Effects of biofouling on the uptake of perfluorinated alkyl acids by organic-diffusive gradients in thin films passive samplers

While organic-diffusive gradients in thin films (o-DGT) passive samplers have been used to assess organic contaminants in water, the effects of biofouling on accurate analyte quantification by o-DGT are poorly...

Lipogenic Potency of Individual Perfluorinated Alkyl Acids (PFAAs) and Persistent Organic Pollutant (POP) Mixtures at Human Blood-Based Exposure Levels on Adipogenesis in 3T3-L1 Cells

Background In recent decades, the incidence of metabolic disorders has increased internationally. This increase has been linked to exposure to persistent organic pollutants (POPs) but little is known about the metabolic effects of realistic human exposure mixtures at relevant concentrations. Objectives In this study we tested if POPs, representing real life exposure profiles and concentrations, were able to disrupt development and functions of adipose tissue in a direct way. Methods The lipogenic potency of a POP mixture modelled on levels found in human blood as detected in the Scandinavian population was assessed. The Total mixture comprises 29 compounds divided over three groups: chlorinated (Cl), brominated (Br), and perfluorinated compounds (PFAA). Individual PFAA chemicals, the Total mixture, and sub-mixtures (Cl, Br, PFAA, Cl + Br, Cl + PFAA, and Br + PFAA) at five (× 1/10, × 1, × 50, × 100, and × 500) human blood levels were tested in an optimised high content analysis (HCA) 3T3-L1 adipogenesis assay. Results Individual PFAAs; perfluorohexanesulfonic acid (PFHxS), perfluorooctanesulfonic acid (PFOS), perfluorononanoic acid (PFNA), and perfluoroundecanoic acid (PFUnDA) promoted lipid accumulation in 3T3-L1 cells. The Total mixture, and the Cl, PFAA, Cl + Br, and Cl + PFAA sub-mixtures, promoted adipogenic differentiation and lipid accumulation. Increased lipid accumulation promoted adipose tissue expansion. Conclusions To the authors knowledge, this is the first in vitro bioassay study assessing the adipogenic effects of POP mixtures modelled on real-life human exposure levels. The findings highlight that such exposures may alter adipose tissue development and function, thus potentially playing a role in the globally increasing escalation of metabolic disorders.

Uptake of perfluorinated alkyl acids by crops: results from a field study

Variability of plant uptake of PFAAs from soil is explored with measured uptake factors for 13 PFAAs in 4 crops.

Exposure to Perflouroalkyl acids and foetal and maternal thyroid status: a review

Background Exposure to perfluorinated-alkyl-acids (PFAAs) is ubiquitous. PFAAs are hormone-disrupting compounds that are strongly suspected to affect mother-child-health such as fetal growth. Thyroid disruption is a plausible mechanism of action. We aim to summarize the epidemiological evidence for the relation between prenatal and postnatal exposure to PFAAs and disruption of thyroid homeostasis in mothers and/or infants. Method Fifteen original publications on PFAAs concentrations and thyroid hormones (TH) in pregnant women and/or infants were found upon a literature search in the PubMed database. Information on exposure to seven PFAAs congeners [Perfluorooctane sulfonate (PFOS), Perfluorooctanoate (PFOA), Perfluorohexane sulfonate (PFHxS), Perfluorononanoic acid (PFNA), Perfluorodecanoic acid (PFDA), Perfluoroundecanoic acid (PFUnA), and Perfluorododecanoic acid (PFDoA)] and thyroid stimulating hormone (TSH), free and total thyroxine (FT4 and TT4), free and total triiodothyronine (FT3 and TT3), T3RU (Free triiodothyronine resin uptake) and FT4-index (FT4I) levels were recorded. We evaluated sampling of maternal TH by trimester, and infant TH by sex stratification. Reported associations between mother or infant PFAAs and TH were not uniformly assessed in the selected studies. Results Ten out of the fifteen studies examined maternal PFAAs concentration and TSH level. Seven studies showed significant associations between TSH and exposure to six PFAAs congeners, most of them were positive. Maternal T4 and T3 were investigated in nine studies and five studies found inverse associations between exposure to six PFAAs congeners and TH (TT3, TT4, FT3, FT4 and FT4I) levels. Eight of the fifteen studies investigated PFAAs concentrations and infant TSH. Infant TSH level was significantly affected in four studies, positively in three studies. Nine studies investigated infant T4 and T3 and seven studies found significant associations with PFAAs exposure. However, both inverse and positive significant associations with infant TH were found eliciting no clear direction. Conclusion Results indicate a mainly positive relationship between maternal PFAAs concentrations and TSH levels, and suggestion of an inverse association with T4 and/or T3 levels. Associations of infant TH with PFAAs concentration were less consistent.