Early postnatal benzo(a)pyrene exposure in Sprague-Dawley rats causes persistent neurobehavioral impairments that emerge postnatally and continue into adolescence and adulthood.

Previous studies have demonstrated that benzo(a)pyrene (BaP) may disrupt the development of key biological systems, thus leaving children more vulnerable to functional impairments in adulthood. The current study was conducted to determine whether neurotoxic effects of postnatal BaP exposure on behavioral performance persist in juvenile and young adult stages. Therefore, neonate Sprague-Dawley pups were given oral doses of BaP (0.02, 0.2, and 2 mg/kg/day) continuing through a period of rapid brain development (on postnatal days [PNDs] 5-11). Further, developmental milestones and behavioral endpoints assessing sensory and motor maturation were examined. Also, in this study, Morris water maze and elevated plus maze were used for evaluating the cognitive function and anxiety-like behavior. Our results showed that there was altered ontogeny in a few measures of neuromotor development; however, other developmental milestones and sensory responses were not altered significantly. Moreover, the locomotor activity deficit in BaP-treated pups was evident at PND 36 and was most pronounced in the PND 69. Also, exposure to BaP during early postnatal development had an adverse effect on adult rats (PND 70) in the elevated plus maze, and the swim maze suggests that low doses of BaP impair spatial learning functions at adult test period. In contrast, BaP exposure had no evident effect on behaviors in these two mazes for adolescent animals. These data clearly indicate that behavioral impairments resulting from postnatal BaP exposure are potentially long-lasting and may not be apparent in juveniles, but are present in young adulthood.