ABSTRACT
UNLABELLED: Based on our own findings from a previous study we aimed to establish if cognitive deficit, shown to be induced by perinatal exposure to polychlorinated biphenyls (PCBs) at earlier ages, persists into school-age. Seventy-seven percent of a cohort last examined at 42 months of age using the Kaufman Assessment Battery for Children were reexamined with the same test at 72 months. At this point, and contrary to the results at 30 and 42 months no adverse PCB-effects were found. However, the positive effect of the home environment became even more pronounced. CONCLUSION: early PCB-exposure at current environmental background levels possibly induces transient delay in cognitive development rather than irreversible deficit.
ABSTRACT
Polychlorinated biphenyls (PCBs) cross the placenta and expose the fetus to the body burden of the mother. Additionally, the breastfed baby is postnatally exposed to PCBs in maternal milk. Among the broad spectrum of biological effects interaction with endocrine systems and developmental neurotoxicity are prominent features of these chemical mixtures. Associations between neurodevelopmental delay and prenatal or early postnatal PCB-exposure at environmental levels have been reported in several cohort studies. Adverse effects were found to be associated with early developmental PCB-exposure, although there are discrepancies between studies in terms of confounding, effective PCB-matrix, as well as spectrum and persistence of effects. From these cohort studies alone the causative role of PCBs in producing neurodevelopmental adversity still cannot be considered proven, but experimental findings do provide evidence for the developmental neurotoxicity of PCBs. The underlying mechanisms of this action is still unknown. However, interaction with endocrine systems, namely the estrogen/androgen and, particularly, the thyroid hormone systems are discussed as a possible explanation for PCB-induced neurodevelopmental adversity. Some evidence in this respect is being reviewed.
