气载微塑料对呼吸系统的影响及机制研究进展

范姿; 卞倩

doi:10.7524/j.issn.0254-6108.2022011301

气载微塑料对呼吸系统的影响及机制研究进展

范姿^1,,
卞倩^1,2, ,

1.
南京医科大学，南京，210009
2.
江苏省疾病预防控制中心毒理与风险评估研究所，南京，210009

通讯作者: Tel：025-83759450，E-mail：biaqian@jscdc.cn

基金项目:
江苏省自然科学基金（BK20211374）资助

Research progress on the effects and mechanisms of airborne microplastics exposure on the respiratory system

FAN Zi^1,,
BIAN Qian^1,2, ,

1.
Nanjing Medical University, Nanjing, 210009, China
2.
Institute of Toxicology and Risk Assessment, Jiangsu Center for Disease Control and Prevention, Nanjing, 210009, China

Corresponding author: BIAN Qian, biaqian@jscdc.cn

Fund Project: Natural Science Foundation of Jiangsu Province（BK20211374）

摘要: 近年来，号称“海中PM_2.5”的微塑料污染已成为全世界广泛关注的环境问题之一. 微塑料是一类新兴环境污染物，它的来源广泛、种类丰富、形态各异等特征使其可在水、土壤等环境介质中长期存在. 然而，有研究已检测到空气中也存在着微塑料. 大气环境中存在的微塑料不仅来源于纺织业、建筑工地、家具等，还可以来源于海洋. 存在于海洋中的微塑料可随季风运动继而悬浮于空气中，并在世界各地范围内广泛移动. 微塑料不仅本身具有一定的生物毒性，它还可携其它污染物构成复合污染. 由此可见，微塑料不仅可以通过食物链进入体内，微（纳米）塑料及其附着的有害物质还可通过吸入途径进入生物体内，从而对人类的健康构成潜在威胁. 由于该领域当前研究主要集中在海洋和陆地环境中存在的微塑料对生物体的毒性研究而对气载微塑料的研究大多仅仅停留在监测或其对生物体的表观效应上，尚缺乏气载微塑料对生物机体构成潜在健康风险的深入机制探索. 因此，本文依据大气环境中微塑料的相关研究报道，主要从大气环境中微塑料的来源与化学组成、主要类型和检测方法、气载微塑料致机体呼吸系统损伤作用、气载微塑料致呼吸系统疾病损伤机制四个方面对大气微塑料暴露对呼吸系统的影响进行综述探讨，并展望今后的研究重点和方向.
- 大气环境 /
- 微塑料 /
- 吸入 /
- 损伤 /
- 毒性效应 /
- 机制
Abstract: In recent years, the pollution of microplastics ("PM_2.5 in the sea") has become one of the environmental issues of widespread concern all over the world. Microplastics are a kind of emerging environmental pollutants, the characteristics of the wide range of sources, rich types, and different shapes that make them long-lived in environmental media such as water and soil. However, some studies have detected the presence of microplastics in the air. The microplastics present in the atmospheric environment not only come from the textile industry, construction industry, furniture, etc., but also the microplastics existing in the ocean can float in the air with the movement of the monsoon and move widely around the world. Microplastics not only have certain biological toxicity, it can also form compound pollution by carrying other pollutants. For the reason that microplastics can not only enter the body through the food chain, but micro (nano) plastics and their attached harmful substances can also enter the organism through inhalation, thus posing the potential threats to human health. Since the current research to microplastics is mainly focused on the toxicity of microplastics existing in the marine and terrestrial environment, the majority of studies on airborne microplastics only focus on monitoring or just the effects on organisms, and there is still a lack of in-depth mechanism exploration of the potential health risks of airborne microplastics to biological organisms. Therefore, based on the relevant research reports of microplastics in the atmospheric environment, this article reviews the impact of atmospheric microplastics exposure on the respiratory system from four aspects: the source and chemical composition of microplastics in the atmospheric environment, the main types and detection methods, the damage effect of airborne microplastics on the respiratory system, and the mechanisms of airborne microplastics-induced respiratory damage, while envisaging the focus and direction for future research.
- atmospheric environment /
- airborne microplastics /
- inhalation /
- injury /
- toxic effects /
- mechanism
图 1 大气环境中微塑料的来源

Figure 1. Sources of microplastics in the atmospheric environment

下载: 全尺寸图片幻灯片

图 2 大气环境中微塑料的主要类型和检测方法

Figure 2. The main types and detection methods of MPs in atmospheric environment

下载: 全尺寸图片幻灯片

图 3 大气中存在的MPs在肺部的吸入与清除

Figure 3. Inhalation and clearance of airborne MPs in the lungs

下载: 全尺寸图片幻灯片

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随着经济社会的不断发展、现代化工业进程的不断加深，塑料的使用在人们日常生活中无处不在. 从食品包装，电子产品，家具到常见的一次性使用物品等. 2016年全球产生了19—2300万吨塑料垃圾，每年塑料排放量到2030年预计可达5300万吨^[1]. 塑料制品经紫外辐射、物理磨损、（微）生物降解等一系列过程后可解离成颗粒状、碎片状或其它形态的塑料，其中直径小于5 mm的塑料被称之为微塑料（microplastic, MPs），纳米级尺寸的塑料为纳米微塑料（nanoplastics，NPs）^[2-3].

据报道，预计到2050年，自然环境中存在的塑料垃圾将达1.20×10¹¹亿吨，它的污染及潜在危害已成为日益关注的环境问题^[4]. MPs所导致的潜在健康危害逐渐引起了全世界的广泛关注，联合国环境规划署已明确将MPs列为全球新兴环境污染物之一^[5-7]. 有研究指出，土壤中的MPs可在阳光照射下，产生环境持久性自由基以及活性氧（reactive oxygen species, ROS），引起生物体的氧化应激而造成机体损伤^[8]. 很多报道已揭示海洋MPs污染会对生物体的消化系统、生殖系统、神经系统等产生不良效应^[9-12]. 然而MPs不仅只存在于海洋中，还广泛浮游在空气里且可随季风等影响，而在全球范围内移动^[13].

近年来，有研究团队在大气环境中检测到了MPs且在人肺组织中也检测到了塑料合成纤维，这引发了人们对空气中存在的MPs与职业病关系的关注^[14-15]. 关于大气中存在的MPs，2021年研究者在我国北部和东南部五个城市-北京、天津、上海、南京和杭州进行了大气MPs浓度检测，结果显示，北部城市空气中的 MPs 浓度（358±132）个·m⁻³高于东南部城市（230±94）个·m^−3[16]. 在中国东莞市进行的调查指出该市大气环境中约存在175—313个·m⁻²·d⁻¹，其平均沉积率为（36 ± 7）个·m⁻²·d^−1[17]. 早前在巴黎进行的调查研究显示，该地区大气沉降物中的MPs浓度可达335个·m⁻²·d^−1[18]. Dris等^[19]在后期研究中指出，巴黎市区总大气沉降物的平均沉降速率为（110 ± 96）个·m⁻²·d⁻¹ ，郊区为（53 ± 38）个·m⁻²·d⁻¹. 由此可见，城市中气载MPs的问题可能比城郊更严峻^[19]. 最近的一项荟萃分析数据显示，成年女性每天平均接触258个MPs颗粒，其中吸入的MPs颗粒达132个^[20]. 鉴于MPs不仅能从海洋传播到陆地环境中，其还能在空气中进行远距离传播^[21]；且空气中的MPs比海洋中的MPs体积更小，肉眼完全看不见，所以很难掌握其移动途径和扩散范围，因而对大气中存在的MPs进行研究刻不容缓.

然而，目前MPs对呼吸系统毒性影响的研究暂仅停留在MPs的肺部沉积及表观毒性效应上^[22]. 本综述旨在总结归纳MPs暴露对呼吸系统的影响及其机制研究进展，并对当前研究存在的不足以及仍待解决的问题进行探讨.

1. 大气环境中MPs的来源（Sources of MPs in the atmospheric environment）

2. 大气环境中MPs的主要类型和检测方法（The main types and detection methods of MPs in the atmospheric environment）

3. 气载MPs的吸入与清除（Inhalation and removal of airborne MPs）

4. 气载MPs致机体呼吸系统损伤作用（Respiratory system injury caused by airborne MPs）

人体呼吸系统包括呼吸道和肺两大部分，其主要功能是进行气体交换. 呼吸道包括鼻、咽、喉、气管和各级支气管. 其中鼻、咽、喉为上呼吸道；气管和各级支气管为下呼吸道. 肺由肺实质（支气管树和肺泡）以及肺间质（结缔组织、血管、淋巴管、淋巴结和神经）组成. 空气中的超细颗粒和非矿物纤维可穿过管腔或通过清除机制而作为吸入异物停留在肺中，这些异物通过影响正常的降解作用继而可能诱发炎症^[46].

生物体吸入MPs后可引起呼吸道粘膜及肺组织产生局部生物反应. 有研究在人的肺部样品中检测到了微量塑料纤维，并猜测此纤维与肺部恶性肿瘤间存在着相关关系^[49]. 在Song等^[50]进行的一组病例报告中，8名工人暴露于弥漫聚丙烯酸酯混合物的工作环境5—13个月后，均因出现呼吸急促，胸腔积液，肺纤维化，异物肉芽肿和低氧血症等症状入院. 经一系列临床检查，患者肺组织中均出现炎症、纤维化和胸膜异物肉芽肿等不良症状. 通过透射电子显微镜在肺部观察到了30 nm的颗粒，同时在胸腔积液中也观察到了颗粒沉积现象^[50]. 另外，Atis等^[51]对生产加工塑料袋的工人和纺织工人进行健康检查发现，与对照组未暴露在工厂环境的人相比，受试工人支气管周围出现了增厚和弥漫性玻璃样变，同时受试组工人出现呼吸道症状的风险增加了3.6倍且血清中IL-8 和 TNF-α水平显著升高. 工厂环境中弥漫的PP团簇物经扫描电子显微镜检测到其直径为（6.9 ± 2.1）μm，长度为（96.7 ± 35.2）μm. 由于该物质空气动力学直径≤ 10 μm，故PP团簇物可能是工人在纺织制造过程中吸入的物质之一. 另外有研究指出：纤维状PP的直径取决于制造工艺，单丝纱线可以从153 μm分解到1—5 μm不等的超细纤维^[52]. 由此可见，弥漫在空气中的MPs可对机体呼吸系统产生一定的损伤作用. 职业暴露是气载MPs成为健康风险的重要方式之一，今后应加强对塑料制厂、纺织工厂等的环境检测以及严格履行对工人的定期例行健康检查来做到早发现、早预防以减少环境暴露对人健康的负面影响.

早在2012年，Varela等^[53]在体外将PS-NPs（polystyrene-Nanomicroplastic, PS-NPs）作用于腺癌人类肺泡基底上皮细胞（A549）的研究表明，NPs能被吸收，其吸收率取决于颗粒大小，40 nm PS-NPs的内化速度快于20 nm、100 nm PS-NPs. 但NPs与肺泡上皮细胞相互作用的机制及其内化后的潜在不良影响未得到很好的理解，故需进一步研究. Dong等^[54]在调查MPs对肺毒性的研究发现，人正常肺上皮细胞（BEAS-2B）暴露于10 μg·cm⁻²和1000 μg·cm⁻² 浓度下（1.72 ± 0.26） μm （1.67—2.17 μm）的PS-NPs后紧密连接蛋白（zona occludens protein 1，ZO-1）表达下降、跨上皮电阻（transepithelial electrical resistance, TEER）降低，导致气道上皮通透性变差从而使得肺屏障功能受损. 因此，外来物质和毒素更容易进入间质及血液中，从而增加了患肺部炎症及慢性阻塞性肺疾病（Chronic obstructive pulmonary disease，COPD）的风险. 此外，其它研究团队也发现PS-NPs会破坏肺泡上皮屏障而影响正常肺功能^[55].

在模式生物体内，Lim等^[56]发现MPs暴露对生物呼吸系统具有潜在损伤作用，他们对大鼠进行连续14 d全身动态吸入100 nm PS-MPs后观察到雄性大鼠的吸气时间明显减少；雌性大鼠呼吸频率增快，吸气时间和呼气时间均减少的肺功能不良症状. 最近，有研究团队在正常和哮喘模型小鼠鼻腔内每3 d滴注300 μg·20 μL⁻¹ MP，连续24 d后发现两组动物均出现肺部炎性细胞浸润、支气管内肺泡巨噬细胞聚集、支气管肺泡灌洗液（bronchoalveolar lavage fluid, BALF）中 TNF-α 水平升高，以及正常小鼠组血浆 IgG1 产生增加；此外，MP暴露通过增加粘液产生和炎症细胞浸润以及促进巨噬细胞聚集来加重哮喘症状^[57].

5. 气载微塑料致呼吸系统疾病损伤机制（Injury mechanism of airborne microplastics in respiratory diseases）

尽管近几年才日益对大气环境中存在的MPs引起关注，但其吸入毒性研究已有相关报道. 基于研究指出气载MPs致机体呼吸系统具有损伤作用，本文接下来将以具体的机制为着眼点，从氧化损伤、炎症反应、细胞周期紊乱和细胞凋亡的4个方面分别进行阐述.

5.1. 气载MPs与氧化损伤

活性氧（reactive oxygen species, ROS）是由具有活性氧功能的基团物质组成，包括超氧阴离子、羟自由基、过氧化氢及其下游产物过氧化物和羟化物等^[58]，ROS的急剧增多可破坏肺组织细胞，导致中性粒细胞发生炎性浸润，蛋白酶分泌增多等不良作用^[59-60]. 研究者对（1.72 ± 0.26） μm （1.67—2.17 μm）聚苯乙烯微塑料颗粒（PS-MPs）的体外肺毒性研究发现：PS-MPs通过诱导ROS的形成对BEAS-2B产生了细胞毒性和炎症效应^[54]. 当BEAS-2B细胞暴露于高剂量的PS-MPs（1000 μg·cm⁻²）时，大量ROS的形成抵抗了细胞抗氧化酶能力而发生了氧化应激. 其机制可能与IL-8、IL-6表达水平的增高，释放相关细胞因子有关. Shi等^[61]在A549细胞中进行PS-MPs与邻苯二甲酸酯联合暴露的毒性研究也发现PS-MPs可通过抵抗细胞内抗氧化酶的活性而引起氧化应激. 氧化酶和抗氧化酶的失衡导致氧化应激损伤，这可能在MPs致肺部疾病中发挥着潜在作用^[59-60,62].

有研究指出在酚醛树脂（phenol-formaldehyde resin microplastic, PF）的制造、应用、加工等过程中，会将大量粒径小于10 μm的PF微塑料微粒（PF-MPs）释放到空气和其他环境介质内^[63]. 据报道，研磨车间环境中的PF-MPs浓度高达153.6 mg·m⁻³. 考虑到在该车间工作的职业人群在PF-MPs环境中暴露的可能性大， Zhu等^[64]采集了来自不同公司的5个PF-MP样本，其平均直径分别为12.13、14.61、14.20、13.52、12.61 μm并在太阳光模拟照射下对它们的氧化潜力（oxidative potential, OP）进行评估，以通过PF-MP在阳光照射下产生的环境持久性自由基（environmentally persistent free radicals , EPFRs）和ROS浓度来衡量OP与PF-MP活性成分之间的相关性及其潜在毒性影响. 此外，使用A549细胞评估了光老化对PF-MP细胞毒性的作用，以进一步了解对人类健康的潜在不利影响. 该研究指出，长期暴露在光照辐射下，1000 μg·mL⁻¹浓度的PF-MPs可明显增加A549细胞ROS的产生并降低其细胞活力来增强细胞毒性^[64]. 在PS-MPs与人肺泡腔室细胞的生物反应差异性的研究中，将25 μg·mL⁻¹浓度下50 nm和100 nm的PS-MPs悬浮液分别染毒Ⅰ型肺泡上皮细胞、Ⅱ型肺泡上皮细胞和肺泡巨噬细胞24 h后观察到GSSG / GSH比率（氧化型谷胱甘肽与还原型谷胱甘肽的比率）上调，激活了氧化应激的发生，进而诱导了炎症，其中巨噬细胞中ROS表达水平低于Ⅰ型肺泡上皮细胞和Ⅱ型肺泡上皮细胞^[65]. 除此， Kim等^[66]以秀丽隐杆线虫和斑马鱼为模式生物，结合转录因子RNAi筛选、AOP Wiki（http://aopwiki.org）和CTD（comparative toxicogenomics database）分析方法进行基因-疾病相互作用分析，揭示了过氧化物酶体增殖物激活受体γ失活导致肺纤维化在微塑料对人类健康影响过程中可能发挥着重要作用. 近期，有研究通过微阵列检测，获得了正常BEAS-2B细胞和7.5 μg·cm⁻²、30 μg·cm⁻² 40 nm PS-NPs处理BEAS-2B细胞之后的差异表达基因并通过功能分析预测到PS-NPs处理组的差异表达基因在氧化还原酶活性和转录调控方面呈显著富集，这可能在呼吸系统疾病的发病过程中发挥着作用^[55].

氧化应激涉及的通路主要包括：Kelch样环氧氯丙烷相关蛋白1-核因子E2 相关因子2-抗氧化反应序列元件（Keap1-Nrf2-ARE）通路、磷脂酰肌醇-3-激酶/蛋白激酶 B（PI3K/Akt）通路、丝裂原蛋白活化激酶（MAPK）信号通路家族、酪氨酸蛋白激酶/信号转导和转录活化子（JAK/ STAT）信号通路、Toll 样受体（TLRs）信号通路、核因子（NF）-κB 信号通路、Wnt信号通路等^[67]. 它们也可能是气载微塑料通过氧化应激对机体产生不良健康影响的潜在机制，这有待研究者进行深入研究.

5.2. 气载微塑料与炎症反应

炎症在肺部疾病的发生发展过程中起着重要作用. 有关气载微塑料的体内动物研究显示，将受试大鼠暴露于不同浓度剂量的100 nm PS-MPs中发现，TGF-β和促纤维化的TNF-α蛋白水平上升^[56]. 早在20年前，Brown等^[68]对空气中PM ₁₀的研究就已发现，气管滴注1 mg的64 nm、202 nm、535 nm PS-MPs于大鼠肺部后，64 nm PS-MPs相较于其它两种粒径PS-MPs，支气管肺泡灌洗液中的蛋白质浓度和乳酸脱氢酶含量水平呈显著上升趋势，肺内嗜中性粒细胞水平也显著增加，这提示着粒径越小的超细颗粒可能会引起更严重的炎症反应. 在另外一项体外细胞实验发现^[54]：当BEAS-2B细胞暴露于（1.72 ± 0.26） μm （1.67—2.17 μm）粒径范围内10 μg·cm⁻²和1000 μg·cm⁻²的PS-MPs环境中24 h后，IL-6在细胞中的表达水平明显升高. BEAS-2B细胞暴露在浓度1000 μg·cm⁻²的PS-MP环境中24 h后，IL-8表达水平也呈增高趋势. 这与Xu等^[69]利用不同尺寸、浓度的PS对A549细胞进行的毒性研究所发现的结果一致，PS-MPs诱导促炎性细胞因子：IL-8和TNF-α表达的上升. 这些改变的细胞因子值得关注，今后的研究可以此作为依据和基础，进行深入探讨.

肺泡巨噬细胞在维持肺部内环境稳定和防御外来大气污染物危害等方面发挥着重要功能，其发挥吞噬功能后可释放包括白介素在内的具有广泛生物活性的各种致炎细胞因子，进而参与组织损伤、水肿等多种炎症过程^[70]. Ruenraroengsak等^[65]的研究指出25 μg·mL⁻¹浓度下50 nm PS-MPs通过激活肺泡Ⅱ型上皮细胞和肺泡巨噬细胞，释放了IL-6和IL-8，使得IL-6、IL-8水平显著上升产生炎症效应. IL-6、IL-8能激活免疫系统，参与急性免疫反应^[71]，并且在COPD的发生发展过程中发挥着一定的作用^[72-73].

炎症反应在呼吸系统疾病中与肺损伤、肺纤维化及COPD等疾病的发生息息相关，NF-κB、MAPK、JAK/STAT、Toll样受体、NLRP3炎症小体等信号通路在炎症因子释放上起着重要作用^[74]. 目前气载微塑料与炎症反应研究暂仅停留在表观效应上，尚未对潜在机制进行探讨. 在今后的研究中，可以从已观察到的效应水平作为着眼点，首先从经典的炎症机制作为起点，对气载微塑料致炎症反应进行寻因以知晓内在可能的潜在机制，来为预防气载微塑料可能造成的潜在不良影响提供针对性的干预支持.

5.3. 气载微塑料与细胞周期紊乱

细胞周期与多种生命活动的正常运行密切相关，如信号传导、基因转录、细胞凋亡、DNA修复、细胞分化等. 它可调控蛋白降解，控制细胞周期内一系列生物活动. 细胞周期紊乱可影响细胞生长、复制、分裂等. 有研究者将A549细胞暴露于100 μg·mL⁻¹浓度下的1 μm和10 μm PS-MPs后发现：细胞活力和增殖能力均显著降低^[75].

据报道称PS-MPs诱导细胞发生ROS和不平衡的氧化还原反应可导致DNA、脂质、蛋白质和细胞器的过氧化^[76]. DNA过氧化可通过碱基切除修复来延缓细胞周期，从而增加cyclin D、cyclin E、Ki-67的表达^[77]. 细胞周期从G1期进入到S期需要cyclin D和cyclin E的持续磷酸化得以实现^[78]. 在Xu等^[69]进行的细胞周期检测中发现25 μg·mL⁻¹ 25 nm、160 μg·mL⁻¹ 70 nm的PS-MPs均将细胞周期阻滞在S期，且cyclin D、cyclin E蛋白表达增加及在mRNA水平上出现了转录水平升高的现象. 除此以外，Ki-67是细胞增值的关键标志物，该研究结果发现Ki-67水平上调，在细胞周期G1、S、G2期中普遍表达而在G0期不表达，由此可见气载MP在肺部细胞暴露后可使细胞周期变长而细胞周期的改变往往和细胞恶性转化和肿瘤细胞失控性增殖关系密切，其潜在不良影响不容忽视；其中参与细胞周期运转的重要蛋白分子可能对细胞不良病变及在临床肿瘤防治过程中发挥着重要作用^[79]. 此外，由于目前该方面的研究较少，且缺少微塑料与肺部恶性疾病间的临床研究数据，故需研究者进行后续探讨且思考现实意义.

5.4. 气载微塑料与细胞凋亡

细胞凋亡是细胞的一种基本生物学现象，受到多基因调控. 它在生物体进化、维持内环境稳定以及多个系统发育过程中都起着重要的作用. 在PS-NPs对人肺上皮细胞影响的初步研究中发现：25 μg·mL⁻¹ 25 nm、160 μg·mL⁻¹ 70 nm的PS-MPs除了诱导促炎细胞因子上调以外还可以以时间依赖性的方式促进凋亡蛋白BAX、Casepase-3、Casepase-8、Casepase-9及细胞色素c表达水平的显著上调，这提示PS-NPs可启动与TNF-a相关的凋亡路径^[69]. Johnston等^[80]在肝母细胞瘤C3A细胞系和肝癌HepG2细胞系的线粒体中检测到了PS-MPs, 且有研究指出NPs可以改变细胞质血小板中的钙水平^[81]. 因此，PS-MPs在细胞质中可能损害线粒体的正常功能，引起线粒体表面Bax的单体化，诱导Ca²⁺内流和线粒体中细胞色素c外流，导致膜电位降低，ATP不足，从而激活下游的Casepase-9和Casepase-3，最终诱导线粒体发生凋亡. PS-MPs不仅可上调TNF-a和肿瘤坏死因子相关凋亡配体Death receptor 5 （Death receptor 5，DR5）的表达，而且PS-MPs对DR5下游的凋亡蛋白casepase-8、casepase-3、casepase-9均有上调作用，这提示着DR5介导的信号复合体可能参与着PS-MPs诱导细胞凋亡的过程. 另外，有研究者通过Annexin V-FITC/PI双染试剂在荧光显微镜下观察经0 μg·cm⁻²、7.5 μg·cm⁻²、15 μg·cm⁻²、30 μg·cm⁻² 40 nm PS-MPs染毒后的HPAEpiC和 BEAS-2B细胞发现：细胞凋亡的症状呈一定的剂量依赖性，随给药浓度的增加而显著增加^[55].

细胞凋亡是一种特殊的细胞死亡类型，具有重要的生物学意义和复杂的分子生物学机制，凋亡过程的紊乱可能与许多疾病的发生发展有直接或间接的关系. 除了上述已发现的机制外，PS-MPs的直接免疫原性以及其诱导发生的炎症反应而破坏细胞膜的完整性进而导致细胞的进一步坏死可能也是肺部疾病发生发展的潜在机制之一，在后续研究中可对其深入研究.

6. 结论（Conclusion）

MPs作为一种新型气载环境污染物，其来源广泛，形态各异. 现阶段研究对海洋和陆地中存在的MPs关注度较高，而对大气环境中的MPs研究甚少. 目前，对于MPs而言，尚缺乏系统的技术规范和环境评价体系. 因而迫切需要构建微塑料监测分析的标准化方法，包括MPs样品采集、分离、检测、量化技术. 由于检测技术的局限性，尚未能对小于400 nm的MPs进行准确表征. 即使通过扫描电子显微镜、mIRage O-PTIR能识别尺寸达纳米级的MPs，但检测范围仍有限. 在后续研究中，研究者应着力攻克小于400 nm MPs的检测技术.

随着越来越多的研究证实了大气中存在着MPs，人们又无时无刻不暴露于空气中，其潜在的健康风险值得大家关注. 当前已有的研究提示，MPs可通过氧化应激、诱导炎症、干扰细胞正常周期和细胞凋亡等机制，对呼吸系统造成潜在威胁，而这些研究侧重于表观效应的描述尚未对潜在的机制进行深入挖掘. 未来，研究者应在已有研究基础上，通过体内、体外和人群研究相结合的方式来对MPs潜在健康危害机理进行深入探索，以期为将来风险评估及危害防范提供科学依据.

此外，对于此领域的研究可重点关注：①通过人群研究摸清大气环境中的MPs在人体中的内暴露水平，进而评估研究气载MPs的现实意义，并为健康风险评估提供数据支持；②探讨不同粒径MPs的吸入暴露风险和健康危害效应以及着眼于生物毒性效应机制的探索；③关注MPs与其他环境污染物的复合暴露毒性效应与机制研究来增强对MPs暴露的全面认识.

参考文献 (81)

气载微塑料对呼吸系统的影响及机制研究进展

通讯作者: Tel：025-83759450，E-mail：biaqian@jscdc.cn

Research progress on the effects and mechanisms of airborne microplastics exposure on the respiratory system

Corresponding author: BIAN Qian, biaqian@jscdc.cn

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气载微塑料对呼吸系统的影响及机制研究进展

通讯作者: Tel：025-83759450，E-mail：biaqian@jscdc.cn

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