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Welcome to PSR's Environmental Health Policy Institute, where we ask questions -- then we ask the experts to answer them. Join us as physicians, health professionals, and environmental health experts share their ideas, inspiration, and analysis about toxic chemicals and environmental health policy.


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Prenatal Origins of Cancer and Endocrine Disruptors

Posted on June 16, 2011

By Theo Colborn, PhD

This essay is in response to: What are we learning about the relationship between environmental toxicants and cancer? How should our regulatory system respond to this information?

The developing embryo and fetus are uniquely vulnerable to environmental chemicals because of the route of exposure through the placenta, and the timing of exposure when their critical life systems are organizing while their bodies are being constructed. The research we have compiled demonstrates that many factors, particularly prenatal exposure to pesticides, air pollution, and industrial chemicals (including those we encounter on a daily basis) have been found to predict cancer. Other variables such as maternal age, diet, stress, maternal illness, and birth weight are also associated with cancer. Some are likely to be root causes, while others, such as birth weight, may be both symptoms and causes.

What connects all these variables is interference with the many domains of the endocrine system as it is developing. The endocrine system is the exquisitely balanced system of glands and hormones that regulates such vital functions as growth, metabolism, the production and utilization of insulin, intelligence, behavior, sexual development, and the ability to reproduce, just to mention a few. The brain is one of the most important endocrine organs, particularly in the early weeks of prenatal life, as it controls how the rest of the endocrine system develops. In our research on fetal origins of cancer, the most common cancer-related outcomes were in the brain and nervous system. Understanding how the brain develops in utero, and how it experiences and regulates internally- and externally-induced hormonal fluctuations, is critical to understanding the origins of cancer, as well as many other diseases faced by children and adults in the modern world.

The Endocrine Disruption Exchange (TEDX) has spent many years aggregating and analyzing the bio-medical literature on the possible prenatal origins of cancer. Our spreadsheet and summary of this vast body of research is available here.

In1996 the US Congress gave the EPA a mandate to develop a set of protocols to detect endocrine disruptors. For almost 12 years the EPA has struggled to develop crude assays to identify endocrine disruptors, but its research has never approached the depth needed to reveal how endocrine disruptors can undermine development and function throughout all life stages, from fertilization through adulthood and senescence – knowledge that goes well beyond toxicology. Unfortunately, the kind of research EPA has been doing to identify endocrine disruptors does not provide the kind of information needed to regulate them. Chemical and product manufacturers have exploited that gap in knowledge so that today, not a single chemical has been regulated for its endocrine disrupting properties. Fortunately, over the past decade hundreds of teams of multi-discipline academicians on campuses in many nations have published in peer-reviewed journals about the sensitivity of the endocrine system, from the molecular and gene level through to the human population level. They have probed deep into how chemicals can interfere mechanistically with the many endocrine organs and tissues and have clearly provided enough evidence to ban further production of a number of chemicals.

A new Congressional mandate is needed immediately to enable the EPA and other regulatory agencies to take action on endocrine disruptors by using the vast body of peer-reviewed, academic research already available in the open literature. Much of this 21st century research was funded through extramural support from the National Institute of Environmental Health Sciences to scientists on campuses across the US. Congress must continue to support this badly needed, inner-space in-utero research with the same generosity it funds outer-space research. The time is ripe to use this knowledge as a springboard toward effective chemical regulations.

Over the last 70 years, millions of individuals have experienced chemical exposures in utero and little has been done to reduce the threat to future generations. Fortunately, there are examples in which human exposure to carcinogens has been greatly reduced because of research combined with intense public scrutiny and action. One such example is exposure to cigarette smoke, first-hand, second-hand, and in utero. The numerous bans on smoking in public places, Surgeon General’s warnings, and public education about the carcinogenic effects of cigarettes, particularly for pregnant women, are all changes that were produced by the dedicated efforts of scientists, activists, and knowledgeable legislators. Another example is DES, a pharmaceutical that was commonly prescribed between 1938 and 1971 for complications of pregnancy. The risk of DES to the fetus was made a national issue by a strong coalition of DES mothers and daughters. Their efforts, backed by scientific research, led to the 1971 FDA advisement that physicians stop prescribing DES to pregnant women. The DES story stands out as a unique example of action taken to reduce exposure based specifically on a cancer initiated before birth.

Scientists exploring the role of known endocrine disruptors during embryonic and fetal development have built a strong case that certain endocrine related cancers, including breast, prostate, and testicular cancer, can be traced back to exposure in the womb. We must reverse the increasing incidence and associated costs of endocrine-related disorders, which include some cancers. We have nothing to lose and everything to gain by taking steps immediately to assure that future children are conceived in a cleaner womb environment.


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