Endocrine-disrupting chemicals and uterine fibroids
Emerging experimental data in animal models and epidemiologic data in humans support that endocrine-disrupting chemicals may increase the risk of uterine fibroids. Possible mechanisms are reviewed herein.
Volume 106, Issue 4, Pages 967-977
Tiffany A. Katz, Ph.D., Qiwei Yang, Ph.D., Lindsey S. Treviño, Ph.D., Cheryl L. Walker, Ph.D., Ayman Al-Hendy, M.D., Ph.D.
Uterine fibroids are the most frequent gynecologic tumor, affecting 70% to 80% of women over their lifetime. Although these tumors are benign, they can cause significant morbidity and may require invasive treatments such as myomectomy and hysterectomy. Many risk factors for these tumors have been identified, including environmental exposures to endocrine-disrupting chemicals (EDCs) such as genistein and diethylstilbestrol. Uterine development may be a particularly sensitive window to environmental exposures, as some perinatal EDC exposures have been shown to increase tumorigenesis in both rodent models and human epidemiologic studies. The mechanisms by which EDC exposures may increase tumorigenesis are still being elucidated, but epigenetic reprogramming of the developing uterus is an emerging hypothesis. Given the remarkably high incidence of uterine fibroids and their significant impact on women's health, understanding more about how prenatal exposures to EDCs (and other environmental agents) may increase fibroid risk could be key to developing prevention and treatment strategies in the future.