Kwabena Danso Isaac, Woo Jong-Hwan, Hoon Baek Seung, Kim Kilsoo, Lee Kyuhong
Inhalation Toxicology Center for Airborne Risk Factor, Korea Institute of Toxicology, 30 Baehak1-Gil, Jeongeup, Jeollabuk-do 56212 Republic of Korea.
Department of Human and Environmental Toxicology, Korea National University of Science & Technology, Daejeon, 34113 Republic of Korea.
Toxicol Res. 2024 Mar 8;40(2):313-323. doi: 10.1007/s43188-023-00224-x. eCollection 2024 Apr.
Polypropylene (PP), polystyrene (PS), and polyethylene (PE) plastics are commonly used in household items such as electronic housings, food packaging, bottles, bags, toys, and roofing membranes. The presence of inhalable microplastics in indoor air has become a topic of concern as many people spent extended periods of time indoors during the COVID-19 pandemic lockdown restrictions, however, the toxic effects on the respiratory system are not properly understood. We examined the toxicity of PP, PS, and PE microplastic fragments in the pulmonary system of C57BL/6 mice. For 14 days, mice were intratracheally instilled 5 mg/kg PP, PS, and PE daily. The number of inflammatory cells such as macrophages, neutrophils, and eosinophils in the bronchoalveolar lavage fluid (BALF) of PS-instilled mice was significantly higher than that in the vehicle control (VC). The levels of inflammatory cytokines and chemokines in BALF of PS-instilled mice increased compared to the VC. However, the inflammatory responses in PP- and PE-stimulated mice were not significantly different from those in the VC group. We observed elevated protein levels of toll-like receptor (TLR) 2 in the lung tissue of PP-instilled mice and TLR4 in the lung tissue of PS-instilled mice compared with those to the VC, while TLR1, TLR5, and TLR6 protein levels remained unchanged. Phosphorylation of nuclear factor kappa B (NF-κB) and IĸB-α increased significantly in PS-instilled mice compared with that in VC. Furthermore, Nucleotide‑binding oligomerization domain‑like receptor family pyrin domain‑containing 3 (NLRP3) inflammasome components including NLRP3, apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), and Caspase-1 in the lung tissue of PS-instilled mice increased compared with that in the VC, but not in PP- and PE-instilled mice. These results suggest that PS microplastic fragment stimulation induces pulmonary inflammation due to NF-ĸB and NLRP3 inflammasome activation by the TLR4 pathway.
The online version contains supplementary material available at 10.1007/s43188-023-00224-x.
聚丙烯（PP）、聚苯乙烯（PS）和聚乙烯（PE）塑料常用于电子产品外壳、食品包装、瓶子、袋子、玩具和屋顶薄膜等家居用品中。在新冠疫情封锁限制期间，许多人长时间待在室内，室内空气中可吸入微塑料的存在已成为一个备受关注的话题，然而，其对呼吸系统的毒性作用尚未得到充分了解。我们研究了PP、PS和PE微塑料碎片对C57BL/6小鼠肺部系统的毒性。连续14天，每天给小鼠气管内注入5mg/kg的PP、PS和PE。注入PS的小鼠支气管肺泡灌洗液（BALF）中巨噬细胞、中性粒细胞和嗜酸性粒细胞等炎症细胞的数量显著高于载体对照组（VC）。与VC相比，注入PS的小鼠BALF中炎症细胞因子和趋化因子的水平有所升高。然而，PP和PE刺激的小鼠的炎症反应与VC组没有显著差异。与VC相比，我们观察到注入PP的小鼠肺组织中Toll样受体（TLR）2的蛋白水平升高，注入PS的小鼠肺组织中TLR4的蛋白水平升高，而TLR1、TLR5和TLR6的蛋白水平保持不变。与VC相比，注入PS的小鼠中核因子κB（NF-κB）和IκB-α的磷酸化显著增加。此外，与VC相比，注入PS的小鼠肺组织中包含NLRP3、含半胱天冬酶募集结构域的凋亡相关斑点样蛋白（ASC）和半胱天冬酶-1的核苷酸结合寡聚化结构域样受体家族含吡啉结构域3（NLRP3）炎性小体成分增加，但在注入PP和PE的小鼠中未增加。这些结果表明，PS微塑料碎片刺激通过TLR4途径激活NF-κB和NLRP3炎性小体，从而诱导肺部炎症。
在线版本包含可在10.1007/s43188-023-00224-x获取的补充材料。
