AbstractPolychlorinated diphenyl ethers (PCDEs) are structurally similar to polychlorinated biphenyls (PCBs), and some PCDE congeners have been reported to cause toxic responses similar to those caused by some of the non‐ortho‐substituted PCBs, which are mediated by the aryl hydrocarbon receptor (AhR). Twenty‐nine PCDEs were tested for their potency as AhR agonists relative to 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin (2,3,7,8‐TCDD) by measuring their ability to induce the cytochrome P‐450 1A1‐associated enzyme activity, ethoxyresorufin‐O‐deethylase (EROD), in the H4IIE rat hepatoma cell bioassay. All PCDE congeners tested were found to be inactive as EROD inducers except for PCDE 156, which was a weak EROD inducer with a 2,3,7,8‐TCDD equivalency factor of about 1.2 × 10−5. During this study we determined that small amounts of polychlorinated dibenzofurans (PCDFs) that occurred as impurities in the PCDE preparations were the cause of the apparent EROD induction initially measured in our experiments. Once the PCDF impurities were removed by purification on florisil, little or no activity could