People in developed countries are exposed to multiple endocrine disruptors, including bisphenol A (BPA), the monomer of polycarbonate plastics, and triclosan, an antimicrobial agent. Few studies have investigated their distribution and interactions at doses that might represent human exposure. We examined single and repeated low dietary doses of BPA in mice and rats, and determined the influences of concurrent triclosan exposure upon the presence and metabolism of BPA. In females receiving 50 µg/kg ¹⁴C-BPA, radioactivity was found throughout the body, but much less in brain than reproductive tissues. Pre-treatment with estradiol or the estrogen antagonist ICI 182,780 significantly reduced radioactivity in the uterus. GC-MS indicated that the majority of BPA in the uterus was aglycone (receptor-active). Mice given 0.5, 5, or 50 µg/kg ¹⁴C-BPA also showed more radioactivity in the uterus than in other non-metabolic tissues. Females given 7 or 28 daily doses of ¹⁴C-BPA showed significantly more radioactivity in reproductive tissues than did those given just one dose, in measures taken 24 hours after the last dose. We then examined whether triclosan exposure affects the distribution of ingested ¹⁴C-BPA in select tissues. Mice were each injected sc with triclosan, in doses ranging from 0.2 to 18 mg, followed by oral administration of either 5 or 50 µg/kg ¹⁴C‑BPA. In females, radioactivity was elevated in the heart, lungs, muscle, uterus, ovaries, and blood serum in those receiving triclosan compared to those given ¹⁴C-BPA alone. This effect was also observed in the epididymides and serum of males. The effective dose of triclosan depended upon the tissue. These data show that BPA preferentially localizes to reproductive tissues following single and repeated low oral doses. They also indicate that triclosan exacerbates BPA presence in vivo, consistent with in vitro evidence that triclosan utilizes enzymes responsible for the metabolism and excretion of BPA.