Elsevier

Early Human Development

Volume 50, Issue 3, 27 February 1998, Pages 283-292
Early Human Development

Neurological condition in 42-month-old children in relation to pre- and postnatal exposure to polychlorinated biphenyls and dioxins.

https://doi.org/10.1016/S0378-3782(97)00066-2Get rights and content

Abstract

Adverse neurological effects of exposure to PCBs have been found up to 18 months of age. Now we report on the effect of pre- and postnatal exposure to PCBs and dioxins on the neurological condition at 42 months of age. For this purpose, PCB levels were determined in cord and maternal plasma, and used as a measure of prenatal exposure. Breast milk was analyzed for PCBs and dioxins. In addition, PCBs were determined in plasma sampled from the child at 42 months of age. We evaluated the neurological condition of 394 children using the Touwen/Hempel method. After adjustment for covariates, neither prenatal PCB exposure nor postnatal exposure to PCBs and dioxins was found to be related to the neurological condition at 42 months of age.

Introduction

Polychlorinated biphenyls (PCBs) and dioxins are polycyclic aromatic compounds, which are widespread environmental pollutants. PCBs are resistant to high temperatures, they can easily conduct heat, and have electrical insulating properties. They have been produced for use in plasticizers, fire retardants, dielectrical fluids in transformers and capacitators, and in hydraulic fluids. In the late 1970s their environmental persistence was recognized, and they were banned world-wide. Yet, in for example eastern Europe, PCBs have been produced until the mid-1980s [14]. Dioxins are derived from many sources, mainly thermal and industrial processes. The incineration of municipal and industrial waste has a major role in the environmental deposition [1].

PCBs have a total number of 209 possible congeners which differ in the degree of chlorination and the position of the chlorine atoms. Dioxins are a mixture of 75 polychlorinated dibenzo-p-dioxins and 135 dibenzofurans. Both PCBs and dioxins are absorbed readily and, due to their very long half-life and high lipophilicity, they accumulate in the adipose tissue of animals and human beings. The uptake in plants is negligible. In organisms at the top of the food chain, including human beings, high concentrations have been detected in blood and adipose tissue [12]. PCBs and dioxins cross the placenta, and are transferred into human milk [9]. In formula milks, cow milk lipids are replaced by fats of vegetable origin having negligible contents of PCBs and dioxins.

Previously, we have studied the effects of prenatal and lactational exposure to PCBs and dioxins on the neurological condition in the second week after birth [7]and at 18 months of age [8]. For that purpose we followed a group of healthy term infants subjected to background levels of exposure from birth. In the second week after delivery, the combination of a high prenatal and a high lactational exposure was found to result in an adverse effect on the neurological condition and a higher incidence of hypotonia. When the children reached the age of 18 months, we found a negative impact of the prenatal PCB exposure on the neurological condition. No effect of lactational exposure to PCBs or dioxins could be detected. We now report on the effect of prenatal exposure to PCBs, PCB and dioxin exposure via breast-feeding, and the child's 42-month PCB body burden on the neurological condition at 42 months of age.

Section snippets

Subjects

From June 1990 until June 1992, healthy pregnant women were asked to participate in the study in Groningen and Rotterdam. Groningen is a semi-urban area in the north of the Netherlands, whereas the Rotterdam area is a highly industrialized region in the Western parts of the Netherlands. It was intended to include 100 breast-feeding and 100 formula-feeding mothers in each study centre. The women were approached by their midwives or obstetrician between the 32nd and 34th week of pregnancy and

Results

The study group consisted of 418 mother–infant pairs, of which 209 were in the breast-feeding group and 209 in the formula-feeding group. In the last month of pregnancy, 415 maternal blood samples were obtained. At birth, 382 cord blood samples were taken. Due to the limited volumes of blood, in nine children the PCB 118 level in cord plasma was not measurable. In the sixth week after delivery, 195 breast milk samples were collected. The dioxin, planar-, mono-ortho-, and di-ortho PCB TEQ values

Discussion

No adverse effects of prenatal PCB exposure on the neurological condition were found at 42 months of age. Although negative effects have been shown in the neonatal period and at 18 months 7, 8, we found no relationship between the prenatal PCB exposure and the neurological condition at 42 months of age. In addition, neither the lactational exposure nor the child's current body burden was related to the neurological optimality at 42 months of age.

Our results are in accordance with the findings

Acknowledgements

We would like to thank M. Huisman and R.R. Bakker for their critical review of the article, and the parents and the children for their cooperation. This study is part of the `Dutch PCB/dioxin study', which is funded by the `European Community'.

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