Particle and Fibre Toxicology颗粒与纤维毒理学
Particle and Fibre Toxicology(英文缩写 PART FIBRE TOXICOL),ISSN 1743-8977,eISSN 1743-8977,中文译名:颗粒与纤维毒理学 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-27 至 2026-09-27，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 9.112 | Q1 |
| 2022 | 10.000 | Q1 |
| 2023 | 7.200 | Q1 |
| 2024 | 8.200 | Q1 |
| 2025 | 10.600 | Q1 |
Particle and Fibre Toxicology 最新收录文献
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1. Perinatal exposure to nano-polystyrene: deleterious imprinting on inflammatory bowel diseases.
PMID:日期:2026-09-10The extent of production and use of plastics leads to release of nanoplastics (NPL) into the environment, where they undergo weathering that could alter their toxicological properties. NPL enter the human food chain via contaminated food, and food packaging, and within the body they are known to pass through epithelial barriers. In parallel to the increasing exposure to plastics, the incidence of non-communicable diseases, including intestinal diseases, is rising worldwide. This study focuses on how oral exposure of gestating and lactating female mice to 50 nm polystyrene beads, pristine (PS50) or weathered (PS50w) affects intestinal function in offspring. Two aspects of intestinal function were studied: oral tolerance and the onset of intestinal disorders. Gestating mice received 1.25 mg of PS50 or PS50w by oral gavage administered daily from gestational day 15. Exposure was continued during lactation until pups were weaned (Postnatal Day, PND21). To study oral tolerance, offspring were exposed to ovalbumin (OVA) both orally and systemically. To study intestinal disorders, colitis was induced by exposure to Dextran Sulfate Sodium (DSS) from PND63. Perinatal exposure to PS50 or PS50w had no impact on mortality of gestating or lactating dams or sex ratio in litters, but did lead to increased body weight at PND63 in offspring. No impact on tolerance to OVA was observed. However, macroscopic scores for DSS-induced colitis in adult offspring were significantly worsened in both sexes. In this context, in male offspring, PS50w was more deleterious than PS50. Early-life exposure to PS50 or PS50w has long-lasting consequences on gut physiology, and effects show sexual dimorphism. The results presented raise questions on the kinetics of later-life effects linked to perinatal PS50 and PS50w exposure, and introduce the notion of imprinting.
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2. Black phosphorus nanomaterials induce hepatic lipid metabolism disorders by triggering oxidative stress and mitochondrial dysfunction.
PMID:日期:2026-07-15Black phosphorus is the most stable allotrope of phosphorus and possesses a unique layered structure. Black phosphorus nanosheets and black phosphorus quantum dots are the two main forms of black phosphorus nanomaterials (BPNM). BPNM hold significant application potential across various fields, yet a comprehensive evaluation of their biosafety, particularly the impact on hepatic metabolism, remains insufficient. This study investigates the hepatotoxic effects and mechanisms induced by BPNM, with a focus on lipid metabolic disorders. Following a 28-day daily oral administration of black phosphorus quantum dots or black phosphorus nanosheets at doses of 0.1 and 1 mg/kg, mice exhibited reduced insulin sensitivity, increased inflammatory responses, decreased serum levels of triglycerides and very-low-density lipoprotein (VLDL), and exacerbated hepatic lipid accumulation. RNA-sequencing revealed that oxidative stress is a key contributor to BPNM-induced metabolic disruption, accompanied by severe mitochondrial dysfunction. Similarly, BPNM exposure also elevated intracellular reactive oxygen species (ROS), impaired mitochondrial respiratory function and ATP production, consequently disrupted VLDL assembly and secretion in AML12 hepatocyte line. Moreover, ROS scavenger and ATP supplementation restored mitochondrial function and triglycerides transport in vitro. Findings demonstrate that BPNM promote hepatic lipid accumulation possibly by triggering oxidative stress and impairing mitochondrial function, thereby interfering with lipid transport, and resulting in hepatic lipid accumulation. This study highlights the potential metabolic disruption risks of BPNM and provides critical insights for their biosafety assessment and sustainable application.
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3. Plastic signatures in childhood: first evidence of urinary micro- and nanoplastics in primary school children from Cyprus.
PMID:日期:2026-07-03Microplastics (MPs) and nanoplastics (NPs) have recently been detected in several human biological matrices; however, evidence in children remains limited. This exploratory study aimed to investigate the presence and concentration of urinary MPs and NPs (MNPs) in primary school children residing in Cyprus. First-morning urine samples from 29 children were analyzed using scanning electron microscopy coupled with energy-dispersive X-ray analysis (SEM/EDX), applying strict contamination-control measures and focusing on particles < 10 μm. Pyrolysis-GC/MS was additionally used to characterize polymer composition, identifying polyethylene (PE) and polypropylene (PP) as the predominant polymers. MNPs < 10 μm were detected in all samples, with concentrations ranging from 393 to 8050 particles/ml (median: 1217 particles/ml; IQR: 800-2030). Particle diameters ranged from 0.88 μm to 3.44 μm (median: 1.69 μm; IQR: 1.25-2.25 μm; minimum: 0.77 μm; maximum: 4.88 μm). No statistically significant associations were observed between MNP concentrations and body mass index (BMI)-for-age categories or hand-to-mouth behavior. Although direct comparisons with previous studies are limited due to methodological variability among studies and the lack of standardized protocols for MNP quantification in human urine, these findings provide preliminary evidence of urinary MNPs in children. Further large-scale studies using harmonized analytical approaches are needed to better characterize exposure patterns in pediatric populations.
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4. Pulmonary toxicity of micro- and nano polyethylene particles following intratracheal instillation in rats.
PMID:日期:2026-06-16Micro- and nano-sized polyethylene plastics (PE-MPs and PE-NPs) are emerging as potential risk factors for pulmonary disease and risk assessment. Currently, their is no direct evidence suggests this appreciable health risk extends to humans. Furthermore, the toxicological evaluation of PE-MPs and PE-NPs is insufficient to support their safe use. This study was aimed to characterize the toxicity of PE-MPs and PE-NPs after 13 weeks of intratracheal instillation in Sprague-Dawley (SD) rats and to assess the reversibility of any effects during a 4-week recovery period. Exposure levels for PE-MPs and PE-NPs were set at 0, 40, 80, and 120 μg per rat once a week. The results indicated that the treatment administration resulted in observable lung tissue alterations. Inflammatory cells were present in the perivascular and peribronchiolar regions in both sexes at ≥ 40 μg per rat in the PE-MPs and PE-NPs-treated groups, indicating a biological response that can turn into toxicity. Additionally, thickened alveolar ducts and alveolar epithelial hyperplasia were noted in males at 120 μg per rat PE-MPs, in males at ≥ 80 μg per rat PE-NPs, and in females at ≥ 40 μg per rat PE-MPs and PE-NPs-treated groups. Interestingly, when instilled repeatedly with both sizes of polyethylene particles, IL-1β and TNF-α secretion was significantly more enhanced in female rats compared to male rats. At the same time, the pulmonary level of IL-6 increased more clearly in male rats than in female rats. The pulmonary level of C-reactive protein, a marker for acute inflammation, was increased in all treated groups. These findings suggest that the lowest-observed-adverse-effect level (LOAEL) for PE-MPs and PE-NPs based on repeated exposures is below 40 μg per rat for both sexes. However, the toxicological data for PE-MPs and PE-NPs remain insufficient to confirm their safety, and further research is necessary to evaluate their potential risks to human health.
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5. Degradation reshapes the toxic identity of polylactic acid microplastics through MSR1-dependent immune decoding in mouse kidney.
PMID:日期:2026-06-14Biodegradable plastics are increasingly being used as a sustainable alternative, but their degradation in biological environments may produce transformation products with unexpected toxicological characteristics. These products generate a distribution pattern in the kidneys that differs from other organs, with the accumulation of low-molecular-weight polylactic acid microplastics (PLA MPs) being far higher than that of high-molecular-weight tissues. PLA is used as a representative bioplastic. We used polymeric and oligomeric MPs to simulate their original and partially degraded states. Mice were exposed to these MPs through repeated oral administration under controlled experimental exposure conditions for 28 consecutive days to study the accumulation and inflammatory damage caused by PLA oligomer and polymer MPs in the kidneys. In combination with in vitro transcriptomic analysis, we explored the potential mechanisms by which oligomers drive nephrotoxicity. Exposure to PLA oligomer MPs results in significantly higher accumulation in the kidneys compared to PLA polymer MPs, and triggers more severe inflammatory damage. The mechanism is that renal macrophages preferentially phagocytose PLA oligomer MPs and decode them through macrophage scavenger receptor 1 (MSR1), activating phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signaling and inducing chemokine ligand 2 (CCL2)-dependent macrophage recruitment, thereby establishing a self-amplifying inflammatory loop. Inhibiting MSR1 or PI3K/AKT effectively reduces oligomer-driven cytokine production, macrophage infiltration, and renal injury, narrowing the toxicity gap between oligomeric and polymeric PLA MPs in the kidneys. These findings reveal that biodegradation can heighten the inflammatory potential of MPs, and that distinct polymerization states of the same material elicit different immune interpretations. Our work provides mechanistic clarity on how degradability reshapes microplastic toxicity, underscoring the need to incorporate degradation-state profiling into the safety assessment of biodegradable MPs.
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6. Inhalation exposure to surrogate military burn pit emissions impairs systemic microvascular function: linking pulmonary insult and diverse peripheral responses.
6. 吸入暴露于替代军用烧伤坑排放物会损害全身微血管功能：将肺部损伤与多种外周反应联系起来PMID:日期:2026-06-12Millions of U.S. troops and supporting personnel have been deployed to military bases in the Middle East. Essentially all personnel on military bases were exposed to the combustion emissions generated by open pit waste burning. Chronic multisymptom illness (CMI) is a term advanced to characterize the complex health effects of inhalation exposures to military burn pits (BP). Because of the diversity of geography, environmental conditions, and deployment operations, it is very challenging to estimate the number of Veterans affected by CMI, but it has been reported to be in the range of ~ 40-60%. Despite this overwhelming number of patients, the underlying causes of CMI remain to be identified. The purpose of this study was to replicate BP combustion and deliver these representative emissions to a whole-body inhalation exposure chamber with Sprague Dawley rats. We hypothesized that because the microcirculation is a critical component of health and disease, that normal microvascular function may be disrupted after BP inhalation exposures. A surrogate BP emission generator was used to combust mixtures of wood, rubber, plastic and jet fuel. Resultant emissions were complex mixtures of volatile organic chemicals, polyaromatic hydrocarbons, fine and ultrafine particles. The particle aerodynamic count median diameter was 113 nm with a geometric standard deviation of 2.21. The particle mobility diameter was 78.1 nm with a geometric standard deviation of 1.69. The aerosol mass-size size distribution had a mass median aerodynamic diameter of 288 nm with a geometric standard deviation of 1.72 nm. Rats were exposed for ~ 4 h/d at BP emission concentrations of 15.4 ± 1.6 mg/m, for 2, 3, or 6 days. Twenty-four hours later, the spinotrapezius muscle was prepared for intravital microscopy. Tissues were also harvested from different rats in these groups for thorough mechanistic analyses. After 3-6 days of exposure, endothelium-dependent arteriolar dilation was abolished. Adrenergic vasoconstrictor sensitivity was augmented by as much as 50% in the BP exposure groups. Bronchoalveolar lavage revealed robust pulmonary inflammation and cellular infiltration. High-performance liquid chromatography with plasma samples demonstrated significant increases (> 50%) in circulating xanthine oxidase, a known driver of oxidative stress, disruptor of vascular nitric oxide, and thus mediator of endothelial dysfunction. After 3 days of BP exposure, RNA sequencing tissue analyses revealed transcriptional markers of lung inflammation as well as an altered transcriptional immune response in both the lung and spleen. BP inhalation exposure also led to elevated RNA transcripts for the vascular growth factor Vegfa and the immune cell trafficking factor Icam1 in brain hippocampal tissue. These initial microvascular observations demonstrate disruption of typical function and mechanisms that may link pulmonary insult with diverse systemic syndromes characteristic with CMI in Veterans.
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7. Bronchial mucosal nuclear transcription factor expression and inflammatory response in humans after exposure to wood smoke.
PMID:日期:2026-06-12Exposure to wood smoke is associated with negative respiratory health outcomes such as airway infections and development of chronic obstructive pulmonary disease (COPD). Previous controlled exposure studies in humans with bronchoscopy sampling have shown wood smoke-induced bronchial cytotoxicity and impaired macrophage phagocytosis. The present study investigated whether an early and transient acute inflammatory response, as reflected in bronchial mucosal biopsies and lavage fluids, could be detected 6 h after wood smoke exposure. On two separate occasions, fourteen healthy participants were exposed, in a double-blind, randomised crossover design, for 2 h to filtered air and diluted wood smoke generated from incomplete wood log combustion with a mean particulate matter concentration of 409 ± 43 µg/m. Bronchoscopy with endobronchial mucosal biopsies, bronchial wash (BW) and bronchoalveolar lavage (BAL) was performed 6 h post-exposure. Biopsies were immunohistochemically stained, and lavage fluids analysed for soluble mediators. In bronchial mucosal biopsies, nuclear translocation of the transcription factors aryl hydrocarbon receptor (AhR) and phosphorylated c-jun (p-c-jun) was significantly reduced within the bronchial epithelium after wood smoke exposure compared to filtered air. There was no endothelial adhesion molecule-mediated recruitment of neutrophils or other inflammatory cells into the bronchial mucosa. Exposure to wood smoke from incomplete wood log combustion suppressed nuclear translocation of transcription factors and the expected inflammatory response in endobronchial mucosal biopsies at 6 h post-exposure. This contrasts to the strong proinflammatory effects of other air pollutants such as ozone and diesel exhaust. Together with previous findings of increased cytotoxicity and impaired airway macrophage phagocytosis in humans, this response may be in line with compromised immune defence and increased susceptibility to airway infections, chronic bronchitis and COPD observed in populations exposed to high levels of indoor air pollution from wood smoke.
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8. Surface-driven endocrine activity of nanoplastics: polymer- and size-dependent estrogen and androgen receptors modulation without steroidogenesis perturbation.
PMID:日期:2026-06-10Growing production and use of plastics have led to significant environmental pollution including the formation and accumulation of plastic nanoparticles (PNPs). Due to their small size, PNPs easily enter the human food chain; however, humans are also exposed to plastics through other consumer pathways, such as the use of cosmetic products. Despite considerable efforts to investigate the potential adverse effects of plastics, their impact on human health is not yet fully understood. In particular, endocrine disruption has emerged as a potential mechanism underlying reported reproductive and hormonal effects of micro- and nanoplastics. We applied an OECD-aligned in vitro test guidelines (TGs) to a factorial panel of eight PNPs spanning four common polymers (polystyrene (PS), polyethylene (PE), polypropylene (PP), polyethylene terephthalate (PET)) with size-resolved materials and polymer-matched mixtures. Thus, estrogen receptor a (ERα) transactivation (TG 455), androgen receptor (AR) transactivation (TG 458, antagonist mode), and H295R steroidogenesis (TG 456) assays were performed using HeLa-9903, AR-EcoScreen GR KO M1, and NCI-H295R cell models, respectively. Across 0.1-10 mg L⁻¹, no cytotoxicity was observed. PENPs (350 nm) and PPNPs (180 nm) acted as ER agonists, whereas PPNPs (50 and 180 nm) and PENPs (350 nm) antagonized AR; PSNPs and PETNPs showed no activity when tested individually. Notably, several mixtures elicited ER and AR responses even when constituent singles were inactive, indicating mixture-dependent potentiation. In contrast, the H295R assay did not meet the OECD decision rule for altered steroidogenesis: sporadic shifts in pathway intermediates did not propagate to estradiol or testosterone. Altogether, the data support a surface- and polymer-dependent, receptor-proximal mode of action for PNPs and highlight mixture effects as a critical, underappreciated driver. These results move endocrine hazard evaluation beyond polystyrene surrogates and provide decision-useful guidance on which polymers/sizes and mixture contexts merit priority in exposure monitoring and risk assessment.
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9. Oxidative aging facilitates biological barrier penetration of polyethylene microplastics, amplifying systemic lipotoxicity in aquatic species.
PMID:日期:2026-06-07Environmental aging processes, such as oxidation, can substantially modify the physicochemical properties and toxicity of microplastics (MPs). Nevertheless, most studies have focused on pristine MPs, overlooking aged forms that more accurately represent environmental exposure conditions. Understanding the toxicological consequences of oxidative aging is essential for realistic ecological risk assessment. We investigated the toxicological effects of pristine polyethylene (PE) and oxidized polyethylene (OPE) microplastics using a dual-species aquatic model comprising Daphnia magna and zebrafish (Danio rerio) embryos. Physicochemical characterization revealed that OPE particles exhibited increased surface roughness, a more negative surface charge, and a higher proportion of oxygen-containing functional groups on the particle surface compared with PE. Exposure to OPE induced pronounced lipid accumulation and significantly reduced heart rate in both models. Transcriptomic analysis indicated that OPE downregulated key genes related to lipid transport and metabolism, including mttp, apoea, and apobb. These findings were further validated by quantitative PCR and Oil Red O staining. Notably, zebrafish embryos exposed to OPE displayed developmental impairment even with intact chorions, implying enhanced bioavailability and barrier penetration of oxidized particles. Our findings demonstrate that oxidative aging amplifies the biological toxicity of polyethylene microplastics by disrupting lipid metabolism and developmental processes. This study underscores the importance of considering environmentally aged MPs in ecological risk evaluations, as pristine particles may underestimate their actual hazard potential in aquatic ecosystems.
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10. Targeting the PPAR-γ-ABC transporter axis ameliorates secondary pulmonary alveolar proteinosis induced by indium oxide nanoparticles.
PMID:日期:2026-06-07Pulmonary alveolar proteinosis (PAP) is a rare lung disease with primary (usually autoimmune) and secondary forms. Unlike the autoimmune type, which can be treated with cytokine therapy or whole-lung lavage, the secondary form associated with occupational particulate exposure, such as indium compounds, has no established therapy and remains challenging to treat. PAP was experimentally induced in rats through intratracheal exposure to indium oxide nanoparticles (InO NPs). To assess potential therapeutic interventions, we administered four pharmacological agents: aspirin and naproxen, which are expected to attenuate inflammation, and pioglitazone and indomethacin, peroxisome proliferator-activated receptor (PPAR)-γ agonists anticipated to restore impaired surfactant homeostasis. The efficacy of their amelioration of InO NP-induced PAP and the underlying mechanisms were evaluated by bronchoalveolar lavage fluid analysis, histopathology, and gene expression profiling. Treatment with pioglitazone and indomethacin markedly attenuated InO NP-induced PAP by reducing foamy macrophage accumulation and restoring the expression of PPAR-γ and its downstream ATP-binding cassette (ABC) transporters, such as ABCG1 and ABCG4. In contrast, aspirin and naproxen only slightly decreased neutrophil infiltration. Among the tested agents, indomethacin showed relatively pronounced effects on several PAP-related endpoints, suggesting its potential to improve macrophage lipid handling and surfactant balance. Targeting PPAR-γ-dependent macrophage lipid regulation may serve to attenuate InO NP-induced secondary PAP-like pathology by reducing foamy macrophage accumulation and improving surfactant clearance. The effects were more pronounced when treatment was administered before disease establishment, whereas established pathology was only partially reversed, supporting the PPAR-γ-ABC transporter pathway as a potential target for future intervention.