Analysis of studies related to tumorigenicity induced by hydroquinone

Hydroquinone (HQ) produced renal adenomas in male F344 rats, and these tumors appeared to arise from areas of spontaneous progressive nephropathy; the nephropathy itself has been found to be enhanced by HQ. Other neoplasms were not confirmed to be causally related to HQ among the reported bioassays. In the male F344 rat, HQ administered alone was not DNA reactive. HQ produced enhanced proliferation of renal tubular epithelium, presumably through toxicity involving glutathione conjugate formation. In the kidney, bone marrow, and other tissues, HQ may induce toxicity by redox cycling and lipid peroxidation. In bone marrow, HQ may produce microtubulin dysfunction, which is a plausible explanation for positive cytogenetic tests, the only consistently positive genotoxicity effect reported for HQ. Although HQ is a metabolic product of benzene, several lines of evidence suggest that the effects of HQ exposure are significantly different from those of benzene. Based upon the plausible mechanisms by which HQ may produce kidney tumors in male rats, we have concluded that occupational exposure levels of HQ are not predicted to be a cancer risk for humans.