{"title":"人工阳光老化通过降解介导的对苯二甲酸释放对聚对苯二甲酸微塑料雄性小鼠呼吸效应的影响。","authors":"Yasuhiro Ishihara, Mizuo Kajino, Yoko Iwamoto, Tatsuto Nakane, Yu Nabetani, Tomoaki Okuda, Maori Kono, Hiroshi Okochi","doi":"10.1093/toxsci/kfae135","DOIUrl":null,"url":null,"abstract":"<p><p>Microplastics are ubiquitous in the atmosphere, leading to human exposure through inhalation. Airborne microplastics undergo degradation due to sunlight irradiation, yet the respiratory risks associated with degraded microplastics remain poorly understood. In this study, we investigated the respiratory effects of polyethylene terephthalate (PET) degraded by artificial sunlight and created a transport and degradation model of PET for risk assessment. PET fibers were cut and subjected to artificial sunlight irradiation. Mice exposed to aged PET showed increased airway resistance induced by methacholine (MCh) inhalation, along with lung inflammation and neutrophil infiltration. Terephthalic acid (TPA) was continuously released from PET aged by artificial sunlight. Exposure to TPA also caused lung inflammation and enhanced airway resistance induced by MCh in mice. These findings indicate that aged PET can cause respiratory impairment via TPA release. A simple transport and degradation model was developed to quantitatively relate the abundance of aged PET produced in this study (i.e. 4,000 × 96 W m-2 h) and aged fractions of PET that can be generated in the atmosphere. Our results suggested 10% to 60% of PET was degraded as that produced in this study over sunny regions in summer, whereas only lower than 1% in high-latitude cities in Europe in winter. This study demonstrates the importance of considering the abundance of aged PET and further development of a transport and degradation model of PET to assess the risk of degraded PET in the atmosphere.</p>","PeriodicalId":23178,"journal":{"name":"Toxicological Sciences","volume":" ","pages":"242-252"},"PeriodicalIF":3.4000,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Impact of artificial sunlight aging on the respiratory effects of polyethylene terephthalate microplastics through degradation-mediated terephthalic acid release in male mice.\",\"authors\":\"Yasuhiro Ishihara, Mizuo Kajino, Yoko Iwamoto, Tatsuto Nakane, Yu Nabetani, Tomoaki Okuda, Maori Kono, Hiroshi Okochi\",\"doi\":\"10.1093/toxsci/kfae135\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Microplastics are ubiquitous in the atmosphere, leading to human exposure through inhalation. Airborne microplastics undergo degradation due to sunlight irradiation, yet the respiratory risks associated with degraded microplastics remain poorly understood. In this study, we investigated the respiratory effects of polyethylene terephthalate (PET) degraded by artificial sunlight and created a transport and degradation model of PET for risk assessment. PET fibers were cut and subjected to artificial sunlight irradiation. Mice exposed to aged PET showed increased airway resistance induced by methacholine (MCh) inhalation, along with lung inflammation and neutrophil infiltration. Terephthalic acid (TPA) was continuously released from PET aged by artificial sunlight. Exposure to TPA also caused lung inflammation and enhanced airway resistance induced by MCh in mice. These findings indicate that aged PET can cause respiratory impairment via TPA release. A simple transport and degradation model was developed to quantitatively relate the abundance of aged PET produced in this study (i.e. 4,000 × 96 W m-2 h) and aged fractions of PET that can be generated in the atmosphere. Our results suggested 10% to 60% of PET was degraded as that produced in this study over sunny regions in summer, whereas only lower than 1% in high-latitude cities in Europe in winter. This study demonstrates the importance of considering the abundance of aged PET and further development of a transport and degradation model of PET to assess the risk of degraded PET in the atmosphere.</p>\",\"PeriodicalId\":23178,\"journal\":{\"name\":\"Toxicological Sciences\",\"volume\":\" \",\"pages\":\"242-252\"},\"PeriodicalIF\":3.4000,\"publicationDate\":\"2025-02-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Toxicological Sciences\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1093/toxsci/kfae135\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"TOXICOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Toxicological Sciences","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1093/toxsci/kfae135","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"TOXICOLOGY","Score":null,"Total":0}
引用次数: 0
摘要
微塑料在大气中无处不在,导致人类通过吸入接触。由于阳光照射,空气中的微塑料会降解,但与降解微塑料相关的呼吸风险仍然知之甚少。本研究探讨了人造阳光降解的聚对苯二甲酸乙二醇酯(PET)的呼吸效应,并建立了PET的运输和降解模型进行风险评估。将PET纤维切割后进行人工日光照射。暴露于老化PET的小鼠表现出吸入甲胆碱引起的气道阻力增加,并伴有肺部炎症和中性粒细胞浸润。对苯二甲酸(TPA)在人工光照老化的PET中不断释放。暴露于TPA还可引起小鼠肺部炎症和甲胆碱(MCh)诱导的气道阻力增强。这些结果表明,老年PET可通过TPA释放引起呼吸损伤。建立了一个简单的传输和降解模型,以定量地联系本研究中产生的老化PET的丰度(即4,000 × 96 W m-2 h)和可以在大气中产生的PET的老化组分。我们的研究结果表明,在夏季阳光充足的地区,本研究中产生的PET降解率为10-60%,而在冬季欧洲高纬度城市,PET降解率低于1%。这项研究表明,考虑老化PET的丰度以及进一步发展PET的运输和降解模型对于评估大气中降解PET的风险非常重要。
Impact of artificial sunlight aging on the respiratory effects of polyethylene terephthalate microplastics through degradation-mediated terephthalic acid release in male mice.
Microplastics are ubiquitous in the atmosphere, leading to human exposure through inhalation. Airborne microplastics undergo degradation due to sunlight irradiation, yet the respiratory risks associated with degraded microplastics remain poorly understood. In this study, we investigated the respiratory effects of polyethylene terephthalate (PET) degraded by artificial sunlight and created a transport and degradation model of PET for risk assessment. PET fibers were cut and subjected to artificial sunlight irradiation. Mice exposed to aged PET showed increased airway resistance induced by methacholine (MCh) inhalation, along with lung inflammation and neutrophil infiltration. Terephthalic acid (TPA) was continuously released from PET aged by artificial sunlight. Exposure to TPA also caused lung inflammation and enhanced airway resistance induced by MCh in mice. These findings indicate that aged PET can cause respiratory impairment via TPA release. A simple transport and degradation model was developed to quantitatively relate the abundance of aged PET produced in this study (i.e. 4,000 × 96 W m-2 h) and aged fractions of PET that can be generated in the atmosphere. Our results suggested 10% to 60% of PET was degraded as that produced in this study over sunny regions in summer, whereas only lower than 1% in high-latitude cities in Europe in winter. This study demonstrates the importance of considering the abundance of aged PET and further development of a transport and degradation model of PET to assess the risk of degraded PET in the atmosphere.
期刊介绍:
The mission of Toxicological Sciences, the official journal of the Society of Toxicology, is to publish a broad spectrum of impactful research in the field of toxicology.
The primary focus of Toxicological Sciences is on original research articles. The journal also provides expert insight via contemporary and systematic reviews, as well as forum articles and editorial content that addresses important topics in the field.
The scope of Toxicological Sciences is focused on a broad spectrum of impactful toxicological research that will advance the multidisciplinary field of toxicology ranging from basic research to model development and application, and decision making. Submissions will include diverse technologies and approaches including, but not limited to: bioinformatics and computational biology, biochemistry, exposure science, histopathology, mass spectrometry, molecular biology, population-based sciences, tissue and cell-based systems, and whole-animal studies. Integrative approaches that combine realistic exposure scenarios with impactful analyses that move the field forward are encouraged.