Environmental endocrine disruptors and breast cancer: The role of bisphenols, polychlorinated biphenyls, parabens, and dioxins

IF 4.2 3区环境科学与生态学 Q2 ENVIRONMENTAL SCIENCES

Environmental toxicology and pharmacology Pub Date : 2025-10-01 DOI:10.1016/j.etap.2025.104834

Marina Sánchez-Ocaña, Vicenç Ruiz de Porras

{"title":"Environmental endocrine disruptors and breast cancer: The role of bisphenols, polychlorinated biphenyls, parabens, and dioxins","authors":"Marina Sánchez-Ocaña, Vicenç Ruiz de Porras","doi":"10.1016/j.etap.2025.104834","DOIUrl":null,"url":null,"abstract":"<div><div>Breast cancer is the most common malignancy in women, and environmental factors such as endocrine-disrupting chemicals (EDCs) contribute to its development and progression. This review examines the roles of four major EDCs—bisphenols, polychlorinated biphenyls (PCBs), parabens, and dioxins—integrating mechanistic and epidemiological evidence. A key pathway is the cross-talk between estrogen receptor (ER) and aryl hydrocarbon receptor (AhR), which regulates proliferation, survival, and immune evasion. Bisphenol A (BPA) promotes proliferation, migration, epigenetic reprogramming, and immune escape. PCBs, particularly PCB-153, are linked to metabolic alterations, inflammation, and variable epidemiological associations. Parabens, common in cosmetics, display estrogenic activity and affect oxidative stress, tumor marker expression, and metastasis. Dioxins, especially TCDD, act via AhR to induce inflammation, immunosuppression, and metastasis, with epidemiological links to cancer risk near emission sources. Collectively, these EDCs disrupt hormonal pathways, alter gene expression, and modulate the tumor microenvironment, underscoring the need for further research, regulation, and public health interventions.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"119 ","pages":"Article 104834"},"PeriodicalIF":4.2000,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Environmental toxicology and pharmacology","FirstCategoryId":"93","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1382668925002091","RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"ENVIRONMENTAL SCIENCES","Score":null,"Total":0}

引用次数: 0

Abstract

Breast cancer is the most common malignancy in women, and environmental factors such as endocrine-disrupting chemicals (EDCs) contribute to its development and progression. This review examines the roles of four major EDCs—bisphenols, polychlorinated biphenyls (PCBs), parabens, and dioxins—integrating mechanistic and epidemiological evidence. A key pathway is the cross-talk between estrogen receptor (ER) and aryl hydrocarbon receptor (AhR), which regulates proliferation, survival, and immune evasion. Bisphenol A (BPA) promotes proliferation, migration, epigenetic reprogramming, and immune escape. PCBs, particularly PCB-153, are linked to metabolic alterations, inflammation, and variable epidemiological associations. Parabens, common in cosmetics, display estrogenic activity and affect oxidative stress, tumor marker expression, and metastasis. Dioxins, especially TCDD, act via AhR to induce inflammation, immunosuppression, and metastasis, with epidemiological links to cancer risk near emission sources. Collectively, these EDCs disrupt hormonal pathways, alter gene expression, and modulate the tumor microenvironment, underscoring the need for further research, regulation, and public health interventions.

查看原文本刊更多论文

环境内分泌干扰物与乳腺癌：双酚、多氯联苯、对羟基苯甲酸酯和二恶英的作用

乳腺癌是女性中最常见的恶性肿瘤，环境因素如内分泌干扰化学物质（EDCs）有助于其发展和进展。本文综述了四种主要的edcs -双酚、多氯联苯（PCBs）、对羟基苯甲酸酯和二恶英-综合机理和流行病学证据的作用。雌激素受体（ER）和芳烃受体（AhR）之间的串扰是调控细胞增殖、存活和免疫逃避的关键途径。双酚A （BPA）促进增殖、迁移、表观遗传重编程和免疫逃逸。多氯联苯，特别是多氯联苯-153，与代谢改变、炎症和不同的流行病学关联有关。对羟基苯甲酸酯在化妆品中很常见，具有雌激素活性，影响氧化应激、肿瘤标志物表达和转移。二恶英，特别是TCDD，通过AhR诱导炎症、免疫抑制和转移，与排放源附近的癌症风险有流行病学联系。总的来说，这些EDCs破坏激素通路，改变基因表达，调节肿瘤微环境，强调了进一步研究、调控和公共卫生干预的必要性。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Environmental toxicology and pharmacology 医学-毒理学

CiteScore

7.00

自引率

4.70%

发文量

185

审稿时长

34 days

期刊介绍： Environmental Toxicology and Pharmacology publishes the results of studies concerning toxic and pharmacological effects of (human and veterinary) drugs and of environmental contaminants in animals and man. Areas of special interest are: molecular mechanisms of toxicity, biotransformation and toxicokinetics (including toxicokinetic modelling), molecular, biochemical and physiological mechanisms explaining differences in sensitivity between species and individuals, the characterisation of pathophysiological models and mechanisms involved in the development of effects and the identification of biological markers that can be used to study exposure and effects in man and animals. In addition to full length papers, short communications, full-length reviews and mini-reviews, Environmental Toxicology and Pharmacology will publish in depth assessments of special problem areas. The latter publications may exceed the length of a full length paper three to fourfold. A basic requirement is that the assessments are made under the auspices of international groups of leading experts in the fields concerned. The information examined may either consist of data that were already published, or of new data that were obtained within the framework of collaborative research programmes. Provision is also made for the acceptance of minireviews on (classes of) compounds, toxicities or mechanisms, debating recent advances in rapidly developing fields that fall within the scope of the journal.