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POTASSIUM BROMATE
EXPLANATION
Potassium bromate is used in treating barley in beer making in
addition to its use in the treatment of flour, and it has been used
for the improvement of the quality of fish paste products in Japan
(Ministry of Health and Welfare, Japan, 1979). Potassium bromate
has been evaluated for acceptable level of treatment for flour to
be consumed by man by the Joint FAO/WHO Committee on Food Additives
in 1963 and 1983 (Annex 1, references 1 and 62). At the last review
the Committee reiterated that, as a general principle, bromate
should not be present in food as consumed. The previous acceptable
level of treatment of flour used for baking products was made
temporary with a maximum treatment level of 75 mg KBrO3 per kg
flour pending further work to establish the residual levels of
potassium bromate in foods treated with it. No acceptable level of
treatment was established for other foods. Bromate is extensively
reduced to bromide for which an ADI of 0-1 mg/kg bw has been
established by the FAO Working party on Pesticide Residues and the
WHO Expert Committee on Pesticide Residues (Annex 1, reference 62).
Since the previous evaluation, additional data have become
available. The previously published monograph (Annex 1, reference
63) is reproduced in its entirety below and has been expanded to
include a summary and discussion of the new data.
BIOLOGICAL DATA
Biochemical aspects
Metabolism
In a preliminary study, male Wistar rats were given an aqueous
solution of potassium bromate by gavage; urine and faeces were
collected for 24 hrs and the content of bromate and bromide
determined. After this period, the animals were sacrificed and the
bromate and bromide content was determined in the following
tissues/organs: plasma, RBC, spleen, kidney, pancreas, stomach and
small intestine. No bromate was detectable in any tissue after this
time although substantial amounts were found in urine (detection
limits 2.5 g BrO3-/ml urine & plasma, 5.0 g/g tissue).
Conversely, bromide was widely distributed in tissues and urine
(Fujii et al., 1984).
Groups of four small Wistar rats were given a single oral dose
of 100 mg KBrO3 and sacrificed after 15 min, 30 min, 1, 2, 4 or
8 hrs. Bromate was then measured in stomach, small intestine, plasma
and urine in the bladder. Bromate disappeared slowly from the
stomach; in the small intestine the levels peaked after 30 min and
fell to undetectable levels by 4 hrs. The plasma concentration of
bromate was maximal (4 g/ml) at the first sampling at 15 min and
fell rapidly, being undetectable after 2 hrs. Urinary levels
reached a peak after 1 hr and decreased rapidly so that no further
urinary excretion was detectable after 4 hrs (Fujii et al.,
1984).
Groups of four male Wistar rats were given potassium bromate
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by oral gavage at doses of 0, 0.625, 1.25, 2.5, 5, 10, 20, 40, 60,
80, or 100 mg/kg bw and bromate and bromide were determined in the
subsequent 24 hr urine. No bromate was detectable at doses of
2.5 mg/kg or less; at higher doses bromate concentration increased
in a dose related manner. Nonsignificant differences from controls
were seen in the bromide concentration of the urine at dose levels
up to 5 mg/kg but at higher doses the bromide concentration
increased with increasing dose (Fujii et al., 1984).
Bromate is therefore rapidly absorbed from the
gastrointestinal tract, partially converted to bromide in the
tissues, and rapidly excreted. Since unchanged bromate could be
detected in urine at doses of 5 mg/kg and above, it must come into
contact with renal tissues, at least at this dose level (Fujii et
al., 1984).
Effects of baking on potassium bromate-treated flour
When
80 mg/kg,
the flour
(Bushuk &

potassium bromate was present in flour at levels of 5 to

no residual bromate was detected in bread prepared from
by a bulk fermentation process after 20-25 minutes baking
Hlynka, 1960).

Potassium bromate present in flour at 30 mg/kg was

quantitatively converted to bromide in breed prepared from the
flour by a bulk-fermentation process (Lee & Tkachuk, 1960).
Breed was made by bulk fermentation and also by mechanical
development from flour doughs containing 0 to 200 mg/kg potassium
bromate and the amount of residual bromate in the bread was
determined. When the added potassium bromate was 50 mg/kg or less,
no residual potassium bromate could be detected; at higher levels
of addition, increasing amounts of residual potassium bromate were
detected, bulk fermentation giving higher residual levels than
mechanical development (Thewlis, 1974).
In a similar experiment but using a more sensitive analytical
procedure with a detection limit of 0.06 mg bromate/kg in bread, no
residual bromate could be detected at flour treatment levels of 25,
50, or 62.5 mg/kg. Residual levels of bromate in bread made from
flour treated at levels of 75 and 100 mg/kg were 0.14 and 0.22 mg/kg,
respectively (expressed on a 40% moisture basis). Within the
limits of experimental error, all of the added bromate not detected
unchanged was accounted for as bromide (Osborne et al., 1988).
Effects on nutritional value
Treatment of flour with potassium bromate at a concentration
of 45 mg/kg did not cause any decrease in its content of thiamine,
riboflavin or nicotinic acid (Ford et al., 1959). Wheat flours
treated with potassium bromate at a concentration of 25 mg/kg and
stored for 12 months did not show any greater decrease in
tocopherol content than flour, either untreated or treated with
ascorbic acid, stored under the same conditions (i.e., not more
than 35-50% decrease) (Menger, 1957).
At high levels of use, about 200 mg/kg bromate has no
significant effect on the thiamine, riboflavin or nicotinic acid
content of flour, or bread made from it. No statistically
significant differences have been found in essential fatty acid
content in flour treated with 200 mg/kg potassium bromate or in
bread made from such flour (Ministry of Agriculture, Fisheries and
Food, U.K., 1974).
Potassium bromate completely destroys folic acid in solution
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in 10 days (British Food Manufacturing Industries Research

Association, 1980).
Toxicological studies
Studies on bromate-treated flour and bread
Short-term studies
Rats
Bread made from flour treated with 14 mg/kg and with 100 mg/kg
of potassium bromate was fed to two groups of 6 male and 20 female
rats each and these diets continued over three generations, the
entire experiment lasting 10 months. The health, behavior, weight
gain and reproductive performance remained normal throughout.
Histological study of the tissues showed no abnormalities and
analyses of brain and liver showed no accumulation of bromine (Ford
et al., 1959).
Eighteen rats were fed a diet containing 84% of flour treated
with potassium bromate at a level of about 75 mg/kg for a period of
4 weeks. Growth and reproductive performance were normal (Ford et
al., 1959).
Bread made from flour treated with 200 mg/kg of potassium
bromate was fed to 12 rats for 16 days and the flour itself to 16
rats for 10 weeks without adverse effects (Ford et al., 1959).
Dogs
Three dogs were fed for 12 weeks a diet containing 84% of
bread made from flour treated with 75 mg/kg potassium bromate. No
ill-effects were observed. Five dogs were fed for 6-14 weeks flour
treated at a level of 75 mg/kg potassium bromate. Two dogs were fed
for 16 days with bread made from flour treated at a level of
200 mg/kg with potassium bromate. No ill-effects were observed (Ford
et al., 1959).
Three dogs were fed for 6 weeks on diets containing flour
treated with 70 mg/kg potassium bromate showed no ill-effects or
'running fits'. Four dogs fed for 17 months on bread made from
flour containing 200 mg/kg potassium bromate showed no adverse
effects attributable to the diet (Impey et al., 1961).
Monkeys
Three monkeys fed for 8 weeks on a diet containing 84% of
bread made from flour treated with 75 mg/kg potassium bromate
showed no adverse effect (Ford et al., 1959).
Long-term studies
Mice
Groups of mice fed flour treated with 15 mg/kg potassium
bromate showed no ill-effects over 8 generations (Ford et al.,
1959).
Groups of 60 male and 60 female mice were fed for 80 weeks on
five diets containing 79% breadcrumbs; the bread used was prepared
from untreated flour (control), from flour treated with 50 mg/kg or
75 mg/kg potassium bromate, or from flour treated with 50 mg/kg
bromate plus one of two mixtures of other commonly used flour
additives (escorbic acid, benzoyl peroxide and chlorine dioxide).
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Appearance, behavior, health and survival were similar in test and

control groups and there was no evidence that any of the treatments
affected the incidence of neoplasms, the incidence of malignant
tumours being similar in control and test groups. Anaemia was
observed in males of all groups (including controls) and in females
at 18 months. No dose-related differences in blood chemistry were
found in male mice; in the females, dose-related increases in
blood-glucose levels were observed at 1 and 12 months but not at
18 months. Renal concentration and dilution tests, and urine analysis
were indicative of normal renal function. Some dose-related differences
in the weights of heart, pituitary and uterus were found but when
expressed relative to body weight, the values for heart and uterus
were not dose-related. The relative weights of pituitary, brain,
kidneys and thyroid showed dose-related changes in males only, with
relative weights of heart and pituitary being lowered and kidneys
and thyroid elevated. These changes were not associated with any
histopathological abnormalities. No significant dose-related
accumulation of covalently bound bromine was observed in adipose
tissue (Ginocchio et al., 1979).
Rats
Twenty rats were fed 2 years with flour treated at a level of
627 mg/kg potassium bromate. Weight gain, general health and
survival rate were not significantly different than those of
controls (Ford et al., 1959).
Five generations of rats were fed bread made from flour
treated with potassium bromate at a level of 15 mg/kg. No effects
on weight gain, reproductive performance or survival were observed
(Ford et al., 1959).
Five groups of 60 male and 60 female rats were fed for 104
weeks on five diets containing 79% breadcrumbs; the bread was
prepared from untreated flour (control), from flour treated with
50 mg/kg or 75 mg/kg potassium bromate, or from flour treated with
50 mg/kg bromate plus one of two mixtures of other flour additives.
Appearance, behavior and health were similar in test and control
groups. The death rate was lower in the test groups than in controls
in the females and the males of the high dose group had fewer deaths
than the other groups taken together. No evidence of carcinogenicity
nor of chronic toxicity was attributable to the compounds under test
at the dose levels used. There was no evidence of accumulation of
covalently-bound bromine in the adipose tissue (Fisher et al.,
1979).
Studies on potassium bromate
Studies on mutagenicity
Potassium bromate was reported to give positive results for
mutagenicity in the Ames test, chromosome aberration test and
micronucleus test but gave negative results in the Rec-assay and in
a silk-worm assay (Kawachi et al., 1980; Ishidate et al.,
1981).
Studies on carcinogenicity
Mice
A 78 week carcinogenicity study was performed on female B6C3F1
mice given potassium bromate at concentrations of 500 or 1000 mg/l
in drinking water. No carcinogenic effect was detected (Kurokawa
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et al., 1982a).
Rats
Groups of 53 male and 53 female F-344 rats were given
potassium bromate in drinking water at concentrations of 0, 250,
and 500 mg/l for 110 weeks, except that the high concentration was
reduced to 400 mg/l for male rats in week 60 due to severe
inhibition of body weight gain. Animals dying or moribund in the
course of the study were autopsied immediately; survivors were
killed and autopsied at week 111 and a detailed histopathological
examination was carried out, including 10-15 serial step sections
on the kidneys. The mean survival time was shortest in males given
500 mg/l potassium bromate (88.1 18.1 w), the mean survival times
of the other groups were between 101 and 104 weeks. Renal tubules
in potassium bromate-treated rats showed various pathological
changes; degenerative, necrotic and regenerative changes were very
common. All the male animals bore tumours (including controls)
and tumour incidence was very high in females (85%, 92% and 83%
in females receiving 0, 250 and 500 mg/l potassium bromate,
respectively). However, the incidence of tumours of the kidney,
peritoneum and thyroid was statistically significantly higher in
treated animals than in controls. Tumours (adenocarcinomas and
adenomas) of the kidney developed in 6%, 50% and 85% of males
and 0%, 40% and 63% of the females receiving 0, 250 and 500 mg/l
respectively. The incidence of mesotheliomas of the peritoneum was
11%, 32% and 54% in male rats given 0, 250 and 500 mg/l respectively
but there was zero incidence of this type of tumour in females,
either treated or controls. Induction times for renal cell
tumours were relatively long, the shortest being 14 w (male,
500 mg/l). It was concluded by the authors that potassium bromate was
carcinogenic in Fischer 344 rats by oral administration (Kurokawa
et al., 1982a, b; Kurokawa, 1982).
Dose-response studies on the carcinogenicity of potassium
bromate were carried out to examine its effects at low doses. Seven
groups of 20-24 male F344 rats were given potassium bromate in the
drinking water at concentrations of 0, 15, 30, 60, 125, 250 or
500 mg/ml for 104 weeks; the mean respective intakes of potassium
bromate over the test period were 0, 0.9, 1.7, 3.3, 7.3, 16.0 and
43.4 mg/kg bw. Animals dying on test or in a moribund condition
were immediately autopsied; at termination the remaining animals
were given a complete autopsy. At autopsy, the weights of brain,
sub-mandibular gland, lung, heart, liver, spleen, adrenals, kidneys
and testes and of any tumours were recorded. These and other organs
were examined histologically. Marked decrease in body weight gain
and in survival times were observed in the group given potassium
bromate at a concentration of 500 mg/ml. The combined incidences of
renal adenomas and adenocarcinomas were significantly increased in
rats receiving bromate at concentrations of 125 mg/ml and above in
a dose related manner. Significant increases in the number of
dysplastic foci in the kidney were seen at the dose level of
30 mg/ml and above, the incidence varying in a dose related manner.
In addition to the renal lesions, a group treated with drinking water
containing 500 mg/ml displayed increased incidence of combined
follicular adenomas and adenocarcinomas of the thyroid and of
peritoneal mesotheliomas (Kurokawa, 1986).
Observations in Man
A number of case studies of acute human intoxication with
potassium bromate have been reported following accidental ingestion
or attempted suicide. In autopsy cases, degeneration of kidney
tubules and liver parenchymal cells, and acute myocarditis were the
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principal pathological changes observed (Paul, 1966; Stewart et

al., 1969; Niwa et al., 1979; Norris, 1965; Quick et al., 1975).
COMMENTS
The Committee reiterated the recommendation made in the
previous reports that, as a general principle, bromate should not
be present in foods as consumed, and the use of potassium bromate
could only be approved in such circumstances. Evidence was
considered that, at levels of flour treatment up to 62.5 mg/kg, no
bromate residues were detected in the bread with the principle
breakdown product being bromide; at levels of treatment of 75 mg/kg
or higher, detectable residues of bromate were found in bread. In
the light of the previously established ADI for bromide, the
Committee was of the opinion that the bromide arising from flourtreatment with bromate within the acceptable levels of treatment
did not present a toxicological hazard. However, as levels of
treatment of 75 mg/kg resulted in detectable residues of bromate in
bread, the Committee reduced the previous acceptable level of
treatment for flour for bread-making to 0-60 mg potassium
bromate/kg flour. In arriving at this conclusion, the Committee
took cognizance of earlier long-term studies in mice and rats which
showed that products made from flour treated with bromate produced
no adverse effects. The Committee had no toxicological data on
other food products treated with bromate and were aware that some
applications could give rise to significant residues. Accordingly,
no acceptable level of treatment could be established for foods
other than flour intended for baking.
EVALUATION
Level resulting in no detectable residues of bromate
For flour used in bread making 0 - 62.5 mg/kg.
Estimate of acceptable level of treatment of food to be
consumed by man
For flour:

0 - 60 mg/kg flour (providing that bakery

products prepared from such treated flour
contains negligible residues of potassium
bromate)

For other foods: No acceptable level of treatment allocated.

REFERENCES
British Food Manufacturing Industries Research Association (1980).
Annual Report, p. 29.
Bushuk, W. & Hlynka, I. (1960).

Cereal Chem., 37, 573.

Fisher, N., Hutchinson, J.B., Berry, R., Hardy, J., Ginocchio, A.V.
& Waite, V. (1979). Long-term toxicity and carcinogenicity studies
of the bread improver potassium bromate 1. Studies in rats. Fd.
Cosmet. Toxicol., 17, 33-39.
Ford, W.P., Kent-Jones, D.W. & Frazer, A.C. (1959). Unpublished
submission, dated 8th December, 1959, to the Preservatives
Sub-Committee of the United Kingdom Food Standards Committee,
Appendices I-IV.
Fujii, M., Oikawa, K., Saito, H., Fukuhara, K.C., Ouosaka, S. &
Tanaka, K. (1984). Metabolism of potassium bromate in rats 1.
In vivo studies. Chemosphere, 13, 1207-1212.
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Ginocchio, A.V., White, V., Hardy, J., Fisher, N., Hutchinson, J.B.
& Berry, R. (1979). Long-term toxicity and carcinogenicity studies
of the bread improver potassium bromate 2. Studies in mice. Fd.
Cosmet. Toxicol., 17, 41.
Impey, S.G., Moore, T. & Sharman, I.M. (1961).
Agric., 11, 729.

J. Sci. Fd,

Ishidate, M., Sofuni, J. & Yoshikawa, K. (1981). Chromosomal

aberration tests in vitro as a primary screening tool for
environmental mutagens and/or carcinogens. Gann Monograph on
Cancer Research, 27, 95.
Kawachi, T., Komatsu, T., Kada, T., Ishidate, M., Sasaki, M.,
Sugiyama, T., Tazima, Y. & Williams, G.M. (ed) (1980). In: The
predictive value of short-term screening tests in carcinogenicity
evaluation, Elsevier, Amsterdam, pp. 253-267.
Kurokawa, Y. (1982). Communication submitted to WHO.
Kurokawa, Y., Hayashi, Y., Maekawa, Y., Takahashi, M. & Kokubo, T.
(1982a). Induction of renal cell tumors in F-344 rats by oral
administration of potassium bromate, a food additive. Gann, 73,
335.
Kurokawa, Y., Hayashi, Y., Maekawa, Y., Takahashi, M., Kokubo, T.
& Odashima, S. (1982b). Carcinogenicity of potassium bromate by
oral administration to F-344 rats. Report submitted to WHO by Y.
Kurokawa.
Kurokawa, Y., Aoki, S., Matsushima, Y., Takamura, N., Imazawa, T.
& Hayashi, Y. (1986). Dose-response studies on the carcinogenicity
of potassium bromate in F344 rats after long-term oral
administration. J. Nat. Canc. Inst., 77, 977-982.
Lee, C.C. & Tkachuk, R. (1960).
Menger, A. (1957).

Cereal Chem., 37, 575.

Brot und Geback, 11, 167.

Ministry of Agriculture, Fisheries & Food, U.K. (1974). Standards

Committee Second Report on Bread and Flour. FSC/REP/61 H.M.S.O.
Ministry of Health and Welfare, Japan (1979). The Japanese
standards of food additives. 4th edition, p. 367.
Niwa, T., Ho, T. & Matsui, E. (1979). Serial renal biopsy in
potassium bromate intoxication. Jap. Circ. J., 38, 387.
Norris, J.A. (1965). Toxicity of home permanent waving and
neutralizer solutions. Fd. Cosmet. Toxicol., 3, 93-97.
Osborne, B.G., Willis, K.H. & Barrett, G.M. (1988). Survival of
bromate and bromide in bread baked from white flour containing
potassium bromate. J. Sci. Fd. Agric., 42, 255-260.
Paul, A.H. (1966). Chemical food poisoning by potassium bromate.
N. Z. Med. J., 65, 33.
Quick, C.A., Chole, R.A. & Mauer, S.M. (1975). Deafness and renal
failure due to potassium bromate poisoning. Arch. Otolaryngol.,
101, 494.
Stewart, T.H., Sherman, Y. & Politzer, W.M. (1969). An outbreak of
food poisoning due to a flour improver, potassium bromate. S. A.
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Med. J., 43, 200.

Thewlis, B.H. (1974). The fate of potassium bromate when used as a
breadmaking improver. J. Sci. Fd. Agric., 25, 1471.
Viggiano, J. & Turk, E.F.H. (1937).

Analyst, 62, 559.

See Also:
Toxicological Abbreviations
Potassium bromate (ICSC)
Potassium bromate (WHO Food Additives Series 18)
Potassium bromate (WHO Food Additives Series 30)
POTASSIUM BROMATE (JECFA Evaluation)
Potassium Bromate (IARC Summary & Evaluation, Volume 40, 1986)

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