By Craig Turczynski, Ph.D.
There is plenty of evidence that the risk of exposure to environmental estrogens is significant. For an excellent review, read Estrogeneration by Dr. Anthony G. Jay (2017). There are several potential sources of estrogen-like substances, but curiously, an examination of the literature reveals that many studies avoid even mentioning ethinyl estradiol (EE2), the synthetic estrogen found in most oral contraception. Dr. Jay of course, being an exception, begins discussing the potential risks in his first chapter. This brings up an interesting point, that our opinions and world view influence our science and how we report on it. A few other studies are also worth noting on this topic. One was published by the EPA (Zorrilla et al., 2010), reporting the effect of EE2 on spermatogenesis in the adult male rat. Treatment of male rats with EE2 did indeed result in a decrease in sperm counts in a dose-dependent manner. Also, a review of literature was published in 2017 by Adeel et al., a group from China. This group clearly seems to avoid the politically correct posture of not mentioning EE2 as a significant source of environmental estrogen. They state:
“It is worthwhile to comment on the paucity [scarcity] of data on the synthetic EE2 compared with the natural E1 and E2.”
They make a concluding statement:
“Synthetic estrogen, ethinyl estradiol, is more persistent in the environment than natural estrogens and may be a greater cause for environmental concern.”
On the other hand, they make another statement about livestock waste being the largest source of environmental estrogen, which left me somewhat perplexed. Especially since the number of cattle in the US is less than 95 million, down from 120 million in the mid 1970s (USDA-NASS, 2018) and the number of people in the US is over 300 million. This led me to do some research and data crunching which revealed something truly startling on the magnitude of the oral contraception risk. Please indulge me on the calculations below.
The accuracy of these numbers could no doubt be disputed; they are an oversimplification and an estimate. The fact remains, however, that because of the synthetic structure of EE2, it is more resistant to degradation and therefore environmental levels are increasing over time. Dr. Anthony Jay (2017) points out the fact that most estrogens are not removed during the water recycling process and filtering them out is problematic as well. Coupled with the other sources of estrogens in our environment, the chances of health-related effects are a real concern. Concentration, duration, and age of first exposure would have a profound consequence for an individual. For example, exposure during critical times of in-utero development can have a permanent influence on the normal sexual and reproductive development of a person (Hines, 2011; Kilcoyne and Mitchell, 2019). The EPA study I mentioned above (Zorrilla et al., 2010) demonstrated that an exposure of 50 µg of EE2 per kg of weight in adult male rats was enough to reduce sperm counts, and generally rats are more resistant to disease processes than humans.
In conclusion, oral contraception is a significant source of environmental estrogen. If you care about the health of people and you say you want to clean up the environment, you can’t ignore the environmental risks of hormonal contraception, regardless of your social, religious, or political position.
Adeel, M., Song, X., Wang, Y., Francis, D. and Yang, Y. (2017) Environmental Impact Of Estrogens On Human, Animal and Plant Life: A Critical Review. Environment International 99, 107-119.
Brenner, P.F., Goeblesmann, U., Stanczyk, F. Z. and Mishell, D.R. (1980) Serum Levels Of Ethinylestradiol Following Its Ingestion Alone Or In Oral Contraceptive Formulations. Contraception 22(1) 85-95.
Daniels, K. and Abma, J.C. (2018) Current Contraceptive Status Among Women Aged 15–49: United States, 2015–2017. NCHS Data Brief #327.
Hines, M. (2011) Prenatal Endocrine Influences On Sexual Orientation And On Sexually Differentiated Childhood Behavior. Front Neuroendocrinology. 32(2) 170-182 doi:10.1016/j.yfrne.2011.02.006.
Jay, A. G. (2017) Estrogeneration: How Estrogenics Are Making You Fat, Sick and Infertile. Pyrimidine Publishing. Tallahassee FL.
Kilcoyne, K.R. and Mitchell, R.T. (2019) Effect Of Environmental And Pharmaceutical Exposures On Fetal Testis Development And Function: A systematic Review Of Human Experimental Data. Human Reproduction Update 25 (4) 397-421.
USDA-NASS (2018) US All Cattle and Calves Inventory 1867-2019. https://www.nass.usda.gov/Charts_and_Maps/Cattle/inv.php
Zorrilla, L. M., K. H. Brown, L. F. Strader, and T. E. Stoker (2010). The Effects Of Ethinyl Estradiol On Spermatogenesis In The Adult Rat. EPA record 218968, https://cfpub.epa.gov/si/si_public_record_report.cfm?Lab=NHEERL&dirEntryId=218968
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