NanoImpact最新文献

To fully understand and predict the impact of nanotechnologies, a truly multidisciplinary approach is required. However, the practicalities relating to how innovation, commercialisation, risk assessment, informatics, and governance in nanotechnology should intersect remain somewhat of a black box. To begin to shed light on this intersection, we identify a need to place ‘purpose’ at the heart of the nanotechnology innovation ecosystem. There is a growing appetite for responsible, sustainable, and purposeful innovation from business, financiers, regulators, consumers, and other stakeholders – an appetite that we foresee will permeate all spheres of commercialisation, including that of nanotechnology. Ultimately, nanotechnologies will only have the ability to sustainably address the global challenges of the 21st century if they are developed and implemented with purpose, and in full consideration of their social and environmental impacts. We (re)define purpose as it relates to sustainable nanotechnology innovation, in an effort to create a more-broadly shared language that can bridge the diverse stakeholder needs and perspectives that are required to address these challenges. To enable innovation, standardisation, promote interdisciplinarity, increase transparency, and enhance regulatory and corporate accountability, we propose a four stage, principles-based framework for purposeful nanotechnology development. This framework offers a practical way forward for nanotechnology innovation, shedding light on how nano-impact can be approached by multidisciplinary teams and describing how interrelated systems and stakeholders can interact successfully to achieve shared goals.

The widespread presence of micro(nano)plastics (MNPs) in the environment threatens ecosystem integrity, and thus, it is necessary to determine and assess the occurrence, characteristics, and transport of MNPs between ecological components. However, most analytical approaches are cost- and time-inefficient in providing quantitative information with sufficient detail, and interpreting results can be difficult. Alternative analyses integrating novel measurements by imaging or proximal sensing with signal processing and machine learning may supplement these approaches. In this review, we examined published research on methods used for the automated data interpretation of MNPs found in the environment or those artificially prepared by fragmenting bulk plastics. We critically reviewed the primary areas of the integrated analytical process, which include sampling, data acquisition, processing, and modeling, applied in identifying, classifying, and quantifying MNPs in soil, sediment, water, and biological samples. We also provide a comprehensive discussion regarding model uncertainties related to estimating MNPs in the environment. In the future, the development of routinely applicable and efficient methods is expected to significantly contribute to the successful establishment of automated MNP monitoring systems.

Ecotoxicity data on cellulose nanofibers (CNFs) are limited despite their wide potential applications prospects, such as structural and packaging materials, filters, coatings, foods, and cosmetics. In this study, toxicity tests of 2,2,6,6-tetramethylpiperidine-1-oxyl radical (TEMPO)-oxidized CNFs (TEMPO-CNFs), which are one of the major CNF products commercially available in Japan, on the green alga Raphidocelis subcapitata were conducted. As nanomaterials are considered difficult-to-test substances, the Organisation for Economic Co-operation and Development has released a guidance document that provides considerations regarding ecotoxicity tests of nanomaterials. In the algal growth inhibition tests of TEMPO-CNFs, there were specific issues to be examined, including the effects of medium components on the characteristics of TEMPO-CNFs, CNF interference with algal density measurements, algal interference with CNF measurements, and the effects of ion concentration changes in the test medium by the addition of CNFs on algal growth. To examine these issues, we conducted preliminary studies and established a suitable test method for algal growth inhibition tests of TEMPO-CNFs. We confirmed that the components in the medium for algal growth inhibition tests had negligible effects on the characteristics (zeta-potential, viscosity, and morphology) and concentration stability of TEMPO-CNFs and that in vitro and in vivo fluorescence measurements were applicable for estimating the algal densities, without interference by TEMPO-CNFs. In contrast, we observed that the grown algae interfered with the CNF concentration measurements. Therefore, we established a method to correct the measured CNF concentrations by estimating the algal contribution. Furthermore, we found that the nutrient salt concentrations in the medium changed due to interactions with CNFs; however, this change did not affect algal growth. Based on the results of the preliminary studies, algal growth inhibition tests of TEMPO-CNFs were conducted using in vitro and in vivo fluorescence measurements, along with measurements of CNFs and ion concentrations in the test dispersions. The test results showed that no growth inhibition was observed on growth rate or yield even at the maximum CNF concentration of 100 mg/L, suggesting that the ecological effect of TEMPO-CNFs on algae was relatively low. The results of this study will be valuable for conducting ecotoxicity assessments on additional CNFs and comparable nanomaterials in future studies.

The objective of this investigation was to evaluate the influence of micro- and nanoplastic particles composed of polyethylene terephthalate (PET), a significant contributor to plastic pollution, on human brain vascular pericytes. Specifically, we delved into their impact on mitochondrial functionality, oxidative stress, and the expression of genes associated with oxidative stress, ferroptosis and mitochondrial functions. Our findings demonstrate that the exposure of a monoculture of human brain vascular pericytes to PET particles in vitro at a concentration of 50 μg/ml for a duration of 3, 6 and 10 days did not elicit oxidative stress. Notably, we observed a reduction in various aspects of mitochondrial respiration, including maximal respiration, spare respiratory capacity, and ATP production in pericytes subjected to PET particles for 3 days, with a mitochondrial function recovery at 6 and 10 days. Furthermore, there were no statistically significant alterations in mitochondrial DNA copy number, or in the expression of genes linked to oxidative stress and ferroptosis, but an increase of the expression of the gene mitochondrial transcription factor A (TFAM) was noted at 3 days exposure.

These outcomes suggest that, at a concentration of 50 μg/ml, PET particles do not induce oxidative stress in human brain vascular pericytes. Instead, at 3 days exposure, PET exposure impairs mitochondrial functions, but this is recovered at 6-day exposure. This seems to indicate a potential mitochondrial hormesis response (mitohormesis) is incited, involving the gene TFAM. Further investigations are warranted to explore the stages of mitohormesis and the potential consequences of plastics on the integrity of the blood-brain barrier and intercellular interactions. This research contributes to our comprehension of the potential repercussions of nanoplastic pollution on human health and underscores the imperative need for ongoing examinations into the exposure to plastic particles.

The increasing application of quantum dots (QDs) increases interactions with organisms. The inflammatory imbalance is a significant manifestation of immunotoxicity. Macrophages maintain inflammatory homeostasis. Using macrophages differentiated by phorbol 12-myristate 13-acetate-induced THP-1 cells as models, the study found that low-dose (5 μM) cadmium telluride QDs (CdTe-QDs) hindered monocyte-macrophage differentiation. CD11b is a surface marker of macrophage, and the addition of CdTe-QDs during induction resulted in a decrease in CD11b expression. Moreover, exposure of differentiated THP-1 macrophage (dTHP-1) to 5 μM CdTe-QDs led to the initiation of M1 polarization. This was indicated by the increased surface marker CD86 expression, along with elevated level of NF-κB and IL-1β proteins. The potential mechanisms are being explored. The transcription factor EB (TFEB) plays a significant role in immune regulation and serves as a crucial regulator of the autophagic lysosomal pathway. After exposed to CdTe-QDs, TFEB activation-mediated autophagy and M1 polarization were observed to occur simultaneously in dTHP-1. The mTOR signaling pathway contributed to TFEB activation induced by CdTe-QDs. However, mTOR-independent activation of TFEB failed to promote M1 polarization. These results suggest that mTOR-TFEB is an advantageous target to enhance the biocompatibility of CdTe-QDs.

The foreseen increasing application of copper-based nanomaterials (Cu-NMs), replacing or complementing existing Cu-agrochemicals, may negatively impact the soil microbiome. Thus, we studied the effects on soil microbiome function and composition of nano copper oxide (nCuO) or copper hydroxide NMs in a commercial (Kocide®3000) or a lab-synthetized formulation (nCu(OH)₂) or bulk copper hydroxide (Cu(OH)₂-B), at the commonly recommended Cu dose of 50 mg(Cu)kg⁻¹ soil. Microbial responses were studied over 28 days in a designed indoor mesocosm. On day-28, in comparison to non-treated soil (CT), all Cu-treatments led to a reduction in dehydrogenase (95% to 68%), arylsulfatase (41% to 27%), and urease (40% to 20%) activity. There was a 32% increase in the utilization of carbon substrates in the nCuO-treatment and an increased abundance of viable bacteria in the nCu(OH)₂-treatment (75% of heterotrophic and 69% of P-solubilizing bacteria). The relative abundance of Acidobacteria [Kocide®3000, nCuO, and Cu(OH)₂-B treatments] and Flavobacteriia [nCu(OH)₂-treatment] was negatively affected by Cu exposure. The abundance of Cu-tolerant bacteria increased in soils treated with Kocide®3000 (Clostridia) and nCu(OH)₂ (Gemmatimonadetes). All Cu-treated soils exhibited a reduced abundance of denitrification-related genes (0.05% of nosZ gene). The DTPA-extractable pool of ionic Cu(II) varied among treatments: Cu(OH)₂-B > Kocide®3000 ∼ nCuO>nCu(OH)₂, which may explain changes on the soil microbiome composition, at the genera and OTU levels. Thus, our study revealed that Cu-materials (nano and bulk) influence the soil microbiome with implications on its ecological role. It highlights the importance of assessing the impact of Cu-materials under dynamic and complex exposure scenarios and emphasizes the need for specific regulatory frameworks for NMs.

Titanium dioxide nanoparticles (TiO₂ NPs) have been widely employed in various industry fields, which makes consumers concerned about their health impact. Our previous work displayed that TiO₂ NPs participated in the mitigation of TNBS-induced colitis, but the mechanism is still unknown. This work aimed to explore the role of oxidative stress and NF-κB pathway in the effect of TiO₂ NPs on TNBS-induced colitis. The results showed that TiO₂ NPs administration reduced the DAI score of colitis mice after TNBS enema. TiO₂ NPs did not alter oxidative stress status (GSH/GSSG), but repaired the gut dysbacteriosis and inhibited the canonical NF-κB pathway activation in TNBS-induced colitis mice, manifested as a decrease in pathogenic bacteria and an increase in beneficial bacteria, as well as down-regulation of toll-like receptors (TLRs), IKKα, IKKβ, p65 and pro-inflammatory cytokines (IL-1β, IL-6, TNF-α and IFN-γ) in mRNA level, and the increased transcription of anti-inflammatory cytokines (IL-10, TGF-β, and IL-12), along with the declined protein level of TNF-α in TiO₂ NPs treated colitis mice. The present study suggested that oral TiO₂ NPs administration inhibited the canonical NF-κB pathway activation by repairing gut dysbacteriosis, which made a predominant role in alleviating colitis. These findings provided a new perspective for exploring the safety of TiO₂ NPs.

TiO₂ is the most widely used white pigment in plastics and food packaging industry, thus the question of its migration towards food and hence the impact on consumers is raised. Since recent research indicate its potential toxicity, it is necessary to study TiO₂ contamination as a consequence of food storage. For this purpose, plastic containers from commercially-available dairy products and custom-made TiO₂-spiked polypropylene materials were put in contact with 50% (v/v) ethanol and 3% (w/v) acetic acid, which were used here as food simulants. The migration assays were carried out under standard contact conditions of packaging use (as recommended by Commission Regulation (EU) N° 10/2011 for food contact migration testing), and under conditions of extreme mechanical degradation of the packaging. The TiO₂ (nano)particles released in the food simulants were analysed by single particle inductively coupled plasma-tandem mass spectrometry in mass-shift mode and using a high efficiency sample introduction system (APEX™ Ω) to avoid matrix effects from food simulants. For the dairy product containers and for the spiked polypropylene, results showed release of TiO₂ particles of rather large sizes (average size: 164 and 175 nm, respectively) under mechanical degradation conditions, i.e. when the polymeric structure is damaged. The highest amounts of TiO₂ were observed in 50% ethanol after 10 days of storage at 50 °C (0.62 ng cm⁻²) for the dairy product containers and after 1 day of storage at 50 °C (0.68 ng cm⁻²) for the spiked polypropylene. However, the level of Ti released in particle form was very small compared to the total Ti content in the packaging and far below the acceptable migration limits set by European legislation. Release under standard contact conditions of use of the container was not measurable, thus the migration of TiO₂ particles from this packaging to dairy products among storage is expected to be negligible.

To ensure the safe use of materials, one must assess the identity and quantity of exposure. Solid materials, such as plastics, metals, coatings and cements, degrade to some extent during their life cycle, and releases can occur during manufacturing, use and end-of-life. Releases (e.g., what is released, how does release happen, and how much material is released) depend on the composition and internal (nano)structures of the material as well as the applied stresses during the lifecycle. We consider, in some depth, releases from mechanical, weathering and thermal stresses and specifically address the use cases of fused-filament 3D printing, dermal contact, food contact and textile washing. Solid materials can release embedded nanomaterials, composite fragments, or micro- and nanoplastics, as well as volatile organics, ions and dissolved organics. The identity of the release is often a heterogenous mixture and requires adapted strategies for sampling and analysis, with suitable quality control measures. Control materials enhance robustness by enabling comparative testing, but reference materials are not always available as yet. The quantity of releases is typically described by time-dependent rates that are modulated by the nature and intensity of the applied stress, the chemical identity of the polymer or other solid matrix, and the chemical identity and compatibility of embedded engineered nanomaterials (ENMs) or other additives. Standardization of methods and the documentation of metadata, including all the above descriptors of the tested material, applied stresses, sampling and analytics, are identified as important needs to advance the field and to generate robust, comparable assessments. In this regard, there are strong methodological synergies between the study of all solid materials, including the study of micro- and nanoplastics. From an outlook perspective, we review the hazard of the released entities, and show how this informs risk assessment. We also address the transfer of methods to related issues such as tyre wear, advanced materials and advanced manufacturing, biodegradable polymers, and non-solid matrices. As the consideration of released entities will become more routine in industry via lifecycle assessment in Safe-and-Sustainable-by-Design practices, release assessments will require careful design of the study with quality controls, the use of agreed-on test materials and standardized methods where these exist and the adoption of clearly defined data reporting practices that enable data reuse, meta-analyses, and comparative studies.

Polystyrene microplastics, extensively considered endocrine disrupting chemicals, disturb the reproductive system of living organisms. Polycystic ovary syndrome (PCOS), the reproductive endocrinopathy, is longstanding concern due to its eternal impacts as reproductive disorder and infertility. Despite several reports in reproductive and endocrine toxicity, there is inadequate literature regarding the daily intake of polystyrene-microplastics via drinking water in causing PCOS and leading to ovarian fibrosis in long-term. The present study investigated whether daily consumption of polystyrene-microplastics at doses equivalent to human exposure can cause PCOS and progress to ovarian fibrosis, using female zebrafish as model. Resembling letrozole-PCOS zebrafish model, daily intake of polystyrene-microplastics displayed hallmark PCOS pathophysiology; like excess body weight and %Gonadosomatic index, decreased Follicle Stimulating Hormone and β-estradiol, increased Luteinising Hormone, brain and ovarian Testosterone (39.3% and 75% respectively). Correspondingly, ovarian histology revealed more developing (stage I and II) oocytes and less mature oocytes alongwith cystic lesions; like follicular membrane disorganization, zona pellucida invagination, theca hypertrophy, basophilic granular accumulation and oocyte buddings. Lipid deposition in intestinal and ovarian tissues was evidenced and increased fasting blood glucose manifesting insulin resistance. The expression of PCOS biomarkers (tox3, dennd1a, fem1a) was significantly disturbed. Polystyrene microplastics played vital role in inducing PCOS further enhancing oxidative stress, which positively influences inflammation and aggravate ovarian mitophagy, shedding light on its ability to harshen PCOS into ovarian fibrosis, which is characterized by collagen deposition and upregulation of pro-fibrogenic biomarker genes. These findings illustrate the potential of daily microplastics intake via drinking water in triggering PCOS and its progression to ovarian fibrosis.