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Objectives: Exposure to high concentrations of persistent organochlorines may cause fetal toxicity, but the evidence at low exposure levels is limited. Large studies with substantial exposure contrasts and appropriate exposure assessment are warranted. Within the framework of the EU (European Union) ENRIECO (ENvironmental Health RIsks in European Birth Cohorts) and EU OBELIX (OBesogenic Endocrine disrupting chemicals: LInking prenatal eXposure to the development of obesity later in life) projects, we examined the hypothesis that the combination of polychlorinated biphenyls (PCBs) and dichlorodiphenyldichloroethylene (DDE) adversely affects birth weight.Methods: We used maternal and cord blood and breast milk samples of 7,990 women enrolled in 15 study populations from 12 European birth cohorts from 1990 through 2008. Using identical variable definitions, we performed for each cohort linear regression of birth weight on estimates of cord serum concentration of PCB-153 and p,p´-DDE adjusted for gestational age and a priori selected covariates. We obtained summary estimates by meta-analysis and performed analyses of interactions.Results: The median concentration of cord serum PCB-153 was 140 ng/L (range of cohort medians 20–484 ng/L) and that of p,p´-DDE was 528 ng/L (range of cohort medians 50–1,208 ng/L). Birth weight decreased with increasing cord serum concentration of PCB-153 after adjustment for potential confounders in 12 of 15 study populations. The meta-analysis including all cohorts indicated a birth weight decline of 150 g [95% confidence interval (CI): –250, –50 g] per 1-µg/L increase in PCB-153, an exposure contrast that is close to the range of exposures across the cohorts. A 1-µg/L increase in p,p´-DDE was associated with a 7-g decrease in birth weight (95% CI: –18, 4 g).Conclusions: The findings suggest that low-level exposure to PCB (or correlated exposures) impairs fetal growth, but that exposure to p,p´-DDE does not. The study adds to mounting evidence that low-level exposure to PCBs is inversely associated with fetal growth.

Objective40,000 residents in Arnsberg, Germany, had been exposed to drinking water contaminated with perfluorinated compounds (PFCs). Internal exposure of the residents of Arnsberg to six PFCs was assessed in comparison with reference areas.Design and participantsOne hundred seventy children (5–6 years of age), 317 mothers (23–49 years), and 204 men (18–69 years) took part in the cross-sectional study.MeasurementsIndividual consumption of drinking water and personal characteristics were assessed by questionnaire and interview. Perfluorooctanoate (PFOA), perfluorooctanesulfonate (PFOS), perfluorohexanoate, perfluorohexanesulfonate (PFHxS), perfluoropentanoate, and perfluorobutanesulfonate (PFBS) in blood plasma and PFOA/PFOS in drinking water samples were measured by solid-phase extraction, high-performance liquid chromatrography, and tandem mass spectrometry detection.ResultsOf the various PFCs, PFOA was the main compound found in drinking water (500–640 ng/L). PFOA levels in blood plasma of residents living in Arnsberg were 4.5–8.3 times higher than those for the reference population (arithmetic means Arnsberg/controls: children 24.6/5.2 μg/L, mothers 26.7/3.2 μg/L, men 28.5/6.4 μg/L). Consumption of tap water at home was a significant predictor of PFOA blood concentrations in Arnsberg. PFHxS concentrations were significantly increased in Arnsberg compared with controls (p < 0.05). PFBS was detected in 33% of the children, 4% of the women, and 13% of the men in Arnsberg compared with 5%, 0.7%, and 3%, respectively, in the reference areas (p < 0.05). Regression analysis showed that age and male sex were significant predictors of PFOS, PFOA, and PFHxS; associations of other regressors (diet, body mass index) varied among PFCs.ConclusionsPFC concentrations in blood plasma of children and adults exposed to PFC-contaminated drinking water were increased 4- to 8-fold compared with controls.