Toxicology and Industrial Health最新文献

Oxidative DNA damage of lambda-cyhalothrin in model vertebrate organism.

IF 1.7 4区医学

Toxicology and Industrial Health Pub Date : 2025-02-04 DOI: 10.1177/07482337251316771

Rabia Şemsi, Burcu Eser, Gülsüm Koçak, Göktuğ Gül, Pınar Arslan Yüce, Aysel Çağlan Günal, Aylin Sepici Dinçel

{"title":"Oxidative DNA damage of lambda-cyhalothrin in model vertebrate organism.","authors":"Rabia Şemsi, Burcu Eser, Gülsüm Koçak, Göktuğ Gül, Pınar Arslan Yüce, Aysel Çağlan Günal, Aylin Sepici Dinçel","doi":"10.1177/07482337251316771","DOIUrl":"https://doi.org/10.1177/07482337251316771","url":null,"abstract":"Pesticides, widely used for insect control in agriculture, public health, and veterinary medicine, are usually present as pollutants in aquatic environments. After contamination of water bodies, pesticides cause adverse effects on non-target organisms and long-term problems in the ecosystem. Lambda-cyhalothrin (LCH) is a chemical compound belonging to the family of synthetic pyrethroids (type II) and is an active ingredient in several insecticides. This study investigated the toxic effects (DNA damage) of LCH exposure on zebrafish for 24 and 72 h. After zebrafish (Danio rerio) were obtained commercially, acclimated, and adapted to laboratory conditions. They were randomly selected, transferred to the experimental aquariums (their average height is 2.51 ± 0.49 cm long, 10 L aquarium size of 10x20x35), and exposed to 0.1 mg/L LCH concentrations for 24 and 72 h. There was also a control and a solvent control group in the study, and whole body tissues of zebrafish were analyzed for 8-hydroxy-2-deoxyguanosine (8-OhdG) determination (ng/100 mg tissue), using an Agilent LC-MS/MS with electrospray ionization in positive ion mode. It was observed that the whole-body 8-OHdG tissue values were significantly increased in the group exposed to LCH for 72 h (9.82 ± 1.44) compared with the control group (6.60 ± 1.78, p = .004). These results suggest that LCH could lead to oxidative DNA damage by causing an increase in 8-OHdG activities in zebrafish, one of the aquatic ecosystem model organisms, indicating that it may also cause undesirable effects on other non-target species.","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"7482337251316771"},"PeriodicalIF":1.7,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143190363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Perfluorooctane sulfonate causes HK-2 cell injury through ferroptosis and endoplasmic reticulum stress pathways. 全氟辛烷磺酸通过铁突变和内质网应激途径导致 HK-2 细胞损伤

IF 1.7 4区医学

Toxicology and Industrial Health Pub Date : 2025-02-01 Epub Date: 2024-11-19 DOI: 10.1177/07482337241300722

Shuqi Yan, Haoyan Ma, Yuwan Ren, Pingwei Wang, Dongge Liu, Na Ding, Yanping Liu, Qianqian Chen, Shuping Ren, Yan Mou

{"title":"Perfluorooctane sulfonate causes HK-2 cell injury through ferroptosis and endoplasmic reticulum stress pathways.","authors":"Shuqi Yan, Haoyan Ma, Yuwan Ren, Pingwei Wang, Dongge Liu, Na Ding, Yanping Liu, Qianqian Chen, Shuping Ren, Yan Mou","doi":"10.1177/07482337241300722","DOIUrl":"10.1177/07482337241300722","url":null,"abstract":"Perfluorooctane sulfonate (PFOS) is a synthetic persistent organic compound that is widely used in industrial products. Studies have shown that PFOS can accumulate in environment and pose a threat to human health. As the kidney is the main excretory organ for PFOS, it is important to study PFOS damage to the kidney to investigate its toxicity. Human proximal tubular epithelial cells (HK-2) were treated with 200 μM PFOS or 1 μM Fer-1. Cell viability, the levels of MDA, GSH, intracellular iron ion, and GPX-4 were determined. The expression of KIM-1 and endoplasmic reticulum stress (ERS) related proteins were determined. The expression levels of KIM-1, a marker of renal tubular injury, and ERS-related proteins, GRP78, ATF6, IRE1, and PERK, were significantly increased in HK-2 cells exposed to PFOS. The levels of MDA and intracellular total iron ion also were significantly increased in HK-2 cells exposed to PFOS and the levels of GSH and GPX-4 were significantly decreased. PFOS can damage HK-2 cells through ferroptosis and endoplasmic reticulum stress, which provides a theoretical foundation for exploring the toxicity of PFOS to the kidney.","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"73-82"},"PeriodicalIF":1.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142668049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Wnt5a promotes Kupffer cell activation in trichloroethylene-induced immune liver injury. 在三氯乙烯诱导的免疫性肝损伤中，Wnt5a促进了Kupffer细胞的活化。

IF 1.7 4区医学

Toxicology and Industrial Health Pub Date : 2025-02-01 Epub Date: 2024-11-26 DOI: 10.1177/07482337241300953

Lei Gao, Ya-Ni Ding, Peng-Cheng Zhou, Luo-Lun Dong, Xin-Yu Peng, Yi-Ru Tang, Qi-Xing Zhu, Jia-Xiang Zhang

{"title":"Wnt5a promotes Kupffer cell activation in trichloroethylene-induced immune liver injury.","authors":"Lei Gao, Ya-Ni Ding, Peng-Cheng Zhou, Luo-Lun Dong, Xin-Yu Peng, Yi-Ru Tang, Qi-Xing Zhu, Jia-Xiang Zhang","doi":"10.1177/07482337241300953","DOIUrl":"10.1177/07482337241300953","url":null,"abstract":"Trichloroethylene (TCE) is a volatile, colorless liquid that is widely used as a chlorinated organic vehicle in industrial production and processing industries. Many workers exposed to trichloroethylene may develop trichloroethylene hypersensitivity syndrome (THS). However, the underlying mechanism of THS is still unclear, especially liver injury. The present study aimed to investigate whether Wnt5a/c-Jun N-terminal kinase (JNK) is involved in and regulates liver injury caused by TCE exposure and to provide new directions for the prevention and treatment in clinical settings of liver injury caused by TCE exposure. We used 6- to 8-week-old SPF-grade BALB/c female mice to establish a TCE sensitization model and explored the mechanism through inhibitor intervention. We found that the expression of Wnt5a/JNK was significantly elevated in the liver of TCE sensitization-positive mice. Inhibitors of Wnt Production 2 (IWP-2) are known antagonists of the Wnt pathway. TCE-sensitization mice treated with IWP-2 showed downregulated Wnt5a/JNK expression, reduced Kupffer cell activation, and decreased liver injury. At the same time, we found that phosphorylated JNK in TCE-sensitization mouse livers and extracted Kupffer cells showed a significant downward trend after inhibition of Wnt5a function. We also found that a specific JNK inhibitor, SP600125, decreased the secretion of cytokines and chemokines and decreased Kupffer cell activation. We demonstrated that Wnt5a/JNK was involved in the regulation of liver injury in TCE-sensitization mice and that it exacerbated liver injury by activating Kupffer cells and releasing chemokines. We therefore hypothesized that Kupffer cell activation was affected by JNK, which reduced chemokine and cytokine secretion and attenuated liver injury in TCE-sensitization mice.","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"83-96"},"PeriodicalIF":1.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142717161","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Metabolomics reveals that phosphatidylethanolamine can alleviate the toxicity of silica nanoparticles in human lung A549 cells. 代谢组学研究表明，磷脂酰乙醇胺可减轻二氧化硅纳米颗粒对人肺A549细胞的毒性。

IF 1.7 4区医学

Toxicology and Industrial Health Pub Date : 2025-02-01 Epub Date: 2024-11-29 DOI: 10.1177/07482337241304166

Shuang Chen, Chengzhi Liu, Yifan Yang, Jiangliang Chu, Beilei Yuan, Zhe Wang

{"title":"Metabolomics reveals that phosphatidylethanolamine can alleviate the toxicity of silica nanoparticles in human lung A549 cells.","authors":"Shuang Chen, Chengzhi Liu, Yifan Yang, Jiangliang Chu, Beilei Yuan, Zhe Wang","doi":"10.1177/07482337241304166","DOIUrl":"10.1177/07482337241304166","url":null,"abstract":"Silica nanoparticles (SiNPs) are widely utilized in occupational settings where they can cause lung damage through inhalation. The objective of this research was to explore the metabolic markers of SiNPs-induced toxicity on A549 cells by metabolomics and provide a foundation for studying nanoparticle-induced lung toxicity. Metabolomics analysis was employed to analyze the metabolites of SiNPs-treated A549 cells. LASSO regression was applied for selection, and protective measure experiments were conducted to validate the efficacy of selected potential toxicity mitigators. After SiNPs treatment, 23 differential metabolites were identified, including lipids, nucleotides, and organic oxidants. Pathway analysis revealed involvement in various biological processes. LASSO regression further identified six metabolites significantly associated with SiNPs toxicity. Notably, phosphatidylethanolamine (PE (14:1(9Z)/14:0)) showed enrichment in six significant metabolic pathways and with an AUC of 1 in the ROC curve. Protective measure experiments verified its protective effect on A549 cells and demonstrated its considerable inhibition of SiNPs-induced cytotoxicity. This study elucidated SiNPs-induced cytotoxicity on A549 cells and identified PE as a potential toxicity mitigator. These findings contribute to understanding the mechanisms of nanoparticle-induced lung toxicity and inform occupational health preventive strategies.","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"97-107"},"PeriodicalIF":1.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755636","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Transcriptome analysis reveals the molecular mechanisms of neonicotinoid acetamiprid in Leydig cells. 转录组分析揭示了新烟碱啶虫脒在睾丸细胞中的分子机制。

IF 1.7 4区医学

Toxicology and Industrial Health Pub Date : 2025-02-01 Epub Date: 2024-11-11 DOI: 10.1177/07482337241300215

Xun Liu, Ce Wang, Yue Ma, Linxiang Fu, Wanji Luo, Changjie Xu, Ying Tian, Mingyue Ma, Yaping Mao

{"title":"Transcriptome analysis reveals the molecular mechanisms of neonicotinoid acetamiprid in Leydig cells.","authors":"Xun Liu, Ce Wang, Yue Ma, Linxiang Fu, Wanji Luo, Changjie Xu, Ying Tian, Mingyue Ma, Yaping Mao","doi":"10.1177/07482337241300215","DOIUrl":"10.1177/07482337241300215","url":null,"abstract":"At present, the reproductive toxicology of neonicotinoids has received greater attention, however, its potential mechanisms are still not fully understood. Acetamiprid (ACE) is a new-generation neonicotinoid and has become a ubiquitous contaminant in the environment. This study aimed to investigate the toxic effects of ACE in TM3 Leydig cells based on transcriptome analysis. The viability and apoptosis of TM3 cells exposed to different concentrations of ACE were assessed by CCK8 and flow cytometry, respectively. After ACE exposure, transcriptome analysis was performed to screen differential expression genes (DEGs), followed by qPCR verification. Results showed that ACE exposure resulted in a time- and dose-dependent decrease in the viability of TM3 cells (p < .05). ACE also exerted a dose-dependent pro-apoptotic effect on TM3 cells. Results of RNA-seq showed that 1477 DEGs were obtained, of which 539 DEGs were up-regulated and 938 DEGs were down-regulated. GO and KEGG analyses of DEGs showed that DNA replication and cell cycle might be the key mechanisms for the cytotoxicity of ACE. qPCR results demonstrated that Mdm2, Cdkn1a (p21) and Gadd45 were significantly increased, and Pcna, Ccna2 (CycA), Ccnb1 (CycB), Ccne1 (CycE), and Cdk1 were significantly decreased, indicating that ACE exposure might promote G1/S and G2/M cell cycle arrest. Additionally, FoxO, p53, and HIF-1 signaling pathways and ferroptosis might play important roles in ACE-induced reproductive toxicity. Collectively, this study provides new perspectives into the mechanism of ACE-induced reproductive toxicity and lays a theoretical foundation for the in-depth study of non-target toxicity mechanisms of neonicotinoid insecticides.","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"61-72"},"PeriodicalIF":1.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142628737","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

DEHP impairs the oxidative stress response and disrupts trace element and mineral metabolism within the mitochondria of detoxification organs. DEHP 会损害氧化应激反应，破坏解毒器官线粒体内微量元素和矿物质的新陈代谢。

IF 1.7 4区医学

Toxicology and Industrial Health Pub Date : 2025-02-01 Epub Date: 2024-12-09 DOI: 10.1177/07482337241306252

Duygu Aydemir, Gozde Karabulut, Nurhayat Barlas, Nuriye Nuray Ulusu

{"title":"DEHP impairs the oxidative stress response and disrupts trace element and mineral metabolism within the mitochondria of detoxification organs.","authors":"Duygu Aydemir, Gozde Karabulut, Nurhayat Barlas, Nuriye Nuray Ulusu","doi":"10.1177/07482337241306252","DOIUrl":"10.1177/07482337241306252","url":null,"abstract":"Di(2-ethylhexyl) phthalate (DEHP), a widely utilized plasticizer in various consumer products, is classified as an endocrine disruptor and has been implicated in numerous adverse health effects, including oxidative stress, inflammation, and metabolic disturbances. Despite the growing body of literature addressing the systemic effects of DEHP, the specific influence of DEHP-induced oxidative stress on mitochondrial function within detoxification organs, particularly the liver and kidneys, remains largely unexplored. This study evaluated the effects of DEHP exposure (0, 100, 200, and 400 mg/kg/day) on mitochondrial oxidative stress, trace elements, and mineral metabolism associated with signaling pathways in the liver and kidneys of rats. Altered mitochondrial oxidative stress status was indicated by impaired glucose 6-phosphate dehydrogenase (G6PD), 6-phosphoglucerate dehydrogenase (6-PGD), glutathione reductase (GR), glutathione s-transferase (GST), and glutathione peroxidase (GPx) activities, along with significant disruptions in essential minerals and trace elements, including Na, Mg, Cu, Zn, and Fe. Key oxidative stress signaling pathways, such as NF-κB, Akt, STAT3, and CREB, glucose, and tissue homeostasis, displayed dose-dependent responses to DEHP, indicating complex regulatory mechanisms. This study represents the first comprehensive investigation into DEHP-induced mitochondrial dysfunction, highlighting its effects on oxidative stress metabolism, trace element homeostasis, and cellular signaling pathways in detoxification organs. These findings provide novel insights into the mitochondrial mechanisms underlying DEHP toxicity and underscores the need for further research into the implications of plasticizer exposure on human health.","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"108-121"},"PeriodicalIF":1.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142802157","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Methyltrimethoxysilane (MTMS).

IF 1.7 4区医学

Toxicology and Industrial Health Pub Date : 2025-01-30 DOI: 10.1177/07482337241301523

{"title":"Methyltrimethoxysilane (MTMS).","authors":"","doi":"10.1177/07482337241301523","DOIUrl":"https://doi.org/10.1177/07482337241301523","url":null,"abstract":"Methyltrimethoxysilane (MTMS) has been used as a coupling agent in thermoplastics and thermosetting resins, a cross-linker in silicone sealants, a water repellent component, and in silicone hard-coats for plastics. Acute studies in experimental animals showed a low order of toxicity for MTMS via oral, dermal, and inhalation routes. MTMS was slightly irritating to both eyes and skin in rabbits. A weight of evidence assessment supports that MTMS is not a dermal sensitizer. Available in vitro and in vivo assays indicated MTMS has a low potential for genotoxicity. MTMS did not produce any changes in either reproductive or developmental parameters. Short-term, repeated inhalation in rats produced treatment-related observations in the urinary bladder and kidney. In a 90-day inhalation study in rats, MTMS was associated with production of urinary bladder epithelial hyperplasia, calculi formation, and moderate kidney dilation with hyperplasia of the pelvic epithelium and granulomatous inflammation. However, an expert panel review concluded that changes in the bladder and kidney were adaptive responses to physical or chemical irritation. The NOAEL of 100 ppm (557 mg/m3) from the 90-day inhalation study was considered the point of departure for the health-based WEEL derivation. After adjusting to account for duration of exposure and interindividual variability, the resulting 8-h TWA WEEL value of 10 ppm (55 mg/m3) is fully expected to provide a significant margin of safety against potential adverse health effects in workers.","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"7482337241301523"},"PeriodicalIF":1.7,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143068205","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Prepubertal phthalate exposure can cause histopathological alterations, DNA methylation and histone acetylation changes in rat brain.

IF 1.7 4区医学

Toxicology and Industrial Health Pub Date : 2025-01-28 DOI: 10.1177/07482337251315212

Seyda Koc, Ekin Erdogmus, Ozlem Bozdemir, Deniz Ozkan-Vardar, Unzile Yaman, Pınar Erkekoglu, Naciye Dilara Zeybek, Belma Kocer-Gumusel

{"title":"Prepubertal phthalate exposure can cause histopathological alterations, DNA methylation and histone acetylation changes in rat brain.","authors":"Seyda Koc, Ekin Erdogmus, Ozlem Bozdemir, Deniz Ozkan-Vardar, Unzile Yaman, Pınar Erkekoglu, Naciye Dilara Zeybek, Belma Kocer-Gumusel","doi":"10.1177/07482337251315212","DOIUrl":"https://doi.org/10.1177/07482337251315212","url":null,"abstract":"Di-2-(ethylhexyl)phthalate (DEHP) is a phthalate derivative used extensively in a wide range of materials, such as medical devices, toys, cosmetics, and personal care products. Many mechanisms, including epigenetics, may be involved in the effects of phthalates on brain development. In this study, Sprague-Dawley male rats were obtained 21-23 days after their birth (post-weaning) and were exposed to DEHP during the prepubertal period with low-dose DEHP (DEHP-L, 30 mg/kg/day) and high-dose DEHP (DEHP-H, 60 mg/kg/day, 37 days) until the end of adolescence (PND 60). The rats in the study groups were sacrificed during adulthood, and histopathological changes, epigenetic changes, and oxidative stress parameters were evaluated in brain tissues. Histopathological findings indicating the presence of deterioration in brain tissue morphology were obtained, more prominently in the DEHP-H group. Examining the hippocampus under the light microscope, pyramidal neuron loss was detected only in CA1 of the DEHP-L group, while in DEHP-H rats, pyramidal neuron losses were detected in the CA1, CA2, and CA3 regions. No significant change was observed in brain lipid peroxidation levels with DEHP compared to control. Significant increases in total glutathione (GSH) in both dose groups were considered to be an adaptive response to DEHP-induced oxidative stress. The decrease in DNA methylation in the brain, although not statistically significant, and the increase in histone modification showed that exposure to DEHP may cause epigenetic changes in the brain and these epigenetic changes may also take place as one of the mechanisms underlying the damage observed in the brain. The results suggest that DEHP exposure during early development may have a significant effect on brain development.","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"7482337251315212"},"PeriodicalIF":1.7,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143053773","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Relationship of perfluoroalkyl chemicals with chronic obstructive pulmonary disease: A cross-sectional study.

IF 1.7 4区医学

Toxicology and Industrial Health Pub Date : 2025-01-24 DOI: 10.1177/07482337251315216

Xuefang Li, Zhijun Li, Jian Ye, Wu Ye

{"title":"Relationship of perfluoroalkyl chemicals with chronic obstructive pulmonary disease: A cross-sectional study.","authors":"Xuefang Li, Zhijun Li, Jian Ye, Wu Ye","doi":"10.1177/07482337251315216","DOIUrl":"https://doi.org/10.1177/07482337251315216","url":null,"abstract":"Perfluoroalkyl chemicals are one of the most stable substances in industry and have become ubiquitous contaminants owing to their persistence in the environment. This study enrolled 1,953 participants aged ≥40 years old using data from the National Health and Nutrition Examination Survey (NHANES). We selected four perfluoroalkyl chemicals with a detection frequency of more than 80%, including perfluorohexane sulfonic acid (PFHxS), perfluorononanoic acid (PFNA), perfluorooctanoic acid (PFOA), and perfluorooctane sulfonic acid (PFOS). Multivariate logistic regression was performed to determine the relationship of serum perfluoroalkyl chemicals with COPD and airflow limitation. We evaluated the interaction between perfluoroalkyl chemicals and lung function using multivariate linear regression analyses. Our results showed that the prevalence of COPD was not significantly related to serum PFHxS, PFNA, PFOA, and PFOS. Airflow limitation was positively linked with serum PFHxS, PFOA, and PFOS. However, these significant differences were not robust after adjustment of all confounders of interest. Serum PFHxS, PFOA, and PFOS were all positively related to the forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), and peak expiratory flow (PEF). However, only PFOA remained significantly linked with the FEV1 and FVC after covariate adjustment. These results indicated that there was no significant interaction between exposure to perfluoroalkyl chemicals and the prevalence of COPD. Higher levels of serum PFOA appeared to be related to higher measures of FEV1 and FVC.","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"7482337251315216"},"PeriodicalIF":1.7,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143034268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

(E)-1,1,1,2,2,5,5,6,6,6-Decafluoro-3-hexene (HFO-153-10mczz-E). (E) 1, 1, 1、2、2、5、5、6、6、6-Decafluoro-3-hexene(高频振荡器- 153 - 10 - mczz - E)。

IF 1.7 4区医学

Toxicology and Industrial Health Pub Date : 2025-01-09 DOI: 10.1177/07482337241290870

{"title":"(E)-1,1,1,2,2,5,5,6,6,6-Decafluoro-3-hexene (HFO-153-10mczz-E).","authors":"","doi":"10.1177/07482337241290870","DOIUrl":"https://doi.org/10.1177/07482337241290870","url":null,"abstract":"(E)-1,1,1,2,2,5,5,6,6,6-Decafluoro-3-hexene (HFO-153-10mczz-E) (CASRN 1256353-26-0) is a volatile liquid proposed for use as a new low global-warming potential dielectric fluid in cooling applications. Workplace exposures are expected to be by inhalation exposure. The substance has low acute inhalation toxicity as indicated by a 4-h inhalation LC50 value of approximately 8000 ppm. A suite of in vitro assays was negative for skin and eye irritation as well as for skin sensitization potential. The chemical did not induce cardiac sensitization up to 5000 ppm. Repeated inhalation exposure in rats for 4 or 13 weeks did not produce any effects attributable to the substance at 3000 ppm, the maximum tested concentration. No indications of developmental or reproductive toxicity were observed in studies in rats, also conducted with a maximum concentration of 3000 ppm. There was no indication of genotoxicity in the Ames assay, an assay with human TK cells, chromosome aberration in cultured human lymphocytes, or an in vivo rat micronucleus assay. The critical study for the development of the 8-hour TWA WEEL is the 13-week inhalation toxicity study with a NOAEC of 3000 ppm (32,400) mg/m3). This inhalation NOAEC was adjusted by application of appropriate uncertainty factors to account for interindividual variability, subchronic to chronic exposure extrapolation and other sources of uncertainty. A WEEL value of 200 ppm (2160 mg/m3) is expected to provide an acceptable margin of safety for potential adverse health effects in workers.","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"7482337241290870"},"PeriodicalIF":1.7,"publicationDate":"2025-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142955611","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0