Use of this information is subject to copyright laws and may require the permission of the owner of the information, as described in the ECHA Legal Notice.
EC number: 204-701-4 | CAS number: 124-43-6
Histological examinations revealed no changes (examined: all gross lesions, tongue, esophagus, stomach, duodenum, ileum, jejunum, caecum, colon, and rectum from all animals in all groups, and on all major organs including the sex organs in the high dose and control animals).
- The most notable effect was increased water consumption observed among males that had received 3000 ppm, and among females that had received 300, 1000 or 3000 ppm.
- After the recovery period no hyperplasia was seen in any dose group.
Reportedly, the sub-chronic toxicity of hydrogen peroxide was examined in a drinking water study (FMC, 1997; dose levels: 0, 100, 300, 1000, and 3000 ppm) using catalase-deficient male and female mice (15/sex/group). At termination after 90 days, 10 animals/sex/group were sacrificed and examined (blood, body weights, gross pathology, histopathology. The latter included all gross lesions, tongue, esophagus, stomach, duodenum, ileum, jejunum, caecum, colon, and rectum from all animals in all groups, and on all major organs including the sex organs in the high dose and control animals). The remaining 5 animals/sex/group continued on distilled water during a 6-week recovery period.
Effects during the treatment period (Days 0-90): There were no treatment-related deaths. Clear treatment-related, dose-dependent effects were noted among both females and males receiving 300, 1000 or 3000 ppm of H2O2. Body weights were significantly reduced only in male and female high-dose animals receiving 3000 ppm. Dose-related reductions in both food and water consumption were observed in female animals receiving 300 ppm and greater, while among the males consistent reductions were observed only at the top dose level. Among females 300 ppm (103 mg/kg/day) was a LOAEL based on significant reduction in water consumption. Histopathology revealed treatment-related effects only in the duodenum of males and females at 1000 and 300 ppm, and in one male at 300 ppm. Although the general architecture of the affected duodenum was normal, there was an increase in cross sectional diameter and a larger mucosal area with broader, more substantial villi when compared to those of control mice. The change was assessed as mucosal hyperplasia because of the increase in mucosal thickness and size of the villi. Mucosal hyperplasia was not found in 100 ppm group mice, neither among controls. No other histopathological changes were noted on the tongue, esophagus, stomach, duodenum, ileum, jejunum, caecum, colon, and rectum from all animals in all groups, and on all major organs including the sex organs in the high dose and control animals.
Recovery period: the most notable effect was increased water consumption observed in males that had received 3000 ppm, and among females that had received 300, 1000, or 3000 ppm. Mucosal hyperplasia was reversible, as no such lesion was seen in any dose group after the recovery period.
The NOAEL was 100 ppm (26 and 37 mg/kg bw/day) in this study for males and females, respectively, based on dose-related reductions in water and food consumption, and on the observation of duodenal mucosal hyperplasia (ECB, 2003).
Information on Registered Substances comes from registration dossiers which have been assigned a registration number. The assignment of a registration number does however not guarantee that the information in the dossier is correct or that the dossier is compliant with Regulation (EC) No 1907/2006 (the REACH Regulation). This information has not been reviewed or verified by the Agency or any other authority. The content is subject to change without prior notice.Reproduction or further distribution of this information may be subject to copyright protection. Use of the information without obtaining the permission from the owner(s) of the respective information might violate the rights of the owner.
Welcome to the ECHA website. This site is not fully supported in Internet Explorer 7 (and earlier versions). Please upgrade your Internet Explorer to a newer version.
Close Do not show this message again