Pub Date : 2025-12-01Epub Date: 2025-11-17DOI: 10.1177/07482337251387921
Yasemin Aydin, Hatice Kurtel, Emine Cakir, Banu Orta Yilmaz
Chlorpyrifos (CPF) is an insecticide that humans are exposed to when used for agricultural and domestic purposes. Many studies have shown that CPF has adverse effects on human health and causes toxicity in various cells and tissues. Since there are few studies in the literature examining the effects of CPF on the male reproductive system, Sertoli cells, which are crucial to the continuation of spermatogenesis, were chosen as a model in our study. The objective of this study was to investigate the cytotoxic, oxidative stress-related, apoptotic, and genotoxic effects of chlorpyrifos in TM4 Sertoli cells. In this study, Sertoli cells were exposed to two concentrations of CPF (100 and 500 μM) for 24 h. The cytotoxic and genotoxic potential of CPF in Sertoli cells was evaluated by measuring metabolic activity, malondialdehyde content, antioxidant enzyme levels, apoptosis rates, and DNA damage. According to the findings, applied CPF concentrations increased oxidative stress and decreased antioxidant enzyme levels in Sertoli cells. The results indicated that cell viability and the nuclear division index decreased in a concentration-dependent manner, while apoptotic cells, the micronucleus, and comet formation increased. Consequently, the results suggest that DNA damage and apoptosis play a major role in the mechanisms underlying the cytotoxic effects of CPF in Sertoli cells, establishing CPF as a strong genotoxic agent.
{"title":"The insecticide chlorpyrifos leads to genotoxic effects by triggering oxidative stress and apoptosis in Sertoli cells.","authors":"Yasemin Aydin, Hatice Kurtel, Emine Cakir, Banu Orta Yilmaz","doi":"10.1177/07482337251387921","DOIUrl":"10.1177/07482337251387921","url":null,"abstract":"<p><p>Chlorpyrifos (CPF) is an insecticide that humans are exposed to when used for agricultural and domestic purposes. Many studies have shown that CPF has adverse effects on human health and causes toxicity in various cells and tissues. Since there are few studies in the literature examining the effects of CPF on the male reproductive system, Sertoli cells, which are crucial to the continuation of spermatogenesis, were chosen as a model in our study. The objective of this study was to investigate the cytotoxic, oxidative stress-related, apoptotic, and genotoxic effects of chlorpyrifos in TM4 Sertoli cells. In this study, Sertoli cells were exposed to two concentrations of CPF (100 and 500 μM) for 24 h. The cytotoxic and genotoxic potential of CPF in Sertoli cells was evaluated by measuring metabolic activity, malondialdehyde content, antioxidant enzyme levels, apoptosis rates, and DNA damage. According to the findings, applied CPF concentrations increased oxidative stress and decreased antioxidant enzyme levels in Sertoli cells. The results indicated that cell viability and the nuclear division index decreased in a concentration-dependent manner, while apoptotic cells, the micronucleus, and comet formation increased. Consequently, the results suggest that DNA damage and apoptosis play a major role in the mechanisms underlying the cytotoxic effects of CPF in Sertoli cells, establishing CPF as a strong genotoxic agent.</p>","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"550-562"},"PeriodicalIF":1.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145542682","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}
Workers involved in paint production or application are extensively exposed to various hazardous substances like organic solvents, lead-based pigments, adhesives, and residual plastic monomers. Therefore, workers in the paint industry are at high risk of suffering adverse health effects. Studies of the lymphocytes of paint workers have demonstrated that industrial paint induces DNA damage and cellular changes. The aim of the present study was to assess DNA damage in 54 paint workers from paint production and application areas and 54 age-gender matched control subjects using a non-invasive buccal micronucleus (MN) assay. Buccal MN frequencies were significantly increased in workers compared to controls. MN frequencies significantly increased among workers from paint production areas compared with workers from paint application areas. MN frequencies in long-term workers (>10 years) were found to be significantly higher than those of short-term workers (≤10 years), which indicates that the duration of exposure to paints causes cytogenetic damage. MN frequencies increased with increasing age, while smoking status and the use of protective masks had no additional effect on MN frequencies within groups. In conclusion, it appears that long-term exposure to complex chemical mixtures during paint production may increase DNA damage in the workers. Understanding the possible causes of occupational exposure-induced genotoxicity in paint industry workers is of great importance for the protection of public health. Monitoring variables related to genotoxic damage in the paint workers using non-invasive methods will facilitate and improve risk assessment in the paint production sector.
{"title":"Evaluation of DNA damage in long-term paint exposed workers by non-invasive buccal micronucleus assay.","authors":"İzem Bilinmiş, Senanur Durna, Sultan Pınar Çetintepe, Sevtap Aydin Dilsiz, Nurşen Başaran","doi":"10.1177/07482337251383382","DOIUrl":"10.1177/07482337251383382","url":null,"abstract":"<p><p>Workers involved in paint production or application are extensively exposed to various hazardous substances like organic solvents, lead-based pigments, adhesives, and residual plastic monomers. Therefore, workers in the paint industry are at high risk of suffering adverse health effects. Studies of the lymphocytes of paint workers have demonstrated that industrial paint induces DNA damage and cellular changes. The aim of the present study was to assess DNA damage in 54 paint workers from paint production and application areas and 54 age-gender matched control subjects using a non-invasive buccal micronucleus (MN) assay. Buccal MN frequencies were significantly increased in workers compared to controls. MN frequencies significantly increased among workers from paint production areas compared with workers from paint application areas. MN frequencies in long-term workers (>10 years) were found to be significantly higher than those of short-term workers (≤10 years), which indicates that the duration of exposure to paints causes cytogenetic damage. MN frequencies increased with increasing age, while smoking status and the use of protective masks had no additional effect on MN frequencies within groups. In conclusion, it appears that long-term exposure to complex chemical mixtures during paint production may increase DNA damage in the workers. Understanding the possible causes of occupational exposure-induced genotoxicity in paint industry workers is of great importance for the protection of public health. Monitoring variables related to genotoxic damage in the paint workers using non-invasive methods will facilitate and improve risk assessment in the paint production sector.</p>","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"473-486"},"PeriodicalIF":1.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145309405","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}
Air pollution caused by pesticide drift poses a significant environmental health risk. The lungs are directly targeted by airborne pesticide exposure via inhalation; however, their inhalation toxicological data are poorly understood. In the present study, we evaluated the combined toxicity and interactions of lambda-cyhalothrin and its binary mixtures with eight insecticides at a concentration ratio of 1:1 in the non-small-cell lung cancer A549 line cells. Cytotoxicity tests showed that the selected pesticide binary mixtures reduced cell viability in a concentration-dependent manner. The combination index (CI) model indicated that the mixtures of lambda-cyhalothrin with acetamiprid, thiamethoxam, or clothianidin exhibited antagonistic effects, while other combinations shifted from antagonism to synergy at a toxicity level of 40%-60%. A synergistic toxicity occurred between lambda-cyhalothrin and emamectin benzoate with CI values of 0.58-0.95, and the obtained benchmark dose limits (BMDLs) value of their binary mixture was greater than 1.5 times more toxic than that of these pesticides individually. Moreover, combined exposure to the binary mixtures produced greater amounts (1.30- to 2.93-fold increase) of reactive oxygen species, malondialdehyde, and lactate dehydrogenase compared with exposure to these pesticides individually. This result suggested that the synergistic cytotoxicity of lambda-cyhalothrin and emamectin benzoate may be driven by excessive oxidative stress. Our findings serve to better understand the complex toxic pesticide interactions that humans face in the environment.
{"title":"Combined toxicity of nine typical pesticides in binary mixtures on A549 cells.","authors":"Weizhang Qi, Tingting Meng, Shujie Wang, Chang Chen, Zhiyong Cao, Ke Fang, Yuying Liu, Yanhong Shi, Jinjing Xiao","doi":"10.1177/07482337251374930","DOIUrl":"10.1177/07482337251374930","url":null,"abstract":"<p><p>Air pollution caused by pesticide drift poses a significant environmental health risk. The lungs are directly targeted by airborne pesticide exposure via inhalation; however, their inhalation toxicological data are poorly understood. In the present study, we evaluated the combined toxicity and interactions of lambda-cyhalothrin and its binary mixtures with eight insecticides at a concentration ratio of 1:1 in the non-small-cell lung cancer A549 line cells. Cytotoxicity tests showed that the selected pesticide binary mixtures reduced cell viability in a concentration-dependent manner. The combination index (CI) model indicated that the mixtures of lambda-cyhalothrin with acetamiprid, thiamethoxam, or clothianidin exhibited antagonistic effects, while other combinations shifted from antagonism to synergy at a toxicity level of 40%-60%. A synergistic toxicity occurred between lambda-cyhalothrin and emamectin benzoate with CI values of 0.58-0.95, and the obtained benchmark dose limits (BMDLs) value of their binary mixture was greater than 1.5 times more toxic than that of these pesticides individually. Moreover, combined exposure to the binary mixtures produced greater amounts (1.30- to 2.93-fold increase) of reactive oxygen species, malondialdehyde, and lactate dehydrogenase compared with exposure to these pesticides individually. This result suggested that the synergistic cytotoxicity of lambda-cyhalothrin and emamectin benzoate may be driven by excessive oxidative stress. Our findings serve to better understand the complex toxic pesticide interactions that humans face in the environment.</p>","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"497-507"},"PeriodicalIF":1.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145006639","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}
This study aimed to investigate the effect of alpha-lipoic acid (ALA) on liver damage caused by extremely low-frequency magnetic fields (ELF-MFs) in rats. Thirty-two male rats were arbitrarily assigned into four groups: Group 1 (control group), Group 2 (ELF-MF exposure group), Group 3 (ELF-MF exposure + ALA administration), and Group 4 (sham group). Groups 2 and 3 were exposed to ELF-MF at 2 mT intensity emitted by two Helmholtz coils for 4 hours/day throughout 30 days. Group 3 received ALA intraperitoneally (100 mg/kg/day) 1 hour prior to each exposure for 30 days. Group 4 was placed inside the coils, but the generator was turned off. Histopathological analysis of the liver revealed statistically significant increases in hyperemia, inflammation, fibrosis, vacuolization, multiple nuclei, and biliary proliferation in Group 2 compared to all other groups. Immunohistochemical evaluation showed that Group 2 had statistically significantly higher TUNEL and caspase-3 levels than all other groups. ELF-MF-induced alterations, including hyperemia, inflammation, vacuolization, and multiple nuclei, were significantly reduced in Group 3 compared with Group 2. However, no significant difference was observed between Group 2 and Group 3 regarding bile duct proliferation or fibrosis. No pathological changes were observed in Groups 1 and 4. ALA administration effectively reduced some histopathological changes caused by ELF-MF, particularly hyperemia, inflammation, vacuolization, and multiple nuclei, but did not improve fibrosis or biliary proliferation. Additionally, it reduced TUNEL and caspase-3 expression. Our findings suggest that ALA exhibits anti-apoptotic and anti-inflammatory effects against ELF-MF-induced liver damage.
{"title":"The effect of alpha-lipoic acid on liver damage induced by extremely low-frequency electromagnetic fields in a rat model.","authors":"Nur Aydinbelge Dizdar, Aylin Akbulut, Gokhan Koca, Mikail Koray Demirel, Nihat Yumusak, Gaye Umurhan, Ayse Gulnihal Canseven Kursun, Meliha Korkmaz","doi":"10.1177/07482337251383412","DOIUrl":"10.1177/07482337251383412","url":null,"abstract":"<p><p>This study aimed to investigate the effect of alpha-lipoic acid (ALA) on liver damage caused by extremely low-frequency magnetic fields (ELF-MFs) in rats. Thirty-two male rats were arbitrarily assigned into four groups: Group 1 (control group), Group 2 (ELF-MF exposure group), Group 3 (ELF-MF exposure + ALA administration), and Group 4 (sham group). Groups 2 and 3 were exposed to ELF-MF at 2 mT intensity emitted by two Helmholtz coils for 4 hours/day throughout 30 days. Group 3 received ALA intraperitoneally (100 mg/kg/day) 1 hour prior to each exposure for 30 days. Group 4 was placed inside the coils, but the generator was turned off. Histopathological analysis of the liver revealed statistically significant increases in hyperemia, inflammation, fibrosis, vacuolization, multiple nuclei, and biliary proliferation in Group 2 compared to all other groups. Immunohistochemical evaluation showed that Group 2 had statistically significantly higher TUNEL and caspase-3 levels than all other groups. ELF-MF-induced alterations, including hyperemia, inflammation, vacuolization, and multiple nuclei, were significantly reduced in Group 3 compared with Group 2. However, no significant difference was observed between Group 2 and Group 3 regarding bile duct proliferation or fibrosis. No pathological changes were observed in Groups 1 and 4. ALA administration effectively reduced some histopathological changes caused by ELF-MF, particularly hyperemia, inflammation, vacuolization, and multiple nuclei, but did not improve fibrosis or biliary proliferation. Additionally, it reduced TUNEL and caspase-3 expression. Our findings suggest that ALA exhibits anti-apoptotic and anti-inflammatory effects against ELF-MF-induced liver damage.</p>","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"487-496"},"PeriodicalIF":1.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145193097","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}
Non-alcoholic fatty liver disease (NAFLD) is an escalating global health threat that has been linked to environmental pollutants such as the highly toxic dioxin-like congener 3,3',4,4',5-pentachlorobiphenyl (PCB 126). Although PCB 126 is known to impair hepatic function, the precise mechanisms-particularly the contribution of ferroptosis, an iron-dependent, lipid-peroxidation-mediated form of cell death-remain elusive. Here, we tested the hypothesis that ferroptosis underlies PCB 126-induced NAFLD and delineated the key molecular pathways involved. Balb/c mice were intraperitoneally injected with PCB 126 (1, 5, or 10 μM/kg) for 14 days. Hepatic injury was assessed through serum biomarkers (ALT, AST, ALP), histopathology (H&E and Oil Red O staining), and mitochondrial ultrastructure via transmission electron microscopy. Ferroptosis markers (GPX4, 4-HNE, Tf receptor), lipid peroxidation (MDA, GSH, SOD), iron homeostasis, and inflammatory cytokines (IL-1β, IL-6, TNF-α) were evaluated using qPCR, Western blotting, and ELISA. Results demonstrated that PCB 126 exposure induced NAFLD, evidenced by elevated liver-to-body weight ratios, serum liver enzymes, and steatosis. Ferroptosis was implicated through reduced mitochondrial cristae, suppressed GPX4 and SLC7A11 expression, increased lipid peroxidation, and iron accumulation. Additionally, PCB 126 activated the NF-κB pathway, elevating pro-inflammatory cytokines and myeloperoxidase (MPO) activity, while oxidative stress was marked by NRF2/KEAP1/HO-1 axis disruption. In conclusion, PCB 126 promotes NAFLD in mice by triggering ferroptosis, inflammation, and oxidative stress. These findings highlight ferroptosis as a pivotal mechanistic link in PCB 126-induced NAFLD, suggesting potential therapeutic targets for mitigating pollutant-driven liver injury.
{"title":"Oxidative stress and ferroptosis mediate 3,3',4,4',5-pentachlorobiphenyl-induced non-alcoholic fatty liver disease in mice.","authors":"Jingjing Wang, Yichun Chen, Hanpeng Wu, Yingrong Ye, Yifei Li, Ershun Zhou","doi":"10.1177/07482337251376455","DOIUrl":"10.1177/07482337251376455","url":null,"abstract":"<p><p>Non-alcoholic fatty liver disease (NAFLD) is an escalating global health threat that has been linked to environmental pollutants such as the highly toxic dioxin-like congener 3,3',4,4',5-pentachlorobiphenyl (PCB 126). Although PCB 126 is known to impair hepatic function, the precise mechanisms-particularly the contribution of ferroptosis, an iron-dependent, lipid-peroxidation-mediated form of cell death-remain elusive. Here, we tested the hypothesis that ferroptosis underlies PCB 126-induced NAFLD and delineated the key molecular pathways involved. Balb/c mice were intraperitoneally injected with PCB 126 (1, 5, or 10 μM/kg) for 14 days. Hepatic injury was assessed through serum biomarkers (ALT, AST, ALP), histopathology (H&E and Oil Red O staining), and mitochondrial ultrastructure via transmission electron microscopy. Ferroptosis markers (GPX4, 4-HNE, Tf receptor), lipid peroxidation (MDA, GSH, SOD), iron homeostasis, and inflammatory cytokines (IL-1β, IL-6, TNF-α) were evaluated using qPCR, Western blotting, and ELISA. Results demonstrated that PCB 126 exposure induced NAFLD, evidenced by elevated liver-to-body weight ratios, serum liver enzymes, and steatosis. Ferroptosis was implicated through reduced mitochondrial cristae, suppressed GPX4 and SLC7A11 expression, increased lipid peroxidation, and iron accumulation. Additionally, PCB 126 activated the NF-κB pathway, elevating pro-inflammatory cytokines and myeloperoxidase (MPO) activity, while oxidative stress was marked by NRF2/KEAP1/HO-1 axis disruption. In conclusion, PCB 126 promotes NAFLD in mice by triggering ferroptosis, inflammation, and oxidative stress. These findings highlight ferroptosis as a pivotal mechanistic link in PCB 126-induced NAFLD, suggesting potential therapeutic targets for mitigating pollutant-driven liver injury.</p>","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"508-521"},"PeriodicalIF":1.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145070545","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}
Pub Date : 2025-10-01Epub Date: 2025-10-20DOI: 10.1177/07482337251387406
{"title":"Retraction Notice: Toxicity of methomyl insecticides to testicular cells and protective effect of folic acid.","authors":"","doi":"10.1177/07482337251387406","DOIUrl":"10.1177/07482337251387406","url":null,"abstract":"","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"522"},"PeriodicalIF":1.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145337460","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}
Pub Date : 2025-08-01Epub Date: 2025-09-03DOI: 10.1177/07482337251371774
Meşide Gündüzöz, Murat Büyükşekerci, Osman Gökhan Özakıncı, Salim Neşelioğlu, Emine Yurt, Özcan Erel
The aim of this study was to investigate oxidative stress markers in patients with embedded fragments (PEF) using thiol-disulfide homeostasis and ischemia-modified albumin (IMA). The study consisted of a PEF group and a control group. Blood or urine metal concentrations were determined using inductively coupled plasma mass spectrometry (ICP-MS). Plasma thiol/disulfide homeostasis parameters and IMA levels were assessed. In PEF, the concentrations of all metals, including antimony (Sb), arsenic (As), copper (Cu), mercury (Hg), cadmium (Cd), lead (Pb), manganese (Mn), nickel serum (Ni), iron (Fe), cobalt (Co), and selenium (Se), were significantly higher than those in the control group, except chromium (Cr). 64.86% of PEF had elevated concentrations of at least one of these metals: Sb, As, Cu, Cd, Pb, Mn, Ni, and Fe, concerning reference values. It was also found that 64.86% (72/111) of PEF had elevated concentrations of metals, such as Sb, As, Cu, Cd, Pb, Mn, Ni, and Fe, in urine or blood, in accordance with the BEI values recommended by ACGIH and clinical laboratory reference values. The disulfide/native thiol, disulfide/total thiol, and total thiol/native thiol ratios were significantly higher in PEF. There was a strong positive correlation between Pb, Cd, and disulfide and a negative correlation between native thiol and Cd, Pb, and Co. Albumin levels were significantly lower, and IMA levels were significantly higher in the PEF group than in the control group. Metal abnormality was approximately 2.7 times higher in PEF who had retained fragments for longer than 20 years. The increased metal body burden resulting from the embedded fragments may pose significant systemic health effects by inducing oxidative stress. Continuous surveillance of patients with retained fragments is essential to combat chronic metal toxicity.
{"title":"Thiol/disulfide homeostasis and ischemia-modified albumin as oxidative stress markers in patients with embedded fragments.","authors":"Meşide Gündüzöz, Murat Büyükşekerci, Osman Gökhan Özakıncı, Salim Neşelioğlu, Emine Yurt, Özcan Erel","doi":"10.1177/07482337251371774","DOIUrl":"10.1177/07482337251371774","url":null,"abstract":"<p><p>The aim of this study was to investigate oxidative stress markers in patients with embedded fragments (PEF) using thiol-disulfide homeostasis and ischemia-modified albumin (IMA). The study consisted of a PEF group and a control group. Blood or urine metal concentrations were determined using inductively coupled plasma mass spectrometry (ICP-MS). Plasma thiol/disulfide homeostasis parameters and IMA levels were assessed. In PEF, the concentrations of all metals, including antimony (Sb), arsenic (As), copper (Cu), mercury (Hg), cadmium (Cd), lead (Pb), manganese (Mn), nickel serum (Ni), iron (Fe), cobalt (Co), and selenium (Se), were significantly higher than those in the control group, except chromium (Cr). 64.86% of PEF had elevated concentrations of at least one of these metals: Sb, As, Cu, Cd, Pb, Mn, Ni, and Fe, concerning reference values. It was also found that 64.86% (72/111) of PEF had elevated concentrations of metals, such as Sb, As, Cu, Cd, Pb, Mn, Ni, and Fe, in urine or blood, in accordance with the BEI values recommended by ACGIH and clinical laboratory reference values. The disulfide/native thiol, disulfide/total thiol, and total thiol/native thiol ratios were significantly higher in PEF. There was a strong positive correlation between Pb, Cd, and disulfide and a negative correlation between native thiol and Cd, Pb, and Co. Albumin levels were significantly lower, and IMA levels were significantly higher in the PEF group than in the control group. Metal abnormality was approximately 2.7 times higher in PEF who had retained fragments for longer than 20 years. The increased metal body burden resulting from the embedded fragments may pose significant systemic health effects by inducing oxidative stress. Continuous surveillance of patients with retained fragments is essential to combat chronic metal toxicity.</p>","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"429-442"},"PeriodicalIF":1.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144970445","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}
Pub Date : 2025-08-01Epub Date: 2025-09-04DOI: 10.1177/07482337251371763
Mine Caglayan
Neonicotinoid insecticides and triazole fungicides are widely used in agriculture, often in combination with other pesticides, leading to concerns about potential health effects. This study investigated the combined effect of these chemicals using the Comparative Toxicogenomics Database (CTD) to identify common target genes, followed by functional enrichment analysis and gene-gene and protein-protein interaction assessments. In this study, it was determined that pesticides may interfere with biological processes such as steroid hydroxylase activity, oxidoreductase activity, and steroid metabolism, and cause hormonal imbalances and endocrine system disorders. In addition, among the 10 genes identified, CYP3A5 and CYP3A7 gene expression differed significantly between prostate cancer and normal prostate tissues, and this was supported by UALCAN data. In addition, previous studies have confirmed that hsa-miR-27b, one of the prominent miRNAs in this study, and transcription factors (PROX1 and ESR2) are associated with prostate cancer. Similar to our study, previous studies have confirmed that triazole fungicides disrupt testosterone homeostasis and steroidogenesis, while neonicotinoids damage the prostate due to their effects on androgen receptors. These genes, miRNAs, and transcription factors appear to mediate the effects of these pesticides on cancer pathways and suggest a link to prostate cancer. In conclusion, this study demonstrated that concurrent exposure to neonicotinoid insecticides and triazole fungicides may damage the prostate and potentially contribute to the development of prostate neoplasia. These findings emphasise the importance of further invitro and invivo validation to establish a definitive causal relationship and provide insight into the toxicological effects of pesticide exposure on prostate health.
{"title":"The effect of neonicotinoid insecticides and triazole fungicides on prostate cancer progression via CYP enzymes, miRNAs, and TF-mediated disruption of steroidogenesis: An integrated <i>in silico</i> approach.","authors":"Mine Caglayan","doi":"10.1177/07482337251371763","DOIUrl":"10.1177/07482337251371763","url":null,"abstract":"<p><p>Neonicotinoid insecticides and triazole fungicides are widely used in agriculture, often in combination with other pesticides, leading to concerns about potential health effects. This study investigated the combined effect of these chemicals using the Comparative Toxicogenomics Database (CTD) to identify common target genes, followed by functional enrichment analysis and gene-gene and protein-protein interaction assessments. In this study, it was determined that pesticides may interfere with biological processes such as steroid hydroxylase activity, oxidoreductase activity, and steroid metabolism, and cause hormonal imbalances and endocrine system disorders. In addition, among the 10 genes identified, <i>CYP3A5</i> and <i>CYP3A7</i> gene expression differed significantly between prostate cancer and normal prostate tissues, and this was supported by UALCAN data. In addition, previous studies have confirmed that hsa-miR-27b, one of the prominent miRNAs in this study, and transcription factors (PROX1 and ESR2) are associated with prostate cancer. Similar to our study, previous studies have confirmed that triazole fungicides disrupt testosterone homeostasis and steroidogenesis, while neonicotinoids damage the prostate due to their effects on androgen receptors. These genes, miRNAs, and transcription factors appear to mediate the effects of these pesticides on cancer pathways and suggest a link to prostate cancer. In conclusion, this study demonstrated that concurrent exposure to neonicotinoid insecticides and triazole fungicides may damage the prostate and potentially contribute to the development of prostate neoplasia. These findings emphasise the importance of further <i>in</i> <i>vitro</i> and <i>in</i> <i>vivo</i> validation to establish a definitive causal relationship and provide insight into the toxicological effects of pesticide exposure on prostate health.</p>","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"415-428"},"PeriodicalIF":1.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144993310","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}
Pub Date : 2025-08-01Epub Date: 2025-07-27DOI: 10.1177/07482337251362359
Daniel Omeodisemi Omokpariola, Anu Adekunle Daramola
The fertilizer manufacturing industry in Nigeria plays a crucial role in supporting the nation's agricultural sector and, by extension, its economy. However, the industry faces significant challenges regarding occupational safety and health, leading to high-risk factors and common workplace hazards such as chemical exposure, physical injuries, and psychosocial stressors. This paper aims to explore the current practices in workplace safety, identify existing challenges, and highlight opportunities for improvement within the sector. By examining regulatory frameworks, industry practices, and technological advancements, the study offers insights into enhancing safety protocols and fostering a culture of health and safety. Recommendations for stakeholders, including policymakers, industry leaders, and workers, emphasize the need for collaborative efforts and the adoption of global best practices to create a safer working environment. The findings underscore the importance of a comprehensive approach to workplace safety, which is essential for ensuring the well-being of employees and the sustainability of the fertilizer manufacturing industry in Nigeria.
{"title":"Challenges and opportunities in enhancing workplace safety and health for Nigeria's fertilizer manufacturing industry: A discussion on current practices and future directions.","authors":"Daniel Omeodisemi Omokpariola, Anu Adekunle Daramola","doi":"10.1177/07482337251362359","DOIUrl":"10.1177/07482337251362359","url":null,"abstract":"<p><p>The fertilizer manufacturing industry in Nigeria plays a crucial role in supporting the nation's agricultural sector and, by extension, its economy. However, the industry faces significant challenges regarding occupational safety and health, leading to high-risk factors and common workplace hazards such as chemical exposure, physical injuries, and psychosocial stressors. This paper aims to explore the current practices in workplace safety, identify existing challenges, and highlight opportunities for improvement within the sector. By examining regulatory frameworks, industry practices, and technological advancements, the study offers insights into enhancing safety protocols and fostering a culture of health and safety. Recommendations for stakeholders, including policymakers, industry leaders, and workers, emphasize the need for collaborative efforts and the adoption of global best practices to create a safer working environment. The findings underscore the importance of a comprehensive approach to workplace safety, which is essential for ensuring the well-being of employees and the sustainability of the fertilizer manufacturing industry in Nigeria.</p>","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"459-472"},"PeriodicalIF":1.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144733434","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}
Pub Date : 2025-08-01Epub Date: 2025-07-27DOI: 10.1177/07482337251359341
Patrick M Plehiers, Billy W Day, Mark W Spence
The 2015-2016 National Health and Nutrition Examination Survey (NHANES) included biomonitoring of aromatic diamines obtained after acid hydrolysis of urine samples for the first time. Aromatic diamines in hydrolyzed urine are biomarkers that are not unique to a single substance. Without further information, that renders association with potential exposures very difficult. This review provides an overview of potential sources of urinary aromatic diamines, the most important being aromatic diisocyanates (occupational and home-use), aromatic diamines themselves (predominantly from hair dye products), and polyurethanes (medical devices and implants). Expected urinary diamine concentrations from these and other sources as well as background levels are evaluated based on available literature data. Finally, recommendations are made to improve the value of future data collections. These include analytical enhancements, better mapping of potential sources of the biomarkers prior to conducting the survey, and documentation of product use to enable identification of exposure sources. These improvements are indispensable for investigating potential links with medical conditions should this be envisioned.
{"title":"The NHANES 2015-2016 aromatic diamine urinary biomonitoring data: A critical review and suggestions for improved data collection.","authors":"Patrick M Plehiers, Billy W Day, Mark W Spence","doi":"10.1177/07482337251359341","DOIUrl":"10.1177/07482337251359341","url":null,"abstract":"<p><p>The 2015-2016 National Health and Nutrition Examination Survey (NHANES) included biomonitoring of aromatic diamines obtained after acid hydrolysis of urine samples for the first time. Aromatic diamines in hydrolyzed urine are biomarkers that are not unique to a single substance. Without further information, that renders association with potential exposures very difficult. This review provides an overview of potential sources of urinary aromatic diamines, the most important being aromatic diisocyanates (occupational and home-use), aromatic diamines themselves (predominantly from hair dye products), and polyurethanes (medical devices and implants). Expected urinary diamine concentrations from these and other sources as well as background levels are evaluated based on available literature data. Finally, recommendations are made to improve the value of future data collections. These include analytical enhancements, better mapping of potential sources of the biomarkers prior to conducting the survey, and documentation of product use to enable identification of exposure sources. These improvements are indispensable for investigating potential links with medical conditions should this be envisioned.</p>","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"443-458"},"PeriodicalIF":1.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144733435","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}