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Toxicological evaluation of some food additives including anticaking agents, antimicrobials, antioxidants, emulsifiers and thickening agents


The evaluations contained in this publication were prepared by the Joint FAO/ WHO Expert Committee on Food Additives which met in Geneva,
25 June - 4 July 19731

World Health Organization

1Seventeenth Report of the Joint FAO/WHO Expert Committee on Food Additives, Wld Hlth Org. techn. Rep. Ser., 1974, No. 539;
FAO Nutrition Meetings Report Series, 1974, No. 53.



These compounds have been evaluated for acceptable daily intake by the Joint FAO/WHO Expert Committee on Food Additives (see Annex 1, Ref. No. 20) in 1969.

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 is reproduced in its entirety below.



Silica, silicic acid and the calcium, magnesium and aluminium 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, mineral-water 22.5, beer 131 gammaSiO2 per g or cm3 (Baumann, 1960).

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 urine, 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 to 30 mg per day (Thomas, 1965). The silica content of human tissue varies from 10 to 200 mg/100 g dry weight (spleen 15 mg, lung 140 mg) (Anon., 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 extra-cellular fluid. It enters the blood corpuscles at a slower rate (Baumann, 1960).

Silica dust was administered intragastrically 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 5% 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% of the dose (King et al., 1933).

Rats receiving silica flour, powdered sand or magnesium trisilicate orally in large amounts were shown to have crystals of these substances in uninflammated myocardium. Entry was via the intestinal epithelium (Reimann et al., 1965, 1966). Using histochemical techniques lysosomal damage was demonstrated in macrophages which had ingested silica particles (Nadler & Goldfischer, 1970).

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 silico 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 nontreated 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 some of the products in the intestine (King & McGeorge, 1938).

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

Very small amounts of silica are normally present in all body tissues. Recently it was found that silicon meets the criteria for an essential trace element in the chick (see short-term studies).


Special studies on carcinogenicity

See under long-term studies.

Special studies on reproduction

Rat: A two-generation reproduction study with the oral administration of 100 mg/kg bw per day amorphous silica to rats was conducted simultaneously. The parent generation (one male and five females) produced five litters with a total of 25 rats. Half a year later one male and five females of the first generation were mated; the number of animals in the second generation was 21. Neither malformation nor any other adverse effects were noted (Mosinger, 1969).

Acute toxicity
   LD50  Reference  AnimalRoute(mg/kg bw)
    Rat  Oral   3.16 Elsea, 1958a
   The oral LD5 in mice of finely ground silicic acid is >5 g/kg bw (Kimmerle, 1968).

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

The probable lethal dose of silica (oral) for man is over 15 g/kg bw. The probable oral lethal dose of magnesium trisilicate for man is over 15 g/kg bw. There is some 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 (Anon., 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 & Zielhuis, 1964). Micronized silica gel was fed to four groups of 10 male rats each in their diet at 0%, 0.2%, 1.0% and 2.5% 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% level and nearly significantly at the 1.0% level. No other parameters were examined (Keller, 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 on 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% for 90 days. A fifth positive control group received a diet containing 3.0% 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 5% 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 bw 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, erythroctye- 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% 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 bw 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 bw. 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).

Fifteen rats of each sex were fed one of the four silicon compounds (silicon dioxide, aluminum silicate, sodium silicate and magnesium trisilicate) for four weeks at the same levels used in the
dog experiment (see below). Polydipsia, polyuria, and soft stools, seen intermittently in a few animals fed magnesium trisilicate or sodium silicate, were the only clinical symptoms observed. No compound-related lesions were seen in any of the rats (Newberne & Wilson, 1970).


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% 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).


Pure-bred beagles of both sexes about six months of age were  fed either silicon dioxide, aluminum silicate, sodium silicate or magnesium trisilicate for four weeks. The doses used provided approximately equivalent amounts of silicon dioxide as the end product (0.8 g/kg/day). Group sizes ranged from six to nine dogs of each sex. Polydipsia and polyuria were observed in a few animals fed sodium silicate and magnesium trisilicate. All clinical tests on blood and urine were within normal limits. However, histopathologic studies revealed characteristic renal lesions in all dogs fed sodium silicate or magnesium trisilicate but none in the other groups. The lesions were visible grossly in all but one animal (Newberne & Wilson, 1970).



Day-old deutectomized cockerels were kept in a trace element controlled environment and fed a synthetic low silicon diet. The diet of the test groups was supplemented with sodium metasilicate (Na2SiO3œ9H2O) at a level of 100 mg/kg. 114 chickens were in the control groups and 114 chickens in the test groups. Growth rates and the appearance of the animals were evaluated at two- to three- day intervals. The animals were killed at the end of a 25- to 35- day period. Gross pathology and histological examinations were carried out on the organs of each chick. Differences between the chicks on the basal and silicon-supplemented diets were noted after one to two weeks. 

At the twenty-third day of the study the average weight for the low silicon group was 76 g compared to a weight of 116 g for the supplemented group (p <0.02). The average daily weight gain for the control groups was 2.57 g and that of the test groups reached 3.85 g (p < 0.01).

The animals on the basal diet were smaller and all their organs appeared relatively atrophied as compared to the test chickens. The leg bones of the deficient birds were shorter, of smaller circumference and thinner cortex. The metatarsal bones were relatively flexible and the femur and tibia fractured more easily under pressure than those of the supplemented group. Thus the effect of silicon on skeletal development indicates that it plays an important role in an early stage of bone formation (Carlisle, 1972).



Long-term studies


Twenty male and 20 female Wistar rats, with starting weights of  70 g, received daily one feed pellet containing amorphous silica (>98.3% SiO2) prior to feeding for two years. The silica content of pellets was regularly adjusted in order to ensure a steady consumption of 100 mg/kg bw per day. The animals were fed a synthetic diet. At the end of two years the survival rates of both male and female rats were 100%. No adverse effects on behaviour, clinical signs and weight gain were noted. The pathologic results of test groups were comparable with those of the controls. No evidence of carcinogenic effects was obtained.


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 minutes 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 mean 24-hour excretion of SiO2 in five male subjects on regular diet was 16.2 mg. The value varied widely and was related to the amount of SiO2 in the diet. Urinary silica excretion was increased in healthy subjects when Mg2Si3O8 n H2O was taken by mouth (Page et al., 1941).

Sixty to 100 g daily for three to four weeks of 12% 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).

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 700 µg SiO2/cm3 urine, the silicic acid was still present in a molybdate reactive form. Silicic acid polymerizes above 100-150 gammaSiO2/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 concentrations in the order of 700 gammaSiO2/cm3 was taken at longer intervals, such as two hours, the concentration of monomeric silicic acid was below the total SiO2 concentration, thus suggesting that some polymerization had taken place. There was indication of storage breakdown of reabsorption (Baumann, 1960).

Oral administration of a single dose of 2.5 g of amorphous polymeric silicon dioxide (99.8% 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).

Observations in humans indicated that various conditions such as lung diseases, chronic diseases and especially growth retardation in children were associated with silicon deficiency. Therefore he recommended silicon therapy for conditions characterized by under-developed and/or damaged mesenchymal tissues (Monceaux, 1973).

The available data on orally administered silica and silicates, including flumed silicon dioxide, appear to substantiate the biological inertness of these compounds. Any silicate absorbed is excreted by the kidneys without evidence of toxic cumulation in the body, except for the reported damage to dog kidney by magnesium trisilicate and sodium silicate. 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.

Talc and magnesium silicate are specified free from asbestos-like particles. This stipulation is made while acknowledging the fact that existing methods for estimating asbestos-like particles in talc and magnesium silicate are not yet fully adequate.


Estimate of acceptable daily intake for man
(a)  Silicon dioxide and certain silicates except magnesium silicate and talc: Not limited.*
(b)  Magnesium silicate and talc: Temporarily not limited.*

Required by June 1976.
(1)  For magnesium silicate studies to elucidate the reported kidney damage in dogs. Long-term feeding studies on talc demonstrated to be free from asbestos-like particles.
(2)  A satisfactory method for estimating asbestos-like particles in talc and magnesium silicate.

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

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

Carlisle, E. M. (1972) Silicon: an essential element for the chick, Science, 178, 619

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

*See relevant paragraph in the seventeenth report (pages 10-11).

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 Ernührungswis senschaft, 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, p. 204

Monceaux, R. H. (1973) La silice, problème biologique médical et social de grande actualité,
Unpublished report submitted by Degussa, Paris

Mosinger, M. (1969) Unpublished report submitted by Degussa

Nadler, S. & Goldfischer, S. (1970) J. Histochem. Cytochem., 18, 368

Newberne, P. & Wilson, R. B. (1970) Proc. Natl. Acad. Sci., 65, 872

Page, R. C., Hefner, R. R. & Frey, A. (1941) Amer. J. Digest. Dis., 8, 13

Reimann, H. A., Imbriglia, J. E. & Ducanes, Th. (1965) Proc. Soc. exp. Biol. Med., 119, 9

Reimann, H. A., Imbriglia, J. E. & Ducanes, Th. (1966) Amer. J. Cardiol., 17, 269

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

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


Silicon (Silica)

Natural Sources:
Horsetail, Equisetum arvense, herb and extracts are the most concentrated sources of silica for dietary supplements. Many foods also contain silica including alfalfa sprouts, beets, brown rice, bell peppers, soybeans, leafy green vegetables, root vegetables, cooked dried beans and peas, and whole grain breads and cereals. Silicon is also sold as trace silicic acid and sodium metasilicate.

Standardized silica capsules, tablets and liquid supplements; multivitamin pills containing silica.

Therapeutic Uses:
Aging Disorders
Alzheimer's Disease
Back Pain
Bone Health
Bone Mending
Brittle Hair
Broken Bones
Capillary Strength
Dental Health
Fetal Development
Fragile Nails
Hair Health
Immune System Health
Internal Cosmetic
Lower Back Pain
Mineral Deficiency (RDI=5-20mg/day)
Osteomalacia Prevention
Rickets Prevention
Skin Disorders
Torn Ligaments
Vascular Disorders
Wound Healing

Silicon is the second most abundant element of the earth's crust (26%), second only to oxygen in abundance (49%). Silica, also known as silicon dioxide, is a compound made out of the two most abundant elements in the Earth's crust, silicon and oxygen (SiO2). Silicon is not found free in nature but occurs chiefly as silica. Silicon is important to plant and animal life. Silicon was recognized as an essential trace element is 1972. In the human body, silicon is found in the connective tissues, tendons, ligaments, cartilage, and blood vessels and it is thought that the mineral is essential for their integrity. Silicon is also required for healthy nails, skin and hair and for calcium absorption in the early stages of bone formation. Studies have shown that the amount of silicon in arteries starts to decline as atherosclerosis starts to develop. French research suggests that silicon can help to prevent osteoporosis and can be used to treat bone fractures. Aging and low estrogen levels reputedly decrease the body's ability to absorb silicon. A human fetus has an abundant supply of silicon in many tissues. Collagen, a primary component of connective tissue and a third of all body protein, is rich in silicon. Elastin is also rich in silicon. Silica, in close cooperation with vitamin C, has the ability of holding moisture in tissues through compounds known as mucopolysaccharides. Also known as glycosaminoglycanes, these mucilaginous carbohydrates together with collagen and elastin make up our connective tissues. Silica is also vital for tooth structures. It is involved in the hardening of enamel, prevents bleeding gums and recession (a cause of loose teeth) which ultimately can prevent the need for dentures. Horsetail is among the riches plant sources of silicon in the form of monosilicic acid, which the body can readily use.

Silica, also known as silicon dioxide, is a compound made out of the two most abundant elements in the Earth's crust, silicon and oxygen (SiO2). Silica has three main crystalline varieties: quartz (by far the most abundant), tridymite, and cristobalite. Silica is the main constituent of more than 95 percent of rocks that comprise 59 percent of the earth's crust. Quartz makes up about 12 percent of the land surface and about 20 percent of the Earth's crust. The highest levels of silicon in humans are found in the skin and connective tissues. Blood averages about 0.5 milligrams of silicon per liter of blood plasma and amounts in the liver, heart and lungs range from 2 to 10 milligrams per kilogram. Silica from spring horsetail, Equisetum arvense, is much more highly bio-available than purely mineral sources of silica due to the presence of flavonoids and other cofactors in the extract, which enhance silica's uptake. Increased bioavailability can be assured through naturally chelated supplements. Natural chelates present in organic vegetal silica assist in successfully absorbing silica through intestinal walls into the bloodstream and from there into the tissues. Successful supplementation can be ensured if silica is extracted from natural horsetail herb, such as Flora-Sil®, carefully extracted from springtime horsetail herb using an aqueous extraction method that eliminates horsetail's abrasive quality. Note: The silica content of foods is usually found in the skin or other outer layers of a food (i.e. rice polishing) and thus silica is often the first to go in food processing. The current intake of silica by the average person is suspected to be low.

Suggested Amount:
There is currently no established RDA for silica. The recommended daily intake for silica varies greatly between authors. Most authoritative sources recommend that the daily intake should be between 5-20mg daily. Other sources recommend taking between 22-33mg of silica daily obtained from spring horsetail extracts that provide naturally chelated silica. Studies do show marked improvement in bone mending and skin health at this level. Other sources recommend much higher intakes (based on traditional diets) ranging between 100-1000mg daily, although these high levels may not be necessary to obtain the health benefits of silica – and safety above 50mg daily has not been established and so should not be recommended. Silica-rich horsetail herb and extracts can also be made into a poultice for stimulating and accelerating wound healing, as a hair rinse and as a skin conditioner. Silica's greatest benefits come from internal use with a proper formula.

Drug Interactions:
None known.

None known.

Side Effects:
None known.

Brown, M.1990. Present Knowledge in Nutrition, 6th edition. International Life Sciences Institute, Nutrition Foundation. Washington, DC, Pp. 301-302
Duke, J. 1997: The Green Pharmacy, The Ultimate Compendium of Natural Remedies from the World's Foremost Authority on Healing and Herbs. Pp. 37; 132-133; 414-415. Rodale Press.
Graefe EU, Veit M. 1999. Urinary metabolites of flavonoids and hydroxycinnamic acids in humans after application of a crude extract from Equisetum arvense. Phytomedicine 1999 Oct; 6(4): 239-46.
Piekos R, Paslawska S, Grinczelis W. 1976. Studies on the optimum conditions of extraction of silicon species from plants with water. III. On the stability of silicon species in extracts from Equisetum arvense herb. Planta Med. 1976 Jun; 29(4): 351-6.
Piekos R, Paslawska S. 1975. Studies on the optimum conditions of extraction of silicon species from plants with water. I. Equisetum arvense L. Herb. Planta Med. 1975 Mar; 27(2): 145-50.


See Also:
  Toxicological Abbreviations