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Cancers
Par Betsi G, Koumaki D, Kountouri A et 1 autres.
Contenu en anglais
This review investigated whether exposure to certain endocrine-disrupting chemicals (EDCs) increases skin cancer risk.
We performed a comprehensive narrative review of in vitro, animal, and human studies examining the association of EDCs with melanoma and non-melanoma skin cancer (NMSC).
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Chemicals are classified as (i) established EDCs with evidence of skin carcinogenicity; (ii) chemicals that are carcinogenic with endocrine-related effects; and (iii) chemicals with limited or uncertain evidence. Proposed carcinogenic mechanisms include oxidative stress, chronic inflammation, immunosuppression, DNA repair inhibition, and epigenetic alterations; AhR likely mediates the carcinogenicity of dioxin (TCDD), dioxin-like PCBs, and PAHs. Epidemiological evidence linking PCBs with melanoma is inconsistent. High cumulative occupational exposure to PAH-containing mineral oils or tar/pitch increases skin cancer risk. Evidence for PFAS and skin cancer is limited and inconsistent. Increased melanoma incidence has been reported after chronic occupational exposure to certain pesticides, including carbaryl, parathion, and maneb/mancozeb. There is substantial evidence of a dose-response association between chronic arsenic exposure and NMSC risk.
High chronic exposure to specific EDCs (especially arsenic, certain PAHs, and certain pesticides) may increase skin cancer risk. For several chemicals, evidence supports carcinogenicity with endocrine-related effects, but direct mechanistic evidence that endocrine disruption specifically mediates skin carcinogenesis is lacking.
Publié dans Cancers. Le résumé est reproduit tel qu’il a été publié et reste l’œuvre de ses auteurs ; lisez l’article complet à la source.
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