When news isn't new: History of estrogenic chemicals

Twine Line v.16, n.6, Dec94

In 1985 the International Joint Commission slated eleven chemicals among the hundreds polluting the Great Lakes for "virtual elimination" (i.e., zero discharge, where possible). IJC is a treaty organization formed in 1909 by Canada and the U.S. to jointly oversee issues concerning the Great Lakes.

The eleven chemicals were chosen by IJC for their combined toxicity and persistence and resulting bioaccumulative effects. The IJC deemed these substances "toxic" because they are known or suspected to have caused death, disease, or abnormalities in organisms. "Persistence" is a substance's resistance to breaking down into its simpler chemical constituents. It is defined by a chemical's half-life, or how long it takes any amount of chemical to break down to half of its original concentration. The IJC defined eight weeks as persistent. Some chemicals, however, can have a half-life of decades, such as dioxin, which has a half-life from 25 to 100 years.

Of these 11 pollutants, at least four have recently been implicated as "endocrine disruptors" by appearing to exhibit estrogenic effects. That is, they mimic the hormone estrogen, which is essential to reproduction in all male and female vertebrates (i.e., animals with backbones). They have, according to IJC and others, been strongly implicated in the reproductive failures and problems of wildlife and lab animals.

Because humans are also vertebrates, some researchers are suggesting that reproductive problems caused by pollution in some vertebrate populations might explain, or portend, the same reproductive problems or failures in humans. These researchers point to a world-wide decrease in sperm count in males and a higher incidence of breast cancer in females over the last 50 years, among other conditions, that could be associated with elevated exposure to estrogens.

The possibility that a chemical pollutant could act like an animal's hormones may seem like a recent discovery. The popular media treat it as though it were brand new, as did the TV news show 20/20 recently in covering the possible effects of a DDT spill on an alligator population in central Florida's Lake Apopka. Even scientists themselves usually site only recent work in support of their own, leaving the uninitiated to think that scientific insights are newer than they really are.

But experiments dating back to 1933 in the scientific journal Nature show that researchers even then knew about artificial estrogenic activity. Just on the verge of producing synthetic estrogens, they were already publishing what seems like news to us: "Estrogenic properties of a low order are possessed by suitable extracts of such a variety of materials as peat, brown coal, lignite, coal tar and petroleum."¹

These same researchers continue, however, "in view of the fact that many such materials are known to contain carcinogenic constituents, the clinical use of such extracts without very stringent refinement is scarcely to be entertained."

Ironically, only one month later in this same 1933 volume of Nature, two of the scientists revealed the first correlation between estrogen itself and cancer.

These researchers were looking for a "correlation between substances having oestrogenic action and those having carcinogenic properties," because both types of compounds share a similar configuration.² To their surprise, they discovered "oestrus-exciting activity to be possessed by the two most potent carcinogenic hydrocarbons yet known." They write, "we confess that this last result was entirely unexpected; it is very striking that both types of biological activity [hormonal and carcinogenic] should be shown by one and the same compound."

The researchers emphasized that their work said nothing of natural estrogens within a body being carcinogenic. But scientists today do in fact correlate cancer in humans with the presence of estrogen, both synthetic and natural.

So what seems like a ninety's discovery was actually known sixty years ago. Chemists knew that lots of chemicals have estrogenic effects. They learned that "there is no biological action of the naturally occurring estrone which cannot be reproduced by the synthetic estrogenic compounds."³ And they were just as amazed sixty years ago as we are now to learn that something as seemingly delicate and precise as an animal's endocrine system could be altered so easily by chemicals released to the environment. They wrote: "It would have been difficult to imagine that so complicated a series of effects involving an orderly sequence such as that of the estrous phenomena can be induced by anything other than the appropriate hormone."⁴

Other old news comes from research in 1950.⁵ This forty-year-old experiment with DDT revealed the same effects that appeared in Florida's alligator population.

In the experiment, after 25 days of exposure to (injected) DDT, White Leghorn cockerel chicks showed surprisingly retarded growth in their combs and wattles. Because combs and wattles are secondary sex characters (like beards and a deep voice in human males), researchers suspected some effect on the testes.

DDT-treated birds 80 to 90 days old had combs two-and-a-half times smaller than untreated birds of the same age. Their testes, it turns out, were less than one-fifth the size of normal. These researchers suggested that "the effects noted here are such that they might easily be duplicated by the administration of an estrogen. It seems, therefore, that the possibility of an estrogenic action of DDT is at least worthy of consideration."

Other scientists in more elaborate experiments came to the same conclusion nearly 20 years later in 1968 ⁶ and again in 1970.⁷ And now another 24 years later in 1994, a diminished population of Florida alligators, its males exhibiting feminization and reduced genitalia, are once again suggesting the same thing.

1 Cook, J.W., E.C. Dodds, and C.L. Hewett, 1933, Nature, 131:56.
2 Cook J.W. and E.C. Dodds, 1933, Nature, 131:205.
3 Cook, J.W., E.C. Dodds, and W. Lawson, 1933, Proc. Roy. Soc. (London), B121: 133.
4 Solmssen, U.V., 1945, Chemical Reviews, 37:481.
5 Burlington, H. and V.F. Lindeman, 1950, Proc. Soc. Exptl. Biol. Med., 74:48.
6 Welch R.M., W. Levin, and A.H. Conney, 1969, Toxicol. Appl. Pharmacol., 14:358.
7 Bitman, J. and H. Cecil, 1970, J. Agric. Food Chem., 18:1108.

source: http://www.sg.ohio-state.edu/publications/water/tl-1294news.html 11jul01