Department of Occupational Pneumology, Institute of Industrial Ecological Sciences, University of Occupational and Environmental Health, Japan, 1-1 Iseigaoka, Yahata-nishi-ku, Kitakyushu, Fukuoka, 807-8555, Japan.
Department of Environmental Health Engineering, Institute of Industrial Ecological Sciences, University of Occupational and Environmental Health, Japan, 1-1 Iseigaoka, Yahata-nishi-ku, Kitakyushu, Fukuoka, 807-8555, Japan.
Part Fibre Toxicol. 2024 Aug 6;21(1):29. doi: 10.1186/s12989-024-00592-8.
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/m and a high concentration of 10 mg/m 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/m 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.
微塑料已在大气和海洋中被检测到,人们担心它们在肺部的生物效应。我们通过短期吸入暴露和气管内滴注的方式,用大鼠来评估与微塑料相关的肺部疾病。我们对 8 周龄雄性 Fischer 344 大鼠进行了为期 4 周、每天 6 小时、每周 5 天的低浓度(2mg/m³)和高浓度(10mg/m³)的聚丙烯细粉吸入暴露。我们还对 12 周龄雄性 Fischer 344 大鼠进行了低剂量(0.2mg/只)和高剂量(1.0mg/只)的聚丙烯气管内滴注。在两次暴露后的 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,以分析肺部炎症和肺损伤。
两种暴露于聚丙烯的方式都导致炎症细胞持续涌入,BALF 中的 CINC-1、CINC-2 和 MPO 表达从暴露后 1 个月开始增加。基因分析显示,炎症相关因素的增加可持续长达 6 个月。低浓度的聚丙烯吸入暴露也会引起轻度的肺部炎症。
这些发现表明,吸入的微塑料聚丙烯会引起持续的肺部炎症,并可能导致肺部疾病。2mg/m³的暴露引起了炎症变化,被认为是聚丙烯急性效应的最低观察到不良效应水平(LOAEL)。然而,考虑到实际一般环境中微塑料的浓度,对人类造成环境危害的风险可能较低。