Toxicology最新文献

{"title":"Prediction of polybrominated diphenyl ethers (PBDEs) as potential substrates of various human CYP enzymes and laboratory test of BDE-99 for its metabolism-activated mutagenicity","authors":"Lin Wang ,&nbsp;Nyame Mustapha Murtala ,&nbsp;Keqi Hu ,&nbsp;Yijing Chen ,&nbsp;Manxin Chen ,&nbsp;Haiting Sun ,&nbsp;Yungang Liu","doi":"10.1016/j.tox.2024.153992","DOIUrl":"10.1016/j.tox.2024.153992","url":null,"abstract":"<div><div>Polybrominated diphenyl ethers (PBDEs) are persistent organic pollutants, of which BDE-47 could be activated by human cytochrome P450s (CYPs) for chromosome-damaging effects. However, the metabolic activation and mutagenicity of other PBDEs remain unknown. In this study, 14 representative PBDEs were analyzed by molecular docking as potential substrates for several human CYPs. The results showed negative free energies for each pair of binding, however, different CYPs demonstrated largely varied frequencies of binding conformations favoring a substrate potential: CYP2E1, 3A4, and 2B6 being suitable for all/most compounds. Using BDE-99 (5 ∼ 40 μM) as a model compound (exposing for 2 cell cycles), it did not induce micronucleus in a human hepatoma HepG2 cell line, however, positive result was observed in C3A cells (derived from HepG2 but with enhanced expression of CYPs). Pretreatment of HepG2 cells with each of bisphenol A (1 μM, inducer of CYPs) and CITCO (10 μM, inducer of CYP2B6) led to micronucleus formation by BDE-99, while the effect of BDE-99 in C3A cells was abolished by 1-aminobenzotriazole (60 μM, inhibitor of CYPs). In a V79-derived cell line genetically engineered for expressing human CYP2B6 BDE-99 induced micronucleus, while it was negative in V79-Mz and its derivatives expressing several other human CYPs. The micronuclei formed in HepG2 cells pretreated with BPA and CITCO were free of centromere protein B immunofluorescence staining. Finally, BDE-99 weakly induced PIG-A gene mutations in C3A, while negative in HepG2 cells. In conclusion, our study suggest that BDE-99 may be activated by human CYP2B6 for chromosome-breaking effects.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"509 ","pages":"Article 153992"},"PeriodicalIF":4.8,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142628712","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of the ROS/NLRP3/caspase-1 pathway in NiSO4-induced cellular pyroptosis and apoptosis in H9c2 cells","authors":"Xinrui Zhao ,&nbsp;Yuxian Yun ,&nbsp;Danni Zhou ,&nbsp;Yuanyuan Ma ,&nbsp;Xianfeng Luo ,&nbsp;Benzhong Zhang","doi":"10.1016/j.tox.2024.153989","DOIUrl":"10.1016/j.tox.2024.153989","url":null,"abstract":"<div><div>According to comprehensive research, the cardiovascular system is damaged by nickel exposure. The present study selected rat cardiomyocytes (H9c2 cells) and subjected them to varying doses of sodium nickel sulfate (NiSO₄) for 24 hours to better understand the mechanism of cardiovascular damage caused by NiSO₄ exposure. The relevant indicators were detected employing biochemical analysis, real-time quantitative polymerase chain reaction (RT-qPCR), and western blot, and flow cytometry was used to detect the cell apoptosis rate. The study revealed that the survival rate of H9c2 cells fell significantly when the concentration of NiSO₄ exposure rose. Moreover, it caused oxidative stress in H9c2 cells by raising the expression of reactive oxygen species and the concentration of LDH in the cell supernatants. After NiSO₄ exposure, the levels of ASC, NLRP3, gasdermin D, and caspase-1 in H9c2 cells increased, suggesting that H9c2 cells underwent pyroptosis induced by NiSO₄. In addition, NiSO₄ exposure also led to inflammation, with increased levels of interleukin [IL]-18, IL-1β. After adding the antioxidant N-Acetyl-L-cysteine (NAC), the level of ROS indicated that the oxidative stress level in H9c2 cells was reduced, western blot inhibited inflammation, the level of pyroptosis was reduced, and the activity of the NLRP3/caspase1 signaling pathway was reduced. To examine the connection between pyroptosis and apoptosis, the cells were treated with the caspase1 inhibitor Z-YVAD-Fluoromethyl Ketone (Z-YVAD-FMK, YVAD), which resulted in a significant decrease in the rate of cell apoptosis as well as a reduction in the activity of the related protein in the signaling pathway, which in turn decreased the level of pyroptosis. NiSO₄ could induce pyroptosis in H9c2 cells through the ROS/NLRP3/caspase-1 axis. Furthermore, NiSO₄-induced apoptosis and pyroptosis were found to be reduced by the addition of the caspase-1 inhibitor.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"509 ","pages":"Article 153989"},"PeriodicalIF":4.8,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142628733","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigation of a broad diversity of nanoparticles, including their processes, as well as toxicity testing in diverse organs and systems","authors":"Azhar U. Khan ,&nbsp;Mohammad Qutob ,&nbsp;Amel Gacem ,&nbsp;Mohd. Rafatullah ,&nbsp;Krishna Kumar Yadav ,&nbsp;Pankaj Kumar ,&nbsp;Javed Khan Bhutto ,&nbsp;Meenal Rehman ,&nbsp;Sudhakar Bansoid ,&nbsp;Lienda Bashier Eltayeb ,&nbsp;Nazia Malik ,&nbsp;Mohammed Azam Ali ,&nbsp;Maha Awjan Alreshidi ,&nbsp;Mir Waqas Alam","doi":"10.1016/j.tox.2024.153985","DOIUrl":"10.1016/j.tox.2024.153985","url":null,"abstract":"<div><div>Nanotechnology arising in wide-ranging areas, covers extensively different ranges of approaches attained from fields such as biology, chemistry, physics, and medicine engineering. Nanoparticles are a necessary part of nanotechnology effectually applied in the cure of a number of diseases. Nanoparticles have gained significant importance due to their unique properties, which differ from their bulk counterparts. These distinct properties of nanoparticles are primarily influenced by their morphology, size, and size distribution. At the nanoscale, nanoparticles exhibit behaviours that can enhance therapeutic efficacy and reduce drug toxicity. Their small size and large surface area make them promising candidates for applications such as targeted drug delivery, where they can improve treatment outcomes while minimizing adverse effects. The harmful effects of nanoparticles on the environment were critically investigated to obtain appropriate results and reduce the risk by incorporating the materials. Nanoparticles tend to penetrate the human body, clear the biological barriers to reach sensitive organs and are easily incorporated into human tissue, as well as dispersing to the hepatic tissues, heart tissues, encephalum, and GI tract. This study aims to examine a wide variety of nanoparticles, focusing on their manufacturing methods, functional characteristics, and interactions within biological systems. Particular attention will be directed towards assessing the toxicity of nanoparticles in different organs and physiological systems, yielding a thorough comprehension of their potential health hazards and the processes that drive nanoparticle-induced toxicity. This analysis will also emphasize recent developments in nanoparticle applications and safety assessment methodologies.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"509 ","pages":"Article 153985"},"PeriodicalIF":4.8,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142605910","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exposure of RAW264.7 macrophages to exhaust emissions (gases and PAH) and non-exhaust emissions (tire particles) induces additive or synergistic TNF-α production depending on the tire particle size","authors":"Abderrahmane Bouredji ,&nbsp;Riadh Lakhmi ,&nbsp;Bogdan Muresan-Paslaru ,&nbsp;Jérémie Pourchez ,&nbsp;Valérie Forest","doi":"10.1016/j.tox.2024.153990","DOIUrl":"10.1016/j.tox.2024.153990","url":null,"abstract":"<div><div>Road traffic is a major contributor to air pollution and consequently negatively affects human health. Car pollution originates both from exhaust emissions (EE) and non-exhaust emissions (NEE, such as tire and brake wear particles, erosion of road surfaces and resuspension of road dust). While the toxicity of EE and NEE has been characterized separately, their combined effects are poorly documented. However, we are constantly exposed to a mixture of pollutants and their interactions should not be neglected as they may significantly impact their toxicological profile resulting in additive, synergistic or antagonistic effects. To fill this gap, we investigated <em>in vitro</em> the combined toxicity of exhaust gases and benzo[<em>a</em>]pyrene (representative of EE) and tire particles (representative of NEE). Macrophages from the RAW264.7 cell line were exposed for 24 h to tire particles (TP) of variable size (6–113 µm), alone or in combination with exhaust gases (CO₂, CO, NO, NO₂) and benzo[<em>a</em>]pyrene (B[<em>a</em>]P) as an archetype of polycyclic aromatic hydrocarbon (PAH). The cell response was assessed in terms of cytotoxicity, proinflammatory response and oxidative stress. TP, gases and B[<em>a</em>]P, alone or in combination triggered neither cytotoxicity nor oxidative stress. On the contrary, a proinflammatory response was elicited with two different profiles depending on the size of the TP: TNF-α production was either slightly (with the finest TP) or strongly (with coarse TP) increased in the presence of gases and B[<em>a</em>]P, suggesting that the effects of TP, gases and B[<em>a</em>]P were either additive or synergistic, depending on TP size.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"509 ","pages":"Article 153990"},"PeriodicalIF":4.8,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142591356","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Activation of α7 nicotinic acetylcholine receptor augments nerve growth factor action on PCtrk cells","authors":"T. Mutoh,&nbsp;Y. Niimi ,&nbsp;Akihiro Ueda","doi":"10.1016/j.tox.2024.153986","DOIUrl":"10.1016/j.tox.2024.153986","url":null,"abstract":"<div><div>Although cigarette smoking is known to be a critical risk factor for various organ systems and cancers, accumulating evidence indicates that nicotine – a main constituent of cigarette smoking – can exert neuroprotective effects on neuronal cells through nicotinic acetylcholine receptors (nAChRs). However, the precise molecular mechanisms for nicotinic neuroprotective actions remain to be fully elucidated. In this study, we examine the effects of agonists, such as nicotine and PNU282987, on tropomyosin-related kinase (Trk)-dependent neuroprotective pathways in PC12 cells overexpressing a Trk neurotrophin receptor (PCtrk cells). We found that even considerably higher concentrations (mM range for nicotine and µM range for PN282987) of nAChR agonists exert favorable effects, such as the augmentation of nerve growth factor (NGF)-induced Trk neurotrophin receptor autophosphorylation of tyrosine residues and NGF-induced neurite extension. Moreover, nicotine upregulated reactive oxygen species (ROS) levels in the cells. ROS production was completely cancelled by pretreatment with Mito-Tempo, a mitochondria-targeted antioxidant, indicating that the main source of ROS production by nicotine was mitochondria. Furthermore, treatment with nAChR agonists appeared to induce autophagic flux, as evidenced by the upregulation of LC3-II expression in cells. Furthermore, sucrose density ultracentrifugation of nicotine-treated cells clearly disclosed the augmented recruitment of α7nAChR protein into the lipid rafts fraction of the membrane. Intriguingly, a pull-down assay of anti-Trk antibody immunoprecipitates clearly included α7nAChR protein, indicating that Trk and α7nAChR proteins form a complex. These results reveal a new molecular interaction between activated α7nAChR and Trk protein that may serve as a new molecular basis of nicotine-induced neuroprotective action.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"509 ","pages":"Article 153986"},"PeriodicalIF":4.8,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142591290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aflatoxin B1-induced hepatotoxicity through mitochondrial dysfunction, oxidative stress, and inflammation as central pathological mechanisms: A review of experimental evidence","authors":"Tsholofelo P. Moloi,&nbsp;Khanyisani Ziqubu,&nbsp;Sithandiwe E. Mazibuko-Mbeje,&nbsp;Nonduduzo H. Mabaso,&nbsp;Zibele Ndlovu","doi":"10.1016/j.tox.2024.153983","DOIUrl":"10.1016/j.tox.2024.153983","url":null,"abstract":"<div><div>Aflatoxin B₁ (AFB₁) is a class of mycotoxin known to contaminate agricultural products, animal feed and animal food products, subsequently causing detrimental effects on human and animal health. AFB₁ is the most common and potent aflatoxin found in food and contributes significantly to liver injury as well as the development of hepatocellular carcinoma. Although the liver is a primary target organ for AFB₁ toxicity and biotransformation, underlying mechanisms implicated in liver injuries induced by these mycotoxins remain to be fully elucidated for therapeutic purposes. This review aims to dissect the complexities of the pathophysiological and molecular mechanisms implicated in hepatotoxicity induced by AFB₁, including mitochondrial dysfunction, oxidative stress and hepatic inflammation. Mechanistically, AFB₁ disrupt mitochondrial bioenergetics and membrane potential, promotes mitochondrial cholesterol trafficking and induces mitophagy. Moreover, mitochondrial dysfunction may lead to hepatic oxidative stress as a consequence of uncontrolled production of reactive oxygen species and defects in the antioxidant defense system. Retrieved experimental evidence also showed that AFB₁ may lead to hepatic inflammation through gut microbiota dysbiosis, the release of DAMPs and cytokines, and immune cell recruitment. Overall, these mechanisms could be utilized as potential targets to extrapolate treatment for liver injury caused by AFB₁.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"509 ","pages":"Article 153983"},"PeriodicalIF":4.8,"publicationDate":"2024-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142568169","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Amitraz mechanisms of cytotoxicity in a characterized SH-SY5Y cells spheroid model","authors":"Felipe Franco-Campos,&nbsp;Mónica Fernández-Franzón,&nbsp;Yelko Rodríguez-Carrasco,&nbsp;María José Ruiz","doi":"10.1016/j.tox.2024.153987","DOIUrl":"10.1016/j.tox.2024.153987","url":null,"abstract":"<div><div>In recent years, spheroids (tridimensional cell cultures) have emerged as a more physiologically relevant replacement for monolayer models. Their distinctive advantage is the formation of an extracellular matrix that facilitates enhanced cellular interaction and communication, approximating the conditions observed <em>in vivo</em>. Therefore, the potential for conducting intricate cellular and molecular techniques in these models could offer a more precise assessment of pivotal proteins within various cellular pathways of interest. Amitraz (AMZ), an acaricide classified as a formamidine chemical, has been detected in honey at concentrations exceeding legal limits. The objective of this study was to characterize a spheroid model of SH-SY5Y cells and determine the cytotoxic effect of AMZ and its mechanisms of action on this spheroid. The formation of mature spheroids was observed on the seventh day following seeding. The results obtained with SH-SY5Y spheroids were an IC₅₀ of 238.8 ± 17 µM and 224.3 ± 19 µM, respectively, after 24 and 48 h of exposure by the MTT assay. The findings revealed that AMZ did not exhibit any indications of inflammatory over-expression markers in the spheroids. Nevertheless, at 238.8 µM of AMZ, an increase incidence of late apoptosis within spheroid cells and Bcl-2 protein expression in peripheral spheroid cells were observed through annexin V and propidium iodide probe and immunofluorescence analysis. In conclusion, the results demonstrated that spheroids could be useful for an accurate assessment of toxicity, representing a viable alternative method for determining the mechanisms of action of AMZ and related compounds.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"509 ","pages":"Article 153987"},"PeriodicalIF":4.8,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142568312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unraveling the enigma of cardiac damage caused by lead: Understanding the intricate relationship between oxidative stress and other multifactorial mechanisms","authors":"Anjali Rajpoot,&nbsp;Tanya Aggarwal,&nbsp;Veena Sharma","doi":"10.1016/j.tox.2024.153984","DOIUrl":"10.1016/j.tox.2024.153984","url":null,"abstract":"<div><div>Lead (Pb) exposure remains a pressing concern in the realm of public health, with a mounting body of evidence underscoring its adverse impact on cardiovascular well-being. The exposure to Lead instigates the production of reactive oxygen species (ROS), leading to consequential cellular and physiological damage and a perturbation in redox equilibrium. The resultant oxidative stress, induced by ROS, disrupts endothelial functionality, propagates inflammatory processes, and initiates vascular remodeling, collectively contributing to the advancement of cardiovascular diseases (CVDs). The objective of this current review is to comprehensively expound upon the intricate mechanisms through which Lead induced toxicity affects cardiac cells. Additionally, it briefly addresses the ramifications of Lead exposure on the development of three interconnected cardiovascular conditions: atherosclerosis, hypertension, and myocardial infarction. Furthermore, the discourse delves into the specific repercussions of Lead exposure on lipid metabolism, blood pressure regulation, and cardiac performance, culminating in the initiation and progression of atherosclerotic plaque formation, elevated blood pressure, and an augmented risk of myocardial infarction. By understanding these intricate mechanisms, targeted interventions may be devised to counteract the deleterious effects of Lead on cardiovascular health. Thus, this review offers novel avenues for preventive and therapeutic strategies, ultimately serving to alleviate the burden of cardiovascular diseases associated with Lead toxicity.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"509 ","pages":"Article 153984"},"PeriodicalIF":4.8,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142558865","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"E-waste in the environment: Unveiling the sources, carcinogenic links, and sustainable management strategies","authors":"Md Abdullah ,&nbsp;Satadal Adhikary ,&nbsp;Suchandra Bhattacharya ,&nbsp;Sudharani Hazra ,&nbsp;Abhratanu Ganguly ,&nbsp;Sayantani Nanda ,&nbsp;Prem Rajak","doi":"10.1016/j.tox.2024.153981","DOIUrl":"10.1016/j.tox.2024.153981","url":null,"abstract":"<div><div>E-waste refers to the electrical and electronic equipment discarded without the intent of reuse or at the end of its functional lifespan. In 2022, approximately 62 billion kg of e-waste, equivalent to 7.8 kg per capita, was generated globally. With an alarming annual growth of approximately 2 million metric tonnes, e-waste production may exceed 82 billion kg by 2030. Improper disposal of e-waste can be detrimental to human health and the entire biosphere. E-waste encompasses a wide range of materials, including heavy metals, Polychlorinated Biphenyls (PCBs), Per- and Polyfluoroalkyl Substances (PFAS), Polycyclic Aromatic Hydrocarbons (PAHs), Polychlorinated Dibenzo-dioxins and -furans (PCDD/Fs), Polybrominated Diphenyl Ethers (PBDEs), and radioactive elements. E-waste, when disposed inappropriately can directly contaminate the aquatic and terrestrial environment, leading to human exposure through ingestion, inhalation, dermal absorption, and trans-placental transfer. These detrimental contaminants can directly enter the human body from the environment and may fuel carcinogenesis by modulating cell cycle proteins, redox homeostasis, and mutations. Heavy metals such as cadmium, mercury, arsenic, lead, chromium, and nickel, along with organic pollutants like PAHs, PCBs, PBDEs, PFAS, and radioactive elements, play a crucial role in inducing malignancy. Effective collection, sorting, proper recycling, and appropriate disposal techniques are essential to reduce environmental contamination with e-waste-derived chemicals. Hence, this comprehensive review aims to unravel the global environmental burden of e-waste and its links to carcinogenesis in humans. Furthermore, it provides an inclusive discussion on potential treatment approaches to minimize environmental e-waste contamination.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"509 ","pages":"Article 153981"},"PeriodicalIF":4.8,"publicationDate":"2024-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142568415","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hematological, cardiovascular and oxidative DNA damage markers associated with heavy metal exposure in electronic waste (e-waste) workers of Bangladesh","authors":"Sarker Masud Parvez ,&nbsp;M Mamun Huda ,&nbsp;Mahbubur Rahman ,&nbsp;Farjana Jahan ,&nbsp;Masatake Fujimura ,&nbsp;Shaikh Sharif Hasan ,&nbsp;Nirupam Aich ,&nbsp;Abul Hares ,&nbsp;Zahir Islam ,&nbsp;Rubhana Raqib ,&nbsp;Luke D Knibbs ,&nbsp;Peter D Sly","doi":"10.1016/j.tox.2024.153978","DOIUrl":"10.1016/j.tox.2024.153978","url":null,"abstract":"<div><div>Electronic waste (e-waste) contains hazardous elements such as lead (Pb), cadmium (Cd), mercury (Hg), and other toxic elements that pose significant health risks to the population directly exposed. We recruited 199 e-waste recycling workers and 104 non-exposed workers in Bangladesh and analyzed heavy metals in blood and hair, as well as hematological and cardiovascular parameters including, blood lipids and blood pressure. We fitted quantile regression models at 0.5 quantile to evaluate the impact of blood Pb, Cd, and total hair Hg (THg) on hematological and cardiovascular parameters and the role of oxidative DNA damage (8-OHdG as a biomarker) in mediatin the relationship between exposures and outcomes. Exposed workers had elevated median blood Pb (11.89 vs. 3.63 µg/dL), moderate blood Cd (1.04 vs. 0.99 µg/L), and lower level of THg (0.38 vs. 0.57 ppm) in hair than non-exposed workers. Adjusted estimates showed that Pb was positively associated with red blood cell (RBC), eosinophil count, eosinophil percentage; and negatively associated with mean platelet volume (MPV), platelet large cell ratio (P-LCR) and platelet volume distribution width (PDW) (all p≤0.05). Cd was only associated with 0.57 units increase in red blood cell distribution width (RDW) percentage (95 % CI: 0.18, 0.95). In cardiovascular outcomes, Pb was associated with 1.42 units decrease in triglyceride, 1.58 units increase in low-density lipoprotein (LDL), 0.07 units increase in LDL/HDL and 0.49 units increase in systolic blood pressure (all p≤0.05). No associations were observed between THg and hematological or cardiovascular parameters. Urinary 8-OHdG concentrations were lower, and it did not mediate exposure-outcome relationships (all p≥0.05). Our data imply that e-waste exposure impairs hematological parameters, blood lipids, and blood pressure secondary to elevated Pb levels and poses a threat to exposed individuals. As such, continuous monitoring in longitudinal studies is warranted to assess the dose-response relationship and identify effective control measures.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"509 ","pages":"Article 153978"},"PeriodicalIF":4.8,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142508627","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}