Interview with  Louis J.  Guillette, Ph.D.


He is Professor of Zoology at the University of Florida. Guillette has studied alligators in Florida for over ten years. Based on Theo Colborn's work, and the findings at the 1991 Wingspread conference in Wisconsin, he shifted his research to hormones -- asking whether environmental contaminants could be affecting alligator health and development.

Interviewed by Doug Hamilton, producer of FRONTLINE's "Fooling With Nature." Interview conducted November 1997.

DH: Take me back to when we were out in that boat on Lake Apopka. How do you go about catching an alligator?

LG: Very carefully is the way the story goes... Alligators are nocturnal. And most of their activity takes place at night. You go out with a very powerful flashlight, Q-beam, and you look for eye shine. And primarily what we're talking about is the same thing you see in the headlights of a car when you spot a cat or whatever. Alligator eyes shine back to you red. And you approach them.

DH: Is this dangerous?

LG: Certainly there's an element of danger involved. It's like working with any large animal. But if you pay attention, then hopefully you minimize the risk.

DH: Now, why do you catch alligators?

LG: We actually started this work in 1985 to try to determine exactly what the reproductive biology of the American alligator was. They wanted to use this animal as a renewable resource for skin and meat. We began our studies to get some idea of the general health of the alligator population. And the way to do that is to take various body measurements, weights, lengths, et cetera, to get some idea of whether they're healthy, or not healthy.

DH: This sounds like a very unusual, certainly difficult, way of going about testing for the effects of chemicals.

LG: It is very important to recognize that we never started the alligator work to study contaminants. What we were in fact doing is studying the American alligator. That is, we wanted to determine whether this animal could be used as a renewable resource. We also wanted to use this animal as a model, if you will, for other crocodilians worldwide, the majority of which are endangered or threatened However, in hindsight, what we now realize is that it's a beautiful model for studying environmental contaminants. It's a top predator. It's at the top of the food chain. It's long-lived. There are usually reasonable numbers of them in a population. At night, they're very obvious, so you can go out and catch them. They stick around where they were born, once they reach adulthood.

DH: So you didn't start out looking for the effects of environmental contaminants. When was the moment that you knew you were on to something here?

LG: It's like anything in science. There are these moments of clarity when you realize you're gathering a bunch of puzzle pieces. And you finally now have maybe the border, even a corner of this puzzle, and you say, "This isn't the puzzle I thought I was putting together."

So we started this project looking at various aspects of the reproductive biology. Now, my colleagues from the U.S. Fish and Wildlife Service had actually done early work showing that there were problems with the eggs. We came into the question saying, "Okay, well what is that problem with the eggs? Why are females having problems making good eggs?"

Once we started to realize that it wasn't because of the size of the female or the hormones, necessarily, in the female or the male, we started to realize something else was going on. And we tried to erase or remove the typical things we thought might be involved. That is, changes in the moisture of the nest. Or the temperature of the nest. Or aspects of female biology or male biology.

And when we couldn't see any difference there, we started saying, "Well, maybe contaminants were involved." And we started to show that there were hormonal abnormalities in these alligators: problems with their levels of testosterone and estradiol. And we saw abnormalities of the testis and the ovary.

And a colleague of mine came in and started talking to us about work he had done, and a meeting he had been to that summer, in which he had met Theo Colborn, and a number of scientists and said, "You know, environmental contaminants might be acting like hormones."

And it was all of a sudden, "Bam!" It was one of these incredible experiences when you realize, I have hormonal abnormalities. I have possibly a contaminated lake. I know I have a top predator that accumulates contaminants, and then it all just kind of came together as a hypothesis.

Now, it's taken lots and lots of work to try and continue to test that hypothesis. We certainly have not proven it. But the data we have to date suggests that environmental contaminants are a major player in the abnormalities that we're seeing in the populations we study in Florida.

DH: And what are the abnormalities you're seeing?

LG: Well, early on, what we were trying to do was to determine the sex of a hatchling, not only by anatomical features of these little guys, but also hormonally. And what we started to note was that the hatchling and the young juvenile males had severely depressed testosterone, the male sex steroid. Females had elevated estrogens. That is, elevated estradiol, the female estrogen.

So we started looking at the gonads and their anatomy. What we found was that the males had what appeared to be advanced spermatogenic activity. That is, the testes of these newborn and six-month old animals had already begun spermatogenesis, the making of sperm. The females, instead of having a single egg per follicle in the ovary, had multiple eggs per follicle. Completely abnormal. But, interestingly enough, a condition very similar to what we see in rodents if they're exposed to estrogens during embryonic development.

Both abnormalities led us to start looking at the teenagers in the population, to look at the adults in the population. What I can tell you to date is that when we look at the teenagers, the abnormalities we saw in the hatchlings persist. Abnormalities in the ovary. Abnormalities in the testis. Abnormal hormone levels. The abnormal testosterone levels in the males then led us to say, "Well, could we look at something else that is testosterone-dependent?"

And that's when we began to look at phallus or penis size. And sure enough we were able to show that males from contaminated lakes or lakes that have high levels of agricultural contaminants, industrial contaminants, they have significantly reduced phallus size, or penis size, compared to the reference lake.

DH: About a twenty-five percent reduction?

LG: Yes. Depressed testosterone circulating in the blood suggested we should have smaller phallus size. Sure enough, we were able to go out and look at the teenage populations on these lakes. And we show on average, for example, on Lake Apopka, twenty-five to thirty percent reduction in phallus size. In other lakes we showed the same kind of reduction in size, but fewer animals are showing this abnormality.

DH: Is this relevant to humans? Do you draw any kind of connection?

LG: I think it's important that we recognize that you can't necessarily do a one-to-one transference, or that if I find something in an alligator automatically it should appear in a human.

But I think it's very important also to recognize that testosterone and dihydrotestosterone, the two androgens, play fundamental roles in penis development in alligators, just like they do in humans. And so if we in fact have abnormalities, for example, in an alligator due to environmental contaminants, and changes in phallus size, we should in fact be looking at humans.

We know that a group of young boys who were exposed to contaminants in rice oil that their mothers ate have depressed testosterone and smaller phallus size. We know that there are other populations of rodents that have been exposed to various contaminants of this nature and have abnormalities in their phallus size and development.

So we can't say there's an exact one-to-one relationship, but we shouldn't in fact be naive enough to believe that there is no relationship and no caution for humans.

DH: Now, do you as a scientist look for human connections? Or do you try to avoid making such a leap?

LG: I as a scientist am trying to understand a puzzle. So when I tell you that I found this or that or an abnormality, I'm talking about the populations that I'm studying. And I'm talking about the species I'm studying. But I would also be naive myself if I didn't believe that there's a larger connection. That is, humans are in fact a mammal, and they use the same hormones that other mammals use.

Mammals use hormones that are very similar to what reptiles use. In fact, the same hormones in many cases. For example, the same estrogens and androgens. So I would have to be blinded not to ask, does this have larger ramifications? Especially when we're talking about something like environmental contamination and health. At the same time, I try not to jump to conclusions, from one to the other and say automatically what I find in the field has an immediate consequence for public health.

DH: Critics, or scientists with a different perspective, would say that there are a lot of naturally occurring hormone-like substances out there that the alligators are exposed to, in more significant quantities, in their diet. And they would ask, how can you possibly correlate problems you're seeing in alligators to specific manmade chemicals out there?

LG: Well, there are a number of important aspects we have to look at here. There are natural compounds in the environment that act as hormones. We eat them every day. However, the majority of those that we eat are readily excreted from our bodies. We do not bioaccumulate them. We do not biomagnify them. So they're not stored in our bodies and magnified or multiplied in their concentrations.

If we ate exactly the same compound every day, then it might be similar to some of the contaminants that we get in the drinking water every day or whatever. But what we have to recognize is that there are some fundamental differences here.

These alligators are eating the same things they've always eaten. But the problems are new. And so to say that in fact the abnormalities that I'm seeing on one lake versus another lake are due to diet, I think, is inappropriate.

Now in humans, diet plays a fundamental role, possibly. But there is this fundamental difference in a natural product versus at least some manmade products. Many of these manmade products do bioaccumulate and biomagnify.

I think the intriguing part for me is actually the reverse argument. We know that there are dietary compounds that are natural compounds, like phytoestrogens [plant estrogens], that do in fact have an effect on developing embryos if we give them a high enough concentration in the diet.

So the interesting part is that it actually supports the hypothesis that weak estrogens or weak androgens or weak hormonal mimics do have an effect on developing embryos. Whether they be natural or synthetic chemicals.

One can argue that we get more in our diet of the natural than the synthetic, but I think it's important to recognize that they are metabolized differently, they're handled in the body differently, they're excreted differently.

DH: But how can you tell which chemicals are causing the problem?

LG: What I then have to do is to take, for example, healthy animals from the clean lake, bring them back into a laboratory condition and expose them either as embryos or as juveniles, or as adults, to the contaminants that I'm seeing in the lake where abnormal alligators live.

Can I, by doing this, replicate the abnormalities that I see? Yes, I can. We've done that. What we've actually done is gone out and collected eggs on clean lakes. We've brought them into the laboratory. We've said, "We know that compound x, y and z is in the contaminated alligator. Now let's take those and put those on the eggs that we have from the clean lake." And sure enough what we're now showing is that if we take those mixtures that we're seeing from the contaminated lake, and we put them on eggs from the clean lake, we get the same abnormalities in the treated alligators that we've seen out in the wild. We get depressed testosterone. We get abnormal estrogen levels. And we're still doing a lot of our work, but it appears that we get similar anatomical abnormalities.

You have to know what's going on in the wild. Then you have to bring it back and say, "Can we replicate that under controlled conditions in the laboratory?"

DH: Simply put, what is "endocrine disruption"?

[laughter]

LG: I've been on a number of national, and international, panels and we've spent days debating the definition of endocrine disruption.

The idea is the following: There are environmental compounds, some of them natural, some of them synthetic. And what they are able to do is to disrupt or modify the normal functioning of the endocrine system.

The endocrine system is a system of chemical messengers. What you have are signals going throughout your body that are chemicals. They decide whether I should grow, whether I should reproduce, whether my immune system should work in a certain way, what my blood sugar is doing, etc.

Endocrine disruption can happen in a couple of different ways. So, for example, you go into a cell that normally makes testosterone and you say, "You're not making testosterone anymore." Or you can actually go to the liver and say, "Instead of chewing up only a little amount of testosterone, which is normal, you're going to chew up a lot more." So what you're doing is increasing excretion.

It's not just a mimicking of hormones or a blocking of hormones, but it's also changing synthesis, changing excretion.

DH: Starting with a metaphor that we've discussed, the player piano metaphor, how would you describe endocrine disruption?

LG: One has to recognize that the endocrine system is an integrating system. And you can take, for example, a metaphor that many have used, the classic idea of the player piano. You have this sheet of music. It has a bunch of holes in it. It has a very specific pattern. And even though the pattern may vary slightly, depending upon the individual, the same music comes out the other end. So it's many people playing the same music. The same basic notes are there.

But now what happens is, let's say you have environmental contaminants, or you have natural compounds that come in and they put extra holes in the sheet. Or they actually tape up or glue up some of those holes. Sometimes you have the same basic melody, but all the accompanying parts have been changed. And so this is this whole idea of endocrine disruption. It's an idea where you have a normal chemical signaling system that tells you to do certain things at certain times in certain ways. And contaminants may subtract or add to that.

Now we know that in any natural system, there are in fact ways of compensating. The body has to be able to compensate. The question is, have we stretched that music or stretched that sheet to the point where the music is no longer even recognizable? By adding notes, or removing them, we change what in fact is the music. And change the future potential of that developing organism.

DH: How do you know it happens?

LG: Well, take something that's an anti-testosterone. And let's take something like, for example, growth. And a specific example may be phallus growth. Testosterone comes in as a molecule and binds to the receptor in the phallus or the testis. And there in the phallus it stimulates the growth of the penis.

Now, we get normal growth if we have normal levels of testosterone. Now we actually take an animal and we expose it developmentally, or in its early life to something, but now instead of promoting penis growth, what it does is actually blocks it.

Now there are many receptors in the cell. And what we in fact are doing is at least blocking some of them. And so what you now have is you have a phallus but it's only half the size, or three quarters of the size it should be, because it only got three quarters of the signal it should have gotten from testosterone.

The endocrine system is a system of hormones. And you have to have a receptor and the hormone together to get action. Your cells have many of these receptors and the hormone circulates around in the body, whether it be testosterone or any other hormone, interacts with the receptor, and causes something to happen.

The endocrine disruptor hypothesis is one where, in the environment there are other molecules that aren't necessarily a hormone, that can mimic this hormone or block its action. And what we hypothesize in alligators, we believe that that's associated with reduced phallus size in alligators.

DH: How do you prove it?

LG: From a scientific perspective, one never proves a hypothesis, only tests it. Because we know that we could go out and study another hundred and fifty or another thousand or another million animals and we might get slightly different results over time.

I think that the best that we can do scientifically is to go into a laboratory and say, "Under the conditions that we're studying in which we try and replicate nature, this is associated with such and such an action." The presence of p,p'-DDE, when we place it in the alligator egg, causes a reduction in phallus size. So as a scientist, I now say, "That seems to support my hypothesis, but that doesn't necessarily prove it." Maybe it's semantics. But part of it is how we do science.

DH: But you know p,p'-DDE is blocking testosterone.

LG: We know it's happening because we can actually give this compound to an animal and it blocks testosterone-induced actions.

DH: And until you know what's happening at the molecular level, you haven't proved it?

LG: You never prove anything in science. What we do is support things. We falsify hypotheses, or we support hypotheses. We don't prove anything. But in contrast, the public wants me to say, "Compound x causes cancer. Compound y causes decreased penis growth." And I'd say, "Well, in alligators, it appears that under my conditions, yes, that happens. But is it going to happen in all species? All ages? All times?" I don't know.

DH: Does a scientist go into the lab and prove something?

LG: A scientist tests a hypothesis. We go into a laboratory, and although you think that what I'm going to do is prove that statement, what I'm in fact going to do is see if I can falsify it. That is, can I actually show that an environmental contaminant does not cause a birth defect? Or does not cause an abnormality in the endocrine system? That's really what I'm trying to test.

DH: So how do you prove that endocrine disruption exists to a degree necessary for it to be generally accepted?

LG: I think that what you do is support a lot of hypotheses. If we can show that in a wide range of species DDT always acts as an estrogen, there's a weight of evidence. It's almost like in a court of law. We don't definitively say that this defendant did this action. He hasn't admitted to it, okay? But what we say is the weight of evidence suggests that without a reasonable doubt this person did that action.

The weight of evidence supports this observation. It may not happen one hundred percent of the time. But it happens frequently enough that it should be of concern to us.

DH: And where are we now with this hypothesis of endocrine disruption?

LG: What's the weight of evidence? There's no longer really a debate about whether there are contaminants in the environment that appear to be able to cause hormonal disruption. That's clear. There's also not much debate that certain concentrations of these compounds, elevated concentrations, actually cause abnormalities in embryos

I think the major debate that still exists today is whether the background levels that the majority of the population of the world is exposed to in fact constitute a health risk. Now, there are several reports that have come out from the Agency for Toxic Substances and Disease Registry, the ATSDR government registry, suggesting that levels of dioxin and PCBs in many areas of the nation do in fact have a measurable effect on the general population.

I think there's clear evidence now that certain compounds are in fact having a measurable effect on the population. As far as the endocrine disruptor story is concerned, there's still a huge debate within the scientific community about what constitutes a risk, what constitutes a detrimental effect, what constitutes a threshold effect.

That's the scientific process, and what people have to realize is that those debates don't necessarily say there isn't a problem or there is a problem. What we're debating, sometimes, are the nuances of how the mechanisms are taking place and what's going on.

But it's clear that there are compounds in the environment that are endocrine disruptors. There's no question about that. At least in my mind.

DH: Tell me something about Theo Colborn.

LG: Probably the biggest thing that she's done is to bring together scientists from many different backgrounds: from the medical profession, from wildlife, from classic ecologists to endocrinologists to comparative endocrinologists to reproductive biologists like myself. And brought them all together in rooms and made us sit down and share our data.

Now, one supposes science does this all the time, but there are hundreds of journals that come out every week with hundreds of articles. And there's no way that we're going to read all that information. And so what she forced us to do was that she actually looked at individuals and said, "Do you guys have something in common?"

And many of us found that we have something in common, whether we're working on alligators or on humans or on rats. Science actually works by gathering lots of bricks and making walls. And every now and then someone gets to climb on the wall and look out. And they look further than everybody else is looking, and they kind of see a pattern that this wall isn't just a wall by itself, but maybe it's making a house, or making a building.

And I think one of the things that Theo did is to bring some of us together to make us realize that although we were working on different parts of the wall, we were working on the same building.

A lot of this started much earlier with work from John McLachlan of the National Institute of Environmental Health Sciences saying, "There are compounds in the environment that are endocrine disruptors." He was looking at environmental estrogens.

So it's a whole series of people that have brought us together to make us recognize that we were working on the same building.

For me, the "aha" moment involved discussions with professor Howard Bern from Berkeley. And Howard had actually spent years working on diethylstilbestrol, a synthetic estrogen, and birth defects it caused in rodents and humans. The DES daughter/son complex. And Howard had been to the first Wingspread conference.

In fact, a lot of the early data that I found, it's not so much I didn't believe it, but I couldn't put it in context. I was finding these abnormalities. We had the observations in my colleagues in the field of problems with the eggs and population declines. And so we had all of these pieces of information, but they appeared to be disparate pieces of information. They didn't fit together into a puzzle that I could understand.

And it was Howard coming in and saying, "There are environmental contaminants that can mimic hormones. There are in fact environmental contaminants, more than just the DDT." Most of us had read in the '60s and the early '70s about DDT and DDT actions. And many of us knew that it could mimic hormones. But we really believed that this was focused on a few compounds.

The fact that a large number of compounds could be interacting with these receptors, we didn't pull it all together. And I think for me, talking to Howard, starting to recognize that there may in fact be a large number of chemicals that can either mimic or disrupt the endocrine system, then looking at the abnormalities that I had and saying, "Aha! These are abnormalities of development. They're abnormalities apparently of the wrong signals, the wrong chemical, the wrong hormonal signals during development. We need to develop some new hypotheses and start testing those."

DH: What is that moment like for a scientist?

LG: Well, I think it's the moment of excitement. There's a tremendous desire to get more information. They talk about science as being a pursuit of the three best jobs on Earth. It's kind of like the adventurer, the artist, the detective, in that you never have all the pieces of the puzzle, you are using your own creativity to form the picture, and that the adventure part is to find things that people haven't found before, or trying to put together ideas that people haven't put together before.

And so it's a tremendous moment. And one hopes that one has many of these in one's career. Most of them are little ones. But every now and then you get a major one, where you go, "Aha! There, something really is going on here that I don't really understand." But it's an incredible sense of excitement to try and move forward and figure out what the puzzle is.

DH: So you don't see endocrine disruption as a radically new understanding?

LG: No, the interesting thing about endocrine disruption is that it's not radical in some of its principles. In other words, the fact that signals can modify embryos, that's not new.

So it's not so much that endocrine disruption is coming up with whole brand new ideas. But it is a paradigm shift in the field of toxicology, in my perception. What we're in fact doing is asking people to look at effects in organisms in completely different ways. We're no longer saying that death is the appropriate endpoint or cancer is the appropriate endpoint or genetic mutation is the appropriate endpoint. We're saying that by just twisting the signals, an embryo develops in a slightly different way.

The problem is the "slightly." In some cases it may be slight and difficult to detect, and may not have a major detrimental effect on that organism. In some cases that "slight" may be difficult to perceive, but has a major effect on the organism and its health.

DH: What is it like working in an area of science that's so hot?

LG: Working in an area that's this hot is both exciting and it's also very difficult. The exciting part is that you actually feel like you're moving a field forward. You feel like you're on a cutting edge.

The other part of it, however is that science traditionally is a pursuit of trying to find the truth. What you're trying to do is understand how a system works. And so one laboratory finds one result, and another laboratory, let's say, finds an opposite result. Then what you do is to sit down and say, "Why are my results different than your results?" And we try and analyze, together, why we got different results. It's not that I'm wrong and you're right. It's more of a perception of, we're trying to move towards a common understanding.

In contrast, with something as hot as endocrine disruption, in something which is as politically charged and financially charged as this topic, what happens is that the system falls down a lot. And what you in fact find is that someone finds something different than someone else, then automatically one has to be right and the other one's wrong. And depending upon which camp you're coming from, whether in fact you're in some political arena or whether you're in fact in some university setting or whether you're a policy person or whether you're a government regulatory agency or whether you're the industry, you all have different takes on these findings. So therefore you line up behind certain people and certain results.

And in a long-term sense, I think that it really hurts where we're going. Because we are, in fact, trying to find what the truth is. That sounds naive but it was good enough for Einstein and a few other people that I have incredible admiration for, and I think it's good enough for us. We are trying to find the truth, and that means we have to work together to understand why the results are different from different labs.

DH: Is one side of this debate trying to use the retraction of the synergy experiment to attack all of endocrine disruption?

LG: Correct. An interesting ploy is that if you can falsify one experiment then it must be that the whole house of cards falls. And this is this idea that somehow not just the synergy story, but endocrine disruption itself is built on just one or two studies. That it just comes from one or two labs. No, quite honestly. The endocrine disruption story is not based upon one or two studies that were done in the last few years. We're talking about studies that go back to the '40s and '50s. We're talking about hundreds of studies which show that endocrine disruption exists.

This is not a right and wrong issue. And I think this is one of the things that many of us are trying to push forward, and especially make the public understand. People like to think of science as black and white. Maybe mathematics is. Two and two is supposed to always equal four. But in the science that I do, you change just a few things and the whole outcome of an experiment can change. And sometimes we don't recognize that those few things really have an effect.

Science is in fact a creative pursuit, although most people don't think of it as such. [But in a field as "hot" as endocrine disruption,] there's a whole new level that's added to it. And I call it the "politicization of science". It's true political science in this sense because we're now taking science and putting it into the realm of politics. And sometimes it's twisted in ways which amaze the scientist who actually did the work.

DH: The stakes are really high.

LG: Talking about billions. One wants to believe that the vast majority of scientists are ethical and that what they are truly trying to understand is the truth. And this isn't a new issue. We can take these issues back quite honestly especially in the environmental contaminate realm to the release of Rachel Carson's book in the '60s. They said she had to be a Communist. She was anti-America. She was going to destroy the world's food supply. Those were really big stakes that they perceived then. In those days, nature was our enemy. And we were out to modify and control the environment. What we now recognize is the most we can do is hope to modify little patches over little periods of time. And so, there's better perception and there's been a good perception that our health is dependent upon ecosystem health. But I think it's very important for us to recognize there are very large stakes. And that science is supposedly a pursuit for truth. But at the same time, science is a human pursuit.

Industry believes that it has tested these compounds effectively. From a scientific perspective, many consider that to be basically the fox protecting the hen house. What you have in industry is, "We will test our own compounds. We will tell you whether they're safe or not. We will submit that information usually under some privacy law to a regulatory agency like EPA." They'll look at it. They'll then say, "Yes, seems reasonable." But for many of the things that I'm testing, for many of the effects I'm looking at, those haven't been tested as endpoints in industry studies. They certainly don't test alligators. They certainly don't go out into the environment many times and test all of the various kinds of things we're trying to test out there. And rightly so. It would take millions if not billions of dollars to try and test these compounds. So, there are in fact many, many levels of concern behind the whole endocrine disruption dispute. When you go to a university setting, especially in this endocrine disruption world, you have to realize that endocrine disruption is not just an environmental story.

It is a politics story. It's an industry story. It's a business story. Universities, where do they get their money? Part of the money comes from the state. Part of the money comes from private donations. Part of it comes from industry. Many of us are being told at a university setting that the government's no longer going to fund research at the level it's done before. The public doesn't really want science to be supported the way it was before. And so, therefore, you have to make partnerships with industry. Well, many scientists feel that it's a double standard. If we're supposed to be going out and just finding the truth, then how can you do that with money that's coming from somebody who's asking you to basically promote something, in some ways. Study this project so we can promote it. Or study this chemical so we can promote it.

Many of us look at not just endocrine disruption but the whole concept of the environment and public health as being just a continual battle that in fact started with smoking and secondary smoke. This is just a continuing phenomenon that in some ways pits certain groups against an open marketplace. That is, the ability to sell on the market and say, "We're selling it because people want it." With another side that says, "This is a public health issue." And that there's a cost here. And we haven't told the public, or we haven't told society, what the actual cost is going to be. We haven't given them the full cost-benefit analyses.

DH: In 1995, you told a bunch of Congressmen that "every man in this room is half the man his grandfather was."

LG: Yes, I did. I told them they were half the men their grandfathers were. That was actually part of the statement. In fact, that was a great headline. But in fact, it wasn't the whole statement. What we were talking about, and what I was testifying about, was the effect on developing embryos of the environmental contaminants. And what I in fact said was something along the lines that there's a hypothesis suggesting that human sperm count, at least in some populations, has declined by at least 50% compared to our grandfather's time. Therefore, every man in this room is the half the man his grandfather was. But the second part of the statement is that the question is whether our grandsons will be half the men we are. The major question is not whether this happened fifty years ago, or what's happened to us and our generation, but whether in fact there is a problem that we may be perceiving. That is, it appears that there have been dramatic changes in the rate of testicular cancer in some populations. An increase in hypospadias: abnormal penis development. An increase in prostate disease. Not universal in all populations, but in many populations. Does this constitute a continuing public health risk? And that is the fundamental question that I still have.

DH: Some scientists are concerned that this field has gotten too much attention. That it's because of sex, in a way. Certainly a threat to the reproductive system gets more media attention, which can then drive legislation. Is this getting too much attention?

LG: I believe that the public in the United States is tremendously underinformed on this topic compared to the population in Europe. The amount of news coverage, the kinds of stories that have played in England and on the European continent, Scandinavia, compared to the United States has to be an order of a magnitude or two different in the level of coverage. So, is this covered too much in the United States? No. If you ask whether everyone wants answers too fast, probably the answer is "yes." We can only do good science so fast. I think there's enough concern right now to take a precautionary approach and say, "Hey, wait a minute. We really need to start looking at the mixtures that are being found in water and food. And we need to do that rapidly." And that's where in fact the policy issues are right now. And I think appropriately so.

DH: But EDSTAC is trying to come up with new testing procedures for tens of thousands of chemicals, and that will be extremely expensive. There are quite a few people on all sides of this issue that wonder if the policy is ahead of the science here. Are we in the impossible position of trying to make policy without enough information?

LG: Well, I'm not on that panel, although I've thought about this whole idea of screening. I think that it's certainly possible to come up with screens that may in fact be very effective but not absolutely, 100% effective. But that's the nature of science. So, I think that certainly the people that are working on those panels I have the utmost respect for. I think that they are putting together some reasonable plans. Whether this is going to in fact completely answer and screen out endocrine disruption, they don't believe it and I don't believe it.

DH: Should scientists be the people making those decisions?

LG: As far as making decisions about what screens should be in place and the quality of those screens, I think that only the scientists probably have the background to do that. We hope to hit some happy ground where in fact it's a reliable means coupled with the fact that it costs less. Because, quite honestly, if it costs a lot it's going to be passed on to the consumer.

DH: Those are real policy decisions.

LG: Those are real policy decisions. And seldom do scientists get involved with the policy decisions. I think most of the time we're asked to provide the knowledge

DH: To make the hard choice to take away an industry's potential economic gain. Is that something a scientist is able to do? Is that a position the scientist should be in?

LG: That's a really good question. I don't know. Scientists are not trained in policy. That's not one of the things we take when we go to grad school.

I think it's very important for us to recognize that we are dealing with a hypothesis. That we still don't have definitive data on wide scale populational effects. But there's no question in my mind that embryos are being affected. That there are populations of children and populations of wildlife that will never reach their full potential because of exposure to environmental contaminants. I truly believe that. The question is whether that cost is acceptable.

DH: The experiment's going on.

LG: Experiment's going on. We have a worldwide experiment going on. And as I love to tell my students, there are no controls. There is no population that is unaffected. Every population has exposure. We just don't know what the cost is. We don't know what the true effect is at all those different levels. And in fact, the scary part I think for me is that we don't in fact have the records both present or even designed right now to take us into the future to ask what the consequences are going to be a decade or two, or five, from now. We don't have the kinds of birth defect registries and health registries we need, not just for humans but for wildlife. They don't exist. And so we're running an experiment in which we're not even collecting the right data to figure out whether there is an effect or not in most cases.

DH: As a member of the National Academy of Sciences' panel, you're coming up with some sort of definitive statement on endocrine disruption?

LG: Given the excellent laboratory studies, I don't think there's any question it exists. The question is whether it exists as a general phenomenon and as a true public health threat. And it's clearly a threat for some human populations and for some wildlife populations. The big question is it a global phenomenon that we all have to be concerned with.

 

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