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Toxicological evaluation of some food additives including anticaking
agents, antimicrobials, antioxidants, emulsifiers and thickening agents
WHO FOOD ADDITIVES SERIES NO. 5
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.
DIOXIDE AND CERTAIN SILICATES
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
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,
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
Ten gamma monomeric SiO2/cm3 was shown in vitro
to damage the enzymes of isolated mitochondria in rat liver (Hanger et
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).
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.
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
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,
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.
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 <
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).
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
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.*
FURTHER WORK OR
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
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
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
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
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
silica capsules, tablets and liquid supplements; multivitamin pills
Immune System Health
Lower Back Pain
Mineral Deficiency (RDI=5-20mg/day)
|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.
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.
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
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):
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.
Toxicological Abbreviations http://www.inchem.org/documents/eintro/eintro/abreviat.htm