For much of its history, forensic toxicology was built on a core analytical question: what poison or drug is present, and at what concentration? That question still matters, but modern casework increasingly shows that it is no longer sufficient on its own. The field grew from the nineteenth-century chemical toxicology of Mathieu Orfila and the arsenic-detecting Marsh test into a discipline central to medicolegal death investigation, overdose certification, and exposure reconstruction. Yet contemporary practice must now contend with novel psychoactive substances, highly potent synthetic opioids, complex polysubstance deaths, delayed reporting, postmortem redistribution, matrix degradation, and incomplete toxicological context. These pressures are pushing forensic toxicology beyond simple compound detection toward mechanism-aware, data-rich interpretation. This review develops the idea of precision forensic toxicology as a proposed, forward-looking conceptual framework for that transition rather than a description of established or routinely implemented forensic practice. In this model, classical analytical chemistry remains essential, but it is connected to toxicogenomics, transcriptomics, epigenomics, proteomics, metabolomics, exposomics, microbiomics, and spatial multi-omics, then integrated through systems toxicology and artificial intelligence. Recent literature shows that toxicogenomics can reveal early molecular perturbations before overt phenotype, that postmortem metabolomics can assist cause-of-death screening, that RNA- and miRNA-based markers may improve postmortem interval estimation, and that machine learning can strengthen high-resolution mass-spectrometry workflows and multi-omics interpretation. At the same time, routine implementation remains constrained by standardization, validation, explainability, privacy governance, and regulatory uncertainty. None of these components is yet part of routine forensic casework; each remains at a research or early-validation stage, and their translation into daily practice will require dedicated feasibility, validation, and regulatory work, which this review discusses explicitly. Taken together, the evidence suggests that the future of poisoning investigation will depend less on any single assay and more on interoperable workflows that connect toxicant detection with biological response, individual susceptibility, and transparent decision support, and that these workflows are intended to complement, not replace, classical toxicological and medicolegal interpretation.

Arsenic contamination poses a significant environmental health risk, yet the mechanisms underlying its induction of hepatic fibrosis remain incompletely elucidated.Our previous clinical studies in arsenic poisoning areas found that serum inflammatory factors (such as IL-6, IL-1β, TNF-α) levels were significantly elevated, but there were no significant differences in liver function and fibrosis markers, suggesting that the inflammatory response precedes detectable typical pathological alterations. Established theories suggest that persistent inflammation is a key factor in the initiation of hepatic fibrosis. PINK1, a key initiator of mitophagy, was found to be downregulated in the livers of arsenic-exposed mice.Based on this, we propose a scientific hypothesis: arsenic exposure induces a persistent inflammatory response by inhibiting PINK1/Parkin-mediated mitophagy, thereby driving hepatic stellate cells (HSCs) activation and the fibrosis process. Experimental validation demonstrated that arsenic exposure significantly inhibited the PINK1/Parkin pathway, impaired mitophagy, and upregulated the expression of fibrosis markers and inflammatory factors in both liver tissues and cells. Conversely, PINK1 overexpression reversed these pathological phenotypes. In summary, dysregulation of the PINK1/Parkin pathway is a pivotal mechanism connecting arsenic exposure to chronic inflammation and the initiation of hepatic fibrosis, providing new insights for early recognition and targeted intervention of arsenic-related liver diseases.

Objective: To analyze the clinical characteristics and treatment efficacy of occupational acute arsenic poisoning based on literature reports. Methods: Literature on occupational acute arsenic poisoning from domestic and international sources was retrieved to summarize its clinical characteristics and treatment outcomes. Results: Six articles reporting a total of 97 cases of occupational acute arsenic poisoning were identified. The primary routes of occupational exposure are the respiratory tract and skin/mucous membranes, the initial clinical manifestations involve skin and mucosal irritation symptoms (>80%), such as dermatitis, pharyngitis, conjunctivitis and keratitis, as well as tracheitis, bronchitis, and pneumonia. Subsequently, symptoms related to the nervous and digestive systems appear. Timely treatment generally results in a favorable prognosis, cure rate of 92.8%. Conclusion: Occupational acute arsenic poisoning is relatively rare. It primarily presents with skin and mucosal irritation symptoms, alongside respiratory, nervous, and digestive system manifestations. These findings highlight the close relationship between the route of exposure and the clinical presentation and prognosis.

Arsenic poisoning significantly elevates the risk of cancer and other chronic illnesses. The goal of this research is to identify important genes whose expression changes in response to arsenic toxicity, and the molecular pathways affected by arsenic, using computational analysis of arsenic toxicity profiles. This approach will computationally identify and analyze genes whose expression changes in response to arsenic, thereby elucidating the heightened risk of carcinogenesis in arsenic-exposed individuals. This work employed high-throughput arsenic toxicity profiles to computationally identify and analyze expressed genes (DEGs) differentially in Affymetrix microarray datasets from the Gene Expression Omnibus (GEO) database, which were screened using the GEO2R program. A protein-protein interaction (PPI) network was constructed using STRING to elucidate the functional links between these DEGs and DNA repair genes. Interactions between the seven central genes (E2F1, EXO1, EZH2, FEN1, HIST1H3A, POLA1, and TIMELESS) and the repair genes PARP1, NBN, PMS1, MSH3, XRCC5, XRCC6, MGMT, and MLH1 were discovered. We employed the DAVID and Enrichr-KG platforms to investigate the functions of these genes and their associations with cellular and molecular processes in greater detail. Two hundred eighty-one non-synonymous single-nucleotide polymorphisms (nsSNPs) in the 07 genes linked to arsenic toxicity were found using the COSMIC database. Based on our analysis, mutations in E2F1, EXO1, EZH2, FEN1, HIST1H3A, POLA1, and TIMELESS can hinder DNA repair mechanisms, ultimately leading to cancer. Our computational analysis demonstrated that these non-synonymous SNPs can affect gene function, potentially altering protein stability and activity. Furthermore, according to Metal-Protein docking and protein-protein docking, these genes and their mutations appear to affect interactions with repair proteins substantially. Specific dietary consumption may lessen the detrimental effects of arsenic poisoning on protein function. We hypothesized that the mutations might be reversed by attaching particular molecules to these mutants. The protective effects of six curcumin compounds were examined using molecular docking with AutoDock 4.2.6 to assess protein dynamics and binding interactions. Optimal complexes were selected for dynamics simulation using GROMACS, and potential strategies for long-term cancer prevention related to arsenic exposure were identified.

Trace elements arsenic, cadmium, lead, chromium, mercury, nickel, and zinc are high-density, naturally occurring metals notable for their toxicity and environmental persistence. Cadmium and mercury are particularly concerning due to their capacity for bioaccumulation and biomagnification within the food chain. Dispersed through both anthropogenic and natural sources, these elements pose significant threats to ecosystems and animal health. In equines, they induce oxidative stress by disrupting mitochondrial function, generating reactive oxygen species, and inhibiting antioxidant enzymes, leading to cellular damage and organ dysfunction. Clinical presentations including gastrointestinal, neurological, renal, and musculoskeletal disorders vary by element, dose, and exposure duration. This review compiles information on the origins, pathogenesis, clinical signs, and therapeutics for poisoning by these seven elements in horses. Additionally, literature-derived baseline levels in blood, serum, hair, liver, and kidneys are synthesized to propose preliminary species-specific reference values, supporting environmental monitoring, clinical diagnosis, and equine product safety.

Heavy metals including mercury (Hg), lead (Pb), cadmium (Cd), and arsenic (As) remain significant global toxins due to their environmental persistence, widespread anthropogenic release, and serious biological effects. This review consolidates current understanding of their natural and industrial sources, environmental cycling, human exposure routes, and population-level vulnerabilities. It covers their toxicokinetics and toxicodynamics, emphasizing species-specific absorption, distribution, and injury mechanisms, including oxidative stress, thiol binding, mitochondrial dysfunction, endocrine disruption, and cancer risk. Clinical signs range from subtle neurocognitive impairment and kidney damage to severe acute poisoning. The review evaluates evidence-based approaches to risk assessment and biomonitoring, such as blood, urine, hair, and speciation tests, noting issues, including unvalidated provoked testing. Treatment focuses on removing exposure, providing nutritional support, and offering supportive care, with chelation therapy reserved for specific cases. It explains the chemistry, pharmacology, and roles of chelating agents-ALA, DMSA, DMPS, Cys, GSH, and physiologic thiols, comparing their effectiveness, limitations, and costs for various metals. Emerging therapies, precision toxicology, and public health strategies are discussed within a prevention-focused context. Unlike prior reviews focused primarily on toxic mechanisms or isolated clinical management, this review integrates mechanistic toxicology, biomarker interpretation and speciation, evidence-based clinical care, and ethical, cost-conscious decision-making within a single translational framework. This narrative review synthesizes foundational and contemporary literature published through 2025, with particular emphasis on studies published since 2000 that inform toxicokinetics, biomarker interpretation, diagnostics, clinical management, and prevention.

Arsenic poisoning has severe health effects, and accordingly, most research on the arsenite methyltransferase 3 (AS3MT) enzyme has focused on its role in arsenic metabolism, overlooking potential endogenous functions. We discovered an arsenic-independent role for AS3MT in regulating hepatic energy metabolism. as3mt loss in zebrafish caused differential expression of thousands of genes in the liver, with many of the downregulated genes playing roles in mitochondrial energy metabolism. Similar genes were downregulated in AS3MT-depleted human cells. as3mt zebrafish mutants had large, malformed mitochondria, were more sensitive to both arsenic and the mitochondrial toxin rotenone, and impaired swimming velocity. as3mt mutants developed steatosis, a hallmark of mitochondrial dysfunction. Restoring As3mt in hepatocytes of as3mt mutants rescued steatosis and mitochondrial gene expression. Overexpression of As3mt in wild-type hepatocytes protected against steatosis caused by iAs induced. This demonstrates a novel, conserved, endogenous role for As3mt in hepatic energy metabolism, identifies As3mt loss as a previously unrecognized cause of steatosis, and suggests that arsenic may induce mitochondrial dysfunction due to sequestering As3mt from its endogenous role.

Arsenic, a toxic metalloid, may cause significant public health impact due to its cumulative toxicity upon chronic exposure. Continuous low-level ingestion of arsenic, often through contaminated groundwater or food, leads to gradual accumulation and a spectrum of health effects over time. Long-term arsenic exposure is associated with dermatological lesions (pigmentation changes and keratosis), various cancers (skin, lung, bladder, etc.), cardiovascular disease, neuropathy, diabetes, and other systemic effects, reflecting its classification as a Group 1 human carcinogen. Ayurveda Classics describe a unique concept of cumulative toxicity under Dushi Visha (latent poison). A comparative analysis of clinical features shows that many symptoms of chronic arsenic toxicity (fatigue, gastrointestinal disturbances, skin changes, neuropathy, etc.) mirror the descriptions of Dushi Visha. Management of chronic arsenic toxicity is challenging, as no specific antidote exists apart from chelation therapy; hence, modern treatment focuses on eliminating exposure and supportive care. Ayurveda offers detoxification (Shodhana) therapies and herbal formulations aimed at expelling latent toxins and mitigating symptoms. This review paper discusses the concept of cumulative arsenic toxicity in modern toxicology and draws parallels with the Ayurvedic notion of Dushi Visha. An integrative understanding of arsenic's cumulative toxicity through both modern and traditional lenses can enrich prevention and management strategies for arsenic poisoning.

Acute arsenic poisoning, a life-threatening condition, results from exposure to inorganic arsenic compounds such as arsenic trioxide (As2O3). This case report describes a 27-year-old male who ingested 25 g of As2O3 and presented with severe gastrointestinal (GI) toxicity and acute kidney injury. Management involved airway protection, GI decontamination with activated charcoal, chelation therapy using D-penicillamine, and supportive care including N-acetylcysteine (NAC) and dialysis for renal failure. GI endoscopy revealed diffuse mucosal ulceration consistent with arsenic's corrosive effects. The patient recovered following three sessions of sustained low-efficiency dialysis and was discharged with improved renal function. This case highlights the critical role of prompt supportive management, chelation, and hemodialysis in arsenic poisoning. It also highlights novel use of NAC as an adjunctive therapy and the importance of monitoring multi-organ involvement for improved outcomes.

Cobalt (Co) metal is a gray, ductile, magnetic element with an atomic number of 27 and an atomic weight of 58.9 Da. In the environment, cobalt is a component of naturally occurring minerals and is found in combination with other elements such as copper, nickel, manganese, arsenic, sulfur, and oxygen. Due to its ferromagnetic properties, high melting point (1495.05 C), and high boiling point (2927 C), cobalt is widely used in industry to produce hard metals and superalloys. For example, the alloy Alnico is a blend of iron, aluminum, nickel, and cobalt used for its permanent magnetic properties. A common source of chronic cobalt exposure is in the production of tungsten carbide, which is used for its hardness, heat resistance, and strength.  Historically, cobalt chloride (CoCl2) has been used in medicine as a treatment for anemia due to its ability to promote erythropoiesis. However, due to its adverse effects of thyroid dysfunction and the development of goiters, the use of cobalt in treating anemia has fallen out of favor. A biochemically important cobalt compound is cyanocobalamin (vitamin B12) which contains a Co3+-ion. Vitamin B12 is an essential nutrient naturally found in foods of animal origin, such as dairy, eggs, fish, poultry, and meat. Deficiencies in vitamin B12 may lead to pernicious anemia as well as peripheral neuropathy. The precursor hydroxocobalamin is used as an antidote for cyanide poisoning and may have a role in treating vasoplegic shock. Potential cobalt exposure can occur via oral, respiratory, and dermal routes.