Xanthan gum was evaluated for acceptable daily intake at the
eighteenth and twenty-ninth meetings of the Joint FAO/WHO Expert
Committee on Food Additives (Annex 1, references 35 and 70). A
toxicological monograph was published after the eighteenth meeting
(Annex 1, reference 36). An ADI of 0-10 mg/kg b.w. was established at
the eighteenth meeting and maintained at the twenty-ninth meeting,
Since the last evaluation, new information has become available, which
was evaluated by the present Committee. The previously-published
monograph has been expanded and is reproduced in its entirety below.
Caloric availability and digestibility studies indicated that
xanthan gum is not utilized by the body. This conclusion was
substantiated by finding that practically all of the gum fed during a
7-day period could be accounted for in the faeces (Booth et al.,
When 14C-labelled xanthan gum prepared by fermentation of
uniformly-labelled glucose with Xanthomonas campestris was fed to
rats at a level of 2% (50 mg total) in the diet, a maximum of 15% of
the label was metabolized to carbon dioxide in 100 hours. In vitro
tests showed that the acetate content was labile at gastric pH.
Acetate and pyruvate accounted for only 9.8% of the label in the gum
used. The finding that 15% of the label was metabolized to carbon
dioxide indicated that the hexoses were used to a certain extent also.
No accumulation in tissues was found, and the observed metabolism of
labelled material and distribution of 14C in tissues was that
expected from feeding a simple 14C-labelled molecule such as acetate
or a hexose. Analysis of faecal material showed no accumulation of the
five polysaccharide constituents, except acetate. Some 98% of the
radioactivity in the faeces could be attributed to unchanged or only
slightly modified polysaccharide. In vitro tests indicated that
nonenzymatic hydrolysis and the action of faecal micro-organisms are
responsible for the initial breakdown of polysaccharide in vivo
Special study on reproduction
A three-generation reproduction study was carried out using
groups of 10 male and 20 female rats in the first generation and 20
male and 20 female rats in subsequent generations. Dosage levels of 0,
0.25, and 0.5 g/kg/day were administered in the diet. Criteria
evaluated were survival, body weight, general appearance, behaviour,
the number of litters produced, number of live births and still
births, physical condition of the young, weight at birth and weaning,
and survival of the young. Females that had fewer than two litters
were examined to determine whether there was fetal resorption.
Malformations in offspring were recorded and gross and
micropathological examinations were made on the offspring of the
second and third generations. No adverse effects attributable to
xanthan gum were found in this study (Woodard et al., 1973).
Animal Route (mg/kg b.w.) Reference
Mouse oral > 1000 Booth et al., 1963
i.p. > 50 Booth et al., 1963
i.v. 100-250 Hendrickson & Booth (sine data)
Rat oral > 45,000 Jackson et al. (sine data a)
Dog oral > 20,000 Jackson et al. (sine data b)
Daily application of a 1% solution for 15 days to rat skin
produced no signs of irritation. Daily application of a 1% solution
for five days to rabbit conjunctiva produced no signs of irritation.
Intradermal challenge tests in guinea-pigs did not produce evidence of
sensitization (Hendrickson & Booth, sine data).
Five albino rats received single doses of xanthan gum. The
material was administered by inhalation for one hour using a stainless
steel inhalation chamber. A total of 19 g of the test material was
used during the one-hour exposure, which gave a calculated chamber
concentration of approximately 21 mg/liter. Following exposure all
rats were observed periodically for one hour for pharmacologic and
toxicologic signs over a period of 14 days. No signs of toxicity were
seen and the rats retained good physical appearance throughout. No
gross changes were seen at autopsy (Knott & Johnston, 1973).
A study was carried out on an unspecified number of rats fed
diets containing 7.5 or 10% xanthan gum for 99-110 days. No adverse
effects were observed in extensive investigatins on these animals
(Booth et al., 1963).
In a 91-day feeding study, a reduced rate of weight gain was
found in groups of rats receiving 7.5 or 15% xanthan gum in the diet.
Diets containing 3 or 6% gum did not reduce weight gain. No
significant alterations in haemoglobin, red or white cell counts, or
organ weights were observed in these rats. Histological examination of
tissues from rats at the 15% level showed no pathological effects. At
the highest-dose level the animals produced abnormally large faecal
pellets, but diarrhoea did not occur. A paired-feeding test was used
to compare the growth of rats ingesting a diet containing 7.5% xanthan
gum and comparable rats restricted to the same intake of control diet.
No differences in weight gain were found at the end of 18 days,
indicating the absence of a growth-inhibiting factor (Booth et al.,
Groups of 5 male and female weanling rats were fed 0, 2.5, 5.0,
or 10.0% commercial xanthan gum product, which consisted of drum-dried
whole fermentation medium (beer) in which Xanthomas campestris
B-1459 was cultured, for 110 days. A laboratory-prepared whole-dried
ferment was tested at a single dietary level of 7.5%, substituted at
the expense of the entire basal diet, for 99 days. No significant
pathological changes associated with feeding either B-1459
fermentation medium were detected (Booth et al., 1968).
Diets containing a nutritionally adequate, high-maltose nutrient
mixture and either 4% xanthan gum or 4% cellulose were fed
ad libitum to male Wistar rats for 7 days. The feeding of this gum
increased the combined weight of the small intestine and its contents
by 110%. This effect was partially due to an enlarged cell mass and to
extra dry matter in the contents; however, it was chiefly due to a
400% increase in intraluminal water. Xanthan feeding enhanced greatly
the persistence of sugars beyond the proximal quarter of the small
intestine and increased their total recovery in the first
three-quarters of that organ by 150%. The xanthan-induced increase in
intraluminal water in the small intestine was partially due to a
slowed absorption of osmotically-active substances from the gut
(Trout et al., 1983).
Rats were fed a stock diet for at least 3 days. They were then
starved for 2 days and divided into 4 groups of 6 animals each. The
starved rats served as a model for differentiating effects of various
dietary carbohydrates. (The feeding of nutritionally-adequate
high-carbohydrate diets to starved rats causes an elevation of total
liver lipid and of hepatic enzymes associated with lipogenesis.) In
experiment 1, rats were fed nutritionally-adequate diets; the
carbohydrate was starch or glucose with or without xanthan gel
(a suspension containing 4% xanthan gum). Experiment 2 had the same
design as experiment 1, but the diets were fat-free. In experiment 3,
the dose-response relationship was examined by feeding 0.8, 1.4, or
2.0% xanthan gum. In all experiments relative liver size, final body
weight, weight gain, total food intake, utilizable nutrient intake,
glucose-6-phosphate (G-6-P) dehydrogenase activity, malic enzyme
activity, and total liver lipid were measured. Xanthan gel lowered
relative liver size, total liver lipid, G-6-P dehydrogenase, and malic
enzyme activity. In the dose-response experiment xanthan gum, at less
than 2% of the dry diet ingredients, lowered nutrient intake
(Putney et al., 1978).
Eighteen young adult male guinea-pigs were injected
intracutaneously with a 0.1% solution of xanthan gum 3 times per week
for a total of 10 injections. Ten days after the last injection, each
guinea-pig received a challenge injection. The injection sites were
evaluated at 24 hours for size of the erythematous spot and for the
intensity of the color produced. Body weights were recorded at 0, 15,
and 30 days. Xanthan gum did not produce sensitization in the
guinea-pig under the conditions of the experiment (Durloo & Johnston,
Two ml of a 1% solution (W/w) of xanthan gum was applied to the
skin of a group of 3 rabbits for 6 weeks. After macroscopic and
histological evaluation, the cumulative cutaneous irritation index was
zero, indicating that the substance was very well tolerated
(Guillot et al., 1982).
Four groups of 2 male and 2 female young adult beagle dogs were
fed for 2 weeks on diets providing 0, 1, or 2 g/kg b.w./day xanthan
gum or 2 g/kg b.w./day of cellulose powder. Persistent diarrhoea
occurred in the high-dose dogs, and occasional diarrhoea occurred in
dogs in the low-dose group. All dogs, including controls, lost weight
but the weight loss was most marked in animals receiving xanthan gum.
Red blood cell counts, haemoglobin concentrations, and serum
cholesterol concentrations were lowered and the relative adrenal
weight increased in dogs receiving 2 g/kg b.w./day xanthan gum. These
effects were considered to be due to the persistent diarrhoea in this
group. Liver and kidney function tests indicated no disturbance in the
function of these organs. Extensive gross and histopathological
examination failed to detect lesions which could be attributed to
ingestion of the gum (Robbins et al., 1964).
Groups of 3 male and 3 female beagle dogs were fed diets
supplying 0, 0.25, or 0.5 g/kg b.w./day xanthan gum for 12 weeks.
Animals in the high-dose group had softer stools than normal, but no
diarrhoea. Growth was slightly retarded in the males and the serum
cholesterol level was lowered in both sexes of the high-dose group. No
other adverse effects were seen. The no-adverse-effect-level in this
test was considered to be 0.25 g/kg b.w./day (USDA, 1964).
Groups of 30 male and 30 female Charles River CD strain rats were
fed diets for 104 weeks supplying O, 0.25, 0.5, or 1.0 g/kg b.w./day
xanthan gum. No abnormalities which could be attributed to ingestion
of these experimental diets were found with regard to survival,
body-weight gain, food consumption, behaviour, or appearance.
Ophthalmic and haematologic examination yielded normal results.
Analysis of blood for glucose, SGOT, and prothrombin time showed no
abnormalities in test groups. Organ weights were within normal limits
and no lesions attributable to xanthan gum were found on gross and
histopathological examination (Woodard et al., 1973).
Xanthan gum was administered in the diet at levels supplying
0, 0.25, 0.37, or 1.0 g/kg b.w./day to groups of 4 male and 4 female
beagle dogs for 107 weeks. No effects attributable to administration
of the gum were seen in the treated animals with regard to survival,
food intake, body-weight gain, electrocardiograms, blood pressure,
heart rate, body temperature, or ophthalmic and neurological
examinations. Haemoglobin, total and differential white cell counts,
coagulation and prothrombin times, thrombocyte counts, serum alkaline
phosphatase, blood urea nitrogen, blood glucose, SGOT, and SPGT were
the same in control and treated animals. Urine pH, glucose
concentrations, and sediment contents were comparable between test and
control groups, but there was a dose-related increase in urine SG and
a more frequent appearance of urinary albumin in dogs consuming
1.0 g/kg b.w./day of gum than in the other groups. Stool consistency
was normal at the 0.37 g/kg level, but stools were loose at the
top-dose level. The weight of the faeces showed a dose-related
increase, as would be expected from feeding a non-absorbed hydrophilic
gum at high-dose levels. The increased urinary SG is consistent with
physiological adjustment for the extra water excreted in the faeces.
Examination of the appearance and weights of organs and
histopathological examinations failed to detect any adverse effects of
treatment with xanthan gum at any dose level (Woodward et al.,
Observations in man
A study group of 30 individuals who had expressed a commitment to
lose weight in a pre-study interview were medically examined and found
to be psychologically suited for a weight-reduction program. Twenty
participants were given capsules containing 550 milligrams of xanthan
gum (2 capsules 20-30 minutes before meals). These participants were
divided into two groups of 10 each; those in group A were placed on a
fixed low calorie diet (1000-1200 calories per day), while those in
group B were given no numerical dietary caloric restriction, but they
were encouraged to limit their caloric intake. Participants in group C
(control group of 10) were given a placebo and requested to limit
caloric intake to 1000-1200 calories per day. The test was performed
over an 8-week period. Group B did better in terms of the number of
successes and the amount of weight lost than did the A group. Both
groups given capsules containing xanthan gum did better than the
control group (Wong et al., 1974).
Over-weight patients were given capsules for 3 weeks in a
double-blind study. Each capsule contained either 0.25 g xanthan gum
or 0.5 g paraffin oil (placebo). The patients were told to take 4
capsules 30 minutes before each meal together with a glass of water
(12 capsules/day). No significant changes in plasma lipid levels were
observed. The patients tolerated the capsules well. There were no
clear side-effects reported and there was not a tendency toward more
frequent stools. The authors concluded that xanthan gum can effect a
slow but significant weight loss in individuals with varying degrees
of overweight (Ockerman et al., 1983).
Five healthy men (aged 26-50 years) consumed for 23 days
10.4-12.9 g xanthan gum each day in three portions. The daily
ingestion of xanthan gum at this high level had no significant effect
on plasma biochemistry, haematological indices, urinalysis parameters,
glucose and insulin tests, serum immunoglobulins, triglycerides,
phospholipids, HDL cholesterol, or breath hydrogen or methane
concentrations. There was a 10% reduction in serum cholesterol, and a
significant increase in faecal bile acid concentrations following the
ingestion of xanthan gum. The xanthan gum also acted, as expected from
a dose-ranging study, as a bulking agent in terms of its effects on
faecal dry and wet weight and on transit time (Eastwood et al.,
In response to the request of the twenty-ninth meeting of the
Committee, information was provided on the nature of the nitrogenous
constituents of xanthan gum. About half of the nitrogenous matter is
proteinaceous and contains amino acid residues in the same relative
proportions as are present in other food grade gums. The rest is
present as amino sugars, nucleic acids, and nucleotides (personal
communication from W.J. Sander, Marinalg International, Paris, France,
to A.W. Randell, FAO, Rome, May 21, 1986; submitted to WHO by Marinalg
A two-year study in rats failed to show any carcinogenic or other
toxic effects attributable to the gum. A reproduction study in rats
was negative. In addition, the results of several short-term studies
in rats, rabbits, guinea-pigs, and dogs were also available. No toxic
effects were observed in these studies. Several recent studies in
humans indicated no adverse effects at levels up to 10-13 grams daily.
Estimate of acceptable daily intake for man
ADI "not specified".
Further work or information
An adequate long-term study in a second rodent species, because
of the potential high exposure levels of this substance and the fact
that xanthan gum is prepared from a microbial source not normally used
Booth, A.N., Hendrickson, A.P., & De Eds, F. (1963). Physiologic
effects of three microbial polysaccharides on rats.
Toxicol. Appl. Pharmacol., 5, 478-484.
Booth, A.N., Hendrickson, A.P., & De Eds, F. (1968). Rat feeding study
of whole dried ferment containing polysaccharide B-1459 (xanthan
gum). Unpublished report from Western Regional Research
Laboratory, United States Department of Agriculture, Albany, CA,
USA. Submitted to WHO by Marinalg International, Paris, France.
Durloo, R.S. & Johnston, C.P. (1973). Keltrol(R), intracutaneous
sensitization potential in the guinea pig. Unpublished report
from Woodard Research Corporation, Herndon, VA, USA. Submitted to
WHO by Marinalg International, Paris, France.
Eastwood, M.A., Brydon, W.G., & Anderson, D.M.W. (1986). The dietary
effects of xanthan gum in man. Unpublished report submitted to
WHO by Marinalg International.
Guillot, J.P., Giauffret, J.Y., Martini, M.C., Gonnet, J.F., &
Soule, G. (1982). Safety evaluation of gum and thickeners used in
cosmetic formulation. Int. J. Cosmetic Sci., 4, 53-66.
Gumbmann, M.R. (1964). Metabolism of 14C polysaccharide B-1459
(xanthan gum) by the rat. Unpublished report from Western
Regional Research Laboratory, United States Department of
Agriculture, Albany, CA, USA. Submitted to WHO by Marinalg
International, Paris, France.
Hendrickson, A.P. & Booth, A.N. (sine data). Supplementary acute
toxicological studies of polysaccharide B-1459 (xanthan gum).
Unpublished report from Western Regional Research Laboratory,
United States Department of Agriculture, Albany, CA, USA.
Jackson, N.N., Woodard, M.W., & Woodard, G. (sine data a). Xanthan
gum acute oral toxicity to rats. Unpublished report from Woodard
Research Corporation, Herndon, VA, USA.
Jackson, N.N., Woodard, M.W., & Woodard, G. (sine data b). Xanthan
gum acute oral toxicity to dogs. Unpublished report from Woodard
Research Corporation, Herndon, VA, USA.
Knott, W.B. & Johnston, C.D. (1973). Keltrol(R), acute inhalation
toxicity to rats. Woodard Research Corporation, Herndon, VA, USA.
Ockerman, P.A. (1983). Untitled unpublished report discussing clinical
study of xanthan gum used for weight control. Department of
Clinical Chemistry, University Hospital, Lund, Sweden. Submitted
to WHO by Marinalg International, Paris, France.
Putney, J.D., Trout, D.L., Johnson, D.A., Moy, N.L., & Michaelis, O.E.
(1978). Effect of xanthan gel on hepatic lipogenesis in
starved-refed rats. Nutr. Rep. Internatl., 18, 659-669.
Robbins, D.J., Moulton, J.E. & Booth, A.B. (1964). Subacute toxicity
study of a microbial polysaccharide fed to dogs. Food Cosmet.
Toxicol., 2, 545-550.
Trout, D.L., Ryan, R.O., & Bickard, N.C. (1983). The amount and
distribution of water, dry matter and sugars in the digestive
tract of rats fed xanthan gum. Proc. Soc. Exp. Biol. Med.,
USDA (1964). Safety evaluation of polysaccharide B-1459 (xanthan gum)
in laboratory animals - effects of feeding to dogs. Unpublished
report from Western Regional Research Laboratory, United States
Department of Agriculture, Albany, CA, USA,
Wong, G.O. (1974). Method of controlling human appetite. United States
Patent No. 3,843,786.
Woodard, G., Woodard, M.W., McNeely, W.H., Kovacs, P., & Cronin,
M.T.I. (1973). Xanthan gum: safety evaluation by two-year
feeding studies in rats and dogs and a three-generation
reproduction study in rats. Toxicol. Appl. Pharmacol.,