Nationwide distribution of perfluoroalkyl ether carboxylic acids in Chinese diets: An emerging concern.

With the phase-out of perfluorooctanoic acid (PFOA) and its replacement by perfluoroalkyl ether carboxylic acids (PFECAs), there is a potential for increased exposure to various new PFECAs among the general population in China. While there are existing studies on dietary exposure to legacy perfluoroalkyl and polyfluoroalkyl substances (PFASs), research on dietary exposure to PFECAs, especially among the general Chinese populace, remains scarce. In the present study, we investigated the distribution of PFECAs in dietary sources from 33 cities across five major regions in China, along with the associated dietary intake. Analysis indicated that aquatic animal samples contained higher concentrations of legacy PFASs compared to those from terrestrial animals and plants. In contrast, PFECAs were found in higher concentrations in plant and terrestrial animal samples. Notably, hexafluoropropylene oxide dimer (HFPO-DA) was identified as the dominant compound in vegetables, cereals, pork, and mutton across the five regions, suggesting widespread dietary exposure. PFECAs constituted the majority of PFAS intake (57 %), with the estimated daily intake (EDI) of HFPO-DA ranging from 2.33 to 3.96 ng/kg bw/day, which corresponds to 0.78-1.32 times the reference dose (RfD) (3.0 ng/kg bw/day) set by the United States Environmental Protection Agency. Given the ubiquity of HFPO-DA and many other PFECAs in the nationwide diet of China, there is an urgent need for further research into these chemicals to establish relevant safety benchmarks or consumption advisory values for the diet.

Comprehensive Assessment of Exposure Pathways for Perfluoroalkyl Ether Carboxylic Acids (PFECAs) in Residents Near a Fluorochemical Industrial Park: The Unanticipated Role of Cereal Consumption.

With the replacement of perfluorooctanoic acid (PFOA) with perfluorinated ether carboxylic acids (PFECAs), residents living near fluorochemical industrial parks (FIPs) are exposed to various novel PFECAs. Despite expectations of low accumulation, short-chain PFECAs, such as perfluoro-2-methoxyacetic acid (PFMOAA), previously displayed a considerably high body burden, although the main exposure routes and health risks remain uncertain. Here, we explored the distribution of perfluoroalkyl and polyfluoroalkyl substances (PFASs) in diverse environmental media surrounding a FIP in Shandong Province, China. PFECAs were found at elevated concentrations in all tested matrices, including vegetables, cereals, air, and dust. Among residents, 99.3% of the ∑36PFAS exposure, with a 43.9% contribution from PFECAs, was due to gastrointestinal uptake. Dermal and respiratory exposures were negligible at 0.1 and 0.6%, respectively. The estimated daily intake (EDI) of PFMOAA reached 114.0 ng/kg body weight (bw)/day, ranking first among all detected PFECAs. Cereals emerged as the dominant contributor to PFMOAA body burden, representing over 80% of the overall EDI. The median EDI of hexafluoropropylene oxide dimer acid (HFPO-DA) was 17.9 ng/kg bw/day, markedly higher than the USEPA reference doses (3.0 ng/kg bw/day). The absence of established threshold values for other PFECAs constrains a comprehensive risk assessment.

Underlying Mechanisms for the Sex- and Chemical-Specific Hepatotoxicity of Perfluoroalkyl Phosphinic Acids in Common Carp (Cyprinus carpio).

The hepatotoxicities of perfluoroalkyl and polyfluoroalkyl substances (PFASs) have been extensively investigated, while little is known about the sex-specific differences. In this study, common carp were exposed to the emerging perfluoroalkyl phosphinic acids (6:6 and 8:8 PFPiAs) for 14 days to disclose sex-specific hepatotoxicity. Apparent hepatotoxicity, including cell necrosis, apoptosis, and steatosis, was observed in both male and female carp liver. The observed hepatocyte steatosis was predominantly attributed to the dysregulation of hepatic lipid metabolism but was based on sex-specific mechanisms. It was manifested as inhibited oxidative decomposition of fatty acids (FAs) in the female liver, whereas it enhanced the uptake of FAs into the male liver, both of which led to excessive lipid accumulation. Untargeted lipidomics validated that the metabolism pathways of FA, sphingolipid, glycerolipid, and glycerophospholipid were disrupted by both compounds, leading to the generation of reactive oxygen species and oxidative stress. The oxidative stress further evolved into inflammation, manifested as promoted expression of proinflammatory cytokines and repressed expression of anti-inflammatory cytokines. Consistently, all of the changes were more noticeable in male carp, suggesting that male fish were more susceptible to PFPiA disruption. 8:8 PFPiA was less accumulated but caused stronger hepatotoxicity than 6:6 PFPiA, possibly because of the stronger binding capacity of 8:8 PFPiA to nuclear transcription factors mediating lipid metabolism and inflammation. The findings of this study highlight the significance of sex- and chemical-dependent bioaccumulation and the toxicity of PFASs in organisms.

Novel Insight into the Mechanisms of Neurotoxicity Induced by 6:6 PFPiA through Disturbing the Gut-Brain Axis.

As alternatives to traditional per- and polyfluoroalkyl substances, perfluoroalkyl phosphonic acids (PFPiAs) are frequently detected in aquatic environments, but the neurotoxic effects and underlying mechanisms remain unclear. In this study, male zebrafish were exposed to 6:6 PFPiA (1 and 10 nM) for 28 days, which exhibited anxiety-like symptoms. Gut microbiome results indicated that 6:6 PFPiA significantly increased the abundance of Gram-negative bacteria, leading to enhanced levels of lipopolysaccharide (LPS) and inflammation in the gut. The LPS was delivered to the brain through the gut-brain axis (GBA), damaged the blood-brain barrier (BBB), stimulated neuroinflammation, and caused apoptosis as well as neural injury in the brain. This mechanism was verified by the fact that antibiotics reduced the LPS levels in the gut and brain, accompanied by reduced inflammatory responses and anxiety-like behavior. The BBB damage also resulted in the enhanced accumulation of 6:6 PFPiA in the brain, where it might bind strongly with and activate aryl hydrocarbon receptor (AhR) to induce brain inflammation directly. Additionally, as the fish received treatment with an inhibitor of AhR, the inflammation response and anxiety-like behavior decreased distinctly. This study sheds light on the new mechanisms of neurotoxicity-induced 6:6 PFPiA due to the interruption on GBA.

Probing Mechanisms for the Tissue-Specific Distribution and Biotransformation of Perfluoroalkyl Phosphinic Acids in Common Carp (Cyprinus carpio).

This study investigated the tissue-specific accumulation and biotransformation of 6:6 and 8:8 perfluoroalkyl phosphinic acids (PFPiA) in common carp (Cyprinus carpio) during 90 d exposure and 30 d depuration in water in the laboratory. Both 6:6 and 8:8 PFPiAs could quickly accumulate in the carp, and 6:6 PFPiA displayed higher bioaccumulation potential than 8:8 PFPiA. The highest concentrations of PFPiAs were observed in the blood, while the lowest were found in the muscle. The equilibrium dialysis experiment indicated that both PFPiAs had higher binding affinities with the proteins in the fish serum than in liver, which was supported by the molecular docking analysis. The results also indicated that 6:6 PFPiA had higher binding affinities with the serum and liver proteins than 8:8 PFPiA. These results suggested that the tissue-specific distribution of PFPiAs was highly dependent on the binding affinities with the specific proteins. Both in vivo and in vitro experiments consistently indicated that PFPiAs experienced biotransformation and produced perfluoroalkyl phosphonic acids (PFPAs), and biotransformation of 8:8 PFPiA was more active than 6:6 PFPiA. It was worth noting that perfluorohexanonate and perfluorooctanoic acids were identified in fish as metabolites after long-term exposure to PFPiAs for the first time.

Glass fiber supported BiOI thin-film fixed-bed photocatalytic reactor for water decontamination under solar light irradiation.

BiOI powder has been proved to be an efficient photocatalyst, but the difficulty in removing it from water after reaction limits its application in real water treatment. To solve this problem, a thin-film fixed-bed reactor (TFFBR) was set-up by developing a BiOI thin film on glass fiber cloth (GFC). The composition and structure of the as-prepared films were characterized with X-ray diffraction, X-ray photoelectron spectroscopy, field emission microscopy, transmission electron microscopy and Fourier transform infrared spectroscopy. The BiOI thin film was made by painting a silica sol containing BiOI on GFC, which could be tailored to desired sizes to accommodate the TFFBR. The mass of BiOI on the GFC increased with the number of iterations of the painting process. SiO2 sol glued the BiOI particles tightly onto the GFC, making the thin film strong enough to resist fluid flushing in the TFFBR. The photocatalytic activity of the BiOI thin film was investigated by degrading bisphenol A (BPA) under simulated sunlight. Ninety eight percent of BPA (20 mg/L in 2 L) was degraded by the BiOI thin film sample of seven layers (GFC-7) on the TFFBR within 8 hr irradiation. The GFC-7 displayed good photocatalytic ability toward artificial sewage containing BPA in a wide pH range (5-9), and also demonstrated excellent durability and reusability. The working conditions were optimized and it was found that the thickness of the fluid film and residence time over the thin film were key factors affecting the photocatalytic efficiency.