The proliferation of nano-plastic particles (NPs) poses severe environmental hazards, urgently requiring effective biodegradation methods. Herein, a novel method was developed for degrading nano-PET (polyethylene terephthalate) using immobilized cutinases. Nano-PET particles were prepared using a straightforward method, and biocompatible elastin-like polypeptide-magnetic nanoparticles (ELPs-MNPs) were obtained as magnetic cores via biomimetic mineralization. Using one-pot synthesis with the cost-effective precursor tetraethoxysilane (TEOS), silica-coated magnetically immobilized ELPs-tagged cutinase (ET-C@SiO2@MNPs) were produced. ET-C@SiO2@MNPs showed rapid magnetic separation within 30 s, simplifying recovery and reuse. ET-C@SiO2@MNPs retained 86 % of their initial activity after 11 cycles and exhibited superior hydrolytic capabilities for nano-PET, producing 0.515 mM TPA after 2 h of hydrolysis, which was 96.6 % that of free enzymes. Leveraging ELPs biomimetic mineralization, this approach offers a sustainable and eco-friendly solution for PET-nanoplastic degradation, highlighting the potential of ET-C@SiO2@MNPs in effective nanoplastic waste management and contributing to environmental protection and sustainable development.

Sterile inflammation is involved in the lung pathogenesis induced by respirable particles, including micro- and nanoplastics. Their increasing amounts in the ambient and in indoor air pose a risk to human health. In two human cell lines (A549 and THP-1) we assessed the proinflammatory behavior of polystyrene nanoplastics (nPS) and microplastics (mPS) (Ø 0.1 and 1 μm). Reproducing environmental aging, in addition to virgin, the cells were exposed to oxidized nPS/mPS. To study the response of the monocytes to the inflammatory signal transmitted by the A549 through the release of soluble factors (e.g. alarmins and cytokines), THP-1 cells were also exposed to the supernatants of previously nPS/mPS-treated A549. After dynamic-light-scattering (DLS) analysis and protein measurements for the assessment of protein corona in nPS/mPS, real-time PCR and enzyme-linked-immunosorbent (ELISA) assays were performed in exposed cells. The pro-inflammatory effects of v- and ox-nPS/mPS were attested by the imbalance of the Bax/Bcl-2 ratio in A549, which was able to trigger the inflammatory cascade, inhibiting the immunologically silent apoptosis. The involvement of NFkB was confirmed by the overexpression of p65 after exposure to ox-nPS and v- and ox-mPS. The fast and higher levels of IL-1β, only in THP-1 cells, underlined the NLPR3 inflammasome activation.

Limited data exist on the interactions between nanoplastics (NPs) and co-contaminants under diverse environmental conditions. Herein, a factorial composite toxicity analysis approach (FCTA) was developed to analyze the time-dependent composite effects of NPs (0 ∼ 60 mg/L), copper (Cu, 0.2 ∼ 6 mg/L) and phenanthrene (PHE, 0.001 ∼ 1 mg/L) on microalgae under diverse pH (6.7 ∼ 9.1), dissolved organic matter (DOM, 1.5 ∼ 25.1 mg/L), salinity (1 ∼ 417 mg/L) and temperature (23 ∼ 33 °C) within the Canadian prairie context. The toxic mechanism was revealed by multiple toxic endpoints. The combined toxicity of NPs, Cu and PHE within prairie aquatic ecosystems was assessed by the developed FCTA-multivariate regression model. Contrary to individual effects, NPs exhibited a promotional effect on microalgae growth under complex environmental conditions. Although Cu and PHE were more hazardous, NPs mitigated their single toxicity. Environmental conditions and exposure times significantly influenced the main effects and interactions of NPs, Cu and PHE. The synergistic effect of NPs*Cu and NPs*PHE on microalgae growth became antagonistic with increased pH or DOM. Microalgae in the Souris River, Saskatchewan, were projected to suffer the most toxic effects. Our findings have significant implications for the risk management of NPs.

The increasing use of contact lenses, artificial tears, and anti-vascular endothelial growth factor (anti-VEGF) drug injections for age-related macular degeneration has heightened the likelihood of eye exposure to microplastic particles. Extensive research has established that microplastic particles can induce oxidative stress on the ocular surface, resulting in damage. However, the impact of these particles on the retina remains unclear. Therefore, this study investigated whether microplastics/nanoplastics (MPs/NPs) cause retinal damage. In vitro human retinal pigment epithelial (RPE) cells were exposed to polystyrene MPs and NPs for 48 h. Assessment of cell viability using WST-8; evaluation of TNF-α and IL-1β expression; observation of cell morphology and particle invasion via TEM; measurement of ROS levels using the DCFDA reagent; and western blot analysis of SOD2, FIS1, Drp1, and LC3B expression were conducted. In vivo experiments involved intravitreal injection of MPs/NPs in rats, followed by retinal H&E staining 24 h later and evaluation of TNF-α and IL-1β expression. Results indicated that exposure to MPs did not significantly alter RPE cell viability, whereas exposure to NPs led to a noticeable decrease. TEM images revealed NPs\' penetration into cells, causing increased oxidative stress (SOD2), mitochondrial fission (FIS1, Drp1), and mitochondrial autophagy (LC3B). In vivo experiments demonstrated an increase in inflammatory cells in retinal tissues exposed to NPs, along with elevated levels of TNF-α and IL-1β. Conclusively, both MPs and NPs impact the retina, with NPs displaying greater toxicity. NPs significantly elevate ROS levels in the retina and induce mitochondrial fission and mitophagy in RPE cells compared to MPs.

Microplastics, particularly microfibers (MFs), pose a significant threat to the environment. Despite their widespread presence, the photochemical reactivity, weathering products, and environmental fate of MFs remain poorly understood. To address this knowledge gap, photodegradation experiments were conducted on three prevalent MFs: polyester (POL), nylon (NYL), and acrylic (ACR), to elucidate their degradation pathways, changes in surface morphology and polymer structure, and chemical and colloidal characterization of weathering products during photochemical degradation of MFs. The results showed that concentrations of dissolved organic carbon, chromophoric dissolved organic matter (DOM), and fluorescent components consistently increased during weathering, exhibiting a continuous release of DOM. Scanning electron microscopy and Raman spectroscopy revealed changes in the surface morphology and polymer spectra of the MFs. During the weathering experiments, DOM aromaticity (SUVA254) decreased, while spectral slope increased, indicating concurrent DOM release and degradation of aromatic components. The released DOM or nanoplastics were negatively charged with sizes between 128 and 374 nm. The production rate constants of DOM or the photochemical reactivity of MFs followed the order ACR > NYL ≥ POL, consistent with their differences in chemical structures. These findings provide an improved understanding of the photochemical reactivity, degradation pathways, weathering products, and environmental fate of microfibers in the environment.

A definitive link between the micro- and nano-plastics (NPLs) and human health has been firmly established, emphasizing the higher risks posed by NPLs. The urgent need for a rapid, non-destructive, and reliable method to quantify NPLs remains unmet with current detection techniques. To address this gap, a novel laser-backscattered fiber-embedded optofluidic chip (LFOC) was constructed for the rapid, sensitive, and non-destructive on-site quantitation of NPLs based on 180º laser-backscattered mechanism. Our theoretical and experimental findings reveal that the 180º laser-backscattered intensities of NPLs were directly proportional to their mass and particle number concentration. Using the LFOC, we have successfully detected polystyrene (PS) NPLSs of varying sizes, with a minimum detection limit of 0.23 μg/mL (equivalent to 5.23 ×107 particles/mL). Moreover, PS NPLs of different sizes can be readily differentiated through a simple membrane-filtering method. The LFOC also demonstrates high sensitivity in detecting other NPLs, such as polyethylene, polyethylene terephthalate, polypropylene, and polymethylmethacrylate. To validate its practical application, the LFOC was used to detect PS NPLs in various aquatic environments, exhibiting excellent accuracy, reproducibility, and reliability. The LFOC provides a simple, versatile, and efficient tool for direct, on-site, quantitative detection of NPLs in aquatic environments.

This work reports the production of nanoplastics (NPs) from polypropylene (PP) free of the antioxidant Irgafos® 168 (IRG) and alkane oligomers (ALK). PP pellets were milled into a powder with particle sizes in the 100-500 μm range. Additives and oligomers were removed using dichloromethane, and the powder exposed to UV irradiation, followed by filtration through 1 μm filters. PP suspensions, free of antioxidant and oligomers, were reloaded with IRG and ALK to their original commercial concentrations. This approach allowed testing the aquatic toxicity of IRG at concentrations compromised by water solubility limits. Toxicity assays using the cladoceran Daphnia magna with 24-48 h immobilization of neonates as endpoint showed toxicity for NPs containing IRG, with EC20 (48 h) in the 1.8-3.5 mg/L range, that corresponded to IRG exposure <1.2 μg/L. Suspensions of PP containing ALK, but not IRG, exhibited low toxicity (EC20 > 20 mg/L). The results allowed estimating the toxicity of IRG with a EC50 value of 3.3 ± 1.1 μg/L. Assays with different proportions of IRG and its oxidized form showed no differences. This work demonstrated the aquatic toxicity of IRG, for which there were no previous data, and developed a method for testing the toxicity of non-polar additives without being limited by their solubility.

Polyethylene (PE) is one of the most widely used plastics in the world. Its degradation leads to the production of small particles including microplastics and nanoplastics (NPs). Plastic particles\' presence poses a health risk. The aim of this work was to investigate the toxicity of two model surfactant-free PE NPs prepared by polymerization of ethylene from cationic and anionic water-soluble initiators on human cell lines Caco-2 and HT29-MTX. After physicochemical characterization, their acute and subacute toxicity profile, including cytotoxicity, oxidative stress, and genotoxicity, was evaluated on both cell lines. Results showed a size increase of PE NPs in culture medium. Zeta potential values close to -10 mV were no longer dependent on the initiator charge after adsorption of serum components in culture medium. However, the cellular toxicity of the cationic and anionic PE NPs was very different. A time-and-concentration dependent cytotoxic, oxidative, and genotoxic effects on Caco-2 cells were only observed for PE NPs prepared with cationic initiators. No toxicity was observed on HT29-MTX, likely due to the protective mucus layer. Genotoxicity correlated with oxidative stress of some PE NPs on Caco-2 cells was observed from a concentration of 0.1 mg.mL-1 after 48-h exposure.

BACKGROUND: Plastic-based products are ubiquitous due to their tremendous utility in our daily lives. Nanoplastic (NP) and microplastic (MP) pollution has become a severe threat to the planet and is a growing concern. It has been widely reported that polystyrene (PS) MPs are severely toxic to the male reproduction system, with effects including decreased sperm parameters, impaired spermatogenesis, and damaged testicular structures. However, the molecular mechanisms for impaired spermatogenesis remain poorly understood.
METHODS: C57BL/6 male mice were treated with PS-NPs (80 nm) and PS-MPs (5 μm) by oral gavage every day for 60 days. A series of morphological analyses were completed to explore the influence of PS-NP and PS-MP exposure on the testes. Compared to other cell types in the seminiferous tubule, PS-NP and PS-MP exposure can lead to decreased spermatocytes. Then, more refined molecular typing was further performed based on gene expression profiles to better understand the common and specific molecular characteristics after exposure to PS-NPs and PS-MPs.
RESULTS: There were 1794 common DEGs across the PS-NP groups at three different doses and 1433 common DEGs across the PS-MP groups at three different doses. GO and KEGG analyses of the common DEGs in the PS-NP and PS-MP groups were performed to enrich the common and specific functional progress and signaling pathways, including 349 co-enriched GO entries and 13 co-enriched pathways. Moreover, 348 GO entries and 33 pathways were specifically enriched in the PS-NP group, while 526 GO entries and 15 pathways were specifically enriched in the PS-MPs group.
CONCLUSIONS: PS-NPs were predominantly involved in regulating retinoic acid metabolism, whereas PS-MPs primarily influenced pyruvate metabolism and thyroid hormone metabolism. Our results highlight the different molecular mechanisms of PS-NPs and PS-MPs in the impairment of spermatogenesis in male mammals for the first time, providing valuable insights into the precise mechanisms of PS-NPs and PS-MPs in male reproduction.

Increasing evidence has suggested that nanoplastic pollution has become a global concern. More importantly, transgenerational toxicity can be induced by nanoplastics at predicted environmentally relevant doses (ERDs). Considering that amino modification could increase nanoplastic toxicity, we compared transgenerational neurotoxicity between pristine polystyrene nanoparticle (PS-NP) and amino-modified PS-NP (NH2-PS-NP) in Caenorhabditis elegans. At 0.1-10 μg/L, NH2-PS-NP caused more severe transgenerational toxicity on locomotion and neuronal development. Accompanied with a difference in transgenerational neuronal damage, compared to PS-NP (10 μg/L), NH2-PS-NP (10 μg/L) induced more severe transgenerational activation of mec-4, crt-1, itr-1, and tra-3, which are required for the induction of neurodegeneration. Moreover, NH2-PS-NP (10 μg/L) caused more severe transgenerational inhibition in expressions of mpk-1, jnk-1, dbl-1, and daf-7 than PS-NP (10 μg/L), and RNA interference (RNAi) of these genes conferred susceptibility to the toxicity of PS-NP and NH2-PS-NP on locomotion and neuronal development. NH2-PS-NP (10 μg/L) further caused more severe transgenerational activation of germline ligand genes (ins-3, ins-39, daf-28, lin-44, egl-17, efn-3, and lag-2) than PS-NP (10 μg/L), and RNAi of these ligand genes caused resistance to the toxicity of PS-NP and NH2-PS-NP on locomotion and neuronal development. Our results highlighted more severe exposure risk of amino-modified nanoplastics at ERDs in causing transgenerational neurotoxicity in organisms.