Assessment of the carcinogenicity associated with oral exposures to hydrogen peroxide

Concern regarding hydrogen peroxide (H2O2) carcinogenicity arises from its ability to act as a strong oxidizing agent. In short-term genotoxicity tests, H2O2 has given predominantly positive results; however, these assays have been performed using either bacterial strains engineered to be exquisitely sensitive to oxidant damage, or mammalian cells deficient in antioxidant enzymes. Significantly, the addition of antioxidant protective measures (normally present in vivo) to these assay systems protects against H2O2 genotoxicity. In most whole animal studies, H2O2 exposure neither initiates nor promotes tumors. In mice, however, 0.4% H2O2 in drinking water was reported to induce hyperplastic lesions of the duodenum and to erode areas in the glandular stomach epithelium. Owing to the chemistry of dilute H2O2 solutions and the anatomy/physiology of the gastrointestinal tract, it is unlikely that orally ingested H2O2 reaches the duodenum. Instead, greatly decreased water consumption and the resultant abrasion of the luminal lining on ingestion of pelleted dry rodent chow is the most likely cause of the observed gastric and duodenal lesions following H2O2 administration in drinking water. Significantly, when hamsters received high doses of H2O2 by gastric intubation (and water intake was not affected), the gastric and duodenal epithelia appeared normal. In-depth analysis of the available data supports the conclusion that oral ingestion of H2O2 should not be considered a carcinogenic threat.