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.

The carbamoyloxime pesticides methomyl, oxamyl and aldicarb, together with the oxidation products of aldicarb, are known to break down much more rapidly in certain anaerobic subsoils than in the aerobic topsoils from the same site. Ferrous ions have now been shown to be involved in this reaction. Oxamyl was degraded in aqueous solutions at 30°C containing 250 pg ml-' Fez+ with a half-life of about 10 h, independent of pH in the range of 5.65-7.66; the observed products of this reaction were N,N-dimethyl-1-cyanoformamide and methanethiol. These same products, rather than the oximino hydrolysis product observed from degradation in aerobic soils, were rapidly and quantitatively formed from oxamyl in suspensions of anaerobic reduced subsoils (Fe2+ concentration 27-41 ,ug ml-' soil water), but oxamyl was rather stable in water-saturated Vredepeel subsoil (Fe2+ concentration 0.65 pg m1-l) in which the redox potential was much higher. Methomyl behaved similarly. The rates of reaction in the suspensions of anaerobic subsoils were greater than expected from the concentrations of Fe2+ in the soil water, but most of the Fe2+ resent in soil was bound to the soil particles by cation exchange and this bound Fey+ may have participated. Breakdown of aldicarb was accelerated both in solutions of Fe2+ and in the suspensions of anaerobic reduced subsoils, though the rate enhancement was less than observed with methomyl and oxamyl; 2-methyl-2methylthiopropionitrile and 2-methyl-2-methylthiopropionaldehyde were the observed products from aldicarb in anaerobic soil but only the former was produced in Fe2+ solutions; the corresponding nitriles and aldehydes were also yielded by aldicarb sulphoxide and aldicarb sulphone in the anaerobic, reduced subsoils.

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