für
    Ernährungswissenschaft, 8, 27

    Leuschner, F. (1963) Unpublished report submitted by Degussa

    Leuschner, F. (1964) Unpublished report submitted by Degussa

    Leuschner, F. (1965) Unpublished report submitted by Degussa

    Malten, K. E. & Zielhuis, R. L. (1964) Industrial Toxicology and
    Dermatology in the Production and Processing of Plastics, Elsevier,

    Sarre, H. (1953) Unpublished summary report submitted by Degussa

    Thomas, K. (1965) Dtsch. Zeitschr. f. Verdaunngs-u.
    Stoffwechsel-Krankheiten 25, 260

    Unilever Research Laboratory (1964) Report No. CH 64888, dated 21
    October 1964

    See Also:
       Toxicological Abbreviations