Effects of developmental exposure to polychlorinated biphenyls and/or polybrominated diphenyl ethers on cochlear function.

Developmental exposure to polychlorinated biphenyls (PCBs) causes hearing loss that may be due to reduced thyroxine during cochlear development. Polybrominated diphenyl ethers (PBDEs) are structurally similar to PCBs and reduce thyroxine. This study utilized an environmental PCB mixture and a commercial PBDE mixture, DE-71, that represents the PBDEs found in humans to assess the potential for additive effects of PCBs and PBDEs on cochlear function. Female Long-Evans rats were dosed with corn oil vehicle, PCBs (3 or 6 mg/kg), molar equivalent doses of PBDEs (5.7 or 11.4 mg/kg), 3 mg/kg PCBs + 5.7 mg/kg PBDEs, or 6 mg/kg PCBs + 11.4 mg/kg PBDEs throughout gestation and lactation. At weaning, pup blood was taken to assess thyroxine concentrations. One male and one female from each litter were maintained until adulthood for distortion product otoacoustic emission (DPOAE) measurements of cochlear function. DPOAE amplitudes were decreased and thresholds were elevated in the 6 mg/kg PCB group. Exposure to PBDEs did not cause DPOAE deficits. There was an interactive effect from combined exposure such that the individual low doses of PCBs and PBDEs did not result in DPOAE deficits, but the two combined produced a deficit similar to that in the high-dose PCB group. Serum thyroxine concentrations of all groups were reduced compared with controls, but PBDEs produced a less dramatic reduction than PCBs, which could explain the lack of DPOAE effects. Importantly, there was evidence that the co-exposure to subthreshold doses of PCBs and PBDEs can have an additive effect on cochlear function.