Muhammad Athaya Rahmanardi, Aditya Muhammad Reva, Lestari Bayu, Sulistomo Hikmawan Wahyu
Master Program in Biomedical Science, Faculty of Medicine, Universitas Brawijaya, Malang, Indonesia.
Department of Pharmacology, Faculty of Medicine, Universitas Brawijaya, Malang, Indonesia.
Toxicol Rep. 2025 Jun 10;14:102067. doi: 10.1016/j.toxrep.2025.102067. eCollection 2025 Jun.
Plastic waste, particularly polyethylene (PE) plastic bags and bottles, poses a significant environmental problem and health risk when degraded into microplastics. Recent atmospheric microplastic pollution increases inhalation exposure, necessitating a study on toxicity in the lungs. However, the inhalation toxicology of PE microplastics is poorly understood. This study used Wistar rats that are divided into control and PE group. The PE groups were exposed to PE microplastic through inhalation for 28 days with the daily dose of 15 mg/m. Inflammatory marker such as Inflammatory exudate, Alveolar thickening, and NF-κB were in PE group increased significantly compared to control group. the increment of MDA and decrement of SOD in PE group revealed the oxidative stress occurred. These results suggest that sub-acute PE microplastic inhalation may contribute to inflammation pathogenesis via the NF-κB pathway as a result of oxidative stress.
塑料垃圾，尤其是聚乙烯（PE）塑料袋和塑料瓶，在降解为微塑料时会造成重大的环境问题和健康风险。最近大气中的微塑料污染增加了吸入暴露风险，因此有必要开展一项关于肺部毒性的研究。然而，人们对PE微塑料的吸入毒理学了解甚少。本研究使用了Wistar大鼠，将其分为对照组和PE组。PE组通过吸入方式暴露于PE微塑料中，持续28天，日剂量为15毫克/立方米。与对照组相比，PE组的炎症标志物如炎性渗出物、肺泡增厚和核因子κB（NF-κB）显著增加。PE组丙二醛（MDA）增加和超氧化物歧化酶（SOD）减少表明发生了氧化应激。这些结果表明，亚急性吸入PE微塑料可能由于氧化应激通过NF-κB途径导致炎症发病机制。
