Air Date: Week of November 22, 2002

A growing number of researchers believe that prenatal exposure to endocrine disrupters is linked to the occurrence of certain types of cancers in adult animals. Host Steve Curwood talks with EPA toxicologist Linda Birbaum about some of the latest evidence.

Transcript

CURWOOD: We know that pollutants including PCBs and dioxins can alter the hormone systems of animals and humans. Now, new research suggests that there could be a link between prenatal exposure to these chemicals and cancer in adults. Linda Birnbaum directs the experimental toxicology division of the U.S. Environmental Protection Agency. She recently published a paper that summarizes research in this area. Dr. Birnbaum says some of the most interesting animal studies to date link exposure to dioxin in the womb to breast cancers later in life.

BIRNBAUM: Other researchers had published several years ago, had shown that if you exposed animals to dioxin prenatally and then treated them with a known carcinogen, when they were young adults that, in fact, they got a much greater incidence of breast cancer. And in our work, the work that Sue Fenton conducted in collaboration with me, what we did was we looked at the development of the breast following a single-day exposure to dioxin, the dose of one microgram per kilogram bodyweight of the rats, which is a relatively sort of an intermediate dose. It’s certainly higher than humans are exposed to. And what we observed was that the breast structure was actually changed so that now is much more susceptible to exposure to another carcinogen later on in life.

Those results, the results that we had which sort of explained why you got the higher incidence of breast cancer just got me thinking. And my colleague and I began to raise the issue of were we conducting studies in the right way and were we in our human studies trying to associate exposure and effects at the wrong time.

CURWOOD: What types of cancers are most closely linked to the question of early exposure to endocrine disrupters?

BIRNBAUM: In the female, for example, there are changes in carcinogenesis reported in the ovary and the uterus and in the vagina and in the cervix. There’s suggestion of effects on the mammary gland and on the prostate. Also the liver, which is an endocrine target, appears to be affected in some of these studies, as well.

CURWOOD: What’s your sense of what the process is? Is this a single-step process, an organism, a person is exposed to a chemical and then the cancer is like a time bomb waiting to go off, or does something else have to happen to ignite the cancer later in life?

BIRNBAUM: There are two possibilities, or at least two possibilities. One is the first one, that the exposure to a certain type of chemical early in life can in fact be like a time bomb that eventually explodes.

But the second possibility that you mentioned has equal probability for different kinds of chemicals, chemicals that actually early exposure may actually change the structure of an organ so it is now more susceptible to insult later on in life, either by another chemical or by more of the same.

There is some data for PCBs that that may be the case—again, this is experimental animal data. There is some very recent data that’s about to be published demonstrating that developmental exposure in utero to arsenic in mice is associated with cancer, a greatly increased cancer risk in the offspring. And there is some other data that is being presented, not yet published yet, suggesting that certain pesticides or other kinds of chemicals may, in fact, have a similar effect of altering development and increasing the risk of cancer later on.

CURWOOD: How important is the dose versus the timing of the dose?

BIRNBAUM: The timing, for at least the effect that we’re looking at, was very critical in that it really occurred towards the end of organogenesis, which is when the organs are being formed. If we waited until the animals were born or just before they were born, we didn’t get the effect.

CURWOOD: Recently, the long-awaited results of the Long Island breast cancer study were released. That’s the study that looked at the link between environmental toxins and breast cancer by taking blood and urine samples from women, as well as samples such as their tap water. But the study failed to show a connection between breast cancer and pesticide exposure. Given your concerns about prenatal exposure, how should we view the results of the Long Island study?

BIRNBAUM: I think what the Long Island study demonstrates is that there is no apparent relationship between ongoing exposure and breast cancer. It doesn’t address the issue of whether or not early life stage exposure could be associated.

CURWOOD: How should your findings inform future studies, do you think?

BIRNBAUM: If we want to know whether a chemical might have a delayed impact, we need to consider exposing early in life. At some point, it would be nice to begin to design such studies and in fact right now in the design phase is a multi-agency approach. The idea is to identify as many as 100,000 families, get samples from women before they get pregnant, during pregnancy, and then follow these offspring for as many years as could possibly be done, and eventually, we might be able to answer this question.

CURWOOD: Linda Birnbaum is director of the Environmental Protection Agency’s Experimental Toxicology division. Her paper was published online in the journal Environmental Health Perspectives. Thanks for taking this time today.

BIRNBAUM: My pleasure.