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Microbeads used in personal care products have been one of the important sources of microplastics (MPs), and little has been reported on their environmental behaviors and health risks. The characteristics of environmentally persistent free radicals (EPFRs) and the toxicity assessment of MPs (environmentally relevant concentrations) from cosmetics during photoaging remains largely unknown. In this study, the formation of EPFRs on polyethylene (PE) microbeads from facial scrubs under light irradiation and their toxicity were investigated using C. elegans as a model organism. The results suggested that light irradiation induced the generation of EPFRs, which accelerates the aging process and alters the physicochemical properties of PE microbeads. Acute exposure to PE (1 mg/L) at photoaged times of 45–60 d significantly decreased the physiological indicators (e.g., head thrashes, body bends, and brood size). The oxidative stress response and stress-related gene expression were also enhanced in nematodes. The addition of N-acetyl-l-cysteine induced significant inhibition of toxicity and oxidative stress in nematodes exposed to 45–60 d of photoaged PE. The Pearson correlation results showed that the concentration of EPFRs was significantly correlated with physiological indicators, oxidative stress, and related-genes expression in nematodes. The data confirmed that the generation of EPFRs combined with heavy metals and organics contributed to toxicity induced by photoaged PE, and oxidative stress might be involved in regulating adverse effects in C. elegans. The study provides new insight into the potential risks of microbeads released into the environment during photoaging. The findings also highlight the necessity for considering the role of EPFRs formation in evaluating the impacts of microbeads.

As a major alternative to traditional brominated flame retardants (BFRs), decabromodiphenyl ethane (DBDPE) is widely used and has been commonly detected in various environmental media and organisms. Few previous studies have focused on DBDPE-induced locomotion neurotoxicity, and the exact molecular mechanisms and related health risks remain unclear. In this study, we first analyzed the locomotion indicators of nematodes following DBDPE exposure, demonstrated that DBDPE caused locomotion neurotoxicity, and identified that a series of the transthyretin (TTR)-like genes participated in the regulation of nematode motility by transcriptomic analysis, gene transcription validation and TTR-like mutant verification. Subsequently, this study demonstrated that DBDPE exacerbated amyloid-beta (Aβ) deposition by repressing TTR/TTR-like gene transcription based on Alzheimer’s disease (AD) model nematodes and human SH-SY5Y cells following DBDPE exposure and further revealed that DBDPE reduced the binding between TTR and Aβ by competing with the strand G region sites on the TTR/TTR-like protein, ultimately exacerbating Aβ deposition and the risk of AD. In short, our study demonstrated that DBDPE induced locomotion neurotoxicity and potential AD risks through intensifying Aβ deposition by inhibiting TTR/TTR-like proteins, providing reference support for risk management and policy formulation related to DBDPE and similarly structured novel BFRs.