PDF(Pubmed)
Abstract：
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.
UNASSIGNED: The online version contains supplementary material available at 10.1007/s43188-023-00224-x.
UNASSIGNED: The online version contains supplementary material available at 10.1007/s43188-023-00224-x.
摘要：
聚丙烯(PP),聚苯乙烯（PS），和聚乙烯（PE）塑料通常用于家用物品，例如电子外壳，食品包装,瓶子,袋子,玩具,和屋顶膜。在COVID-19大流行封锁限制期间，许多人在室内呆了很长时间，室内空气中可吸入微塑料的存在已经成为一个令人担忧的话题，然而,对呼吸系统的毒性作用没有得到正确理解。我们检查了PP的毒性，PS,C57BL/6小鼠肺系统中的PE微塑料碎片。14天,小鼠气管内滴注5mg/kgPP，PS,每天体育。巨噬细胞等炎症细胞的数量，中性粒细胞，PS滴注小鼠的支气管肺泡灌洗液（BALF）中的嗜酸性粒细胞显着高于载体对照（VC）。与VC相比，PS滴注小鼠的BALF中炎性细胞因子和趋化因子的水平增加。然而,PP和PE刺激小鼠的炎症反应与VC组无显著差异.我们观察到与VC相比，PP滴注小鼠肺组织中Toll样受体（TLR）2的蛋白水平升高，PS滴注小鼠肺组织中TLR4的蛋白水平升高，而TLR1、TLR5和TLR6蛋白水平保持不变。与VC相比，PS滴注小鼠的核因子κB（NF-κB）和IB-α的磷酸化显着增加。此外，核苷酸结合寡聚化结构域样受体家族pyrin结构域包含3（NLRP3）炎性体成分，包括NLRP3，凋亡相关斑点样蛋白，含有caspase募集结构域（ASC），与VC相比，PS滴注小鼠肺组织中的Caspase-1增加，但不是在PP和PE滴注的小鼠中。这些结果表明，PS微塑料片段刺激可通过TLR4途径引起NFB和NLRP3炎性体活化引起肺部炎症。
■在线版本包含补充材料，可在10.1007/s43188-023-00224-x获得。
■在线版本包含补充材料，可在10.1007/s43188-023-00224-x获得。
