Relationship between Measures of Exposure to PCBs/Dioxins and Behavioral Effects in Recent Developmental Studies

This paper does not reflect official EPA policy. Epidemiological studies on the neurodevelopmental effects of exposure to PCBs initiated in the last decade have had the opportunity to take advantage of modern methodologies for the analysis of congeners of PCBs, dioxins, and related orga-nochlorine compounds. Each of these studies is a longitudinal prospective study, in which women were recruited during pregnancy and the children are being followed for at least several years after birth. The study from which the largest body of data has been published to date is being performed in the Netherlands, in which exposure to PCBs and related compounds is through the general food supply. Mother-infant pairs were recruited in two cities. Half of the infants were bottle-fed and half breast-fed in each city. Four PCB congeners (118, 138, 153, 180) were assessed in maternal and cord plasma, breast milk, and plasma of the child at 3.5 years. TEQ in breast milk was calculated based on PCDDs/PCDFs and dioxin-like PCBs. Various measures of in utero exposure were associated with suboptimal neurological status during infancy, whereas maternal plasma PCB concentration was associated with cognitive deficits (Kaufman scores) at 3.5 years of age. The child's concurrent plasma PCB levels and maternal PCB plasma levels independently predicted performance on various aspects of a vigilance task, and maternal and cord plasma levels predicted impairment of complex play behavior. Poor scores on behavioral ratings were associated with concurrent blood PCB concentrations in the child. A study in Oswego in Lake Ontario fish eaters includes mothers who never ate Great Lakes fish and mothers who consumed greater than 40 PCB-equivalent pounds of Lake Ontario fish over their lifetime. Sixty-eight PCB congeners were measured in cord blood. Suboptimal neurological status during infancy was associated with maternal fish consumption and highly chlorinated cord PCB levels, whereas deficits in short-term memory at 6 months and 1 year of age were associated with total chlorinated cord PCB levels. In a study in Germany of 171 mother-infant pairs, PCB congeners 138, 153, and 180 were measured in cord plasma and milk 2 weeks after birth; both measures are considered markers of in utero exposure. Suboptimal neurological status during infancy, decrements in Bayley scores at 30 months and Kaufman scores at 42 months were associated with PCBs in milk but not cord plasma. These studies, combined with data from previous studies, reveal a consistent relationship between PCB exposure and suboptimal neurological status during infancy, and cognitive deficits associated with in utero exposure. Data from the Dutch study revealed effects on other behavioral domains associated with concurrent (postnatal) exposure. Although it is not possible to identify specific congeners or groups of congeners that may be responsible for the neurotoxic effects observed in these studies, the TEQ approach was not particularly predictive for neurotoxic outcomes.