PDF(Pubmed)
Abstract：
Microplastics have been detected in the atmosphere as well as in the ocean, and there is concern about their biological effects in the lungs. We conducted a short-term inhalation exposure and intratracheal instillation using rats to evaluate lung disorders related to microplastics. We conducted an inhalation exposure of polypropylene fine powder at a low concentration of 2 mg/m3 and a high concentration of 10 mg/m3 on 8-week-old male Fischer 344 rats for 6 h a day, 5 days a week for 4 weeks. We also conducted an intratracheal instillation of polypropylene at a low dose of 0.2 mg/rat and a high dose of 1.0 mg/rat on 12-week-old male Fischer 344 rats. Rats were dissected from 3 days to 6 months after both exposures, and bronchoalveolar lavage fluid (BALF) and lung tissue were collected to analyze lung inflammation and lung injury.
Both exposures to polypropylene induced a persistent influx of inflammatory cells and expression of CINC-1, CINC-2, and MPO in BALF from 1 month after exposure. Genetic analysis showed a significant increase in inflammation-related factors for up to 6 months. The low concentration in the inhalation exposure of polypropylene also induced mild lung inflammation.
These findings suggest that inhaled polypropylene, which is a microplastic, induces persistent lung inflammation and has the potential for lung disorder. Exposure to 2 mg/m3 induced inflammatory changes and was thought to be the Lowest Observed Adverse Effect Level (LOAEL) for acute effects of polypropylene. However, considering the concentration of microplastics in a real general environment, the risk of environmental hazards to humans may be low.
Both exposures to polypropylene induced a persistent influx of inflammatory cells and expression of CINC-1, CINC-2, and MPO in BALF from 1 month after exposure. Genetic analysis showed a significant increase in inflammation-related factors for up to 6 months. The low concentration in the inhalation exposure of polypropylene also induced mild lung inflammation.
These findings suggest that inhaled polypropylene, which is a microplastic, induces persistent lung inflammation and has the potential for lung disorder. Exposure to 2 mg/m3 induced inflammatory changes and was thought to be the Lowest Observed Adverse Effect Level (LOAEL) for acute effects of polypropylene. However, considering the concentration of microplastics in a real general environment, the risk of environmental hazards to humans may be low.
摘要：
背景：已经在大气以及海洋中检测到微塑料，人们担心它们在肺部的生物学效应。我们使用大鼠进行了短期吸入暴露和气管内滴注，以评估与微塑料相关的肺部疾病。我们对8周龄的雄性Fischer344大鼠进行了低浓度2mg/m3和高浓度10mg/m3的聚丙烯细粉吸入暴露，每天6小时，每周5天，共4周。我们还对12周大的雄性Fischer344大鼠以0.2mg/大鼠的低剂量和1.0mg/大鼠的高剂量进行了气管内滴注聚丙烯。在两次暴露后3天至6个月对大鼠进行解剖，收集支气管肺泡灌洗液（BALF）和肺组织，分析肺部炎症和肺损伤。
结果：从暴露后1个月起，两次聚丙烯暴露诱导炎症细胞持续流入，并在BALF中表达CINC-1，CINC-2和MPO。遗传分析显示，炎症相关因素在长达6个月的时间内显着增加。吸入中低浓度的聚丙烯也引起轻度肺部炎症。
结论：这些发现表明吸入聚丙烯，这是一种微塑料，诱导持续的肺部炎症，并有可能导致肺部疾病。暴露于2mg/m3诱导炎症变化,并且被认为是聚丙烯急性作用的最低观察到的不良反应水平(LOAEL)。然而,考虑到微塑料在真实环境中的浓度，环境危害对人类的风险可能很低。
结果：从暴露后1个月起，两次聚丙烯暴露诱导炎症细胞持续流入，并在BALF中表达CINC-1，CINC-2和MPO。遗传分析显示，炎症相关因素在长达6个月的时间内显着增加。吸入中低浓度的聚丙烯也引起轻度肺部炎症。
结论：这些发现表明吸入聚丙烯，这是一种微塑料，诱导持续的肺部炎症，并有可能导致肺部疾病。暴露于2mg/m3诱导炎症变化,并且被认为是聚丙烯急性作用的最低观察到的不良反应水平(LOAEL)。然而,考虑到微塑料在真实环境中的浓度，环境危害对人类的风险可能很低。
