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Plastic particles smaller than 5 mm, termed microplastics, have raised concerns regarding their potential impact on human health. Even smaller particles (<1 µm), classified as nanoplastics, also warrant further investigation. Since these plastic particles have been detected in various human tissues, their biological effects must be thoroughly evaluated. These plastics originate from diverse polymer types and exhibit complex physicochemical properties such as size, shape, and surface degradation in the environment. However, current studies mainly utilize polystyrene beads, which may not exist widely in the environment. Therefore, the use of environmentally relevant micro- and nanoplastics for safety assessments is crucial. Focusing mainly on surface degradation, this study aimed to elucidate detailed mechanisms of cell death caused by micro- and nanoplastics and assess their universality across different polymer types, including polyethylene (PE) and polyvinyl chloride (PVC). Surface-degraded samples of PE and PVC with different particle sizes, including microplastics and nanoplastics, were prepared and their cell death mechanisms were evaluated in murine macrophage RAW264.7 cells. Transcriptomic analysis revealed that degraded PE microplastics upregulated ferroptosis-related gene expressions and increased reactive oxygen species level and lipid peroxidation. Cell death and lipid peroxidation induction were also examined in other polymer types, including PVC microplastics as well as PE and PVC nanoplastics. Notably, only the degraded samples induced cell death and lipid peroxidation for all tested particles. Given the role of lipid peroxidation in various diseases such as neurological dysfunction and ischemia-reperfusion injury, our findings highlight the potential health risks of environmental micro- and nanoplastics.
Manabe et al. (Mon,) studied this question.