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