Bromic acid, potassium salt

Substance overview Plus
Name:
Bromic acid, potassium salt
CAS Number:
7758-01-2
Synonyms:
Potassium bromate
Approval number:
HSR001336, Approved with controls
UN Class:
Class 5: Oxidizing substances and organic peroxides; Division 5.1; Packing group II: Substances presenting medium danger
UN Number:
1484
Molecular weight:
167
Relative density:
3.27
Water solubility:
 
Classification Oxid. Solid 2 Plus
Classification route species:
 
Classification description:
H272: May intensify fire; oxidiser.
Classification key study:
 
Classification Acute Tox. 3 Plus
Classification route species:
(oral)
Classification description:
H301: Toxic if swallowed.
Classification key study:

Oral Route
SPECIES:
ENDPOINT: LD50
VALUE: 157 mg/kg
REFERENCE SOURCE: Eisei Kagaku. Hygienic Chemistry. (Nippon Yakugakkai, 2-12-15 Shibuya, Shibuya-ku, Tokyo 150, Japan) V.1- 1953- (37,258,1991). [RTECS]

Classification Skin Irrit. 2 Plus
Classification route species:
 
Classification description:
H315: Causes skin irritation.
Classification key study:

Skin Irritation
SPECIES:
RESULT: The substance irritates the eyes, the skin and the respiratory tract.
REFERENCE SOURCE: ICSC [INCHEM]

Eye Irritation
SPECIES:
RESULT: The substance irritates the eyes, the skin and the respiratory tract.
REFERENCE SOURCE: ICSC [INCHEM]

Classification Eye Irrit. 2 Plus
Classification route species:
 
Classification description:
H319: Causes serious eye irritation.
Classification key study:

Skin Irritation
SPECIES:
RESULT: The substance irritates the eyes, the skin and the respiratory tract.
REFERENCE SOURCE: ICSC [INCHEM]

Eye Irritation
SPECIES:
RESULT: The substance irritates the eyes, the skin and the respiratory tract.
REFERENCE SOURCE: ICSC [INCHEM]

Classification Repr. 2 Plus
Classification route species:
 
Classification description:
H361: Suspected of damaging fertility or the unborn child <state specific effect if known> <state route of exposure if it is conclusively proven that no other routes of exposure cause the hazard>.
Classification key study:
Effect on fertility: Abstract
The potential toxicity of sodium bromate (CAS No. 7789-38-0) was evaluated using a short-term reproductive and developmental toxicity screen. This study design was selected to identify the process (development; female reproduction; male reproduction; various somatic organs/processes) that is the most sensitive to sodium bromate exposure.
A dose range-finding study was conducted at concentrations of 0, 250, 500, 1000, and 2000 ppm in order to select concentrations for the 35-day study. Based on dose-related body weight reductions and decreased feed and water consumption, the concentrations for the 35-day study were selected to be 0, 25, 80, and 250 ppm. For the main study, Sprague-Dawley rats were administered sodium bromate at these concentrations in the drinking water over a 35-day period. One group of male rats (10 per group) and two groups of female rats designated as Group A (peri-conception, 10 per group) and Group B (gestational exposure, 13 per group) were used at each dose level. Control animals received deionized water, the vehicle.
During the treatment period, all animals survived to the scheduled necropsy and there were no general toxic effects noted at any level. The overall average calculated consumption of sodium bromate for Groups 2-4 was approximately 2.6, 9.0, and 25.6 mg/kg body weight/day, respectively. There were no changes observed in the reproductive data for the Group A and Group B females. The male and female weekly absolute body weights, feed consumption, water consumption, clinical observations, and gross findings were comparable among dose groups. The male organ weights and organ-to-body weight ratios were also comparable across dose groups. Although there was no effect on male fertility, there was a slight decrease in epididymal sperm density, which decreased with increasing concentration and reached significance in the 250 ppm males (reduced by 18%). Sodium bromate resulted in no treatment-related gross or microscopic changes in the kidney, liver, spleen, testis, or epididymis. Serum ALT was decreased by 14% in the 80 and 250 ppm groups. Because this change was small, and in the absence of changes in other liver enzymes, this was deemed to be biologically insignificant.
Results of this study indicate that sodium bromate treatment did not produce any adverse signs of general toxicity in any of the dose levels tested, and based on these findings, a maximum tolerated dose (MTD) was not reached. Female reproductive function was not adversely affected in this study. Sodium bromate appeared to slightly reduce male epididymal sperm density at 250 ppm. Based on the lack of general toxicity findings at any dose, and the epididymal sperm density decrease at 250 ppm , the no-observable-adverse-effect-level (NOAEL) was determined to be 80 ppm. From these data, sodium bromate may be a selective male reproductive toxicant at 250 ppm since male reproductive toxicity was noted in the absence of general toxicity.
Sodium Bromate (rats), CAS No. 7789-38-0 Study Number: RDGT94007
NTIS# PB96-190640
[NTP]
Effect on developmental toxicity: Abstract
The potential toxicity of sodium bromate (CAS No. 7789-38-0) was evaluated using a short-term reproductive and developmental toxicity screen. This study design was selected to identify the process (development; female reproduction; male reproduction; various somatic organs/processes) that is the most sensitive to sodium bromate exposure.
A dose range-finding study was conducted at concentrations of 0, 250, 500, 1000, and 2000 ppm in order to select concentrations for the 35-day study. Based on dose-related body weight reductions and decreased feed and water consumption, the concentrations for the 35-day study were selected to be 0, 25, 80, and 250 ppm. For the main study, Sprague-Dawley rats were administered sodium bromate at these concentrations in the drinking water over a 35-day period. One group of male rats (10 per group) and two groups of female rats designated as Group A (peri-conception, 10 per group) and Group B (gestational exposure, 13 per group) were used at each dose level. Control animals received deionized water, the vehicle.
During the treatment period, all animals survived to the scheduled necropsy and there were no general toxic effects noted at any level. The overall average calculated consumption of sodium bromate for Groups 2-4 was approximately 2.6, 9.0, and 25.6 mg/kg body weight/day, respectively. There were no changes observed in the reproductive data for the Group A and Group B females. The male and female weekly absolute body weights, feed consumption, water consumption, clinical observations, and gross findings were comparable among dose groups. The male organ weights and organ-to-body weight ratios were also comparable across dose groups. Although there was no effect on male fertility, there was a slight decrease in epididymal sperm density, which decreased with increasing concentration and reached significance in the 250 ppm males (reduced by 18%). Sodium bromate resulted in no treatment-related gross or microscopic changes in the kidney, liver, spleen, testis, or epididymis. Serum ALT was decreased by 14% in the 80 and 250 ppm groups. Because this change was small, and in the absence of changes in other liver enzymes, this was deemed to be biologically insignificant.
Results of this study indicate that sodium bromate treatment did not produce any adverse signs of general toxicity in any of the dose levels tested, and based on these findings, a maximum tolerated dose (MTD) was not reached. Female reproductive function was not adversely affected in this study. Sodium bromate appeared to slightly reduce male epididymal sperm density at 250 ppm. Based on the lack of general toxicity findings at any dose, and the epididymal sperm density decrease at 250 ppm , the no-observable-adverse-effect-level (NOAEL) was determined to be 80 ppm. From these data, sodium bromate may be a selective male reproductive toxicant at 250 ppm since male reproductive toxicity was noted in the absence of general toxicity.
Sodium Bromate (rats), CAS No. 7789-38-0 Study Number: RDGT94007
NTIS# PB96-190640
[NTP]
Classification Muta. 2 Plus
Classification route species:
 
Classification description:
H341: Suspected of causing genetic defects <state route of exposure if it is conclusively proven that no other routes of exposure cause the hazard>.
Classification key study:
Genetic toxicity in Vitro: see:
Induction of micronucleated reticulocytes by potassium bromate and potassium chromate in CD-1 male mice.
Authors:
Awogi T
Murata K
Uejima M
Kuwahara T
Asanami S
Shimono K
Morita T
Author Address: Otsuka Pharmaceutical Co., Ltd., Tokushima, Japan.
Source: Mutat Res 1992 Feb-Mar;278(2-3):181-5
[EMIC]
Mutat Res 1988 Dec;206(4):455-8
Acute cytogenetic effects of potassium bromate on rat bone marrow cells in vivo.
Fujie K, Shimazu H, Matsuda M, Sugiyama T.
Department of Natural Science, Osaka Womens University, Japan.[MEDLINE]
Oxidative DNA damage induced by potassium bromate in isolated rat renal proximal tubules and renal nuclei.
Authors:
Sai K
Tyson CA
Thomas DW
Dabbs JE
Hasegawa R
Kurokawa Y
Author Address: Division of Toxicology, National Institute of Health Sciences, Tokyo, Japan.
Source: Cancer Lett 1994 Nov 25;87(1):1-7
[EMIC]
Comparative evaluation of the genotoxic properties of potassium bromate and potassium superoxide in V79 Chinese hamster cells.
Authors:
Speit G
Haupter S
SchÓutz P
Kreis P
Author Address: UniversitÓatsklinikum Ulm, Abteilung Medizinische Genetik, D-89069, Ulm, Germany. guenter.speit@medizin.uni-ulm.de
Source: Mutat Res 1999 Feb 19;439(2):213-21
[EMIC]

Genetic toxicity in Vivo: see:
Induction of micronucleated reticulocytes by potassium bromate and potassium chromate in CD-1 male mice.
Authors:
Awogi T
Murata K
Uejima M
Kuwahara T
Asanami S
Shimono K
Morita T
Author Address: Otsuka Pharmaceutical Co., Ltd., Tokushima, Japan.
Source: Mutat Res 1992 Feb-Mar;278(2-3):181-5
[EMIC]
Mutat Res 1988 Dec;206(4):455-8
Acute cytogenetic effects of potassium bromate on rat bone marrow cells in vivo.
Fujie K, Shimazu H, Matsuda M, Sugiyama T.
Department of Natural Science, Osaka Womens University, Japan.[MEDLINE]
Oxidative DNA damage induced by potassium bromate in isolated rat renal proximal tubules and renal nuclei.
Authors:
Sai K
Tyson CA
Thomas DW
Dabbs JE
Hasegawa R
Kurokawa Y
Author Address: Division of Toxicology, National Institute of Health Sciences, Tokyo, Japan.
Source: Cancer Lett 1994 Nov 25;87(1):1-7
[EMIC]
Comparative evaluation of the genotoxic properties of potassium bromate and potassium superoxide in V79 Chinese hamster cells.
Authors:
Speit G
Haupter S
SchÓutz P
Kreis P
Author Address: UniversitÓatsklinikum Ulm, Abteilung Medizinische Genetik, D-89069, Ulm, Germany. guenter.speit@medizin.uni-ulm.de
Source: Mutat Res 1999 Feb 19;439(2):213-21
[EMIC]

Classification Carc. 2 Plus
Classification route species:
 
Classification description:
H351: Suspected of causing cancer <state route of exposure if it is conclusively proven that no other routs of exposure cause the hazard>.
Classification key study:
Key information: 5.4 Evaluation
There is sufficient evidence for the carcinogenicity of potassium bromate in experimental animals.
No data were available on the carcinogenicity of potassium bromate to humans.
N.B. - After the meeting, the Secretariat became aware of a study in which 9% of male hamsters administered potassium bromate in the drinking-water developed kidney tumours (Takamura et al., 1986).
Subsequent evaluation: Suppl. 7 (1987) (p. 70: Group 2B)
IARC
[INCHEM]

Classification STOT Rep. Exp. 2 Plus
Classification route species:
 
Classification description:
H373: May cause damage to organs <or state all organs affected, if known> through prolonged or repeated exposure <state route of exposure if it is conclusively proven that no other routes of exposure cause the hazard>.
Classification key study:
Repeated dose toxicity:

Oral Route
Primary Organ Effected: Renal toxicity (Kidney)
Secondary Organ(s) Effected: Hepatotoxicity (liver)
Long term
DRINKING WATER
Groups of 27 male B6C3F1, BDF1 or CDF1 mice received 750 mg potassium bromate/l of drinking water (approx. 60-90 mg/kg bw) for 88 weeks. A control group of 15 male/strain was used. One renal adenocarcinoma was found in a B6C3F1 treated mouse and a renal adenoma was found in 2, 1 and 0 treated mice of the B6C3F1, BDF1 and CDF1 strain, respectively. No renal adenocarcinomas or adenomas were found in the control group. Renal dysplastic foci were seen in 2, 4 and 0 treated mice of B6C3F1, DBF1 and CDF1 strain, respectively (in control groups 1, 1 and 0, respectively). In addition, significant increased incidences of liver adenomas in B6C3F1 mice and adenomas of the small intestine in CDF1 mice were observed (Kurokawa et al.,1990).
Male Slc:Wistar rats received 0.04% potassium bromate in their drinking water (equal to 400 mg/l). Markedly decreased growth was seen after one month. After 7-11 weeks karyopicnotic foci of tubules in the inner stripe of the medulla were seen. Markedly increased BUN levels were observed after 1 year and 3 months accompanied by marked structural abnormalities of the cortical tubules. Degeneration, regeneration atypism and cystic changes of the renal cortex were seen. Renal adenocarcinoma were seen in 2 out of 9 rats (only English summary of Japanese publication available) (Nakano et al., 1989).
Potassium bromate was administered to groups of 8-20 male F344 rats at a dose-level of 500 mg/l of drinking water for periods of 13, 26, 39, 52 or 104 weeks. The animals were sacrificed immediately or were given drinking water up to 104 weeks. In the kidneys the number of dysplastic foci, adenomas and adenocarcinomas in all discontinued treatment groups were approximately equal to or even higher than those in the group given potassium bromate continuously for 104 weeks. The minimum induction time for the development of renal adenomas was 26 weeks and the minimum treatment period and minimum total dose for the induction of renal adenomas and adenocarcinomas were 13 weeks and 4 g/kg bw, respectively, when the rats were maintained thereafter on drinking water for 2 years. In this study, also, induction of mesothelioma of the peritoneum was observed (Kurokawa et al., 1987a).
Groups of 20 male Syrian golden hamsters received 0, 125, 250, 500 or 2000 mg potassium bromate/l of drinking water for 89 weeks. Survival times did not show differences. Mean final body weights in the 2000 mg/l group were significantly reduced. Mean absolute and relative kidney weights were significantly increased at the 2000 and 250 mg/l levels. One, two and four hamsters in 250, 500 and 2000 mg/l group developed a renal adenoma. No renal tumours were seen in the control group. Structural and cellular morphological characteristics of the renal tumours as well as the dysplastic foci found in the treated groups, were similar to those induced in rats (Takamura et al., 1985).
762. Potassium bromate (WHO Food Additives Series 30) [INCHEM]