Environmental toxicology and pharmacology最新文献

{"title":"Relationship of fractalkine with arsenic exposure and the risk of cardiovascular diseases","authors":"Nesar Uddin ,&nbsp;Rajoana Karim Rimi ,&nbsp;Osman Goni ,&nbsp;Nayan Chandra Mohanto ,&nbsp;Kamrun Nahar Rossi ,&nbsp;Faysal Abedin ,&nbsp;Sharmin Akter Beauty ,&nbsp;Biplob Ahmed ,&nbsp;Sobuj Mia ,&nbsp;Sharon Jahan Sarder ,&nbsp;Sajib Hossain ,&nbsp;Mainul Islam ,&nbsp;Abu Shadat M. Noman ,&nbsp;Md Ashraful Hoque ,&nbsp;Daigo Sumi ,&nbsp;Koren K. Mann ,&nbsp;Zahangir Alam Saud ,&nbsp;Seiichiro Himeno ,&nbsp;Khaled Hossain","doi":"10.1016/j.etap.2025.104824","DOIUrl":"10.1016/j.etap.2025.104824","url":null,"abstract":"<div><div>Cardiovascular diseases (CVDs), the leading cause of arsenic-related morbidity and mortality, are a major public health concern in many countries, including Bangladesh. Understanding the mediators of increased CVD risk associated with arsenic exposure is decisive. Fractalkine (CX3CL1), a CX3C chemokine with both chemotactic and adhesive functions, acts by interacting with its specific receptor, CX3CR1. Fractalkine is implicated in atherosclerosis, leading to CVDs. However, the association between chronic arsenic exposure and serum fractalkine levels and its implication in CVDs have not yet been documented. The present study aimed to investigate the relationship between arsenic exposure and serum fractalkine levels, especially regarding the risk of CVDs. The study included 413 participants from low- and high-arsenic exposure rural areas in Bangladesh. Fractalkine levels in serum were measured by immunoassay, and the risk of CVDs was assessed by measuring the serum high-density lipoprotein cholesterol (HDL-C) and hypertension. We found that participants from high-exposure areas had nearly twice the serum fractalkine levels compared to those in low-exposure area (<em>p</em> &lt; 0.001). A one-unit increase of log₂-transformed water, hair, and nail arsenic showed significantly higher propensity score adjusted odd ratios (aORs) in the second and third tertiles of serum fractalkine in comparison to the first tertile. Serum fractalkine levels were inversely associated with HDL-C levels and positively linked to blood pressure and ORs of hypertension. Finally, the associations between arsenic exposure and hypertension were found to be mediated by serum fractalkine. These results suggest that arsenic-exposure-related increases in fractalkine levels may be implicated in the pathogenesis of CVDs.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"119 ","pages":"Article 104824"},"PeriodicalIF":4.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145180854","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dеvеlоpmеntаl nеurоtоxісіty study оf pesticide Асеtаmіprіd in Wistar Hannover rats","authors":"Inna Rashkivska ,&nbsp;Mykola Produnchuk ,&nbsp;Nadiia Nedopytanska ,&nbsp;Petro Zhminko ,&nbsp;Mojmir Mach ,&nbsp;Yana Kolianchuk","doi":"10.1016/j.etap.2025.104833","DOIUrl":"10.1016/j.etap.2025.104833","url":null,"abstract":"<div><div>Available data on pesticide Acetamiprid (ACE) are insufficient to clarify the uncertainties identified neurotoxicity. The current DNT study of ACE was conducted according to the OECD TG 426 and GLP requirements to clarify uncertainties. ACE was administered orally by gavage Wistar Hannover rats at dose levels of 0, 2.5, 10 and 45 mg/kg/bw/day. Maternal toxicity was expressed at a dose level of 45 mg/kg/bw/day. Developmental toxicity was indicated at a dose level of 45 mg/kg/bw/day. Regarding ACE developmental neurotoxicity, administration at 10 and 45 mg/kg body weight/day affected the acoustic startle response and locomotor activity, with no observed structural brain changes. Based on the study findings, the No-Observed-Adverse-Effect Level (NOAEL) for maternal toxicity was determined to be 10 mg/kg bw/day. The NOAEL was identified as 2.5 mg/kg bw/day for developmental neurotoxicity. A developmental neurotoxicity study of ACE demonstrated that neurotoxicity is a critical limiting factor for the compound's overall toxicity.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"119 ","pages":"Article 104833"},"PeriodicalIF":4.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145216741","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biomarker-based assessment of sublethal metal exposure in brown trout and parasites acanthocephalans from a protected karst river","authors":"Sara Šariri ,&nbsp;Tatjana Mijošek Pavin ,&nbsp;Zuzana Redžović ,&nbsp;Zoran Kiralj ,&nbsp;Dušica Ivanković ,&nbsp;Vlatka Filipović Marijić","doi":"10.1016/j.etap.2025.104823","DOIUrl":"10.1016/j.etap.2025.104823","url":null,"abstract":"<div><div>Karst freshwater ecosystems are especially susceptible to metal pollution, even in protected areas. Present study assessed biomarker responses in intestine of <em>Salmo trutta</em> and their intestinal parasites acanthocephalans at three sites along the karst Krka River: river source, a wastewater-impacted site, and a site within the Krka National Park. Biomarkers of metal exposure, general stress, lipid peroxidation, antioxidant defense, and tissue metabolic activity were analyzed in relation to season, fish biometry, cytosolic metal(loid) concentrations, and parasite burden. Fish from both the wastewater-impacted site (KRK) and the national park site (KNP) showed moderate stress and significantly elevated lipid peroxidation compared to the river source. Correlation analysis revealed stronger biomarker–metal associations in spring, and higher stress in smaller fish with lower parasite burdens. This study provides rare data on biomarker responses in fish intestine and the first data on metallothionein and cytosolic protein levels in acanthocephalans, which exhibited higher biomarker values than host tissue. These results support biomarker use for early detection of sublethal contamination.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"119 ","pages":"Article 104823"},"PeriodicalIF":4.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145182454","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Can bystander effects of metals in Daphnia magna be mediated by DNA methylation?","authors":"Guilherme Jeremias ,&nbsp;Joana Lourenço ,&nbsp;Cristiano V.M. Araujo ,&nbsp;Filip Van Nieuwerburgh ,&nbsp;Fernando J.M. Gonçalves ,&nbsp;Jana Asselman ,&nbsp;Joana L. Pereira","doi":"10.1016/j.etap.2025.104832","DOIUrl":"10.1016/j.etap.2025.104832","url":null,"abstract":"<div><div>The bystander phenomenon can be described as the detection of effects in non-exposed cells/individuals when these come in contact with exposed ones. Bystander literature has focused mostly on the detection of effects rather than understanding the underlying mechanisms, thus these remain largely unknown from a molecular perspective. Epigenetic mechanisms play a major role in biological responses to environmental stressors, with limited evidence suggesting their involvement in the mechanisms behind bystander effects as well. To gain further insight on this specific topic, we performed bystander experiments with <em>Daphnia magna</em> and an essential (copper) and non-essential (cadmium) metal. In short, metal-exposed organisms were left to co-habit with bystander (not previously exposed) organisms in blank medium for further assessment of gene-specific DNA methylation changes in both groups. In exposed organisms, methylation changes mostly occurred in genes involved in general stress responses and in the offset metal toxicity and oxidative stress. DNA methylation changes were also detected in bystander organisms for both metals, and bystander epigenetic responses targeted specifically the <em>Alpha-ketoglutarate-dependent dioxygenase alkB</em> and <em>Tetraspanin 47 F</em> genes, therefore relating to the cellular signalling of metal stress and the coping with metal-induced DNA damage. Taken together, these insights into the molecular mechanisms underpinning bystander effects contribute to a better understanding of their ecological and ecotoxicological consequences.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"119 ","pages":"Article 104832"},"PeriodicalIF":4.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145208635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High concentrations of Printex 90 carbon black ultrafine particles disturb the epithelial barrier in human primary respiratory mucosa models","authors":"Totta Ehret Kasemo ,&nbsp;Maximilian Oppmann ,&nbsp;Sofia Dembski ,&nbsp;Maria Steinke ,&nbsp;Elena Lajtha ,&nbsp;Helena Moratin ,&nbsp;Manuel Stöth ,&nbsp;Agmal Scherzad ,&nbsp;Mathilde Noémie Delaval ,&nbsp;Ralf Zimmermann ,&nbsp;Sebastiano Di Bucchianico ,&nbsp;Stephan Hackenberg ,&nbsp;Till J. Meyer","doi":"10.1016/j.etap.2025.104829","DOIUrl":"10.1016/j.etap.2025.104829","url":null,"abstract":"<div><div>Airborne pollutants harm human health, but the mechanisms involved remain unclear. Impaired epithelial barrier function is, as in respiratory diseases, one possible pathomechanism. To investigate this, carbon black (CB) as a model for ultrafine particles (UFP), was applied to respiratory mucosa models of primary fibroblasts and epithelial cells cultured at the air-liquid interface (ALI). Models were assessed for the mucociliary phenotype. Cytotoxicity, DNA damage, and barrier integrity were evaluated by the lactate dehydrogenase (LDH) and comet assays, and by transepithelial electrical resistance (TEER) measurements. Cilia movement and ultrastructure, secretory cells, and intact cell-cell contacts were confirmed. Subtle changes were observed: the LDH release had increased 2 h post exposure and barrier disturbance 24 h post exposure was detected, both without mucosal damage or genotoxic effects. Donor-specific differences were present. Barrier disruption without cell detachment or death suggests model feasibility for long-term studies of, <em>e.g.</em>, tissue regeneration or fibrosis following UFP exposure.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"119 ","pages":"Article 104829"},"PeriodicalIF":4.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145188103","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Environmental endocrine disruptors and breast cancer: The role of bisphenols, polychlorinated biphenyls, parabens, and dioxins","authors":"Marina Sánchez-Ocaña,&nbsp;Vicenç Ruiz de Porras","doi":"10.1016/j.etap.2025.104834","DOIUrl":"10.1016/j.etap.2025.104834","url":null,"abstract":"<div><div>Breast cancer is the most common malignancy in women, and environmental factors such as endocrine-disrupting chemicals (EDCs) contribute to its development and progression. This review examines the roles of four major EDCs—bisphenols, polychlorinated biphenyls (PCBs), parabens, and dioxins—integrating mechanistic and epidemiological evidence. A key pathway is the cross-talk between estrogen receptor (ER) and aryl hydrocarbon receptor (AhR), which regulates proliferation, survival, and immune evasion. Bisphenol A (BPA) promotes proliferation, migration, epigenetic reprogramming, and immune escape. PCBs, particularly PCB-153, are linked to metabolic alterations, inflammation, and variable epidemiological associations. Parabens, common in cosmetics, display estrogenic activity and affect oxidative stress, tumor marker expression, and metastasis. Dioxins, especially TCDD, act via AhR to induce inflammation, immunosuppression, and metastasis, with epidemiological links to cancer risk near emission sources. Collectively, these EDCs disrupt hormonal pathways, alter gene expression, and modulate the tumor microenvironment, underscoring the need for further research, regulation, and public health interventions.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"119 ","pages":"Article 104834"},"PeriodicalIF":4.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145216846","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unveiling the molecular responses of human lung cells to retene: Transcriptomics insights and implications for toxicity","authors":"Francisco Carlos da Silva Junior ,&nbsp;Junyi Lin ,&nbsp;Markus Hecker ,&nbsp;Silvia Regina Batistuzzo de Medeiros","doi":"10.1016/j.etap.2025.104828","DOIUrl":"10.1016/j.etap.2025.104828","url":null,"abstract":"<div><div>While retene (RET) ecotoxicity has been studied, its molecular mechanisms remain unclear despite its prevalence in forest fires. This study investigated RET’s effects in BEAS-2B cells using whole transcriptome (RNA-seq) analysis, cell viability, ATP level, cell adhesion, cell migration, and cell invasiveness endpoints after 24 h and 72 h of exposure. RNA-seq revealed dynamic transcriptional changes, including dysregulated long non-coding RNAs (lncRNAs), microRNAs (miRNAs), and pseudogenes. Pathway analysis implicated disrupted fatty acid metabolism and mitochondrial function, suggesting energy imbalance. RET induced hormesis effects, with low doses stimulating cell proliferation and increase in ATP levels. Altered cytoskeletal and extracellular matrix genes likely drove enhanced adhesion, migration, and invasiveness. Wound healing and transwell assays suggested RET may promote epithelial-mesenchymal transition-like functional phenotype (EMT). The present findings suggested metabolic adaptation and transcriptional regulation as key to RET’s effects on proliferation and invasiveness, revealing complex cellular responses to environmental stressors with implications for PAH-linked respiratory diseases and carcinogenesis.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"119 ","pages":"Article 104828"},"PeriodicalIF":4.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145181260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ER stress links HSP90/NLRP3-mediated pyroptosis in grass carp brain under synergistic exposure to cypermethrin and sulfamethoxazole","authors":"Yingxue Zhang,&nbsp;Boran Zhou,&nbsp;Yufei Cao,&nbsp;Shuni Wang,&nbsp;Mingwei Xing,&nbsp;Hongjing Zhao","doi":"10.1016/j.etap.2025.104831","DOIUrl":"10.1016/j.etap.2025.104831","url":null,"abstract":"<div><div>With the aggravation of pesticide and antibiotic pollution, drug residues in water increasingly threaten the stability of aquatic ecosystems, which has aroused widespread social concern. The nervous system plays a leading role in the organism, but the mechanism of brain damage induced by cypermethrin (CMN) and sulfamethoxazole (SMZ) is still unclear. In this study, the effects of CMN (0.65 μg/L) and SMZ (0.30 μg/L) alone and combined exposure for 42 days on the brain tissue of grass carp (<em>Ctenopharyngodon idella</em>) were investigated. We noted that co-exposure to CMN and SMZ resulted in more pronounced pathological damage and ultrastructural disruptions in brain tissue, accompanied by endoplasmic reticulum stress (ERS), heat shock response (HSR), and pyroptosis. A detailed mechanistic investigation indicated that the ERS pathway (PERK) was activated, which may trigger cell protection against the damage caused by CMN and SMZ exposure. Excessive ERS was also accompanied by the HSR and the pyroptosis response, which were supported by increased expression levels of heat shock proteins (HSP60, HSP70, and HSP90) and related molecular mechanisms of pyroptosis (NLRP3, ASC, IL-18, Caspase-1) from mRNA and protein levels. This study suggested that CMN and SMZ induced neurotoxicity in grass carp through activating the HSP90/NLRP3 signaling pathway, providing valuable data for the ecological risk assessment of SMZ and CMN to aquatic organisms and theoretical support for the conservation of aquatic organisms.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"119 ","pages":"Article 104831"},"PeriodicalIF":4.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145215068","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adipose tissue cadmium concentrations as potential determinants of serum PON1 status in an adult cohort from Southern Spain","authors":"Maria Cruz Gomez Pellin ,&nbsp;Eduardo Linares-Ruiz ,&nbsp;Javier Esteban ,&nbsp;Inmaculada Salcedo-Bellido ,&nbsp;Gonca Çakmak ,&nbsp;María Eugenia Velasco García ,&nbsp;Jose Barril ,&nbsp;Suylen Galbán-Velázquez ,&nbsp;Celia Pérez-Díaz ,&nbsp;Francisco M. Pérez-Carrascosa ,&nbsp;Petra Vrhovnik ,&nbsp;Željka Fiket ,&nbsp;María de la Cruz Pellín ,&nbsp;Juan P. Arrebola","doi":"10.1016/j.etap.2025.104827","DOIUrl":"10.1016/j.etap.2025.104827","url":null,"abstract":"<div><div>Paraoxonase 1 (PON1) is an antiatherogenic enzyme inhibited by environmental stressors such as cadmium (Cd). Thus, this human study aimed to assess (1) the associations between adipose tissue Cd concentrations and serum PON1 status and (2) the influence of the PON1_Q192R phenotype on the susceptibility of PON1 status to Cd. As a continuation from previous work, a subsample from the GraMo cohort (Granada, Spain) was studied. Three PON1 activities using non-organophosphorous substrates {PALS (phenyl acetate in the absence of NaCl), PAHS (phenyl acetate in 2 M NaCl) and CMPA [4-(chloromethyl)phenyl acetate]} were assayed in serum (n = 296) to obtain the three functional PON1_Q192R phenotypes (QQ, QR and RR). Complementarily, Cd concentrations in adipose tissue (n = 226) and information on socio-demographic characteristics, lifestyle, diet and health status acquired by face-to-face interviews were available. The associations between PON1 activities in serum and Cd concentrations in adipose tissue (subset of n = 138) were explored by using linear regression models, which were adjusted for sex, alcohol consumption and PON1_Q192R phenotype. Additionally, benchmark dose (BMD) modelling was performed. Higher adipose tissue Cd concentrations were associated with lower PON1 activities. PON1_Q192R specific susceptibility to Cd increased in the order QQ &lt; QR &lt; RR. The Cd BMD ranges for an averaged subject were 0.002–0.016 and 0.046–0.115 mg_Cd/kg_{adipose-tissue} for RR and QR, respectively. For QQ cases, the BMD were higher than the Cd concentrations found in adipose tissue. These results suggest that part of the increased susceptibility of the RR cases to cardiovascular diseases might putatively be mediated by its higher sensitivity to Cd, with adipose tissue Cd levels serving as a biomarker of chronic exposure.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"120 ","pages":"Article 104827"},"PeriodicalIF":4.2,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145182421","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adverse pulmonary effects and metallic characteristic of size-resolved welding fumes in human lung epithelial BEAS-2B cells","authors":"Pin-Hao Qiu ,&nbsp;Chia-Hua Lin ,&nbsp;Yen-Ping Peng ,&nbsp;Ku-Fan Chen ,&nbsp;Yi-Chun Chen ,&nbsp;Yung-Chang Lin ,&nbsp;Chia-Hsiang Lai","doi":"10.1016/j.etap.2025.104826","DOIUrl":"10.1016/j.etap.2025.104826","url":null,"abstract":"<div><div>Welding produces complex metal fumes containing fine and ultrafine particles that can penetrate different regions of the respiratory tract and cause adverse health effects. Analyses based solely on total particulates overlook the size-dependent toxicity of these aerosols. This study employed human lung epithelial cells to elucidate the effects of different sizes (2.5–10 μm, 1.0–2.5 μm, and &lt; 1.0 μm) of metallic fume particles (MFPs) in a stainless steel arc welding workplace. High concentrations of iron (106.09 μg/m³), chromium (40.94 μg/m³), and manganese (27.43 μg/m³), which are the main components of stainless steel welding materials, were detected in the MFPs. The total concentrations of 23 metal elements in the MFPs were in the order of MFP_1.0 (79.74 %) &gt; MFP_2.5–10 (12.89 %) &gt; MFP_1–2.5 (7.37 %). The total deposited MPS flux was highest in the nasal cavity (87.90 %), followed by the alveolar region (5.16 %) and the tracheobronchial region (1.17 %), using the International Commission on Radiological Protection model. Cell viability decreased with increasing metal concentration. Ultrafine MFPs (50 μg/cm²) increased intracellular reactive oxygen species (ROS) levels by more than 4.24-fold compared to control levels. Principal component analysis highlighted iron, molybdenum, barium, and lead as the primary contributors to ROS generation. In conclusion, fine particles (MFP_1–2.5) posed a greater risk of lung injury, and welding fumes induced cytotoxicity via ROS even in the absence of classical carcinogenic metals. These findings highlight the critical role of particle size and metal composition in driving pulmonary toxicity and emphasize the need for size-specific exposure limits to better protect welders’ respiratory health.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"119 ","pages":"Article 104826"},"PeriodicalIF":4.2,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145154968","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}