Dioxins [polychlorinated dibenzo-p-dioxins (PCDD), dibenzofurans (PCDF)] and polychlorinated biphenyls (PCB) are potentially hazardous compounds. Animal studies have demonstrated that PCDD, PCDF, and PCB can alter thyroid hormone homeostasis. We investigated thyroid hormone levels in 105 mother-infant pairs. To estimate maternal and infant exposure, four nonplanar PCB congeners were measured in maternal plasma during the last month of pregnancy and in umbilical cord plasma. Seventeen PCDD and PCDF congeners, three planar PCB congeners, and 23 nonplanar PCB congeners were measured in human milk. Higher PCDD, PCDF, and PCB levels in human milk, expressed as toxic equivalents, correlated significantly with lower plasma levels of maternal total triiodothyronine and total thyroxine, and with higher plasma levels of TSH in the infants in the 2nd wk and 3rd mo after birth. Infants exposed to higher toxic equivalents levels had also lower plasma free thyroxine and total thy-PCDD and PCDF, summarized as dioxins, are tricyclic aromatic compounds. Because the number of chlorine atoms can vary between one and eight, there are potentially 75 different PCDD and 135 PCDF congeners. They are mainly formed as by-products during the synthesis of organochlorine chemicals and during the combustion of municipal and hazardous waste (1). PCB are a compilation of 209 possible congeners with different chlorine substitutions. Because of their unique physical properties and chemical stability, mixtures were used for diverse

Polychlorinated biphenyls (PCBs) and dioxins (polychlorinated dibenzo-p-dioxins (PCDDs), and dibenzofurans (PCDFs)) are widespread environmental contaminants which are neurotoxic in animals. Perinatal exposure to PCBs, PCDDs, and PCDFs occurs prenatally via the placenta and postnatally via breast milk. To investigate whether such an exposure affects the neonatal neurological condition, the neurological optimality of 418 Dutch newborns was evaluated with the Prechtl neurological examination. Half of the infants were breast-fed, the other half were formula-fed, representing a relatively high against a relatively low postnatally exposed group, respectively. As an index of prenatal exposure, four non-planar PCBs in cord and maternal plasma were used. These PCB levels were not related to neurological function. As measures of combined pre- and early neonatal exposure, 17 dioxin congeners, three planar, and 23 non-planar PCB congeners were determined in human milk in the second week after delivery. Higher levels of PCBs, PCDDs, and PCDFs in breast milk were related to reduced neonatal neurological optimality. Higher levels of planar PCBs in breast milk were associated with a higher incidence of hypotonia. This study confirms previous reports about the neurotoxic effects of these compounds on the developing brain of newborn infants.

The neurological optimality of 418 Dutch children was evaluated at the age of 18 months, in order to determine whether prenatal and breast milk mediated exposure to polychlorinated biphenyls (PCBs) and dioxins affected neurological development. Half of the infants were breast-fed. the other half were formula-fed. PCB concentrations in cord and maternal plasma were used as a measure of prenatal exposure to PCBs. To measure postnatal exposure, PCB and dioxin congeners were determined in human milk and in formula milk.After adjusting for covariates, transplacental PCB exposure was negatively related to the neurologkal condition at 18 months. Althc.ugh greater amounts of PCBs and dioxins are transferred via nursing than via placental passage, an effect of lactational exposure to PCBs and dioxins could not be detected. We even found a beneficial effect of breast-feeding on the fluency of movements.We conclude that transplacental PCB passage has a small negative effect on the neurological condition in 18-month-old toddlers.

Public Health Briefs breast-feeding" as an analytic category may dilute the true association between intentions of pregnancy and breastfeeding because of the heterogeneous nature of that category. In our study, however, the same associations were observed for both any breast-feeding and exclusive breast-feeding.This study highlights the importance of identifying women with unplanned pregnancies and specifically targeting that group for breast-feeding promotion interventions. Finally, the study provides yet further evidence that children bom to women who did not intend to become pregnant are at higher risk than other children of not having sufficient resources-in this instance, the benefits of breast-feeding-for healthy development.4 z Acknowledgments

We analyzed polychlorinated biphenyls (PCBs) in s.c. adipose tissue, liver, and brain of nine fetuses who died in utero. Their median (range) gestational ages and birth weights were 34 (17-40) wk and 2050 (162-3225) g. Three fetuses were small for gestational age. The levels of PCB congener nos. 118, 138, 153, and 180, and the sum of these (sigmaPCB), were calculated in terms of tissue total fat content (ng/g fat). The median (range) sigmaPCB (in ng/g fat) amounted to adipose tissue 235 (97-768), liver 198 (67-362), and brain 50 (22-122). Median (range) sigmaPCB levels in liver and brain were 0.8 (0.4-0.9) and 0.2 (0.1-0.3) times, respectively, as high as the sigmaPCB levels in adipose tissue. There were strong relations between sigmaPCB in adipose tissue and sigmaPCB in liver (r=0.98; p < 0.01), and between sigmaPCB in adipose tissue and sigmaPCB in brain (r=0.91; p < 0.01). Adipose tissue, liver, and brain did not show differences in the distribution of congeners 118, 138, 153, and 180, and there was no statistically significant association between tissue PCB levels and gestational age (r varied between 0.22 and 0.47). Median sigmaPCB levels in fetal adipose tissue proved to be comparable with our previously established sigmaPCB levels in mature breast milk of 93 Dutch women (median 414; range 158-969 ng/g of fat). The PCB congeneric distribution of fetal adipose tissue was not different from that of human milk. We conclude that maternal PCBs have a tendency to accumulate notably in fetal tissues with high triglyceride contents. They are easily transferred across the placenta and seem to become equilibrated among the apolar parts of maternal and fetal lipids.