Developmental delays and locomotor activity in the C57BL6/J mouse following neonatal exposure to the fully-brominated PBDE, decabromodiphenyl ether.

After several decades of commercial use, the flame retardant chemicals polybrominated diphenyl ethers (PBDEs) and their metabolites have become pervasive environmental contaminants with a global distribution. PBDEs have entered the food chain and increasing levels can be detected in the human body. Decabrominated diphenyl ether (decaBDE) is currently the most widely used of the PBDEs in the United States. Despite its widespread use, little is known about the health effects of decaBDE. The current study examined the effects of neonatal exposure to decaBDE in the inbred C57BL6/J mouse. Neonatal male and female mice were exposed to a daily oral dose of 0, 6, or 20 mg/kg decaBDE from postnatal day 2 to 15. Three groups of endpoints were examined: the ontogeny of sensorimotor responses and serum thyroxine levels in immature animals, and locomotor activity in adult animals. In immature animals, 20 mg/kg/day produced developmental delays in the acquisition of the palpebral reflex. At this age, exposed males also showed a dose-related reduction of serum thyroxine levels. As adults, decaBDE exposure altered the normal sex- and age-specific characteristics of spontaneous locomotor activity. The most striking effect was an increase of activity during the first 1.5 h of the 2 h assessment in males exposed to 20 mg/kg/day decaBDE. These effects suggest that decaBDE is a developmental neurotoxicant that can produce long-term behavioral changes following a discrete period of neonatal exposure.