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Intranasal exposure to UV-irradiated polystyrene nanoplastics triggers vital organ inflammation and cognitive impairment

Journal of Environmental Sciences 2025 1 citation ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 53 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Huiqin Liu, Xidong Wu, Dan Luo, Luxuan Liu, W L Zhang, Yan Jun Ge, Yaqi Peng, Chengshuai Liu, Chengyu Chen, Tao Liu

Summary

Researchers exposed rats to polystyrene nanoplastics through nasal passages and found that UV-irradiated particles caused more severe damage than pristine ones, triggering inflammation in the lungs, liver, and kidneys. Smaller 100-nanometer particles caused more serious liver damage than larger 600-nanometer particles, as indicated by elevated liver enzyme levels. The study also found that learning and memory abilities declined as the duration of nanoplastic photoaging increased.

Polymers
Models
Study Type In vivo

Nanoplastics (NPs) are emerging environmental contaminants that can undergo photoaging before inhalation. However, it remains unclear how intranasal exposure to photoaged NPs triggers vital organ inflammation and cognitive impairment. This study investigated the health impact of intranasal exposure to polystyrene NPs (PSNPs) of 100 nm (PS100) and 600 nm (PS600), both before and after ultraviolet (UV) irradiation. Irradiation generated reactive oxygen species, lowered zeta potentials, reduced particle sizes, and decreased solution pH. Both in vitro and in vivo experiments indicated that UV-irradiated PSNPs caused significant damage to the nasal mucosa. In rats, exposure to PSNPs, particularly those irradiated for 3 and 6 h, resulted in pronounced pulmonary inflammation. Additionally, inflammatory lesions were observed in the liver and kidneys, with smaller PS100 particles causing more severe liver damage. Notably, rats exposed to PS100 showed significantly elevated levels of alanine aminotransferase (72.27 ± 34.34 U/L) and aspartate aminotransferase (173.55 ± 35.13 U/L) (P < 0.05). Blood tests revealed increased white blood cells, lymphocytes, and neutrophils post-exposure. Furthermore, learning and memory abilities in rats declined as the duration of PSNPs photoaging increased, with up to a 48-second delay observed in the hidden platform test. These findings demonstrate that intranasal exposure to photoaged PSNPs induced inflammation in vital organs and impaired cognitive function, highlighting potential health risks associated with their inhalation.

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