Evaluation of the Adequacy of Published Studies of Low-Dose Effects of Bisphenol A on the Rodent Prostate for Use in Human Risk Assessment

• Published in: Regulatory toxicology and pharmacology Vol. 35; no. 3; pp. 338 - 346
• Main Authors: Milman, Harry A., Bosland, Maarten C., Walden, Paul D., Heinze, John E.
• Format: Journal Article
• Language: English
• Published: San Diego, CA Elsevier Inc 01.06.2002; Elsevier
• Subjects: Air Pollutants - adverse effects; Air Pollutants - toxicity; Animals; Benzhydryl Compounds; Biological and medical sciences; Chemical and industrial products toxicology. Toxic occupational diseases; Dose-Response Relationship, Drug; Estrogens, Non-Steroidal - adverse effects; Estrogens, Non-Steroidal - toxicity; Female; Humans; Hyperplasia - chemically induced; Hyperplasia - pathology; Male; Maternal Exposure; Medical sciences; Mice; Organ Size - drug effects; Phenols - adverse effects; Phenols - toxicity; Pregnancy; Prenatal Exposure Delayed Effects; Prostate - drug effects; Prostate - pathology; Prostatitis - chemically induced; Prostatitis - pathology; Rats; Risk Assessment; Species Specificity; Toxicology; Various organic compounds; prostatitis; testosterone; phenylephrine; bisphenol A; 17β-estradiol; prostate; endocrine disrupters; benign prostatic hyperplasia; hormonally active agents; Evaluation; Prostate disease; Rat; Toxicity; Low dose; Rodentia; Pregnancy; Bisphenol A; Progeny; Vertebrata; Mammalia; Mouse; Animal; Methodological bias; Prostate
• ISSN: 0273-2300; 1096-0295
• DOI: 10.1006/rtph.2002.1553

Studies conducted in our laboratories and by others found no consistent correlation between prostate size, prostate pathology, or the development of prostate cancer under a variety of experimental conditions. Furthermore, an evaluation of eight published studies that were conducted in mice and rats following in utero exposure by oral treatment of dams with low levels of bisphenol A (BPA) and that focused on the prostate identified several discrepancies that affect their adequacy for use in human risk assessment. For example, there was inadequate reporting of the purity of BPA and the animal supplier used, and housing of offspring was not the same among the studies. In addition, there were differences between studies with mice and rats in exposure regimen, route of exposure, and numbers of dams or pups used per BPA dose group. Poor inter- and intraspecies correlation (i.e., mouse to rat or between mouse or rat strains) further complicates the ability to use results from these studies to predict potential prostate effects in humans. Thus, we conclude that a finding of increased prostate weight in rodent studies with perinatal exposure in the absence of associated pathologic and/or functional changes is meaningless and not indicative of a potential adverse effect in humans.