"CHEMICALLY-INDUCED ALTERATIONS IN SEXUAL AND FUNCTIONAL DEVELOPMENT: THE WILDLIFE/HUMAN CONNECTION"1

In July, 1991, scientists from many different fields, including reproductive physiology, medicine, law, psychiatry, wildlife management, toxicology, and immunology, gathered at the Wingspread Conference Center in Racine, Wisconsin. Individually, they were concerned about certain disturbing results from their research. For example, female fish in the effluent from a pulp and paper mill on the Gulf coast of Florida developed the conspicuous external feature and some of the behavior of the male of their species.2 Other scientists had observed reproductive stress and other problems in many species of birds, fish, mud snails, and mammals in the Great Lakes of North America, the coast of southern California, Puget Sound, and Europe.

Encouragement for the [Wingspread Work Session] came from lengthy conversations with biologists who had observed the anomalies in wildlife, with basic scientists who had demonstrated the sensitivity to perturbation of the developing endocrine system, with toxicologists who had reported on the results of exposing laboratory animals to endocrine-system-disrupting chemicals found in the environment, and with researchers who had documented the similarity in the anomalies in laboratory animals and humans exposed to diethylstilbestrol (DES) in the womb.3


"Furthermore, it is of concern that many of the abnormalities are not expressed during fetal and neonatal life and only become apparent after puberty. . ."


In the textbook stemming from the Wingspread Conference the scientists have written chapters giving information that led them to their powerful consensus statement. From the "Wingspread Consensus Statement":

We are certain of the following:

A large number of man-made chemicals that have been released into the environment, as well as a few natural ones, have the potential to disrupt the endocrine system of animals, including humans. Among these are the persistent, bioaccumulative, organohalogen compounds [organic compounds containing, for example, chlorine, bromine, or fluorine] that include some pesticides (fungicides, herbicides, and insecticides) and industrial chemicals, other synthetic products, and some metals. . . . The patterns of effects vary among species and among compounds. Four general points can nonetheless be made: (1) the chemicals of concern may have entirely different effects on the embryo, fetus, or perinatal organism than on the adult; (2) the effects are most often manifested in offspring, not in the exposed parent; (3) the timing of exposure in the developing organism is crucial in determining its character and future potential; and (4) although critical exposure occurs during embryonic development, obvious manifestations may not occur until maturity.

We estimate with confidence that:

Some of the developmental impairments reported in humans today are seen in adult offspring of parents exposed to synthetic hormone disrupters. . . released in the environment. The concentrations of a number of [them] measured in the US human population today are well within the range and dosages at which effects are seen in wildlife populations. In fact, experimental results are being seen at the low end of the current environmental concentrations [emphasis added].4

Professor Richard E. Peterson and his team at the University of Wisconsin, Madison, fed pregnant rats tiny doses of the most toxic dioxin (TCDD). Unfortunately, along with many other similar chlorine-containing compounds, dioxins are ubiquitous in our environment. Dioxins are contaminants of many pesticides; they are released in incinerator plumes; and they are a by-product of the chlorine bleaching of paper. PCBs are similar to the dioxins. In fact, many of the biological effects of all these other chlorine-containing compounds, although lesser, can still be ranked relative to the same effects from TCDD.


Unfortunately, along with many other similar chlorine-containing compounds, dioxins are ubiquitous in our environment. Dioxins are contaminants of many pesticides; they are released in incinerator plumes; and they are a by-product of the chlorine bleaching of paper. PCBs are similar to the dioxins.


Knowing the stages of development and the fragility of the fetus, Professor Peterson's team fed the female rats a single dose of TCDD on "Day 15 of pregnancy." The four groups of treated rats each received a dose of a different potency. The largest dose was one microgram (one millionth of a gram) per kilogram (one thousand grams) of the rat's weight—far too small a dose for any apparent effect on the adult rats or on their litter size. Also, at birth "no male or female offspring with gross external malformations were found."5 However, the males at maturity had significantly smaller sex organs, lowered sperm count ("75 percent decrease" even at the much smaller maternal dose of 0.064 micrograms of TCDD per kilogram),6 and a more than 200 percent increase in "feminine sexual behavior."7

During sexual differentiation there are a number of critical periods when the reproductive system is uniquely susceptible to chemically-induced perturbations. At these times an inappropriate chemical signal can result in irreversible lesions that often result in infertility, whereas similarly exposed young adults are only transiently affected. The serious reproductive abnormalities that resulted from human fetal exposure to DES, synthetic hormones, and other drugs provide grim examples of the types of lesions that can be produced by interfering with this process. Furthermore, it is of concern that many of the abnormalities are not expressed during fetal and neonatal life and only become apparent after puberty. . . . The list of known developmental reproductive toxicants includes a broad spectrum of drugs, pesticides, and [other] toxic substances. Some of the xenobiotics, like the PCBs and dioxins, are of particular concern because they persist in the environment and bioaccumulate in the food chain. The fact that these toxicants alter sex differentiation through a wide variety of relatively well understood physiological mechanisms that are common to all mammals allows scientists to use rodent models to predict potential adverse outcomes in humans, domestic animals, and wildlife.8


"Some of the xenobiotics, like the PCBs and dioxins, are of particular concern because they persist in the environment and bioaccumulate in the food chain."


Most of the food sold in the United States has been treated with pesticides, which are registered to kill target organisms but which have not been tested for endocrine and multigeneration effects on either us or other "nontarget" organisms. Even those of us who carefully buy "certified organic" food know that it is only chemically less contaminated than the regular products in supermarkets. Drift of pesticides, PCBs, and other man-made contaminants is worldwide—"these chemicals have reached both the Arctic and Antarctic via the atmosphere."9

"Nearly all cultivated cropland in the United States is treated annually with at least one herbicide."10 We are also exposed to pesticides from contaminated drinking and rain water. Unfortunately, especially children can ingest pesticides from house dust and yard soil. There are many excellent alternatives to using pesticides and other toxic chemicals in our homes and gardens. We need to pursue these alternatives.


The compelling conclusion to this experiment and its repeatable results in the organic community is that the highly touted benefit assumptions for pesticide and fertilizer inputs are nonexistent.


Also, for our agricultural production there is no need for pesticides and chemical fertilizers. When government scientists make a "risk/benefit analysis" for a pesticide, they often assume that benefits are great because they believe that production is higher than when no pesticides are used. However, the test plots that they don't spray with pesticides are still contaminated by past sprayings so that the natural biological controls have had no opportunity to return. It takes at least three years of no chemical treatment for some balance to return. John Bell Clark, holder of a PhD in biochemistry from the University of California, Berkeley, and an organic farmer on 1800 acres in Michigan since 1980, describes how he and his wife, Merrill, have increased production on their farm above the level of production when chemicals were used there. "Yields get better as organic practices are continued, and pest problems virtually disappear. Natural pest controls, which are suppressed in chemical farming, get healthier and more effective every year. Plant and livestock health improves, soil tilth improves every year, and so does soil moisture retention. . . . The compelling conclusion to this experiment and its repeatable results in the organic community is that the highly touted benefit assumptions for pesticide and fertilizer inputs are nonexistent.11

___________

1Colborn, Theo and Coralie Clement, Chemically-Induced Alterations in Sexual and Functional Development: The Wildlife/Human Connection, Volume XXI, Advances in Modern Environmental Toxicology, Princeton Scientific Publishing Co., Inc., Princeton, NJ, 1992.

2Ibid., pp. 113-127.

3Ibid., p. xiii.

4Ibid., pp.1-3.

5Ibid., p. 148.

6Ibid., p. 181.

7Ibid., p. 185.

8Ibid., p. 203.

9Ibid., p. xiv.

10Ibid., p. 348.

11Clark, John Bell, "Notes from an Organic Farmer," The Human Ecologist,  Spring 1990, Number 45, p. 5.

*This article was first published in the Spring 1970 issue of the Human Ecology Study Group newsletter. Dr. Randolph has kindly given us his permission to publish it again.

Article from NOHA NEWS, Vol. XVIII, No. 2, Spring 1994, pages 1-2.