Wednesday, March 11, 2009

The urinary estrogen theory. Part I

What is the main source of estrogen in the environment? Birth control pills? An industrial compound with estrogenic properties, like DDT, PCBs, and dioxins?

No, it’s women’s urine. The stuff that gets flushed down toilets millions of times a day. There is also testosterone in wastewater but at much lower levels, being less water‑soluble (Tabak et al., 1981). What happens, then, to this estrogen as it wends it way through the environment?

The question has attracted little interest. And perhaps we have no cause for worry. On the one hand, natural estrogen is quickly consumed by nitrifying bacteria if left in a warm stagnant medium with organic matter (Vader et al., 2000). These were the conditions of traditional wastewater disposal, i.e., privies, cesspools, and ditch sewers (Rockefeller, 1996). On the other hand, modern wastewater disposal is very good at removing urinary estrogen. Primary treatment alone removes 35‑55 percent and the proportion rises to 50‑70 percent for primary and secondary treatment combined (Tabak et al., 1981). Today, state‑of‑the­-art treatment plants remove 90 percent of all natural and synthetic estrogenic compounds (LeQuire, 1999).

If there had existed only a traditional system of disposal and a modern system, we would indeed have no cause for worry. But there was a long transitional period with a third system: central collection of wastewater and separation from fecal waste, followed by discharge into local bodies of water without treatment. This kind of sewage system was available to one million Americans in 1860. By 1900, the total had risen to over twenty‑four million, including a million served by primary wastewater treatment (Hyde, 1938). By 1960, untreated wastewater was being produced by 70 million Americans—an all-time high that fell to 2 million after passage of the Clean Water Act in 1972 and subsequent upgrading to secondary treatment of almost all U.S. sewer systems (Copeland, 1993; U.S. Council on Environment Quality, 1984).

As stated above, wastewater treatment currently removes 50 to 90 percent of all wastewater estrogen. Such removal is impaired by two factors: cold temperatures, as shown by seasonal variation in estrogen removal, and lack of bacteria due to short sludge retention (Desbrow et al., 1998; Ternes et al., 1999; Belfroid et al., 1999; Vader et al., 2000). Thus, urinary estrogen persists in the environment only when wastewater is untreated and rapidly discharged into a cold, clear, and largely aqueous medium. From the late 19th century to the 1970s, this was the way we dealt with wastewater in North America and northern Europe.

Cold bodies of water were not just destinations for sewage. They were also sources of drinking and bathing water. Did this situation pose a serious risk of estrogen exposure? No one seems to know. But there is some suggestive evidence.

Estrogen feminizes male rainbow trout (as measured by production of female egg yolk protein) at levels as low as 10 ng per liter of water for estradiol and 25 ng per liter for estrone; above these thresholds the response follows a dose-related curve (Routledge et al., 1998). By comparison, treated wastewater in Great Britain contains 1 to 10 ng of estrogen (either estradiol or estrone) per liter, with levels exceeding 30 ng at the outflow from some sewage treatment plants (Desbrow et al., 1998). Drinking water generally has low or undetectable concentrations. To date, the record seems to be 14 to 22 ng/L for drinking water from Lake Kinneret, Israel (Desbrow et al., 1998, Shore et al., 1993). It should be noted, however, that before the 1980s no one was testing drinking water or wastewater for estrogen pollution (Tabak et al., 1981).

If the public water supply used to be a significant source of estrogen, either via drinking or bathing, the effects should be more serious in young children, whose body tissues are much less sexually differentiated. If serious enough, such effects ought to show up in statistics on male reproductive health, some of which go back to the late 19th century. What do these statistics tell us?

To be continued in my next post


Belfroid, A.C., Van der Horst, A., Vethaak, A.D., Schäfer, A.J., Rijs, G.B.J., Wegener, J., and Cofino, W.P. (1999). Analysis and occurrence of estrogenic hormones and their glucuronides in surface water and waste water in The Netherlands. Sci. Total Environ., 225, 101‑108.

Copeland, C. (1993). Wastewater Treatment: Overview and Background [93-138 ENR] Washington, D.C.: Congressional Research Service.

Desbrow, C., Routledge, E.J., Brighty, G.C., Sumpter, J.P., and Waldock, M. (1998). Identification of estrogenic chemicals in STW effluent. 1. Chemical fractionation and in vitro biological screening. Environ. Sci. Technol., 32, 1549‑1558.

Hyde, C.G. (1938) A review of progress in sewage treatment during the past fifty years in the United States. In: L. Pearse, (ed.) Modern Sewage Disposal. Anniversary Book of the Federation of Sewage Works Associations, pp. 1‑15.

LeQuire, E. (1999). Something in the Water. InSites, 7(1),

Rockefeller, A.A. (1996). Civilization and sludge: Notes on the history of the management of human excreta. Current World Leaders, 39, 99‑113.

Routledge, E.J., Sheahan, D., Desbrow, C., Brighty, G.C., Waldock, M., and Sumpter, J.P. (1998). Identification of estrogenic chemicals in STW effluent. 2. In vivo responses in trout and roach. Environ. Sci. Technol., 32, 1559-1565.

Shore, L.S., Gurevitz, M., and Shemesh, M. (1993). Estrogen as an environmental pollutant. Bull. Environ. Contam. Toxicol., 51, 361‑366.

Tabak, H.H., Bloomhuff, R.N., and Bunch, R.L. (1981). Steroid hormones as water pollutants II. Studies on the persistence and stability of natural urinary and synthetic ovulation‑inhibiting hormones in untreated and treated wastewaters. Dev. Ind. Microbiol., 22, 497‑519.

Ternes, T.A., Stumpf, M., Mueller, J., Haberer, K., Wilken, R.-D., and Servos, M. (1999). Behavior and occurrence of estrogens in municipal sewage treatment plants ‑ I. Investigations in Germany, Canada and Brazil. Sci. Total Environ., 225, 81‑90.

U.S. Council on Environment Quality. (1984). Annual Report. Washington D.C.

Vader, J.S., van Ginkel, C.G., Sperling, F.M.G.M., de Jong, J., de Boer, W., de Graaf, J.S., van der Most, M., and Stokman, P.G.W. (2000). Degradation of ethinyl estradiol by nitrifying activated sludge. Chemosphere, 41, 1239‑1243.


Anonymous said...

In girls estrogen exposure might have caused earlier menarche
Encyclopedia of Children and Childhood in History and Society :Menarche

The median age at menarche in North America, estimated to be around 15.5 years in 1850, decreased by three to four months each decade after 1850, but has remained relatively stable since the 1970s when it reached 12.5 years.

Anonymous said...

Thus, we may see a reduction in the number of male homosexuals over time then.

Anonymous said...


There are other suggested reasons for the decline in the age of menarche, particularly imrovements in nutrition and perhaps changes in the ethnic composition of the American population (age of menarche varies with ethnic/racial background).


I suspect the proportion of male homosexuals will decrease from the current level of 3-5% of all men to about 1%, which may have been the historic baseline level. As I stated earlier, there are probably many causes for male homosexuality, although some are undoubtedly more important than others. So there will always be a certain baseline number.

Anonymous said...

If homosexuality was due to an unnatural exposure to estrogen it would alter a lot more than sexual preference.

Homosexual men would be more likely to have undescended testicles and other physical abnormalities.

Many have suspected hormones as a cause of homosexuality since before World War 2. If it was hormones we'd know something by now.

Anonymous said...

In head to head competition the Urinary Estrogen Theory loses decisively to the Gay Germ Theory for one simple reason. Cochran continues to rack up "wins" at an ever increasing rate.

Maternal flu linked to Schizophrenia and Autism

Stealth Adapted Cytomegalovirus Infections as a Cause of Autism

Toxoplasmosis Parasite May Trigger Schizophrenia And Bipolar Disorders

Link found between TBE and schizophrenia

Do Autoantibodies Cause Narcolepsy?

Herpes Virus Link To Preterm Birth And High Blood Pressure During Pregnancy

Cerebral palsy 'infection link'

Cold Sore Virus Linked To Alzheimer's Disease: New Treatment, Or Even Vaccine Possible

Glandular fever link offers hope of vaccine for MS

I could go on forever.

Anonymous said...

Uggh... I screwed up my first link. Here it is correct.

Maternal Flu Linked To Schizophrenia, Autism In Child

My bad, ok here are some bonus links. 8-)

Schizophrenia linked to immune response in womb

Study Of Human Pancreases Links Virus To Cause Of Type 1 Diabetes

Common Toxoplasma Gondii infection alters personality

Chapter 2.2.
More likely left-handed after more serious childhood bacterial meningitis: support for the pathological left-handedness hypothesis

Anonymous said...


Intuitively, I believe that male homosexuality has many causes, i.e., more than one factor can and probably does disrupt the chain of developmental events that leads to a masculine sexual orientation in the male brain.

Yes, a pathogen may be one such factor. And yes, pathogens can alter behavior (this was a subject of a previous post). But where is the evidence that a pathogen is responsible for male homosexuality? Hmm? I'm not hostile to the Gay Germ theory. I'd just like to see some evidence.

When talking about hormonal effects, we should also distinguish between transient effects (due to current hormonal levels) and organizational effects (due to hormonal levels at some critical phase of development). The first hormonal theory is no longer taken seriously, but the second one is still in the running.

Anonymous said...

Hi Peter,

But where is the evidence that a pathogen is responsible for male homosexuality?

Scientists in the western world do not have the academic freedom to investigate Cochran's hypothesis.

Anonymous said...

What's missing is a molecular biologist willing to actually LOOK for evidence of a pathogen attack on the brain.

According to Greg Cochran, such a person has been impossible to find--too many people worried about careers.

What I wonder is this: why don't reseachers seek to identify the brain structures/chems that are responsible for a male heterosexual
search image? Find that and you've found it's opposite, haven't you?

Yes, of course, I realize that it would appear to be easier to identify brain cell damage than to identify "non-damage," but can't researchers frame the research request in such a way?

Here we are in 2009 and we don't know the biological mechanisms of our urge to mate? Can't THAT get funding?

So, yes, Peter, there is no direct evidence supporting the pathogen theory--just sound evolutionary reasoning and a great hypothesis that no one wants to test.

Anonymous said...


If hormones organized the male brain for homosexuality shouldn't we find dozens of common, physical markers? For instance if extra estrogen in utero produced men with lower than average sperm counts shouldn't gay men tend to have low sperm counts? I don't know if that particular is true but shouldn't there be dozens of known markers that point to estrogen?

In addition if hormones are key why would MZ concordance be so low? Depending on what I've read it ranges from 20% to 30% or so. That doesn't sound obviously hormonal. By comparison MZ twins are about 40% concordant for Type I Diabetes which appears to be triggered by the common Enterovirus.

Anonymous said...

Many people in the field of science have asked of what use would a discovery of the cause(s) of homosexuality be?

There are lots of strong and valid responses to that, but here's the most important one: lots, in fact most boys who wind up gay suffer greatly through their early childhood and adolescence because of gender dysphoria or feelings of being markedly different.

Seems to me it's pretty arrogant of the adult gays who've finally come to terms with who they are (having suffered themselves along the way), to argue that if only society were more understanding, kids would no longer suffer. Their argument assumes a great deal: first, that even if there were no scorn directed at the effiminate or "different" kid, he'd feel perfectly happy; two, that childhood peers themselves would, because of society's new "enlightened" ideas toward homosexuality, no longer view the effeminate male as an odd duck.

These are easy but conveniently myopic and selfish views. I suppose though that they are a bit understandable coming from a minority that has suffered.

Not understandable, however, is that such arguments are offered or adopted by researchers, people who are engaged in looking for the causes (then treatments/cures) of all kinds of things that cause human suffering.

To somehow pretend to conclude or to ignore that homosexuality or the gender dysphoria which often precedes a homosexual orientation will not continue to cause suffering for many children is disingenuous at the very least.