Levels of certain metals, organochlorine pesticides and dioxins in cord blood, maternal blood, human milk and some commonly used nutrients in the surroundings of the Aral Sea (Karakalpakstan, Republic of Uzbekistan)

Since the 1960s a massive decline in the volume of the Aral Sea has occurred as a result of the diversion of the supplying rivers to cotton irrigation schemes. The contaminated sediment of the former seabed has been disseminated over the surrounding area by strong winds. This deterioration of the ecosystem has created a hazardous situation for the health of approximately 3.5 million people. This pilot study was undertaken to assist Karakalpak health workers in investigating the degree of exposure to metals, persistent organochlorine pesticides (OCPs) and dioxins during the most vulnerable prenatal and postnatal period and to provide guidelines for future research. All subjects came from areas located within 200 km of the southern border of the Aral Sea. Blood was obtained from 18 pregnant women and 28 newborns (cord blood) to determine the levels of metals, lead, cadmium, zinc and selenium and the OCPs alpha-, beta- and gamma -hexachlorocyclohexane (HCH; lindane is the product name of gamma -hexachlorocyclohexane), hexachlorobenzene (HCB), and isomers and metabolites of dichlorodiphenyltrichloroethane (DDT), i.e. op-DDT, pp-DDT, pp-DDE and pp-TDE. Levels of metals were also determined in blood from 28 non-pregnant women. In addition, levels of 17 dioxins were determined in 41 human milk samples and I batch of formula. Information about possible dietary sources of the fat-soluble OCPs and dioxins was obtained from a pooled sample of butter and from seven cottonseed oil samples. A mass-selective detector coupled to a gas chromatograph equipped with a large volume injector was used to analyse the selected OCPs, whereas the dioxins were determined by gas chromatography with high-resolution mass spectrometry. The levels of metals in cord and maternal blood were consistent with concentrations observed in European countries. Only three women (7%) had lead levels greater than 100 ppb. The most notable pollutants in maternal and cord blood were the OCPs, notably HCB, beta -HCH, pp-DDE and the most toxic dioxin, 2,3,7,8-TCDD, when calculated as TEQs. A similar pattern was observed in human milk: beta -HCH and pp-DDE levels of more than 1000 ng g(-1) fat were found in 68 and 43% of the subjects, respectively. Levels of 2,3,7,8-TCDD were six times higher than those observed in Western Europe. Traces of pp-DDE were detected in the batch of formula milk. Contaminated animal fat, but not cottonseed oil, is the most likely dietary source of OCPs and dioxins. Conclusion: Further epidemiological research is needed to elucidate the health implications of these pollutants on perinatal and maternal health, including lactation. More importantly, an investigation should be initiated to identify the emission sources of persistent organic pollutants in Karakalpakstan and adjacent regions

Prenatal exposure to organochlorine compounds and neonatal thyroid stimulating hormone levels.

It has been suggested that prenatal exposure to some organochlorine compounds (OCs) may adversely affect thyroid function and may, therefore, impair neurodevelopment. The main aim of this study was to examine the relationship of cord serum levels of 1,1,1-trichloro-2,2-bis(4-chlorophenyl)ethane (4,4'-DDT), 1,1-dichloro-2,2-bis(4-chlorophenyl)ethylene (4,4'-DDE), β-hexachlorocyclohexane (β-HCH), hexachlorobenzene (HCB), four individual polychlorobiphenyl (PCB) congeners (118, 138, 153, and 180), and their sum, with neonatal thyroid stimulating hormone (TSH) levels in blood samples in a mother-infant cohort in Valencia, Spain. This study included 453 infants born between 2004 and 2006. We measured OC concentrations in umbilical cord serum and TSH in blood of newborns shortly after birth. Associations between neonatal TSH levels and prenatal OC exposure adjusted for covariates were assessed using multivariate linear regression analyses. Neonatal TSH levels tended to be higher in newborns with β-HCH levels in umbilical cord above 90th percentile (104 ng/g lipid) than in those with levels below the median (34 ng/g lipid), with an adjusted increment in neonatal TSH levels of 21% (95% confidence interval=-3, 51; P=0.09). No statistically significant association was found between the remaining OCs and TSH at birth. Prenatal exposure to β-HCH may affect neonatal thyroid hormone status and its function in neurological development