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.

For both substances a crossing of the placental barrier could be shown. For PFOS we observed a decrease from maternal to cord plasma concentrations by a factor of 0.41-0.80. To the contrary, PFOA crosses the placental barrier obviously unhindered. These findings show that neonates are exposed to PFOS and PFOA via their mothers' blood. Given the current situation that only little is known about the consequences of PFOS and PFOA exposure in the early state of development of humans and the fact that in animal studies both substances showed developmental toxic effects further research regarding human health effects is indispensable.

Our data agree well with results of other recent studies in Europe and suggest that the current exposure of the adult German population is lower than the exposure of the US and Canadian population. The sources of human exposure are currently not well understood. Toxicological implications are restricted to animal studies and occupational investigations not adequate for quantitative risk assessment in humans. Overall, more scientific research is necessary to characterize the body burden of PFCs (especially for relevant subsets of the population) and the main sources and routes, which are responsible for human exposure and possible health implications of these compounds.

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