[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"doc-seo-349466-105":3,"detail-sidebar-cat-0-en-105":80,"doc-detail-349466-en":130},{"code":4,"msg":5,"data":6},0,"ok",{"site_id":7,"language":8,"slug":9,"title":10,"keywords":11,"description":12,"schema_data":13,"social_meta":73,"head_meta":75,"extra_data":77,"updated_unix":79},105,"en","arsenic-exposure-and-skin-cancer-mechanisms-clinical-evidence-and-public-health-implications-review","Arsenic exposure and skin cancer: Mechanisms, clinical evidence and public health implications - Review","","Skin is among the most frequent sites of cancer diagnosis, and global skin cancer incidence continues rising despite extensive public health initiatives. Arsenic, a ubiquitous environmental metalloid classified as a Group 1 carcinogen, is driven by exposure through contaminated drinking water, food sources, and occupational contact. Mechanistic evidence links arsenic-associated skin carcinogenesis to disrupted redox signaling, altered DNA damage and repair, and epigenetic reprogramming, with additional context-dependent roles in microRNA networks, telomere dynamics, and mitochondrial homeostasis. Clinical data support dose-responsive risk for non-melanoma skin cancer, while melanoma evidence is more heterogeneous due to confounding.",{"@graph":14,"@context":72},[15,34,55],{"@type":16,"itemListElement":17},"BreadcrumbList",[18,23,27,31],{"item":19,"name":20,"@type":21,"position":22},"https://docshare.wps.com","Home","ListItem",1,{"item":24,"name":25,"@type":21,"position":26},"https://docshare.wps.com/document/","Document",2,{"item":28,"name":29,"@type":21,"position":30},"https://docshare.wps.com/document/research-report/","Research & Report",3,{"item":32,"name":10,"@type":21,"position":33},"https://docshare.wps.com/document/arsenic-exposure-and-skin-cancer-mechanisms-clinical-evidence-and-public-health-implications-review/349466/",4,{"url":32,"name":10,"@type":35,"image":36,"author":41,"headline":10,"publisher":44,"fileFormat":47,"inLanguage":8,"description":12,"dateModified":48,"datePublished":49,"encodingFormat":47,"isAccessibleForFree":50,"interactionStatistic":51},"DigitalDocument",{"url":37,"@type":38,"width":39,"height":40},"https://docshare.wps.com/thumbnails/arsenic-exposure-and-skin-cancer-mechanisms-clinical-evidence-and-public-health-implications-review/349466.png","ImageObject",300,407,{"name":42,"@type":43},"Anna Hans","Person",{"url":19,"name":45,"@type":46},"DocShare","Organization","application/pdf","2026-09-23","2026-09-22",true,{"@type":52,"interactionType":53,"userInteractionCount":22},"InteractionCounter",{"@type":54},"ViewAction",{"@type":56,"mainEntity":57},"FAQPage",[58,64,68],{"name":59,"@type":60,"acceptedAnswer":61},"What exposure routes make arsenic a concern for skin cancer risk?","Question",{"text":62,"@type":63},"Arsenic exposure occurs through contaminated drinking water, food sources, and occupational contact, leading to persistent environmental exposure relevant to cutaneous carcinogenesis.","Answer",{"name":65,"@type":60,"acceptedAnswer":66},"Which molecular mechanisms are associated with arsenic-induced skin cancer?",{"text":67,"@type":63},"Evidence links arsenic to disrupted redox signaling, altered DNA damage signaling and repair, and epigenetic reprogramming; additional effects may involve microRNA networks and telomere/mitochondrial homeostasis.",{"name":69,"@type":60,"acceptedAnswer":70},"How strong is the clinical evidence for arsenic in non-melanoma skin cancer versus melanoma?",{"text":71,"@type":63},"For non-melanoma skin cancer, clinical data from high-exposure endemic regions and occupational cohorts suggest a dose-responsive association. For melanoma, evidence is more heterogeneous and susceptible to confounding, though modest risk elevations have been reported in some high-exposure or occupational settings.","https://schema.org",{"og:url":32,"og:type":74,"og:title":10,"og:site_name":45,"og:description":12},"article",{"robots":76,"canonical":32},"index,follow",{"doc_id":78,"site_id":7},349466,1790156404,{"code":4,"msg":81,"data":82},"success",[83,87,91,95,100,105,110,114,119,122,126],{"id":22,"doc_module":4,"doc_module_name":25,"category_name":84,"show_sort_weight":85,"slug":86},"Story & Novel",90,"story-novel",{"id":26,"doc_module":4,"doc_module_name":25,"category_name":88,"show_sort_weight":89,"slug":90},"Literature",80,"literature",{"id":33,"doc_module":4,"doc_module_name":25,"category_name":92,"show_sort_weight":93,"slug":94},"Exam",70,"exam",{"id":96,"doc_module":4,"doc_module_name":25,"category_name":97,"show_sort_weight":98,"slug":99},5,"Comic",60,"comic",{"id":101,"doc_module":4,"doc_module_name":25,"category_name":102,"show_sort_weight":103,"slug":104},6,"Technology",50,"technology",{"id":106,"doc_module":4,"doc_module_name":25,"category_name":107,"show_sort_weight":108,"slug":109},7,"Healthcare",40,"healthcare",{"id":111,"doc_module":4,"doc_module_name":25,"category_name":29,"show_sort_weight":112,"slug":113},8,30,"research-report",{"id":115,"doc_module":4,"doc_module_name":25,"category_name":116,"show_sort_weight":117,"slug":118},9,"Religion & Spirituality",20,"religion-spirituality",{"id":117,"doc_module":4,"doc_module_name":25,"category_name":120,"show_sort_weight":117,"slug":121},"World Cup","world-cup",{"id":123,"doc_module":4,"doc_module_name":25,"category_name":124,"show_sort_weight":123,"slug":125},10,"Lifestyle","lifestyle",{"id":127,"doc_module":4,"doc_module_name":25,"category_name":128,"show_sort_weight":96,"slug":129},19,"General","general",{"code":4,"msg":81,"data":131},{"doc_id":78,"user_id":132,"nickname":42,"user_avatar":133,"doc_module":4,"category_id":111,"category_name":29,"doc_title":10,"doc_description":12,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":22,"is_deleted":4,"is_public":22,"is_downloadable":22,"audit_status":22,"page_count":139,"language":140,"language_code":8,"site_id":7,"html_lang":8,"table_of_contents":141,"faqs":142,"seo_title":143,"seo_description":12,"update_tm":144,"read_time":145},5909892332657,"https://ap-avatar.wpscdn.com/davatar_994ba38a5ba835b3df7d355c54d3ed8d","INTERNATIONAL JOURNAL OF MOLEcULAR MEdIcINE 58: 222, 2026  \nArsenic exposure and skin cancer: Mechanisms, clinical evidence and public health implications (Review)  \n1 2 1  \ndIMITRIOS A. ANdREIKOS , MIcHAEL AScHNER , dIMITRIOS c. ZIOGAS , ARISTIdIS TSATSAKIS3 and dEMETRIOSA. SPANdIdOS4  \n1  \nFirst department of Medicine, National and Kapodistrian University of Athens School of Medicine, 11527 Athens, Greece; 2  \ndepartment of Molecular Pharmacology, Albert Einstein college of Medicine, New York, NY 10461, USA;  \n3 4  \nLaboratory of Toxicology, School of Medicine, University of crete, 71003 Heraklion, Greece; Laboratory of clinical Virology,  \nSchool of Medicine, University of crete, 71003 Heraklion, Greece  \nReceived September 4, 2025; Accepted May 22, 2026  \ndOI: 10.3892/ijmm.2026.5893  \nAbstract. Skin is among the most frequent sites of cancer diagnosis, and the global incidence of skin cancer continues to rise despite extensive public health initiatives and preven‑ tive strategies. Arsenic, a ubiquitous environmental metalloid classified as a Group 1 carcinogen, remains an important concern due to widespread exposure through contaminated drinking water, food sources and occupational contact . Arsenic‑associated skin carcinogenesis involves complex, interdependent molecular processes and has been linked to the disruption of redox signalling, altered dNA damage signalling and repair responses as well as epigenetic reprogramming. In keratinocytes, arsenic perturbs redox and stress‑response pathways and may disrupt genome maintenance and cellular stress signalling in experimental systems. Arsenic may also alter microRNA networks and affect telomere and mitochon‑ drial homeostasis, although the contribution of these processes to malignant transformation remains context‑dependent; in melanoma, the carcinogenic mechanisms of arsenic are less well characterized. clinically, arsenic is recognized as a carcinogen in non‑melanoma skin cancer (NMSc) and evidence from high‑exposure endemic regions, together with occupational cohorts, suggest a dose‑responsive association. For melanoma, clinical evidence is more heterogeneous and subject to substantial potential confounding, although some studies suggest modest risk elevation in high‑exposure or occupational settings. collectively, convergent mechanistic, experimental and epidemiological data support arsenic as an independent carcinogen, particularly in NMSc. These find‑ ings underscore the need for heightened clinical vigilance,  \nCorrespondence to: dr dimitrios A. Andreikos, First department of Medicine, National and Kapodistrian University of Athens School of Medicine, 75 Mikras Asias Street, 11527 Athens, Greece  \nE‑mail: [jim.andrei@outlook.com](jim.andrei@outlook.com)  \nKey words: arsenic, skin cancer, cutaneous carcinogenesis, non‑melanoma skin cancer, melanoma, heavy metals  \nparticularly in exposed populations, and call for renewed public health strategies and regulatory frameworks to mitigate the persistent global burden of arsenic‑associated skin cancer.  \nContents  \n1. Introduction  \n2. Arsenic exposure, biotransformation and toxicity  \n3. Arsenic and carcinogenesis  \n4. Mechanistic pathways in arsenic‑induced skin cancer  \n5. Arsenic and melanoma: clinical and epidemiological evidence  \n6. Arsenic and NMSc: clinical and epidemiological evidence  \n7. conclusions  \n1. Introduction  \nThe global cancer burden is projected to climb from 19.3 million incident cases in 2020 to 28.4 million by 2040 (1) . The International Agency for Research on cancer (IARc) attributes a portion of malignancies to chronic exposure to environmental toxicants, especially redox‑active trace elements released by mining, smelting, intensive agricul‑ ture, food consumption and fossil‑fuel combustion (2,3) . In caucasian populations, the skin is the most common site for cancer diagnosis, and incidence continues to climb worldwide despite extensive educational and preventive efforts (4‑6) . Skin cancer incl","cbCaiputDIoqILis","https://ap.wps.com/l/cbCaiputDIoqILis","pdf",3979250,17,"English","# Introduction\n# Arsenic exposure, biotransformation and toxicity\n# Arsenic and carcinogenesis\n# Mechanistic pathways in arsenic-induced skin cancer\n# Arsenic and melanoma: clinical and epidemiological evidence\n# Arsenic and NMSc: clinical and epidemiological evidence\n# Conclusions","[{\"question\":\"What exposure routes make arsenic a concern for skin cancer risk?\",\"answer\":\"Arsenic exposure occurs through contaminated drinking water, food sources, and occupational contact, leading to persistent environmental exposure relevant to cutaneous carcinogenesis.\"},{\"question\":\"Which molecular mechanisms are associated with arsenic-induced skin cancer?\",\"answer\":\"Evidence links arsenic to disrupted redox signaling, altered DNA damage signaling and repair, and epigenetic reprogramming; additional effects may involve microRNA networks and telomere/mitochondrial homeostasis.\"},{\"question\":\"How strong is the clinical evidence for arsenic in non-melanoma skin cancer versus melanoma?\",\"answer\":\"For non-melanoma skin cancer, clinical data from high-exposure endemic regions and occupational cohorts suggest a dose-responsive association. For melanoma, evidence is more heterogeneous and susceptible to confounding, though modest risk elevations have been reported in some high-exposure or occupational settings.\"}]","Arsenic exposure and skin cancer: Mechanisms, clinical evidence and public health implications - Review | PDF",1790083438,43]