The Environmental Protection Agency defines an endocrine disruptor as an external agent that interferes in some way with the role of natural hormones in the body. (Hmm. Doesn’t sound too bad.). Compounds which earn the title as an endocrine disruptor include a variety of chemical classes, including drugs, pesticides, compounds used in the plastics industry and in consumer products, industrial by-products and pollutants, and even some naturally produced botanical chemicals. Specific chemicals which are known to be endocrine disruptors include Bisphenol A, phthalates, alkylphenols, polychlorinated biphenyls and polybrominated diphenyl ethers – all used in textile processing.
The endocrine system includes the glands (e.g., thyroid, pituitary gland, pancreas, ovaries, or testes) and their secretions (i.e., hormones), that are released directly into the body’s circulatory system. The endocrine system controls blood sugar levels, blood pressure, metabolic rates, growth, development, aging, and reproduction. “Endocrine disruptor” is a much broader concept than the terms reproductive toxin, carcinogen, neurotoxin, or teratogen. Scientists use one or more of these terms to describe the types of effects these chemicals have on us.
How do they work? This is from The Society of Environmental Toxicology and Chemistry (SETAC):
Humans and wildlife must regulate how their bodies function to remain healthy in an ever-changing environment. They do this through a complicated exchange between their nervous and endocrine systems. The endocrine systems in humans and wildlife are similar in that they are made up of internal glands that manufacture and secrete hormones. Hormones are chemical messengers that move internally, start or stop various functions, and are important in determining sleep/wake cycles, stimulating or stopping growth, or regulating blood pressure. Some of the most familiar hormones in humans or wildlife are those that help determine male and female gender, as well as control the onset of puberty, maturation, and reproduction. An endocrine disruptor interferes with, or has adverse effects on, the production, distribution, or function of these same hormones. Clearly, interference with or damage of hormones could have major impacts on the health and reproductive system of humans and wildlife, although not all of the changes would necessarily be detrimental.
But why the fuss over endocrine disruptors - and why now? After all, scientists had known for over fifty years that DDT can affect the testes and secondary sex characteristics of young roosters1.
And for almost as long, it has been well known that daughters born to women who took the drug diethylstilbestrol (DES), a synthetic estrogen, early in their pregnancies had a greatly increased risk of vaginal cancer. 2
And it has been known for over 25 years that occupational exposures to pesticides could “diminish or destroy the fertility of workers.”3
It wasn’t until Theo Colborn, a rancher and mother of four who went back to school at age 51 to get her PhD in zoology, got a job at the Conservation Foundation and began to put the pieces together that the big picture emerged. Theo’s job was to review other scientists’ data, and she noticed that biologists investigating the effects of presumably carcinogenic chemicals on predators in and around the Great Lakes were reporting odd phenomena:
- Whole communities of minks were failing to reproduce;
- startling numbers of herring gulls were being born dead, their eyes missing, their bills misshapen;
- and the testicles of young male gulls were exhibiting female characteristics.
- And frogs were born in many different configurations!
Colborn correlated this data with the presence in the water of organochlorine compounds such as PCBs, DDT, and dieldrin, some of which have hormone-mimicking effects and build up in fatty tissue. Often, the offspring of creatures exposed to chemicals were worse off than the animals themselves. Colborn concluded that nearly all the symptoms could be traced to things going awry in the endocrine system.
In 1991, Colborn called together a conference, whose participants included biologists, endocrinologists and toxicologists as well as psychiatrists and lawyers, at the Wingspread Conference Center in Racine, Wisconsin. They produced what become known as the “Wingspread Statement,” the core document of the endocrine-disruption hypothesis, in which these researchers concluded that observed increases in deformities, evidence of declining human fertility and alleged increases in rates of breast, testicular and prostate cancers, as well as endometriosis are the result of “a large number of man-made chemicals that have been released into the environment”.4
Endocrine disruption—the mimicking or blocking or suppression of hormones by industrial or natural chemicals— appeared to be affecting adult reproductive systems and child development in ways that far surpassed cancer, the outcome most commonly looked for by researchers at the time. Potential problems included infertility, genital abnormalities, asthma, autoimmune dysfunction, even neurological disorders involving attention or cognition. In one early study that Colborn reviewed, for instance, an Environmental Protection Agency (EPA) commissioned psychologists to study children whose mothers ate fish out of the Great Lakes. The researchers found that the children “were born sooner, weighed less, and had smaller heads” than those whose mothers hadn’t eaten the fish. Moreover, the more PCBs that were found in the mother’s cord blood, the worse the child did on tests for things such as short-term memory. By age eleven, the most highly exposed kids had an average IQ deficit of 6.2.5
The endocrine disruptor hypothesis first came to widespread congressional attention in 1996, with the publication of the book Our Stolen Future – by Theo Colborn, Dianne Dumanoski and John Peterson Myers.6
In the years since the Wingspread conference, many of its fears and predictions have been fleshed out by new technologies that give a far more precise picture of the damage that toxins can wreak on the human body – and especially on developing fetuses, which are “exquisitely sensitive to both the natural hormone signals used to guide its development, and the unexpected chemical signals that reach it from the environment”7
Thanks to a computer-assisted technique called microarray profiling, scientists can examine the effects of toxins on thousands of genes at once (before they could study 100 at a time at most). They can also search for signs of chemical subversion at the molecular level, in genes and proteins. This capability means that we are beginning to understand how even tiny doses of certain chemicals may switch genes on and off in harmful ways during the most sensitive period of development.
The endocrine disruption hypothesis has also unleashed a revolution in toxicity theory. The traditional belief that “the dose makes the poison” (the belief that as the dose increases, so does the effect; as the dose decreases, so does its impact) has proven inadequate in explaining the complex workings of the endocrine system, which involves a myriad of chemical messengers and feedback loops.
Experimental data now shows conclusively that some endocrine-disrupting contaminants can cause adverse effects at low levels that are different from those caused by high level exposures. For example, when rats are exposed in the womb to 100 parts per billion of DES, they become scrawny as adults. Yet exposure of just 1 part per billion causes grotesque obesity.8 Old school toxicology has always assumed that high dose experiments can be used to predict low-dose results. With ‘dose makes the poison’ thinking, traditional toxicologists didn’t pursue the possibility that there might be effects at levels far beneath those used in standard experiments. No health standards incorporated the possibility.
Jerry Heindel, who heads a branch of the National Institute of Environmental Health Science (NIEHS) that funds studies of endocrine disruptors, said that a fetus might respond to a chemical at “one hundred-fold less concentration or more, yet when you take that chemical away, the body is nonetheless altered for life”. Infants may seem fine at birth, but might carry within them a trigger only revealed later in life, often in puberty, when endocrine systems go into hyperdrive. This increases the adolescent’s or adult’s chances of falling ill, getting fat, or becoming infertile – as is the case with DES, where exposure during fetal development doesn’t show up until maturity.
And not just the child’s life, but her children’s lives too. “Inside the fetus are germ cells that are developing that are going to be the sperm and oocytes for the next generation, so you’re actually exposing the mother, the baby, and the baby’s kids, possibly,” says Heindel.9
So it’s also the timing that contributes to the poison.
According to Our Stolen Future, “the weight of the evidence says we have a problem. Human impacts beyond isolated cases are already demonstrable. They involve impairments to reproduction, alterations in behavior, diminishment of intellectual capacity, and erosion in the ability to resist disease. The simple truth is that the way we allow chemicals to be used in society today means we are performing a vast experiment, not in the lab, but in the real world, not just on wildlife but on people.”
1 Burlington, F. & V.F. Lindeman, 1950. “Effect of DDT on testes and secondary sexcharacteristics of white leghorn cockerels”. Proc. Society for Experimental Biologyand Medicine 74: 48–51.
2 Herbst, A., H. Ulfelder, and D. Poskanzer. “Adenocarcinoma of the vagina: Association of maternal stilbestrol therapy with tumor appearance in young women,” New England Journal of Medicine, v. 284, (1971) p. 878-881.
3 Moline, J.M., A.L. Golden, N. Bar-Chama, et al. 2000. “Exposure to hazardous substances and male reproductive health: a research framework”. Environ. Health Perspect. 108: 1–20.
4 Shulevitz,Judith, “The Toxicity Panic”, The New Republic, April 7, 2011.
6 Colborn, Theo, Dianne Dumanoski, and John Peterson Myers. Our Stolen Future: Are We Threatening Our Fertility, Intelligence, and Survival? A Scientific Detective Story. New York: Penguin. (1996) 316 p.
9 Shulevitz,Judith, op. cit.