塑料在全球水体分布广泛并且数量巨大，粒径小于5 mm的“微塑料”作为一种新型污染物受到了高度的关注。微塑料具有较强的疏水性，可强烈吸附有机污染物，使有机污染物在微塑料表面高浓度富集。微塑料易被生物摄食，有机污染物可通过微塑料被摄食进入生物体，进而影响其生物富集和生物毒性效应。当前，微塑料作为污染物对其生物毒性效应的研究较多，但微塑料作为载体其对有机物的生物毒性影响的研究较少。在不同浓度、不同粒径的微塑料存在条件下，微塑料影响污染物对低营养级生物毒性的机制仍不了解。本研究通过典型芳香族化合物在微塑料上的吸附、微塑料对微藻的毒性效应和微塑料存在条件下典型芳香族化合物对微藻的毒性影响三方面，揭示微塑料胁迫下典型芳香族化合物对微藻的毒性效应。 通过开展菲、硝基苯和萘在毫米微塑料和微米微塑料上的吸附实验，揭示菲、硝基苯和萘在微塑料上的吸附机制和关键影响因素。结果表明：①比表面积和表面官能团是影响微塑料吸附的重要因素；②比表面积归一化后不同材质微米微塑料吸附菲、硝基苯和萘的能力顺序为：高密度聚乙烯(HDPE)>聚苯乙烯(PS)>低密度聚乙烯(LDPE)>聚氯乙烯(PVC)；③菲和硝基苯在PS微塑料的吸附能力先随着粒径的减小而增加(170 μm~235 nm)，而后再缓慢减小(235~ 50 nm)。团聚作用是纳米级微塑料单位比表面积吸附能力减弱的原因。通过研究微塑料与污染物的相互作用关系，可明晰污染物和微塑料在不同相间的分配机制，是研究微塑料对污染物毒性影响的基础。 选取典型绿藻(小球藻，Chlorella vulgaris)和典型蓝藻(聚球藻，Synechococcus)为代表微藻，开展不同粒径、不同浓度条件下PS微塑料对两种微藻的96 h毒性效应研究。通过微塑料暴露条件下微藻生长、细胞体积、叶绿素a含量、抗氧化系统酶、丙二醛、酯酶活性、细胞膜通透性以及细胞亚显微结构观察等多个指标揭示微塑料对微藻的毒性效应。结果表明：50 nm~110 μm微塑料均抑制小球藻的生长，增加活性氧物质(ROS)水平，改变抗氧化酶活性，增大脂质过氧化程度，降低细胞活性，使小球藻产生氧化应激。其中50~200nm微塑料能够诱导小球藻细胞死亡数量增加，50nm~3μm微塑料显著减小小球藻细胞体积、增大细胞疏松程度，6 ~110 μm微塑料减弱小球藻光合作用。50和90 nm微塑料能够减弱聚球藻光合作用、降低细胞活性；200 nm~3 μm微塑料不仅减弱聚球藻光合作用，还显著抑制生长、减小细胞体积、增加细胞结构疏松度、增加ROS水平，改变抗氧化酶活性，但是没有使聚球藻产生明显的氧化应激；6 μm ~110 μm微塑料也能够减弱聚球藻光合作用。暴露于同样浓度微塑料中，小球藻比聚球藻毒性反应更敏感。1~1000mg/L微塑料引起小球藻ROS水平显著增加、酯酶活性降低，以及聚球藻酯酶活性降低和叶绿素a含量的减少。100~1000mg/L微塑料促进聚球藻生长，但是抑制小球藻生长，同时增加小球藻细胞死亡数量，改变小球藻抗氧化酶活性，使小球藻产生脂质过氧化。微塑料对小球藻和聚球藻生长、脂酶活性和细胞死亡有显著的剂量效应。通过添加不同电子传递链的抑制剂，证明小球藻的叶绿体是细胞中ROS产生和积累的位点，由ROS过量引起的脂质过氧化作用是微塑料引起小球藻毒性的主要机制之一。 最后选取纳米级PS微塑料(50 nm)，开展微塑料存在条件下菲和硝基苯对小球藻毒性效应的影响研究。结果表明：在微塑料存在条件下，硝基苯、菲使小球藻生长受到更显著抑制，细胞体积增加明显，细胞表面粗糙度增加，ROS水平增高，酯酶活性降低，微塑料显著增加硝基苯和菲对小球藻的毒性。微塑料和硝基苯、菲混合物引起的联合毒性效应中，微塑料是造成毒性的主要因素。在微塑料存在条件下，硝基苯、菲使小球藻死细胞数量增加，细胞死亡是微塑料和高浓度硝基苯、菲共同作用的结果。微塑料对菲影响小球藻生长抑制、ROS产生和细胞死亡的程度比硝基苯更明显。微塑料显著减少菲的生物富集，对硝基苯的生物富集没有显著影响。微塑料虽然减弱了硝基苯和菲对藻的暴露浓度，但是却增加了微藻的毒性，因此微塑料对芳香族化合物的毒性影响不完全依赖于芳香族化合物的生物富集程度。鉴于微塑料也有一定的生物毒性，今后对微塑料影响污染物毒性的研究中应将微塑料的毒性贡献比例作为重要的考虑因素。

Generally, plastic particles with size less than 5 mm are defined as “microplastics”. It has led to enormous concerns in the past few years due to wide distribution and increasing concentration in the ocean. It has been reported that microplastics can strongly sorb some organic pollutants owning to hydrophobic property. As a result, the accumulation of harmful organic pollutants on microplastics in the ocean may affect its local or global transport in the marine environment. These organic pollutants concentrated by microplastics can be swallowed by some aquatic organisms with microplastics, and change the toxicity effect of organic pollutants on organisms. Therefore, the toxicity effect of organic pollutants on organisms was complex in the presence of microplastics. Toxicity of microplastics on organisms has been studied extensively, but the study of toxic effect of organic pollutants on microalgae in the presence of microplastics is rare. It is significant to study the toxicity effect of organic pollutants on microalgae in the presence of microplastics with various concentrations, particle sizes, etc. In this study, the sorption mechanisms of typical aromatic compounds on microplastics, toxic effect of microplastics on microalgae, and toxic effect of typical aromatic compounds on microalgae in the presence of microplastics, were investigated. The main conclusions were as follows: Sorption experiments of phenanthrene, nitrobenzene and naphthalene on mesoplastics and microplastics were performed to reveal the mechanisms and key factors of sorption. The results suggested that specific surface area (SSA) and functional groups on the surface of plastics were important for sorption abilities of phenanthrene, nitrobenzene and naphthalene on mesoplastics and microplastics. After normalized by SSA, the sorption abilities of microplastics followed the order as HDPE > PS > LDPE >PVC. In addition, for micron-polystyrene and submicron-polystyrene, the sorption abilities increased with decreasing particle size, whereas for nano-polystyrene, the sorption abilities decreased slightly and were lower than that of 235 nm microplastics. The aggregation of nano-polystyrene reduced the sorption capacitiesy of phenanthrene and nitrobenzene. The results can help understand the distribution of typical aromatic compounds in different phases and contribute to exploring the toxic mechanism of typical aromatic compounds in the presence of microplastics. The toxicity test of PS microplastics with different particle size and concentration on Chlorella vulgaris and Synechococcus was performed in 96 h. The results showed that microplastics with size from 50 nm to 110 μm caused growth inhibition, increased the production of reactive oxygen species (ROS), changed the antioxidant enzyme activity, caused lipid peroxidation, reduced cellular activity and caused oxidative stress in Chlorella vulgaris. The 50 - 200 nm sized microplastics induced cell apoptosis, the 50 nm - 3 μm sized microplastics reduced the cell volume and increased the intracellular porosity, and the 6 - 110 μm microplastics weakened the photosynthesis of Chlorella vulgaris. The 50 nm - 3 μm sized microplastics weakened the photosynthesis and reduced the cell activity of Synechococcus, the 200 nm - 3 μm sized microplastics caused growth inhibition, weakened the photosynthesis, reduced the cell volume, increased the intracellular porosity, induced the production of ROS, changed the antioxidant enzyme activity without oxidative stress occurring and lowered the mortality rate of Synechococcus. The 6 μm - 110 μm sized microplastics weakened the photosynthesis of Synechococcus. Microplastics with concentration from 1 to 1000 mg/L weakened the cell activity of Chlorella vulgaris and Synechococcus，induced the production of ROS of Chlorella vulgaris and weakened the photosynthesis of Synechococcus. Microplastics with concentration between 100 and 1000 mg/L promoted the growth of Synechococcus but inhibited the growth of Chlorella vulgaris. Meanwhile, microplastics with concentration between 100 and 1000 mg/L changed the antioxidant enzyme activity, caused lipid peroxidation and increased cell mortality of Chlorella vulgaris. Toxicity in Chlorella vulgaris was more significant than in Synechococcus induced by microplastics. By adding inhibitors of different electron transfer chains, the chloroplast was proved to be the site of ROS production and accumulation in Chlorella vulgaris. Lipid peroxidation induced by ROS accumulation was one of the main mechanisms of toxicity in Chlorella vulgaris induced by microplastics. The toxic tests of phenanthrene and nitrobenzene in Chlorella vulgaris in the presence of microplastics were performed by 50 nm PS microplastics. The results showed that microplastics reduced the exposure concentration of phenanthrene and had no significant effect on the exposure concentration of nitrobenzene to Chlorella vulgaris. Nitrobenzene and phenanthrene significantly caused growth inhibition, increased the cell volume, increased the roughness of the cell surface, induced the production of ROS, weakened the cell activity in the presence of microplastics. Microplastics significantly increased toxicities of nitrobenzene and phenanthrene on Chlorella vulgaris and microplastics played a major effect on the joint toxicity of microplastics and aromatic compounds. Nitrobenzene and phenanthrene increased the mortality rate of Chlorella vulgaris in the presence of microplastics due to the joint toxicity of microplastics and compounds. The effects of phenanthrene on the growth inhibition, ROS production and cell apoptosis were more significant than those of nitrobenzene in the presence of microplastics. Although microplastics reduced the exposure concentrations of nitrobenzene and phenanthrene to Chlorella vulgaris, the mixture of microplastics and aromatic compounds still increased the toxicity of Chlorella vulgaris. Therefore, the effect of microplastics on toxicity of aromatic compounds did not depend on the bioaccumulative concentrations of these compounds. Considering that microplastics have the dual identity of toxic substances and vehicle, the contribution of microplastics to the joint toxicity of microplastics and organic pollutants should be taken into account in future studies.