Endocrine Disruptors and Endometriosis Risk

In: ISGE Series · 2020 · pp. 1–8 · doi:10.1007/978-3-030-57866-4_1 · W3110866202
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Endometriosis pathogenesis involves hormonal influence, which may be linked to endocrine disruptors' effects on hormone-sensitive tissues.

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This paper reviews evidence on whether endocrine-disrupting chemicals contribute to endometriosis risk, framing endometriosis pathogenesis as involving hormonal influences alongside inflammatory theories. It summarizes findings across environmental epidemiology and mechanistic studies, including associations between in utero or biomarker-based exposure to compounds such as bisphenol A and phthalates (and also dioxin-related pathways) and endometriosis, as well as animal and in vitro data showing estrogenic activity, immune/inflammatory effects, and endometrial receptor changes. A key caveat is that the chapter does not establish a single consensus pathogenic mechanism and synthesizes heterogeneous study designs and exposure measures. This paper is centrally about endometriosis — it specifically reviews endocrine-disruptor exposures (e.g., bisphenol A, phthalates, and dioxin-related factors) and their links to endometriosis risk and pathogenesis.

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Abstract

Endometriosis is defined as the presence of endometrial-type mucosa outside the uterine cavity. Several theories have been proposed during the last 20 years to explain the disease pathogenesis; however, a unique consensus has not yet been established. Although the most recent pathogenic theory is based on inflammatory causes [1], hormonal influence is certainly involved not only in the endometriosis pathogenesis but also in its development and progression [2]. Access this chapter Tax calculation will be finalised at checkout Purchases are for personal use only Similar content being viewed by others

References

Sourial S, Tempest N, Hapangama DK. Theories on the pathogenesis of endometriosis. Int J Reprod Med. 2014;2014:179515. Di Guardo F, et al. Management of women affected by endometriosis: are we stepping forward? J Endo Pelvic Pain Dis. 2019;11(2):77–84. Roy D, et al. Integrated bioinformatics, environmental epidemiologic and genomic approaches to identify environmental and molecular links between endometriosis and breast Cancer. Int J Mol Sci. 2015;16(10):25285–322. Preciados M, et al. Estrogenic endocrine disrupting chemicals influencing NRF1 regulated gene networks in the development of complex human brain disease. Int J Mol Sci. 2016;17(12):2086. Welshons WV, et al. Large effects from small exposures. I. Mechanisms for endocrine-disrupting chemicals with estrogenic activity. Environ Health Perspect. 2003;111(8):994–1006. Borgeest C, et al. The effects of endocrine disrupting chemicals on the ovary. Front Biosci. 2002;7:d1941–8. Zoeller RT, et al. Endocrine-disrupting chemicals and public health protection: a statement of principles from the Endocrine Society. Endocrinology. 2012;153(9):4097–110. Street ME, et al. Current knowledge on endocrine disrupting chemicals (EDCs) from animal biology to humans, from pregnancy to adulthood: highlights from a national Italian meeting. Int J Mol Sci. 2018;19(6):1647. Skinner MK. Endocrine disruptors in 2015: epigenetic transgenerational inheritance. Nat Rev Endocrinol. 2016;12(2):68–70. Craig ZR, et al. Endocrine-disrupting chemicals in ovarian function: effects on steroidogenesis, metabolism and nuclear receptor signaling. Reproduction. 2011;142(5):633–46. Li X, Frank AA. Improvement of bisphenol A quantitation from urine by LCMS. Anal Bioanal Chem. 2015;407(13):3869–74. Kim JH. Analysis of the in vitro effects of di-(2-ethylhexyl) phthalate exposure on human uterine leiomyoma cells. Exp Ther Med. 2018;15(6):4972–8. Germaine M, et al. Bisphenol A and phthalates and endometriosis, the ENDO study. Fertil Steril. 2013;100(1):162–9. Michalowicz J. Bisphenol A-sources toxicity and biotransformation. Environ Toxicol Pharmacol. 2014;37(2):738–58. Li Y, et al. Differential in vitro biological action, coregulator interactions, and molecular dynamic analysis of bisphenol A (BPA), BPAF, and BPS ligand-ERa complexes. Environ Health Perspect. 2018;126(1):017012. Watson CS, et al. Nongenomic signaling pathways of estrogen toxicity. Toxicol Sci. 2010;115(1):1–11. Xu J, et al. Developmental Bisphenol A exposure modulates immune-related diseases. Toxics. 2016;4(4):23. North ML, et al. Effects of phthalates on the development and expression of allergic disease and asthma. Ann Allergy Asthma Immunol. 2014;112(6):496–502. Okubo T, et al. Estimation of estrogenic and anti-estrogenic activities of some phthalate diesters and monoesters by MCF-7 cell proliferation assay in vitro. Biol Pharm Bull. 2003;26:1219–24. Ferguson KK, et al. Associations between maternal biomarkers of phthalate exposure and inflammation using repeated measurements across pregnancy. PLoS One. 2015;10(8):90135601. Upson K, et al. Organochlorine pesticides and risk of endometriosis: findings from a population-based case-control study. Environ Health Perspect. 2013;121(11–12):1319–24. Igarashi T, et al. Expression of Ah receptor and dioxin-related genes in human uterine endometrium in women with or without endometriosis. Endocr J. 1999;46:765–72. Bruner-Tran KL, et al. Dioxin may promote inflammation-related development of endometriosis. Fertil Steril. 2008;89(5 Suppl):1287–98. Missmer SA, et al. In utero exposures and the incidence of endometriosis. Fertil Steril. 2004;82(6):1501–8. Aldad TS, et al. Bisphenol-A exposure alters endometrial progesterone receptor expression in the nonhuman primate. Fertil Steril. 2011;96(1):175–9. Cho YJ, Park SB, Han M. Di-(2-ethylhexyl)-phthalate induces oxidative stress in human endometrial stromal cells in vitro. Mol Cell Endocrinol. 2015;407:9–17. Signorile PG, et al. Pre-natal exposure of mice to bisphenol A elicits an endometriosis-like phenotype in female offspring. Gen Comp Endocrinol. 2010;168(3):318–25. Cobellis L, et al. High plasma concentrations of di-(2-ethylhexyl)-phthalate in women with endometriosis. Hum Reprod. 2003;18(7):1512–5. Kim SH, et al. Increased plasma levels of phthalate esters in women with advanced-stage endometriosis: a prospective case-control study. Fertil Steril. 2011;95(1):357–9. Cobellis L, et al. Measurement of bisphenol A and bisphenol B levels in human blood sera from healthy and endometriotic women. Biomed Chromatogr. 2009;23(11):1186–9. Weuve J, et al. Association of exposure to phthalates with endometriosis and uterine leiomyomata: findings from NHANES, 1999–2004. Environ Health Perspect. 2010;118(6):825–3. Louis B, et al. Bisphenol A and phthalates and endometriosis, the ENDO study. Fertil Steril. 2013;100(1):162–169.e2. Itoh H, et al. Urinary bisphenol-A concentration in infertile Japanese women and its association with endometriosis: a cross-sectional study. Environ Health Prev Med. 2007;12:258–64. Upson K, et al. A population-based case-control study of urinary bisphenol A concentration and risk of endometriosis. Hum Reprod. 2014;29(11):2457–64. Rashidi BH. A case-control study of Bisphenol A and endometrioma among subgroup of Iranian women. J Res Med Sci. 2017;22:7. Author information Authors and Affiliations Corresponding author Editor information Editors and Affiliations Rights and permissions Copyright information © 2021 International Society of Gynecological Endocrinology About this chapter Cite this chapter Palumbo, M., Di Guardo, F. (2021). Endocrine Disruptors and Endometriosis Risk. In: Genazzani, A.R., Nisolle, M., Petraglia, F., Taylor, R.N. (eds) Endometriosis Pathogenesis, Clinical Impact and Management. ISGE Series. Springer, Cham. https://doi.org/10.1007/978-3-030-57866-4_1 Download citation DOI: https://doi.org/10.1007/978-3-030-57866-4_1 Published: Publisher Name: Springer, Cham Print ISBN: 978-3-030-57865-7 Online ISBN: 978-3-030-57866-4 eBook Packages: MedicineMedicine (R0)

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