Per- and polyfluoroalkyl substances in waterbird feathers around Poyang Lake, China: Compound and species-specific bioaccumulation.

As a nondestructive means of environmental monitoring, bird feathers have been used to analyze levels of per- and polyfluoroalkyl substances (PFASs) in specific environments. In this study, feather samples from 10 waterbird species around Poyang Lake were collected, and a pretreatment method for PFASs in feathers was optimized. The results showed that a combined cleaning method using ultrapure water and n-hexane effectively removed external PFASs. Twenty-three legacy and emerging PFASs were identified in the feathers of waterbirds, of which hexafluoropropylene oxides (HFPOs), chlorinated polyfluoroalkyl ether sulfonates (Cl-PFESAs), and sodium p-perfluorinated noneoxybenzene sulfonate (OBS) were reported for the first time, with their concentrations ranging from 0.060-2.4 ng·g-1 dw, 0.046-30 ng·g-1 dw, and lower than the method detection limit to 30 ng·g-1 dw, respectively. Compound- and species-specific bioaccumulation of PFASs was observed in the feathers of different waterbird species, suggesting that different PFAS types can be monitored through the selection of different species. Moreover, the concentrations of most PFCAs (except perfluorobutyric acid), perfluorooctane sulfonate (PFOS), and perfluorooctane sulfonamide (FOSA) were significantly positively correlated with δ15N (p < 0.05), while the concentrations of HFPOs, Cl-PFESAs, and OBS had significant positive correlations with δ13C. This indicates that the bioaccumulation of legacy and emerging PFASs in waterbird feathers is affected by their trophic level, feeding habits, and foraging area.

Per- and polyfluoroalkyl substances induce lipid metabolic impairment in fish: Integration on field investigation and laboratory study.

The biotoxicity of perfluoroalkyl and polyfluoroalkyl substances (PFASs) to aquatic organisms has been widely concerned. However, studies on toxic effects of PFASs are usually evaluated directly by using laboratory exposure rather than laboratory validation based on data obtained in the field. In this study, wild catfish (Silurus meridinalis) was explored on the relationship between PFASs bioaccumulation and lipid disorders. Nine and thirteen lipid metabolites were significantly associated with perfluorooctane sulfonate (PFOS) and 6:2/8:2Cl-PFESA (trade name F-53B) exposures, respectively; and the correlated lipid metabolites were the fatty acid (FA) and conjugates, FA esters, steroids, and glycerophosphate subclasses. The effects of PFASs on lipid metabolism of fish and its mechanism were further analyzed through exposure experiments. Zebrafish (Danio rerio) of different sexes underwent PFOS and F-53B exposures for 21 days at 100 ng/L and 100 µg/L. By determining gene expression levels, hepatic lipid contents, and histopathological change, the adverse effects order on lipid metabolism in male or female was 100 µg/L F-53B > 100 µg/L PFOS > 100 ng/L F-53B > 100 ng/L PFOS; the stress response in male was more intensive than that in female. PFOS and F-53B activated the peroxisome proliferator-activated receptor pathway, promoting the processes of FA and total cholesterol (T-CHO) transport, FA ß-oxidation, FA synthesis, and finally induced FA and T-CHO transportation from blood into liver, then accelerated FA to FA ester transformation, and CHO into steroids. Laboratory experiments confirmed the field analysis. This study innovatively explored the adverse effects of PFOS and F-53B on lipid metabolism and their mechanisms at field and laboratory levels, highlighting concerns regarding PFASs health risks.

Novel PFOS alternative OBS inhibits body growth of developing zebrafish by triggering thyroid function disorder and osteoclast differentiation.

The extensive use of the perfluorooctane sulfonate (PFOS) alternative sodium p-perfluorous nonenoxybenzene sulfonate (OBS) has resulted in its widespread detection in the environment and enrichment in wildlife and humans. However, little is known about its potential toxicity, particularly in terms of body development. In this study, zebrafish embryos were acutely exposed to PFOS and OBS for a comparative developmental toxicity assessment. Both PFOS and OBS led to lower body weight and shorter body length, and the damaging effects of PFOS were more severe than those of OBS at the same exposure concentration. Biochemical assays of THs and transcription profiles correlated to the HPT axis demonstrated that OBS-induced body development inhibition resulted mainly from interference in THs synthesis, transfer, coupling with receptors, and conversion from T4 to T3, which was similar to the case of PFOS, except that the disruptive effects of OBS on thyroid function were more intense. Further transcriptome analysis showed that PFOS and OBS also promoted osteoclast differentiation, aggravating the inhibitory effects on body growth, and that PFOS had more obvious inhibitory effects than OBS. This study systematically explored the inhibitory effects of PFOS and OBS exposure on body development and tightly linked the toxic effects to thyroid function disorder and osteoclast differentiation. Our findings highlight that the health risks associated with OBS, an emerging substitute for PFOS, should not be ignored.

A new mechanistic insight into the association between environmental perfluorooctane sulfonic acid (PFOS) exposure and attention deficit and hyperactivity disorder (ADHD)-like behavior.

Perfluorooctane sulfonic acid (PFOS) is one of the main residual environmental pollutants that threaten human health. PFOS exposure is positively correlated with the prevalence of attention deficit hyperactivity disorder (ADHD); however, the underlying mechanism is unknown. Given that dopamine (DA) is a crucial target for PFOS and that its dysfunction is a key role in ADHD development, it is speculated that PFOS exposure contributes to the occurrence of ADHD to some extent by disrupting DA homeostasis. To establish the relationship between PFOS exposure, DA dysfunction, and ADHD-like behavior, adult zebrafish were exposed to PFOS for 21 days using PFOS concentrations in the serum of patients with ADHD as the reference exposure dose. Results showed that PFOS caused ADHD-like behaviors, with the presence of the slightly elevated percentage of time spent in movement and prolonged time spent in reaching the target zone in the T-maze. Hyperactivity and cognitive ability impairment were more severe with increasing PFOS concentrations. Further investigation showed that PFOS exposure resulted in a decrease in the DA content, accompanied by a decrease in the number of dopaminergic neurons and a disturbance in the transcription profiles of genes associated with the dopaminergic system. Treatment with Ritalin effectively alleviated PFOS-induced ADHD-like behavior and restored DA levels, number of dopaminergic neurons, and expression of DA metabolism-related genes, suggesting that PFOS exposure induced ADHD-like behavior by triggering DA secretion disorder. This study enriches our understanding of the pathogenic mechanisms underlying ADHD development and emphasizes the importance of focusing on the health risks pertaining to environmental exposure.