Toxicity Of Nanoplastics Research Articles

Polystyrene nanoplastics exacerbated Pb-induced liver toxicity in mice.

Nanoplastics are widely distributed in the environment and can adsorb heavy metals, which poses a potential threat to human health through food chain. It is necessary to assess the combined toxicity of nanoplastics and heavy metals. The adverse effect of Pb and nanoplastics on liver, single or in combination, was evaluated in this study. The results showed that the Pb content in co-exposure group of nanoplastics and Pb (PN group) was higher than the group exposed to Pb alone (Pb group). And more severe inflammatory infiltration was observed in liver sections of PN group. The level of inflammatory cytokines and malondialdehyde were increased, while the superoxide dismutase activity was decreased in liver tissues of PN group. Moreover, the gene expression level of nuclear factor-erythroid 2-related factor 2, nicotinamide adenine dinucleotide phosphate:quinine oxidoreductase 1 and catalase, which is related to antioxidation, was downregulated. And the expression level of cleaved-Caspase9 and cleaved-Caspase3 were increased. However, with the supplementation of oxidative stress inhibitor N-Acetyl-L-cysteine, liver damage shown in PN group was evidently alleviated. In summary, nanoplastics evidently exacerbated the deposition of Pb in liver and potentially aggravated the Pb-induced liver toxicity by activating oxidative stress.

The ovarian-related effects of polystyrene nanoplastics on human ovarian granulosa cells and female mice

Nanoplastics (NPs) have recently emerged in the context of global plastic pollution. They may be more toxic than macroplastics litter and microplastic fragments due to its abundances, tiny sizes, and cellular accessibility. The female reproductive toxicity of NPs has been widely documented for aquatic animals, but their effects and underlying mechanisms remain poorly understood in mammals. This study aimed to explore the effects of NPs on female reproduction using human ovarian granulosa cells (GCs) and female mice. The accumulation of polystyrene NPs (PS-NPs) in human granulosa-like tumor cells (KGN cells) and the ovaries of female Balb/c mice were evaluated by exposure to fluorescent PS-NPs. Proliferation and apoptosis, reactive oxygen species (ROS), and Hippo signaling pathway-related factors were analyzed in KGN cells. In addition, fertility rate, litter size, ovarian weight and microstructure, follicle development, serum level of anti-Mullerian hormone, and apoptosis in ovaries were examined in female mice. Here, the PS-NPs can penetrate the KGN cells and accumulate in the ovaries. In vitro, 100 μg/ml PS-NPs inhibited proliferation, induced apoptosis, accumulated ROS, activated three key regulators of the Hippo signaling pathway (MST1, LATS1, and YAP1), and downregulated the mRNA levels of CTGF and Cyr61 in KGN cells. Furthermore, salidroside, an antioxidative compound extracted from Rhodiola rosea, alleviated the damage of PS-NPs to KGN and inhibited the activation of the Hippo signal pathway. In vivo, exposure to 1 mg/day PS-NPs resulted in decreased fertility, abnormal ovarian function, and increased ovarian apoptosis in female mice. Overall, our data suggest that PS-NPs cause granulosa cell apoptosis and affect ovarian functions, leading to reduced fertility in female mice, by inducing oxidative stress and dysregulating the Hippo pathway.

Toxicity interaction of polystyrene nanoplastics with sulfamethoxazole on the microalgae Chlamydomonas reinhardtii: A closer look at effect of light availability

The coexistence of nanoplastics and antibiotics in the aquatic environment has raised a complicated risk for ecosystems and human health. How the environmental factors e.g., light, regulate the interaction between nanoplastics and antibiotics and the resulting combined toxicity is poorly understood. Here, we investigated the individual and combined toxicity of polystyrene nanoplastics (nPS, 100 mg L1) and sulfamethoxazole (SMX, 2.5 and 10 mg L−1) toward the microalgae Chlamydomonas reinhardtii under low (LL, 16 μmol m−2·s−1), normal (NL, 40 μmol m−2·s−1), and high light (HL, 150 μmol m−2·s−1) in terms of cellular responses. Results indicated that the joint toxicity of nPS and SMX commonly exhibited a strong antagonistic/mitigative effect under LL/NL at 24 h, and under NL at 72 h. nPS could adsorb more SMX under LL/NL at 24 h (1.90/1.33 mg g−1) and under NL at 72 h (1.01 mg g−1), thereby alleviating SMX toxicity to C. reinhardtii. However, the self-toxicity of nPS had a negative influence on the degree of antagonism between nPS and SMX. The experimental results coupled with computational chemistry further revealed that the adsorption capacity of SMX on nPS was stimulated by low pH under LL/NL at 24 h (∼7.5), while by less co-existing saline ions (0.83 ppt) and algae-derived dissolved organic matter (9.04 mg L−1) under NL at 72 h. nPS toxicity that was responsible for the toxic action modes was mainly attributed to the shading effect induced by hetero-aggregation and hindrance of light transmittance (>60%), as well as being regulated by additives leaching (0.49–1.07 mg L−1) and oxidative stress. Overall, these findings provided a critical basis for the risk assessment and management of multiple pollutants in the complex natural environment.

Reproductive toxicity of polystyrene nanoplastics in Drosophila melanogaster under multi-generational exposure

Micro-nanoplastics have become a new type of pollutant worldwide and have attracted widespread attention for their potential toxicity. However, the toxicity of polystyrene nanoplastics (PS-NPs) under continuous exposure of multi-generations is still unclear. In the present study, Drosophila melanogaster was selected as an in vivo biological model to investigate the reproductive toxicity and underlying mechanism induced by PS-NPs (100 nm; 1, 10, 50, and 100 mg L−1) after continuous exposure of five generations. The results showed that PS-NPs accumulated in the crop, gut and ovaries after 5 d of exposure. It was also observed that the number of egg production and eclosion rate decreased significantly (P < 0.05) accompanied by delayed development during continuous exposure PS-NPs of multi-generations. Further analysis revealed that the degree of apoptosis and necrosis of oocytes in the F5 generation increased with the increasing exposure dose. To elucidate the underlying toxicity mechanism mediated by PS-NPs, transcriptomic analysis was performed on the ovaries of the F5 generation. The results showed that there were 102 and 208 differentially expressed genes (DEGs) in the 1 mg L−1 and 100 mg L−1 PS-NPs treatment groups, respectively, compared with the control group. The transcriptome analysis further detected the KEGG pathway with significant enrichment of DEGs, revealing obvious reproductive toxicity at the molecular level. In conclusion, this research not only highlighted the negative physiological effects of multi-generational exposure to PS-NPs on Drosophila melanogaster, but also explored potential mechanisms by transcriptomic analysis to better understand reproductive toxicity induced by multi-generational exposure.

Short term exposure to polystyrene nanoplastics in mice evokes self-regulation of glycolipid metabolism

With the detection of nano-plastics (NPs) in daily essentials and drinking water, the potential harm of NPs to human health has become the focus of global attention. Studies have shown that long term exposure to NPs can lead to disorders of glucose and lipid metabolism in organisms, while the effects of short term exposure are rarely reported. Moreover, environmental factors cause the aging of NPs, and it is unclear whether this has an effect on their toxicity. In this study, we use 100 nm polystyrene (PS) NPs and ultraviolet (UV) aging PS (aPS) NPs to gavage mice for 7 days at an exposure dose of 50 mg/kg/day. To evaluate the effects of exposure on mice hepatic glucose lipid metabolism, we performed blood biochemical, pathological and metabolomic analyses. The results showed that exposure to PS NPs and aPS NPs increased serum glucose, disrupted serum lipoprotein levels, and up-regulated the expression levels of phosphatidylinositol 3-kinase (PI3K)/ phosphoprotein kinase B (p-AKT)/Glucose transporter 4 (GLUT4) proteins in the glucose metabolism pathway. The expression levels of key proteins sterol regulatory element binding protein-1 (SREBP-1)/peroxisome proliferator-activated receptor-γ (PPARγ)/adipose triglyceride lipase (ATGL) in the lipid metabolism signaling pathway were significantly increased. These findings suggest that short term exposure to PS NPs and aPS NPs induces glycolipid metabolism disturbance in mice, which may subsequently awaken the mice to self-regulate the serum levels of various lipoproteins and the expression of related key proteins. Compared with PS NPs, the aPS NPs interfered more strongly with glucose metabolism, and the corresponding self-regulation in mice was also more obvious. These findings not only provide a basis for environmental factors to increase the health risk of NPs but also provided a reference for the selection of test substances for further studies on the toxicity of NPs.

Adverse effects of polystyrene nanoplastics on sea cucumber Apostichopus japonicus and their association with gut microbiota dysbiosis

The mariculture environment is a sink of microplastics (MPs) due to its enclosed nature and mass use of plastics. Nanoplastics (NPs) are MPs with a diameter <1 μm that have a more toxic effect on aquatic organisms than other MPs. However, little is known about the underlying mechanisms of NP toxicity on mariculture species. Here, we performed a multi-omics investigation to explore gut microbiota dysbiosis and associated health problems induced by NPs in juvenile sea cucumber Apostichopus japonicus, a commercially and ecologically important marine invertebrate. We observed significant differences in gut microbiota composition after 21 days of NP exposure. Ingestion of NPs significantly increased core gut microbes, especially Rhodobacteraceae and Flavobacteriaceae families. Additionally, gut gene expression profiles were altered by NPs, especially those related to neurological diseases and movement disorders. Correlation and network analyses indicated close relationships between transcriptome changes and gut microbiota variation. Furthermore, NPs induced oxidative stress in sea cucumber intestines, which may be associated with intraspecies variation in Rhodobacteraceae in the gut microbiota. The results suggested that NPs were harmful to the health of sea cucumbers, and they highlighted the importance of the gut microbiota in the responses to NP toxicity in marine invertebrates.

Toxicity of polystyrene nanoplastics to human embryonic kidney cells and human normal liver cells: Effect of particle size and Pb2+ enrichment

Nanoplastics pollution in drinking water has aroused wide concern, but their effects on human health are still poorly understood. Herein we explore the responses of human embryonic kidney 293T cells and human normal liver LO2 cells to polystyrene nanoplastics, mainly focusing on the effects of particle sizes and enrichment of Pb2+. When the exposed particle size is higher than 100 nm, there is no obvious death for these two different cell lines. As the particle size decreases from 100 nm, cell mortality goes up. Although the internalization of polystyrene nanoplastics in LO2 cells is at least 5 times higher than that in 293T cells, the mortality of LO2 cells is lower than that of 293T cells, illustrating that LO2 cells are more resistant to polystyrene nanoplastics than 293T cells. Additionally, the Pb2+ enrichment on polystyrene nanoplastics in water can further enhance their toxicity, which should be taken seriously. The cytotoxicity of polystyrene nanoplastics to cell lines works through a molecular mechanism involving oxidative stress-induced damage of mitochondria and cell membranes, resulting in a decrease in ATP production and an increase in membrane permeability. Referenced to nanoplastics pollution in drinking water, there is no necessary to panic about the adverse effects of plastic itself on human health, but the enrichment of contaminants should get more attention. This work provides a reference for the risk assessment of nanoplastics in drinking water to human health.

Brassinosteroids alleviate nanoplastic toxicity in edible plants by activating antioxidant defense systems and suppressing nanoplastic uptake

As emerging pollutants of global concern, absorbed nanoplastics might have negative impacts on plant development and nutrient uptake, thereby decreasing yields. If nanoplastics are transferred to the edible parts of plants, they may pose a threat to human health when large quantities are ingested. While nanoplastic-induced phytotoxicity is attracting increasing attention, little is known about how to inhibit nanoplastic accumulation in plants and reduce the subsequent adverse effects. Here we investigated the absorption and accumulation of polystyrene nanoplastics (PS-NPs) in different plant species and the role of brassinosteroids in alleviating PS-NP toxicity. Brassinosteroids inhibited accumulation of PS-NPs in tomato fruit and reversed PS-NP-induced phytotoxicity to promote plant growth and increase fresh weight and plant height. Brassinosteroids also reversed the induction of aquaporin-related genes by PS-NPs including TIP2-1, TIP2-2, PIP2-6, PIP2-8, PIP2-9, SIP2-1, and NIP1-2, providing a potential stress mechanism by which PS-NPs accumulate in the edible parts and targets for inhibition. In transcriptomic analyses, brassinosteroids enhanced fatty acid and amino acid metabolism and synthesis. In conclusion, exogenous application of 50 nM brassinosteroids alleviated the adverse effects of PS-NPs on plants, and exogenous application of brassinosteroids might be an effective means to minimize PS-NP-induced phytotoxicity.

Nanoplastics Toxicity Specific to Liver in Inducing Metabolic Dysfunction—A Comprehensive Review

Plastic pollution in the world is widespread and growing. The environment is swamped with nanoplastics (<100 nm), and the health consequences of these less visible pollutants are unknown. Furthermore, there is evidence that microplastics can release nanoplastics by digestive disintegration, implying that macroplastic exposure can cause direct and indirect disease via nanoplastics. The existence and impact of nanoplastics in numerous tissues from invertebrates to larger vertebrates that consume significant amounts of plastics were investigated, and histopathological techniques were utilized to determine physiological reactions and inflammation from the plastics. Nanoplastics enters an organism through the respiratory and gastro-intestinal tract where they accumulate into the liver through blood circulation via absorption, or epidermal infiltration. It is stated that macroplastics can cause damage directly at the site of exposure, whereas nanoplastics can influence the liver, causing subsequent damage to other organs. Multi-organ dysfunction is brought on by liver changes, and nanoplastics can readily enter the gut-liver axis and disturb the gut microflora. By exploring the literature and summarizing the research that has been published to date, this review article reveals the deleterious effect and mechanisms of nanoplastics on the pathophysiological functions of the hepatic system.

Neurotoxicity and endocrine disruption caused by polystyrene nanoparticles in zebrafish embryo

Nanoplastics (NP) are present in aquatic and terrestrial ecosystems. Humans can be exposed to them through contaminated water, food, air, or personal care products. Mechanisms of NP toxicity are largely unknown and the Zebrafish embryo poses an ideal model to investigate them due to its high homology with humans. Our objective in the present study was to combine a battery of behavioral assays with the study of endocrine related gene expression, to further explore potential NP neurotoxic effects on animal behavior. Polystyrene nanoplastics (PSNP) were used to evaluate NP toxicity. Our neurobehavioral profiles include a tail coiling assay, a light/dark activity assay, two thigmotaxis anxiety assays (auditory and visual stimuli), and a startle response - habituation assay in response to auditory stimuli. Results show PSNP accumulated in eyes, neuromasts, brain, and digestive system organs. PSNP inhibited acetylcholinesterase and altered endocrine-related gene expression profiles both in the thyroid and glucocorticoid axes. At the whole organism level, we observed altered behaviors such as increased activity and anxiety at lower doses and lethargy at a higher dose, which could be due to a variety of complex mechanisms ranging from sensory organ and central nervous system effects to others such as hormonal imbalances. In addition, we present a hypothetical adverse outcome pathway related to these effects. In conclusion, this study provides new understanding into NP toxic effects on zebrafish embryo, emphasizing a critical role of endocrine disruption in observed neurotoxic behavioral effects, and improving our understanding of their potential health risks to human populations.

Molecular mechanisms of toxicity and detoxification in rice (Oryza sativa L.) exposed to polystyrene nanoplastics

Nanoplastics (NPs) are an emerging threat to higher plants in terrestrial ecosystems. However, the molecular of NP-related phytotoxicity remains unclear. In the present study, rice seedlings were exposed to polystyrene (PS, 50 nm) NPs at 0, 50, 100, and 200 mg/L under hydroponic conditions to investigate the induced physiological indices and transcriptional mechanisms. We found that 50, 100, and 200 mg/L PS significantly reduced root (53.05%, 49.61%, and 57.58%, respectively) and shoot (54.63%, 61.56%, and 62.64%, respectively) biomass as compared with the control seedlings. The activities of antioxidant enzymes, including catalase (CAT), peroxidase (POD), superoxide dismutase (SOD), and ascorbate peroxidase (APX), were significantly activated in all PS treatment groups, indicating that PS inhibited plant growth and induced oxidative stress. Transcriptome analyses showed that PS modulated the expression of the genes involved in cell detoxification, active oxygen metabolism, mitogen-activated protein kinase (MAPK), and plant hormone transduction pathways. Our study provides new insights into phytotoxicity by demonstrating the potential underlying toxicity of PS NPs in higher plants.

Nanoplastics induce epigenetic signatures of transgenerational impairments associated with reproduction in copepods under ocean acidification

Ocean acidification (OA) is one of many major global climate changes that pose a variety of risks to marine ecosystems in different ways. Meanwhile, there is growing concern about how nanoplastics (NPs) affect marine ecosystems. Combined exposure of marine organisms to OA and NPs is inevitable, but their interactive effects remain poorly understood. In this study, we investigated the multi- and transgenerational toxicity of NPs on copepods under OA conditions for ten generations. The findings revealed that OA and NPs have a synergistic negative effect on copepod reproduction across generations. In particular, the transgenerational groups showed reproductive impairments in the F1 and F2 generations (F1T and F2T), even though they were never exposed to NPs. Moreover, our epigenetic examinations demonstrated that the observed intergenerational reproductive impairments are associated with differential methylation patterns of specific genes, suggesting that the interaction of OA and NPs can pose a significant threat to the sustainability of copepod populations through epigenetic modifications. Overall, our findings provide valuable insight into the intergenerational toxicity and underlying molecular mechanisms of responses to NPs under OA conditions

Toxicity of nanoplastics to aquatic organisms: Genotoxicity, cytotoxicity, individual level and beyond individual level.

Due to the small size, high mobility and large surface area, nanoplastics (NPs) showed high potential risks to aquatic organisms. This paper reviews the toxicity of NPs to aquatic organism at various trophic levels including bacteria, plankton (algae), zooplankton, benthos, and nekton (fish). The effects at individual level caused by NPs were explained and proved by cytotoxicity and genotoxicity, and the toxicity of NPs beyond individual level was also illustrated. The toxicity of NPs is determined by the size, dosage, and surface property of NPs, as well as environmental factors, the presence of co-contaminants and the sensitivity of tested organisms. Furthermore, the joint effects of NPs with other commonly detected pollutants such as organic pollutants, metals, and nanoparticles etc. were summarized. In order to reflect the toxicity of NPs in the real natural environment, studies on toxicity assessment of NPs with the coexistence of various environmental factors and contaminants, particularly under the concentrations in natural environment are suggested.

Investigating nanoplastics toxicity using advanced stem cell-based intestinal and lung in vitro models.

Plastic particles in the nanometer range-called nanoplastics-are environmental contaminants with growing public health concern. As plastic particles are present in water, soil, air and food, human exposure via intestine and lung is unavoidable, but possible health effects are still to be elucidated. To better understand the Mode of Action of plastic particles, it is key to use experimental models that best reflect human physiology. Novel assessment methods like advanced cell models and several alternative approaches are currently used and developed in the scientific community. So far, the use of cancer cell line-based models is the standard approach regarding in vitro nanotoxicology. However, among the many advantages of the use of cancer cell lines, there are also disadvantages that might favor other approaches. In this review, we compare cell line-based models with stem cell-based in vitro models of the human intestine and lung. In the context of nanoplastics research, we highlight the advantages that come with the use of stem cells. Further, the specific challenges of testing nanoplastics in vitro are discussed. Although the use of stem cell-based models can be demanding, we conclude that, depending on the research question, stem cells in combination with advanced exposure strategies might be a more suitable approach than cancer cell lines when it comes to toxicological investigation of nanoplastics.

Nanoplastics induce molecular toxicity in earthworm: Integrated multi-omics, morphological, and intestinal microorganism analyses.

The toxicity of nanoplastics (NPs) at relatively low concentrations to soil fauna at different organismal levels is poorly understood. We investigated the responses of earthworm (Eisenia fetida) to polystyrene NPs (90-110nm) contaminated soil at a relatively low concentration (0.02% w:w) based on multi-omics, morphological, and intestinal microorganism analyses. Results showed that NPs accumulated in earthworms' intestinal tissues. The NPs damaged earthworms' digestive and immune systems based on injuries of the intestinal epithelium and chloragogenous tissues (tissue level) and increased the number of changed genes in the digestive and immune systems (transcriptome level). The NPs reduced gut microorganisms' diversity (Shannon index) and species richness (Chao 1 index). Proteomic, transcriptome, and histopathological analyses showed that earthworms suffered from oxidative and inflammatory stresses. Moreover, NPs influenced the osmoregulatory metabolism of earthworms as NPs damaged intestinal epithelium (tissue level), increased aldosterone-regulated sodium reabsorption (transcriptome level), inositol phosphate metabolism (proteomic level) and 2-hexyl-5-ethyl-furan-3-sulfonic acid, and decreased betaine and myo-inositol concentrations (metabolic level). Transcriptional-metabolic and transcriptional-proteomic analyses revealed that NPs disrupted earthworm carbohydrate and arachidonic acid metabolisms. Our multi-level investigation indicates that NPs at a relatively low concentration induced toxicity to earthworms and suggests that NPs pollution has significant environmental toxicity risks for soil fauna.

Organosilicon and inorganic silica inhibit polystyrene nanoparticles uptake in rice.

Nanoplastics (NPs) have become an emerging global environmental problem, and the toxicity of polystyrene nanoplastics (PS-NPs) in rice plants has received widespread attention. However, few studies have focused on silicon (Si)-mediated interactions between PS-NPs and rice. Thus, two forms of Si (organosilicon/inorganic silica) treated rice cells were exposure of positively or negatively charged NPs, PS-NH2 and PS-COOH, to evaluate the effects of Si for defense against PS-NPs toxicity in rice. The result showed PS-NH2 nanoparticles were accumulated at relatively low levels in cells compared with that of PS-COOH, but induced a higher accumulation of hydrogen peroxide (H2O2) and superoxide radicals (O2•-). However, both organosilicon and inorganic silica can generate more negative potential on the surfaces of cell wall to absorb large numbers of positively charged PS-NH2. In addition, they can prevent the uptake of both PS-NH2 and PS-COOH through reducing the porosity on the surface of the cell walls. These finally alleviated the toxicity of oxidative stress caused by PS-NPs and improved the viability of rice cells. Our findings demonstrated the significant contribution of Si in combating PS-NPs in rice.

Exposure to polystyrene nanoplastics induces an anxiolytic-like effect, changes in antipredator defensive response, and DNA damage in Swiss mice.

Although the in vivo toxicity of nanoplastics (NPs) has already been reported in different model systems, their effects on mammalian behavior are poorly understood. Thus, we aimed to evaluate whether exposure to polystyrene (PS) NPs (diameter: 23.03±0.266nm) alters the behavior (locomotor, anxiety-like and antipredator) of male Swiss mice, induces brain antioxidant activity, and erythrocyte DNA damage. For this, the animals were exposed to NPs for 20 days at different doses (6.5ng/kg and 6500ng/kg). Initially, we did not observe any effect of pollutants on the locomotor activity of the animals (inferred via open field test and Basso mouse scale for locomotion). However, we noticed an anxiolytic-like behavior (in the open field test) and alterations in the antipredatory defensive response of mice exposed to PS NPs, when confronted with their predator potential (snake, Pantherophis guttatus). Furthermore, such changes were associated with suppressing brain antioxidant activity, inferred by lower DPPH radical scavenging activity, reduced total glutathione content, as well as the translocation and accumulation of NPs in the brain of the animals. In addition, we noted that the treatments induced DNA damage, evaluated via a single-cell gel electrophoresis assay (comet assay) applied to circulating erythrocytes of the animals. However, we did not observe a dose-response effect for all biomarkers evaluated and the estimated accumulation of PS NPs in the brain. The values of the integrated biomarker response index and the results of the principal component analysis (PCA) and the hierarchical clustering analysis confirmed the similarity between the responses of animals exposed to different doses of PS NPs. Therefore, our study sheds light on how PS NPs can impact mammals and reinforce the ecotoxicological risk associated with the dispersion of these pollutants in natural environments and their uptake by mammals.

Nanoplastic-induced vascular endothelial injury and coagulation dysfunction in mice

Nanoplastics are the persistent pollutants in a variety of environments, representing a potential threat to human health. Notably, plastic particles have been detected in sample of human bloodstream. It is thus significant to investigate the effects of nanoplastics on the cardiovascular system owing to its ease transfer through the bloodstream to other organs. However, few studies have been performed to evaluate the cardiovascular toxicity of nanoplastics. Herein, we pursued to investigate the adverse cardiovascular impacts of polystyrene (PS), PS-NH2 and PS-COOH nanoplastics on mice. Experimental results demonstrated that the exposure to these nanoplastics could result in structural damage of vascular endothelial cells and inflammatory response. Moreover, it was found out that the dysfunctions of coagulation and prethrombotic state were caused by nanoplastics, which could be ascribed to the activation of JAK1/STAT3/TF signaling pathway. In summary, results clearly indicated that nanoplastic exposure lead to vascular toxicity to mice, which serves as a basis for future studies about the potential physiological threat of nanoplastics to humans.

Charge-dependent negative effects of polystyrene nanoplastics on Oryzias melastigma under ocean acidification conditions

Marine nanoplastics (NPs) have attracted increasing global attentions because of their detrimental effects on marine environments. A co-existing major environmental concern is ocean acidification (OA). However, the effects of differentially charged NPs on marine organisms under OA conditions are poorly understood. We therefore investigated the effects of OA on the embryotoxicity of both positively and negatively charged polystyrene (PS) NPs to marine medaka (Oryzias melastigma). Positively charged PS-NH2 exhibited slighter aggregation under normal conditions and more aggregation under OA conditions than negatively charged PS-COOH. According to the integrated biomarker approach, OA reversed the toxicity of positively and negatively charged NPs towards embryos. Importantly, at environmental relevant concentrations, both types of PS-NPs could enter the embryos through chorionic pores and then transfer to the larvae. OA reversed the internalization of PS-NH2 and PS-COOH in O. melastigma. Overall, the reversed toxicity of PS-NH2 and PS-COOH associated with OA could be caused by the reversed bioavailability of NPs to O. melastigma, which was attributed to altered aggregation of the NPs in acidified seawater. This finding demonstrates the charge-dependent toxicity of NPs to marine fish and provides new insights into the potential hazard of NPs to marine environments under OA conditions that could be encountered in the near future.

Micro(nano)plastic size and concentration co-differentiate the treatment performance and toxicity mechanism in aerobic granular sludge systems

Microplastics (MPs) and nanoplastics (NPs) released into wastewater may pose threats to the biological treatment process. Aerobic granular sludge (AGS), a prospective biotechnology for wastewater treatment, can effectively intercept MPs and NPs, but the effect of these emerging contaminants on the AGS system lacks investigation. This study showed that low concentrations of MPs and NPs (1 mg/L) posed negligible inhibitory effects on the characteristics and performance of the AGS system. Yet, increasing MPs concentrations to higher levels (20 and 100 mg/L) impaired the granular integrity and diminished the total nitrogen (TN) removal efficiency by 3.8 %–17.8 %, especially for the denitrification process. Compared to MPs, prolonged exposure to NPs at the same levels showed greater adverse effects on the AGS, as evidenced by overgrowth of filamentous bacteria and lower TN removal efficiency (decreased by 11.4 %–22.8 %). This was possibly due to biofilm formation on the surface of MPs and excessive secretion of extracellular polymeric substances served as barriers to mitigate the toxic effects of MPs. In contrast, microorganisms were directly exposed to the toxicity of NPs, resulting in greater oxidative stress, impaired cytomembrane structure, deteriorated cell viability, and decreased proteins production. Metagenomic analysis further revealed that the populations of key functional bacteria (e.g. denitrifiers Acidovorax and Flavobacterium) decreased after long–term exposure to MPs and NPs. The key enzymes and genes (e.g. nirK, napAB, nirS, norBC and nosZ) related to nitrogen transformation processes, electron donor and energy production (e.g. mdh) were declined accordingly, unravelling the inherent mechanism for the decreased nitrogen removal. This study indicated that NPs have more detrimental impacts on AGS system, which needs to be taken into account when treating plastic containing wastewaters.