Particle and Fibre Toxicology最新文献

{"title":"A simple and reliable method for the qualitative and quantitative analysis of nano- and microplastics in organs for controlled preclinical studies.","authors":"Soyeon Jeon, Gyuri Kim, Jun Hui Jeon, Sung Ik Yang, Kyuhong Lee, June-Woo Park, Wan-Seob Cho","doi":"10.1186/s12989-026-00677-6","DOIUrl":"10.1186/s12989-026-00677-6","url":null,"abstract":"<p><strong>Background: </strong>Toxicity studies of microplastics increasingly emphasize the importance of particle retention, transformation, and physicochemical properties within biological systems, as these factors critically influence hazard identification and dose-response interpretation. However, quantitative and qualitative analyses of microplastics in biological matrices remain technically challenging, and many existing digestion-based methods can alter particle properties, thereby confounding toxicological outcomes. Herein, we propose a novel methodology to provide quick, easy, non-destructive, cost-efficient, and reliable outcomes by offering a particle collection method for microplastics as-present in organs using proteinase K (PK) digestion and a simple quantification method based on ultraviolet-visible (UV-Vis) spectrophotometry.</p><p><strong>Results: </strong>The test microplastic samples comprised three spherical polystyrene (0.1, 1, and 100 μm), two fragmented polystyrene (1 and 100 μm), one spherical polyethylene (10 μm), one fragmented polyethylene (100 μm), and two fragmented polypropylene (1 and 100 μm). Particles as-present in organs were successfully collected by conducting PK tissue digestion at 5 µg PK per mg dried tissue. The collected particles were then quantified using a standard curve, with absorbance measured at 750 nm. Spiking experiments with microplastics in mouse lung and mussel tissues showed > 90% accuracy and recovery for all test particles. Because the PK-based particle collection method is non-destructive, the collected particles can be further used to evaluate their physicochemical properties, such as size, shape, composition, and oxidative potential. However, the plastics treated with both acids and alkalis exhibited significant morphological, optical, and chemical changes, indicating that these methods are destructive to particles.</p><p><strong>Conclusion: </strong>Therefore, this simple, non-destructive approach enables quantitative and qualitative analyses for laboratory toxicological studies and qualitative identification of microplastics in unknown biological samples, providing a valuable tool for future toxicity and environmental research.</p>","PeriodicalId":19847,"journal":{"name":"Particle and Fibre Toxicology","volume":" ","pages":""},"PeriodicalIF":10.6,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13104356/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147639511","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Maternal exposure to titanium dioxide nanoparticles disrupts ultrasonic vocalization development in mouse offspring.","authors":"Marie Boulain, Taner Aktas, Gilles Courtand, Grégory Barrière, Muriel Thoby-Brisson, Didier Morin, Laurent Juvin","doi":"10.1186/s12989-026-00668-7","DOIUrl":"10.1186/s12989-026-00668-7","url":null,"abstract":"<p><strong>Background: </strong>Early neurodevelopment is a critical period during which environmental exposures can have lasting effects on brain function and behavior. One key indicator of early neurodevelopmental integrity in rodents is the production of neonatal ultrasonic vocalizations (USVs), which are essential for maternal-offspring communication. Given the widespread use of titanium dioxide nanoparticles (TiO2NPs) in food and consumer products, there is growing concern that perinatal exposure to these particles may interfere with normal neurodevelopment. However, the effects of TiO2NPs exposure on USV production remain poorly investigated.</p><p><strong>Results: </strong>In the present study, pregnant mice were orally exposed to TiO2NPs (200 µg/g) from conception to weaning, and their offspring underwent a maternal separation test to assess USVs between postnatal day P2 and P13. TiO2NP-exposed pups exhibited a significant reduction in the number of USVs at P6-7, accompanied by a delayed peak vocalization period. This reduction was primarily attributable to shorter vocalization series rather than fewer isolated calls. Additionally, acoustic analysis revealed that pups emitted two types of USVs, simple and complex, both of which were significantly reduced in number at P6-7 in the exposed group. Fast Fourier transform (FFT)-based analysis showed that complex USVs had a lower mean frequency, while both call types exhibited increased variability in mean frequency. Furthermore, TiO2NP-exposed pups displayed alterations in USV syntax, including a lower proportion of simple USVs and disrupted developmental maturation of call structure. Electrophysiological recordings revealed that the intermediate reticular oscillator (iRO), a key brainstem center involved in vocalization control, exhibited reduced excitability and an increased activity variability in exposed pups, suggesting that nanoparticle exposure compromises vocal motor regulation at the neural level. Lastly, playback experiments demonstrated that USVs from TiO2NP-exposed pups failed to elicit appropriate maternal attraction, indicating impaired communicative effectiveness.</p><p><strong>Conclusions: </strong>Perinatal exposure to TiO2NPs disrupts the normal development of USVs, impairing both vocalization patterns and neural excitability of the iRO. These changes may contribute to altered maternal-offspring interactions and highlight the potential neurodevelopmental risks of early-life TiO2NPs exposure. Given the widespread presence of TiO2NPs in consumer products, further research is necessary to assess their long-term consequences on neural circuits underlying communication and social behavior.</p>","PeriodicalId":19847,"journal":{"name":"Particle and Fibre Toxicology","volume":" ","pages":""},"PeriodicalIF":10.6,"publicationDate":"2026-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13104461/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147609587","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A comprehensive review on the role of PM2.5 in modulating transplant immunity and graft survival.","authors":"Muhammad Adil Malik, Quan Zhuang, Junjie Huang, Xu Cao","doi":"10.1186/s12989-026-00660-1","DOIUrl":"10.1186/s12989-026-00660-1","url":null,"abstract":"<p><p>Organ transplantation is an indispensable therapeutic approach for patients experiencing end-stage organ failure. Despite ongoing advancements and refinements in immunosuppressive therapies aimed at mitigating graft rejection and enhancing graft longevity, environmental influences including particulate matter 2.5 (PM2.5) have emerged as significant determinants of post-transplant health. PM2.5, a prevalent environmental contaminant, is particularly concerning due to its widespread presence and detrimental biological effects. Notably, the living environment of transplant recipients further exacerbates the complexity of post-transplant outcomes. Evaluating findings from recent investigations, this review delves into the influence of PM2.5 exposure on the immune system. The findings identify its capacity to provoke systemic inflammation, disrupt cytokine profiles, and compromise immune tolerance mechanisms. Such immune dysfunction poses direct risks to graft integrity, with potential implications for both graft health and the prospects of achieving long-term graft survival in affected patients.</p>","PeriodicalId":19847,"journal":{"name":"Particle and Fibre Toxicology","volume":"23 1","pages":""},"PeriodicalIF":10.6,"publicationDate":"2026-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13036968/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147593828","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Maternal PM_2.5 exposure induces insulin resistance in adult male mouse offspring via gut-liver axis.","authors":"Renjie Hu, Wenbin Zhao, Wenjun Fan, Ran Li, Lu Zhang, Li Qin, Huanhuan Zhu, Xuan Zhu, Qinghua Sun, Guifen Qiang, Cuiqing Liu","doi":"10.1186/s12989-026-00676-7","DOIUrl":"10.1186/s12989-026-00676-7","url":null,"abstract":"<p><strong>Background: </strong>The rising prevalence of metabolic diseases represents a global health challenge, with metabolically unhealthy normal-weight (MUHNW) individuals remaining largely overlooked. In addition to direct fine particulate matter (PM_2.5) inhalation, there is growing recognition that maternal PM_2.5 exposure may be a contributing environmental factor for metabolic disorders. However, the mechanisms by which maternal PM_2.5 exposure induced metabolic disorders in the offspring remain unknown.</p><p><strong>Methods: </strong>Eight-week-old pregnant C57BL/6N mice were exposed to either filtered air (FA) or ambient PM_2.5 throughout gestation, from gestational day 0 to 18, using a whole-body inhalation exposure system. Eight-week-old male C57BL/6N mice were treated once daily for three consecutive days with an antibiotic cocktail containing 1 g/L ampicillin, 0.5 g/L neomycin, 0.5 g/L vancomycin, and 1 g/L metronidazole to generate pseudo-germ-free mice. Subsequently, fecal microbiota from maternal PM_2.5-exposed three-week-old male mouse offspring (donor) were transplanted to pseudo-germ-free mice (recipient) via oral gavage twice weekly for five weeks. After fecal microbiota transplantation (FMT), fecal samples from donor and recipient mice were collected for full-length 16S rRNA sequencing. Liver tissue from donor mice was analyzed by 5R 16S rRNA sequencing.</p><p><strong>Results: </strong>Maternal PM_2.5 exposure induced non-obese insulin resistance in adult male mouse offspring, with the liver identified as a susceptible organ characterized by suppressed AKT phosphorylation. Subsequently, systemic and hepatic insulin resistance were recapitulated in pseudo-germ-free mice, which received gut microbiota from maternal PM_2.5-exposed mouse offspring via FMT. Mechanistically, the increased abundance of Helicobacter hepaticus contributed to DNA damage-mediated colonic barrier injury. This impaired colonic barrier facilitated gut-to-liver translocation of bacteria and lipopolysaccharide (LPS), which triggered hepatic inflammation via activation of TLR4 signaling pathway, ultimately leading to insulin resistance.</p><p><strong>Conclusions: </strong>These findings indicated a causal role for gut microbiota dysbiosis in maternal PM_2.5 exposure-induced non-obese insulin resistance in the offspring, providing potential insights into the developmental origins of MUHNW from the perspective of maternal exposure to air pollution.</p>","PeriodicalId":19847,"journal":{"name":"Particle and Fibre Toxicology","volume":" ","pages":""},"PeriodicalIF":10.6,"publicationDate":"2026-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13085421/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147593880","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Small particles, large questions: unravelling the toxicity and potential health risks of PET micro-/nanoplastics.","authors":"Michaela Hanzlova, Drahomira Holmannova, Tereza Svadlakova, Zdenek Fiala","doi":"10.1186/s12989-026-00673-w","DOIUrl":"10.1186/s12989-026-00673-w","url":null,"abstract":"<p><p>Despite the extensive use of polyethylene terephthalate (PET), the public health implications of its micro- and nanoparticles (MNPs) remain poorly understood, raising credible concerns about human exposure and health risks. We conducted a comprehensive literature search to synthesise evidence on human exposure to PET MNPs, their detection in human tissues and biological fluids, and the human-relevant toxicity of PET particles in vitro and in vivo. Studies consistently identify PET MNPs across consumer and environmental sources, and several investigations have detected PET in human matrices, supporting the plausibility of systemic translocation across biological barriers. Toxicological findings consistently indicate size- and shape-dependent uptake and effects: smaller particles exhibit greater cellular internalisation, reactivity, and biodistribution, with predominant oxidative, inflammatory, metabolic, and genotoxic responses, whereas larger microplastics more often provoke mechanical irritation. Key gaps include limited protocol harmonisation, unrealistic exposure levels, scarce long-term/kinetic data, and insufficiently standardised, well-characterised PET MNPs preparations. While evidence for exposure, detection in human matrices, and biological activity is growing, these deficits still hinder robust cross-study comparisons and clinically meaningful quantitative risk assessment.</p>","PeriodicalId":19847,"journal":{"name":"Particle and Fibre Toxicology","volume":" ","pages":""},"PeriodicalIF":10.6,"publicationDate":"2026-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13064395/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147530749","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Macrophages bend long fibres with flexural rigidity lower than 3 mN·nm² to avoid frustrated phagocytosis.","authors":"Dirk Broßell, Asmus Meyer-Plath, Oliver Gräb, Elisabeth Heunisch, Kerstin Kämpf, Andrea Haase, Martin Wiemann","doi":"10.1186/s12989-026-00666-9","DOIUrl":"10.1186/s12989-026-00666-9","url":null,"abstract":"<p><strong>Background: </strong>It is an established toxicological principle that the inhalation pathogenicity of respirable and biodurable fibres is caused by excessive fibre length as alveolar macrophages fail to uptake and remove such fibres. However, studies on carbon nanotubes showed that this principle needs revision, as thin, flexible variants showed reduced fibre-specific toxicity. One potential explanation is that the low flexural rigidity of thin fibres enables macrophages to bend and internalize even those that are long relative to the cell size. To evaluate this proposed \"rigidity hypothesis,\" the mechanisms governing the uptake of flexible long fibres that determine a critical threshold value for flexural rigidity require clarification.</p><p><strong>Methods: </strong>We exposed NR8383 rat alveolar macrophages to three silver nanowire variants differing in diameter and length. Time-lapse microscopy captured fibre uptake processes. Successful internalization of long fibres was found to require fibre bending during uptake. A mechanical model was developed by combining established cytoskeletal biophysics with the observed fibre deformation dynamics. As flexural rigidity describes fibre behaviour under load, our model estimated rigidity by reproducing the observed bent fibre shape. By defining limit cases for physically 'weak' and 'strong' NR8383 macrophages, i.e., assuming upper bounds on the forces generated by their cytoskeletal nanomachinery, our model enabled us to derive a range for the critical fibre rigidity threshold.</p><p><strong>Results and conclusion: </strong>A macrophage was observed bending an exceptionally long fibre (~ 140 μm) first into an arc and then a spiral for full internalization, initiated by a pseudopod extending along the fibre and buckling the internalized segment. Our model can reproduce such behaviour. It yielded a flexural rigidity of 20 mN·nm² for this fibre. Predicted critical rigidity limits for fibres that just fit into NR8383 macrophages range from 3 to 62 mN·nm². Using the conservative lower bound, long and biodurable fibres with a rigidity lower than 3 mN·nm² are expected to be readily phagocytized by this cell line. Although this rigidity scale may not be directly translatable to human alveolar macrophages, our experimental findings and their modeling emphasize the key role of rigidity in fibre-cell interactions. Fibre rigidity is therefore central for material safety aspects and sustainable product design.</p>","PeriodicalId":19847,"journal":{"name":"Particle and Fibre Toxicology","volume":"23 1","pages":""},"PeriodicalIF":10.6,"publicationDate":"2026-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12998087/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147474873","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A quantitative definition for poorly soluble particles.","authors":"Lan Ma-Hock, Heidi Stratmann, Matthias Hufnagel, Anthony M Bowden, Blanca Serrano Ramón, David Warheit, Rüdiger Battersby, Shannon M Krieger, Marco Kellert, Nils Krueger, Bennard van Ravenzwaay, Robert Landsiedel, Helmut Greim","doi":"10.1186/s12989-026-00670-z","DOIUrl":"10.1186/s12989-026-00670-z","url":null,"abstract":"<p><p>Poorly soluble low toxicity particles (PSLT) have long been a concept in particle toxicology and regulatory frameworks addressing inhalation hazards. The term PSLT refers to particles that exhibit low toxicity and minimal solubility in biological fluids, leading to prolonged retention in the lungs and potential overload effects. Historically, PSLT has been used to distinguish materials whose adverse effects are primarily driven by particle burden rather than intrinsic chemical toxicity. While the \"low toxicity\" (LT) component of the definition has been examined to a certain degree (Driscoll and Borm in Inhal Toxicol 32(2):53-62, 2020), the poorly soluble (PS)-criterion does not yet have a precise definition although it is critically influencing the interpretation of toxicological inhalation repeated dose studies and hazard classifications. An ECETOC Task Force (TF) was formed to define criteria for \"poorly soluble\" particles (PSPs). This paper presents a quantitative non-animal approach for defining PSP using a model particle, with a focus on its potential to cause volumetric lung overload and affect macrophage clearance mechanisms. The analysis allows to calculate a dissolution rate that would lead to a lung burden of about 1 µL/g of lung tissue (lung overload threshold according to Morrow (Morrow in Fundam Appl Toxicol 10(3):369, 1988)). Below this threshold dissolution rate, this specific model particle would qualify as PSP. In addition, a formula was presented to translate abiotic dissolution rates into biotic (rat) dissolution rates to allow a PS-assessment in an animal-free system. As proof of concept, the TF collected existing in vivo data from member companies, publicly available literature of presumed PS-substances, and reference materials. The collected data revealed that most substances exhibited dissolution rates below the critical threshold and that the lung burden at no observed adverse effect concentrations (NOAECs) remained below the lung overload limit. Importantly, this threshold dissolution rate can differ from particle to particle, depending on factors such as agglomerate density, particle size distribution, and expected concentration. Thus, it should be evaluated on a case-by-case basis.</p>","PeriodicalId":19847,"journal":{"name":"Particle and Fibre Toxicology","volume":"23 1","pages":""},"PeriodicalIF":10.6,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12983584/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147444538","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effects of ingested cellulose nanomaterials on DNA methylation in intestinal cells.","authors":"Nádia Vital, Célia Ventura, Camila Fernandes, Luís Vieira, Ana Valente, Michel Kranendonk, Maria João Silva, Henriqueta Louro","doi":"10.1186/s12989-026-00672-x","DOIUrl":"10.1186/s12989-026-00672-x","url":null,"abstract":"<p><strong>Background: </strong>Cellulose nanomaterials (CNMs) are emerging materials under development for various applications in biomedicine and the food industry. Consequently, their potential human health effects warrant evaluation, particularly after oral exposure. Previous studies on two innovative CNMs, CNF-TEMPO and CMF-ENZ, indicated that genotoxicity could not be ruled out, as DNA damage was observed in Caco-2 cells. Whether these CNMs may affect gene expression regulation and induce downstream effects not assessed through genotoxicity testing, is still an open question. This work presents a new approach methodology coupling in vitro simulated digestion with epigenomics, to investigate changes in DNA methylation upon exposure of intestinal cells to these CNMs.</p><p><strong>Results: </strong>DNA methylation patterns differed upon cell exposure to undigested or digested samples, showing a trend towards hypermethylation for undigested and hypomethylation for digested samples. Using Reduced Representation Bisulfite Sequencing, significant differentially methylated regions (DMR) and genes were identified in undigested and digested CNMs-exposed cells. Pathway analysis revealed that CNMs targeted multiple signal transduction pathways. CMF-ENZ and CNF-TEMPO impacted glycosaminoglycan metabolism and glycosylation pathways, possibly involved in cell proliferation. CMF-ENZ affected a DNA repair pathway, while CNF-TEMPO impacted pathways associated with glucose metabolism, independently of the digestion process. Both CNMs seemed to affect pathways implicated in overall cytoskeletal and extracellular matrix dynamics. For digested CNMs, particularly digested CNF-TEMPO, the epigenetic modifications suggested a possible deleterious disturbance given the involvement of ERBB2/PIK3 signaling.</p><p><strong>Conclusions: </strong>This study shows that CNMs may have a biological effect on Caco-2 cells, affecting DNA methylation, and highlights the importance of epigenetic analysis in pointing out the way for unraveling the mechanisms underlying their toxicity.</p>","PeriodicalId":19847,"journal":{"name":"Particle and Fibre Toxicology","volume":" ","pages":""},"PeriodicalIF":10.6,"publicationDate":"2026-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13335175/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147444465","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of PADI2-mediated vimentin citrullination alleviates silica-induced pulmonary fibrosis in mice.","authors":"Fuyu Jin, Yaqian Li, Tian Li, Shupeng Liu, Dingjie Xu, Heliang Liu, Zhongqiu Wei, Xuemin Gao, Na Mao, Wenchen Cai, Yiwei Shi, Haibo Zhang, Hong Xu","doi":"10.1186/s12989-026-00671-y","DOIUrl":"10.1186/s12989-026-00671-y","url":null,"abstract":"<p><p>Silicosis remains a critical occupational health concern worldwide, lacking effective treatments due to unclear mechanisms. In this study, we investigated the citrullinated proteomic profile and its effects in mice exposed to silica. Our findings demonstrated elevated levels of citrullinated peptides and citrullinated vimentin (Cit-Vim) in silicotic mice and silica-treated macrophages, regulated by peptidylarginine deiminase (PADI2). Unlike vimentin, Cit-Vim amplified the production of tumor necrosis factor-α (TNF-α), Interleukin-6 (IL-6), and IL-1β in silica-treated macrophages through interaction with Toll-like receptor 4 (TLR4) signaling. RNA sequencing revealed that early growth response protein 1 (EGR1) is a target of PADI2, with Cit-Vim inducing lung inflammation via EGR1 signaling. Pharmacological inhibition or genetic knockout of Padi2 attenuated silica-induced lung inflammation and fibrosis. These findings suggest that targeting PADI2 may represent a novel therapeutic strategy of silicosis.</p>","PeriodicalId":19847,"journal":{"name":"Particle and Fibre Toxicology","volume":" ","pages":""},"PeriodicalIF":10.6,"publicationDate":"2026-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13019754/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147373062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations of prenatal fine particulate matter mixtures with neurodevelopmental outcomes in early childhood: component- and source-specific insights.","authors":"Haonan Li, Elizabeth A Holzhausen, Devendra Paudel, Nathan D Young, Jonatan Ottino-González, Frederick W Lurmann, Douglas I Walker, Howard H Chang, Donghai Liang, Ravi Bansal, Michael I Goran, Bradley S Peterson, Tanya L Alderete","doi":"10.1186/s12989-025-00657-2","DOIUrl":"10.1186/s12989-025-00657-2","url":null,"abstract":"<p><p>This study investigates independent and joint effects of fine particulate matter (PM2.5) components on early childhood neurodevelopment and explores emission sources of key toxic components. We included 165 mother-infant dyads from Southern California. Annual average concentrations of 15 PM2.5 components, including carbonaceous components, secondary inorganic salts, and trace elements, were estimated for the birth year. Neurodevelopment across cognitive, language, motor, social-emotional, and adaptive behavior domains was assessed at age 2 using Bayley-III Scales. Mixture effects and key contributors were evaluated using weighted quantile sum (WQS) and Bayesian kernel machine regression (BKMR). Source inference was conducted through inter-component clustering and spatial analysis. Linear regression showed PM2.5, sulfate (SO42−), nitrate (NO3−), ammonium (NH4+), copper (Cu), nickel (Ni), lead (Pb), and vanadium (V) were inversely, while calcium (Ca) and zinc (Zn) were positively, associated with adaptive behavior scores (p < 0.05). WQS showed negative associations between the mixture and adaptive behavior (p = 0.02–0.06), with Ni, Cu, V, and SO₄²⁻ as key contributors. BKMR showed similar trends. Ni, V, and SO42− likely originate from heavy oil combustion, and Cu from brake wear. Findings suggest that PM2.5 components, particularly from traffic and marine fuel combustion, may adversely affect adaptive behavior in early childhood.</p>","PeriodicalId":19847,"journal":{"name":"Particle and Fibre Toxicology","volume":" ","pages":""},"PeriodicalIF":10.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12990619/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147326835","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}