Toxicology Reports最新文献

{"title":"Silymarin attenuates oxidative, inflammatory and apoptotic damage induced by a fungicide mixture in rat liver, kidney and brain","authors":"Hamada S. Salem,&nbsp;Asmaa M.R. Gouda,&nbsp;Nesreen M. Essam,&nbsp;Hanaa T. El-Bahnasy","doi":"10.1016/j.toxrep.2026.102287","DOIUrl":"10.1016/j.toxrep.2026.102287","url":null,"abstract":"<div><div>Fungicide exposure is associated with significant health hazards in both animals and humans. The present study examined the toxicological effects of a mixture of copper oxychloride, propiconazole, boscalid, and pyraclostrobin on the liver, kidney, and brain of male rats, and evaluated whether silymarin could counteract fungicide-associated injury. Forty male Sprague–Dawley rats were randomly allocated to four groups: control, fungicide-treated, silymarin-treated, and fungicide and silymarin-treated. A panel of biochemical indices, oxidative stress measures, and inflammatory and apoptotic markers was quantified. In fungicide-treated rats, serum liver enzymes, bilirubin, urea, creatinine, and uric acid were higher than in controls. Total protein, neurochemical, and electrolyte markers also decreased significantly. Fungicide exposure increased malondialdehyde and lowered total antioxidant capacity and other antioxidant defences; at the same time, inflammatory and apoptotic markers rose. When silymarin was given alongside the fungicide mixture, it substantially dampened these biochemical disturbances and strengthened antioxidant status; inflammatory and apoptotic responses were also reduced. In conclusion, the findings support the potential use of silymarin supplements as an additional protective agent against chemical toxicity.</div></div>","PeriodicalId":23129,"journal":{"name":"Toxicology Reports","volume":"16 ","pages":"Article 102287"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148230896","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acute and subacute oral toxicity assessment of Karanjin in Sprague Dawley rats","authors":"Natasha Sura Anak Lubau ,&nbsp;Vinod Balasubramaniam ,&nbsp;Christina Gertrude Yap ,&nbsp;Alina Arulsamy ,&nbsp;Vetriselvan Subramaniyan","doi":"10.1016/j.toxrep.2026.102207","DOIUrl":"10.1016/j.toxrep.2026.102207","url":null,"abstract":"<div><div>Karanjin (KRN) is a benzofuran flavonoid derived from <em>Pongamia pinnata</em> seeds, known for its antihyperglycemic and anti-inflammatory properties. Despite its traditional use, comprehensive toxicological data are limited. This study evaluated the acute and subacute oral toxicity of KRN in Sprague Dawley rats. In the acute study, single doses of 5, 500, or 2000 mg/kg were administered, and animals were observed for 14 days. In the subacute study, daily doses of 5, 50, or 250 mg/kg were given for 28 days. Clinical signs, body weight, food and water intake were monitored throughout. At termination, organs (liver, kidney, heart, etc.) were weighed, blood was analysed for biochemical parameters (ALT, AST, ALP, total protein, albumin, lipids), and tissues were examined histopathologically. No mortality or treatment-related clinical signs occurred at any dose. Body weight, food/water intake, and organ weights did not differ significantly between treated and control groups. Serum biochemical values remained within normal limits, showing only minor, non-dose-dependent variations. Histopathology revealed normal architecture of major organs without evidence of necrosis, inflammation, or degeneration. These findings demonstrate a wide margin of safety for oral KRN and support its potential for further pharmacological development.</div></div>","PeriodicalId":23129,"journal":{"name":"Toxicology Reports","volume":"16 ","pages":"Article 102207"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146022731","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessing aflatoxin exposure risk from imported nuts in the Jordan market","authors":"Abdalmajeed M. Alajlouni ,&nbsp;Dima Alkadri ,&nbsp;Mohammad S. Abu-Hardan ,&nbsp;Amer A. Al-Sakaji","doi":"10.1016/j.toxrep.2025.102190","DOIUrl":"10.1016/j.toxrep.2025.102190","url":null,"abstract":"<div><div>This study assessed the contamination levels and health risk of aflatoxins in nuts from the markets in Jordan. A total of 180 nut samples (pistachios, almonds, walnuts, and cashews) were analyzed using high-performance liquid chromatography (HPLC) following immunoaffinity column clean-up and QuEChERS extraction. Aflatoxins were detected in 13 % of the samples, with pistachios showing the highest contamination rate. The Estimated Daily Intake (EDI) and Margin of Exposure (MOE) were calculated using deterministic risk assessment methods, based on the mean contamination levels and average nut consumption patterns in Jordan. All MOE values were below the safety threshold of 10,000, indicating a potential health risk. These findings emphasize the need for strengthened monitoring programs and regulatory actions to ensure food safety and minimize the public health risk.</div></div>","PeriodicalId":23129,"journal":{"name":"Toxicology Reports","volume":"16 ","pages":"Article 102190"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145791813","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessing the hepatic and renal parameters of breast cancer patient blood samples before and after chemotherapy","authors":"Ghaith B. Heilat ,&nbsp;Tahani Alwidyan ,&nbsp;Amjad Z. Alrosan ,&nbsp;Aseel O. Rataan ,&nbsp;Khaled Alrosan ,&nbsp;Rehaf B. Ahmad ,&nbsp;Kinda R. Al-Kammash","doi":"10.1016/j.toxrep.2026.102283","DOIUrl":"10.1016/j.toxrep.2026.102283","url":null,"abstract":"<div><div>Breast cancer (BC) is the most common malignancy in women, with chemotherapy as a fundamental treatment despite its potential to cause hepatotoxicity and nephrotoxicity. Although routine assessment of organ function is customary, the predictive value of composite liver-kidney biomarkers for post-chemotherapy survival remains inadequately investigated. This retrospective study sought to assess the influence of chemotherapy on hepatic and renal parameters in 132 BC patients treated at King Abdullah University Hospital (KAUH) in Jordan from January 2011 to April 2025, with a particular focus on the prognostic relevance of the Albumin-Creatinine Ratio (ACR), Alkaline Phosphatase-to-Creatinine Ratio (ALP/Cr), and Albumin-Bilirubin (ALBI) score. Liver and kidney function tests were evaluated pre- and post-four chemotherapy cycles utilizing Wilcoxon signed-rank tests, Kaplan-Meier survival curves, and Cox proportional hazards regression. Post-treatment analysis demonstrated a moderate yet statistically significant reduction in total protein (<em>p = 0.035</em>) and serum creatinine (<em>p = 0.019</em>). Significantly, whereas routine enzymes (ALT, AST, ALP) exhibited no notable alterations, the composite biomarkers ACR and ALP/Cr ratio demonstrated substantial increases post-treatment (<em>p = 0.036</em> and <em>p = 0.030</em>, respectively). Using ROC-derived cut-offs, the survival analysis revealed that patients with a low post-treatment ACR (&lt;1045) had significantly longer overall survival (OS) than those in the high-ACR group (8.14 vs. 2.35 years; <em>p = 0.009</em>). Further, a lower post-treatment ALP/Cr ratio (&lt;1491.7) was associated with longer survival (8.94 vs. 6.12 years; <em>p = 0.017</em>). These data suggest that, whereas individual liver and kidney indicators were relatively stable, composite biomarkers—specifically ACR and ALP/Cr—were more susceptible to treatment-induced physiological stress. Thus, these ratios serve as crucial indicators of OS, suggesting that incorporating hepatic and renal evaluations into composite markers provides greater predictive value for monitoring BC patients than standalone organ function tests.</div></div>","PeriodicalId":23129,"journal":{"name":"Toxicology Reports","volume":"16 ","pages":"Article 102283"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148167647","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Study of exposure to benzene, toluene, ethylbenzene, and xylenes (BTEX) and protective effects of Gallic acid on oxidative stress on peripheral lymphocytes of workers in the paint unit of an automobile industry","authors":"Enayatollah Seydi ,&nbsp;Asghar Ghahri ,&nbsp;Fatemeh Pasbin ,&nbsp;Jalal Pourahmad","doi":"10.1016/j.toxrep.2026.102284","DOIUrl":"10.1016/j.toxrep.2026.102284","url":null,"abstract":"<div><div>Exposure to workplace chemicals is a major concern across various industries, with serious consequences for workers' health and safety. The paint unit of the automotive industry exemplifies a workplace where hazardous chemicals are common. This unit is a significant source of volatile organic compounds (VOCs), which are highly harmful. Monitoring workers is a common method for evaluating chemical exposure levels in occupational settings. Gallic acid (GA) acts as an antioxidant at low doses and has beneficial effects on human health. In this study, we examined oxidative stress in peripheral lymphocytes of workers exposed to benzene, toluene, ethylbenzene, and xylenes (BTEX) in a paint unit of an automotive industry, and evaluated the protective role of GA in this context. Exposure to BTEX was assessed using the NIOSH 1501 method. Additionally, oxidative and antioxidant stress parameters in peripheral lymphocytes were measured. The study results showed that workers' exposure to benzene exceeded the national occupational exposure limits (OEL), while exposure to toluene, ethylbenzene, and xylene was below these limits. Furthermore, GA at concentrations of 12.5, 25, and 50 µg/ml reduced oxidative stress levels in peripheral blood lymphocytes of paint unit workers and increased antioxidant enzyme levels and reduced glutathione (GSH). It is recommended that workers in this unit be continuously monitored and use personal protective equipment and control methods to reduce exposure. It is also recommended to use antioxidant compounds continuously to reduce the side effects of exposure.</div></div>","PeriodicalId":23129,"journal":{"name":"Toxicology Reports","volume":"16 ","pages":"Article 102284"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148167652","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Kelulut honey (Heterotrigona itama) as a multi-target neuroprotective strategy against bisphenol A-induced neurotoxicity","authors":"Siti Khadijah Azmi ,&nbsp;Nur Faizah Ali ,&nbsp;Rosfaiizah Siran","doi":"10.1016/j.toxrep.2026.102278","DOIUrl":"10.1016/j.toxrep.2026.102278","url":null,"abstract":"<div><div>Bisphenol A (BPA) is a synthetic chemical widely used in the production of plastics and epoxy resins due to its low cost, durability, and heat resistance.Recognised as an endocrine-disrupting chemical, BPA has raised growing concern regarding its potential effects on brain development, particularly during prenatal and early postnatal life. BPA-induced neurotoxicity involves multiple interconnected mechanisms, including oxidative stress, neuroinflammation, mitochondrial dysfunction, synaptic impairment, and neuroendocrine disruption, which collectively contribute to cognitive and behavioural abnormalities. Kelulut honey, produced by stingless bees (<em>Heterotrigona itama</em>), contains various bioactive compounds such as polyphenols, flavonoids, organic acids, and trehalulose. These compounds possess antioxidant, anti-inflammatory, and neuroprotective properties and may modulate pathways involved in neuronal survival, synaptic plasticity, inflammatory regulation, NMDA receptor signalling, and estrogen-related pathways. This narrative review summarises current findings on the neuroprotective potential of kelulut honey against BPA-induced neurotoxicity, highlights existing research gaps, and discusses future directions for further mechanistic and translational studies.</div></div>","PeriodicalId":23129,"journal":{"name":"Toxicology Reports","volume":"16 ","pages":"Article 102278"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148167657","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Emerging multisystem disease mechanisms of e-cigarette vaping on human health","authors":"Md Mohaimenul Islam Tareq,&nbsp;Sreejayan Nair,&nbsp;Guanglong He","doi":"10.1016/j.toxrep.2026.102282","DOIUrl":"10.1016/j.toxrep.2026.102282","url":null,"abstract":"<div><div>Electronic cigarettes (e-cigarettes) have quickly grown from a niche smoking cessation design to a ubiquitous nicotine-delivery device, causing ever-growing debate concerning their safety and long-term health outcomes. This review critically summarizes the available evidence from current literature on the development of e-cigarette technologies, nicotine pharmacodynamics, and systemic biological effects, especially pulmonary, cardiovascular, and neurological outcomes. Although noncombustible, e-cigarette aerosols contain hazardous compounds such as nicotine, metallic particulates, and aldehyde-reactive species, which can interact with the endothelial surfaces, immune effector cells, and neuronal networks, leading to oxidative stress, inflammation, and tissue remodeling. Clinical and preclinical evidence shows that e-cigarette vaping is linked to acute and chronic pulmonary injury, endothelial dysfunction, suppressed neurodevelopment, and behavioral dysregulation in adolescents. Additionally, the so-called nicotine-free and flavored products often contain unreported toxicants and do not have standardized safety tests. The consumption trends among young people and the vulnerable have been on the increase due to unsubstantiated assumptions about its controversial harm-reduction effects and overly zealous advertising campaigns. This review will also discuss controversial issues of the harm-reduction paradigm, gaps in regulatory control, and future research areas, such as longitudinal cohort studies. An evidence-based, multidisciplinary framework is firmly needed to guide innovation, policy, and clinical practice and, as such, make sure that responses to public health are aligned with sound scientific knowledge.</div></div>","PeriodicalId":23129,"journal":{"name":"Toxicology Reports","volume":"16 ","pages":"Article 102282"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148167735","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lycopene supplementation during pregnancy and lactation attenuates thermally oxidized cooking oil-induced hepatic and cerebral damage in rat offspring: A comprehensive histomorphometric and molecular analysis","authors":"Ahmad Aulia Jusuf ,&nbsp;Fadilah ,&nbsp;Nimas Ayu Nirwanti","doi":"10.1016/j.toxrep.2026.102290","DOIUrl":"10.1016/j.toxrep.2026.102290","url":null,"abstract":"<div><h3>Background</h3><div>Thermally oxidized cooking oil (TOCO) generates reactive oxygen species and lipid peroxidation products that cross the placental barrier, posing risks to offspring organ development in low-to-middle income countries where cooking oil reuse is endemic. Lycopene, a potent carotenoid antioxidant, possesses neuroprotective and hepatoprotective properties, yet its capacity to prevent maternal-to-offspring oxidative damage through maternal supplementation remains unexplored.</div></div><div><h3>Methods</h3><div>Twenty-four female Sprague Dawley rats were randomized into six groups (n = 4 dams each): Control, CMC vehicle, TOCO1 × , TOCO3 × , TOCO1 × + Lycopene, and TOCO3 × + Lycopene. Lycopene (0.24 mg/kg) was administered via oral gavage from gestational day 1 through postnatal day 14 (total duration: 35 days encompassing pregnancy and early lactation). Dam was used as the experimental unit for all inferential statistics to avoid pseudo-replication. Statistical analysis employed Kruskal-Wallis and Mann-Whitney U tests with Benjamini-Hochberg FDR correction, effect size estimation (Cohen’s d with 95% CI), and post-hoc power analysis.</div></div><div><h3>Results</h3><div>TOCO3 × exposure significantly reduced normal hippocampal CA1 neurons (60% vs 85% controls; Cohen’s d=2.2, p &lt; 0.05), cerebellar Purkinje cells (55% vs 90%; d=2.5, p &lt; 0.05), and increased hepatocyte damage (27% vs 8%; d=2.8, p &lt; 0.05). Lycopene supplementation provided substantial protection: hippocampal recovery to 75% (PI 60%), cerebellar recovery to 78% (PI 66%), liver recovery to 15% damaged (PI 63%), with NNT of 4–5. Biochemical markers (MDA, GSH) showed non-significant trends (post-hoc power 15–42%). Caspase-3 expression showed dose-dependent elevation with TOCO and suppression with lycopene.</div></div><div><h3>Conclusions</h3><div>Maternal lycopene supplementation provides significant multi-organ protection against TOCO-induced developmental toxicity. These findings are supported by convergent evidence from histopathology (d=2.2–2.8), molecular markers (caspase-3 dose-response), and exposure characterization, consistent with oxidative stress-mediated mechanisms. The translational HED (2.7 mg/day from 150 g fresh tomatoes) supports investigation of dietary lycopene as a public health intervention for pregnant women in TOCO-endemic populations.</div></div>","PeriodicalId":23129,"journal":{"name":"Toxicology Reports","volume":"16 ","pages":"Article 102290"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148230948","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circulating miR-126 and miR-155 are associated with environmental lead exposure: A translational approach via human biomonitoring and bioinformatic networks","authors":"Alejandra González-Bravo ,&nbsp;Velia Verónica Rangel-Ramírez ,&nbsp;Carlos Gabriel de la Trinidad-Chacón ,&nbsp;Myrna Lizbeth López-Ramírez ,&nbsp;Claudia Iveth Almendárez- Reyna ,&nbsp;Ciria Berenice Salazar-Rodríguez ,&nbsp;Leticia Carrizales-Yáñez ,&nbsp;Iván N. Pérez-Maldonado ,&nbsp;Ángeles C. Ochoa-Martínez","doi":"10.1016/j.toxrep.2026.102210","DOIUrl":"10.1016/j.toxrep.2026.102210","url":null,"abstract":"<div><div>Exposure to environmental contaminants, particularly lead (Pb), has increased due to anthropogenic activities and has been associated with epigenetic alterations, including changes in microRNA (miRNA) expression. Certain miRNAs have emerged as potential biomarkers of environmental exposure and early biological effects. Among them, miR-126 and miR-155 have been reported to be responsive to lead exposure. In this exploratory study, we evaluated circulating levels of miR-126 and miR-155 in a Mexican population environmentally exposed to lead and performed bioinformatic analyses to investigate the biological pathways potentially regulated by these miRNAs. Our results showed a mean blood lead concentration of 7.6 ± 5.8 μg/dL, with more than 50 % of participants exceeding the Mexican reference value (≥5 μg/dL; NOM-199-SSA1–2000). Both miRNAs showed significantly altered expression patterns associated with elevated blood lead levels (p &lt; 0.05). Gene Ontology and KEGG pathway analyses of predicted target genes revealed enrichment in pathways related to inflammation, angiogenesis, lipid metabolism, and atherosclerosis, including AGE–RAGE signaling, TNF, Toll-like receptor, and fluid shear stress–related pathways. Protein–protein interaction network analysis identified MYC as a shared regulatory node, suggesting coordinated regulation of biological processes relevant to cardiovascular function. Together, these findings indicate that lead exposure is associated with altered circulating miR-126 and miR-155 expression and with modulation of pathways related to cardiovascular health. Although causal inferences cannot be drawn due to the observational design, these results provide a framework for future large-scale epidemiological and functional studies aimed at elucidating epigenetic responses to environmental lead exposure.</div></div>","PeriodicalId":23129,"journal":{"name":"Toxicology Reports","volume":"16 ","pages":"Article 102210"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146166810","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polycyclic aromatic hydrocarbon exposure in battlefield and beyond: Implications for environmental- and human health","authors":"Markis’ D. Hamilton ,&nbsp;Ritu Chauhan ,&nbsp;Anthony E. Archibong ,&nbsp;Aramandla Ramesh","doi":"10.1016/j.toxrep.2026.102208","DOIUrl":"10.1016/j.toxrep.2026.102208","url":null,"abstract":"<div><div>Polycyclic aromatic hydrocarbons (PAHs) are combustion pollutants that are released into the environment through natural events and anthropogenic activities. Exposures to PAHs occur in military personnel during garrison (non-combat) and active deployment (combat) environments. Exposures that occur at low levels during deployment could lead to health issues, post-deployment. A scoping review was conducted to address the pathways of exposure, and the adverse effects caused by PAHs in active-duty personnel and veterans. Out of 50,171 scientific publications screened from 5 databases, 296 studies were identified that focused on the relationship between exposure to PAHs from various point sources and debilitating health issues reported in veterans. The findings revealed that in combat conditions, PAHs are released into the environment through explosions caused by bombing, artillery fire, and missile attacks on military installations, petrochemical industries, oil well fires set by saboteurs, and burn pits used to incinerate ammunition waste and military base refuse. Significant exposure of troops to PAHs occurred during active combat in the Operation Desert Shield, Operation Desert Storm, and Operation Enduring Freedom campaigns launched against hostile forces. The PAH releases contaminated not only the affected service personnel and staff, but also the surrounding environment. The coastal environment, including its flora and fauna, were affected by oil tanker fires, petroleum storage tanks that caught fire during conflict and subsequent release of PAHs into the marine environment. The human health effects resulting from PAH exposures included severe lung-, kidney-, and reproductive dysfunctions, as well as an increased risk of cancer, mostly manifested in Veterans as part of the Gulf War Syndrome. The Exposome approach utilizing the omics-based biomarkers to characterize individual service member profile with wearable monitors (wrist bands and sensors) to characterize the external environment when combined with biomonitoring studies holds significant promise for treatment of troops during combat and post deployment.</div></div>","PeriodicalId":23129,"journal":{"name":"Toxicology Reports","volume":"16 ","pages":"Article 102208"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146077718","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}