scholarly journals Endocrine disrupting chemicals and breast cancer: a systematic review of epidemiological studies

Author(s):  
Murphy Lam Yim Wan ◽  
Vanessa Anna Co ◽  
Hani El-Nezami
2020 ◽  
Vol 21 (23) ◽  
pp. 9139
Author(s):  
Louisane Eve ◽  
Béatrice Fervers ◽  
Muriel Le Romancer ◽  
Nelly Etienne-Selloum

Breast cancer (BC) is the second most common cancer and the fifth deadliest in the world. Exposure to endocrine disrupting pollutants has been suggested to contribute to the increase in disease incidence. Indeed, a growing number of researchershave investigated the effects of widely used environmental chemicals with endocrine disrupting properties on BC development in experimental (in vitro and animal models) and epidemiological studies. The complex effects of endocrine disrupting chemicals (EDCs) on hormonal pathways, involving carcinogenic effects and an increase in mammary gland susceptibility to carcinogenesis—together with the specific characteristics of the mammary gland evolving over the course of life and the multifactorial etiology of BC—make the evaluation of these compounds a complex issue. Among the many EDCs suspected of increasing the risk of BC, strong evidence has only been provided for few EDCs including diethylstilbestrol, dichlorodiphenyltrichloroethane, dioxins and bisphenol A. However, given the ubiquitous nature and massive use of EDCs, it is essential to continue to assess their long-term health effects, particularly on carcinogenesis, to eradicate the worst of them and to sensitize the population to minimize their use.


2001 ◽  
Vol 1 ◽  
pp. 653-655 ◽  
Author(s):  
Jennifer E. Fox ◽  
Matthew E. Burow ◽  
John A. McLachlan

Endocrine disrupting chemicals (EDCs) include organochlorine pesticides, plastics manufacturing by-products, and certain herbicides[1]. These chemicals have been shown to disrupt hormonal signaling in exposed wildlife, lab animals, and mammalian cell culture by binding to estrogen receptors (ER-α and ER-β) and affecting the expression of estrogen responsive genes[2,3]. Additionally, certain plant chemicals, termed phytoestrogens, are also able to bind to estrogen receptors and modulate gene expression, and as such also may be considered EDCs[4]. One example of phytoestrogen action is genistein, a phytochemical produced by soybeans, binding estrogen receptors, and changing expression of estrogen responsive genes which certain studies have linked to a lower incidence of hormonally related cancers in Japanese populations[5]. Why would plants make compounds that are able to act as estrogens in the human body? Obviously, soybeans do not intentionally produce phytoestrogens to prevent breast cancer in Japanese women.


Cancers ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1063 ◽  
Author(s):  
Kaoutar Ennour-Idrissi ◽  
Pierre Ayotte ◽  
Caroline Diorio

Persistent organic pollutants (POPs) bioaccumulate in the food chain and have been detected in human blood and adipose tissue. Experimental studies demonstrated that POPs can cause and promote growth of breast cancer. However, inconsistent results from epidemiological studies do not support a causal relationship between POPs and breast cancer in women. To identify individual POPs that are repeatedly found to be associated with both breast cancer incidence and progression, and to demystify the observed inconsistencies between epidemiological studies, we conducted a systematic review of 95 studies retrieved from three main electronic databases. While no clear pattern of associations between blood POPs and breast cancer incidence could be drawn, POPs measured in breast adipose tissue were more clearly associated with higher breast cancer incidence. POPs were more consistently associated with worse breast cancer prognosis whether measured in blood or breast adipose tissue. In contrast, POPs measured in adipose tissue other than breast were inversely associated with both breast cancer incidence and prognosis. Differences in biological tissues used for POPs measurement and methodological biases explain the discrepancies between studies results. Some individual compounds associated with both breast cancer incidence and progression, deserve further investigation.


Biomedicines ◽  
2020 ◽  
Vol 8 (6) ◽  
pp. 137 ◽  
Author(s):  
Eleonora Rotondo ◽  
Francesco Chiarelli

The purpose of this article is to review the evidence linking background exposure to endocrine-disrupting chemicals (EDCs) with insulin resistance in children. Although evidence in children is scarce since very few prospective studies exist even in adults, evidence that EDCs might be involved in the development of insulin resistance and related diseases such as obesity and diabetes is accumulating. We reviewed the literature on both cross-sectional and prospective studies in humans and experimental studies. Epidemiological studies show a statistical link between exposure to pesticides, polychlorinated bisphenyls, bisphenol A, phthalates, aromatic polycyclic hydrocarbides, or dioxins and insulin resistance.


2010 ◽  
Vol 75 (4) ◽  
pp. 471-492 ◽  
Author(s):  
Yan Cheng ◽  
Hui-ming Chen ◽  
Wen-lian Yu ◽  
Yuan Cui ◽  
Li-li Zhou ◽  
...  

Perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) have become emerging persistent organic pollutants (POPs), but their health effects on humans remain controversial because of contradictory experimental and epidemiological studies. In this study, we used three-dimensional quantitative structure–activity relationship (3D-QSAR) method by applying Surflex-dock to study and compare the binding modes between PFOS, PFOA and eight other endocrine disrupting chemicals, and human estrogen receptor (hERα), human androgen receptor (hAR) and human thyroid receptor (hTRβ). Molecular docking and hydrogen bond studies indicated that PFOS and PFOA had high affinity potency toward hERα, hAR and hTRβ due to low free binding energies, while the highest value was obtained toward hTRβ. This means that PFOS and PFOA might have more disrupting effects on thyroid than on estrogen and androgen receptors. Hydrogen bonding interactions revealed that Met313 in hTRβ might act as the critical amino acid residue in the binding of ligand–receptor complex, which would provide an explanation for the interaction mechanisms. Our results provide an important reference and direction for the interaction mode and mechanism study between PFOS/PFOA and human endocrine systems.


Author(s):  
Elvira V Bräuner ◽  
Youn-Hee Lim ◽  
Trine Koch ◽  
Cecilie S Uldbjerg ◽  
Laura S Gregersen ◽  
...  

Abstract The incidence of many hormone-dependent diseases, including testicular cancer, have sharply increased in all high-income countries during the 20th century. This is not fully explained by established risk factors. Concurrent, increasing exposure to antiandrogenic environmental endocrine disrupting chemicals (EDCs) in fetal life may partially explain this trend. This systematic review assessed available evidence regarding the association between environmental EDC exposure and risk of testicular cancer (seminomas and non-seminomas). Following PRISMA guidelines, a search of English peer-reviewed literature published prior to December 14 th, 2020, in the databases PubMed and Embase® was performed. Among the 279 identified records, 19 were eligible for quality assessment and 10 for further meta-analysis. The completeness of reporting was high across papers, but over 50% were considered subject to potential risk of bias. Mean age at diagnosis was 31.9 years. None considered effects of EDCs multipollutant mixtures. The meta-analyses showed that maternal exposure to combined EDCs was associated with a higher risk of testicular cancer in male offspring (summary RRs: 2.16, (95% CI:1.78-2.62); 1.93 (95% CI:1.49-2.48); 2.78 (95% CI:2.27-3.41) for all, seminoma, non-seminoma respectively). Similarly, high maternal exposures to grouped organochlorines and organo-halogens were associated with higher risk of seminoma and non-seminoma in the offspring. Summary estimates related to postnatal adult male EDC exposures were inconsistent.Maternal but not postnatal adult male, EDC exposures were consistently associated with a higher risk of testicular cancer, particularly risk of non-seminomas. However, the quality of studies was mixed and considering the fields complexity, more prospective studies of prenatal EDC multipollutant mixture exposures and testicular cancer are needed.


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