RESUMEN

Electronic waste (e-waste) dismantling facilities are well-known bisphenol chemical (BP) sources. In this study, non-targeted screening combined with targeted analysis of BPs in surface soil from e-waste dismantling facilities and their surroundings revealed their presence, distribution, and exposure risk. A total of 14 BPs were identified including bisphenol A (BPA) and its novel structural analogs and halogenated BPs. The total concentrations of BPs ranged from 963 to 47,160 ng/g (median: 6970 ng/g) in e-waste soil, higher than those measured in surface soil from surrounding areas, i.e., 10-7750 ng/g (median 197 ng/g). BPA, tetrabromobisphenol A (TBBPA), and bisphenol F (BPF) were the dominant ones from the two areas. Concentrations of TBBPA and its debromination product from the surrounding area significantly decreased with increasing distances from the e-waste dismantling facilities. Estimation of daily intake via oral ingestion of soil suggests that current contamination scenarios are unlikely to pose health risks for e-waste dismantling workers and adults and toddlers living in the surrounding areas, with their intakes generally well below the tolerable daily intakes proposed for several BPs. However, the BPA intakes of workers exceeded the more strict tolerable daily intake for BPA established recently, which merits continuous environmental surveillance.

RESUMEN

Hyperuricemia is characterized by elevated blood uric acid (UA) levels, which can lead to certain diseases. Epidemiological studies have explored the association between environmental contaminant exposure and hyperuricemia. However, few studies have investigated the role of chemical exposure in the development of hyperuricemia. Here, we sought to investigate the effects of bisphenol exposure on the occurrence of hyperuricemia. Fifteen bisphenol chemicals (BPs) were detected in human serum and urine samples collected from an area with a high incidence of hyperuricemia in China. Serum UA levels positively correlated with urinary bisphenol S (BPS), urinary bisphenol P (BPP), and serum bisphenol F (BPF). The effects of these three chemicals on UA levels in mice were explored at various exposure concentrations. An increase in serum UA levels was observed in BPS- and BPP-exposed mice. The results showed that BPS exposure increased serum UA levels by damaging the structure of the kidneys, whereas BPP exposure increased serum UA levels by disturbing purine metabolism in the liver. Moreover, BPF did not induce an increase in serum UA levels owing to the inhibition of guanine conversion to UA. In summary, we provide evidence of the mechanisms whereby exposure to three BPs disturbs UA homeostasis. These findings provide new insights into the risks of exposure to bisphenol chemicals.

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RESUMEN

Exposure to bisphenols chemicals could cause various adverse health effects, including non-alcoholic fatty liver disease (NAFLD), which have been associated with cellular mitochondria stress. However, the biological mechanism underlying the mitochondria stress-mediated cell death by bisphenols was poorly understood. Here, CRISPR screens were performed to identify the critical genes which were involved in cell death caused by exposure to four bisphenols (BPA, BPB, BPE and BPS). Results of CRISPR screens showed that UGT1A9 was the primary genetic factor facilitating cell death induced by all of the four bisphenols. Systematic toxicological tests demonstrated that UGT1A9 was required for BPA-induced mitochondria dyshomeostasis in vitro and in vivo, and UGT1A9-mediated mitochondria dyshomeostasis was an important cause of facilitating cell death. Liver injury caused by exposure to BPA in wild-type mice was accompanied with suppression of mitophagy and increased expression of C-Caspase 3, but UGT1A9 knockout attenuated these adverse effects induced by BPA. Finally, molecular epidemiology analysis suggested that the five genetic variants of UGT1A9 could be potential genetic risk factors of NAFLD when people were exposed to BPA. The biological mechanism uncovered here provided mechanistic evidence for identification of susceptible populations of liver injury associated with exposure to BPA.

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