The Teratogenic Effects of Atrazine.
-Review articles for Endocrine Disruptions by Hayes et al
– Hayes TB. Welcome to the revolution: integrative biology and assessing the impact of endocrine disruptors on environmental and public health. Integr Comp Biol. 2005 Apr;45(2):321-9
-Main research articles on Atrazine by Hayes et. al. (Main presentation article):
-Hayes TB, Khoury V, Narayan A, Nazir M, Park A, Brown T, Adame L, Chan E, Buchholz D, Stueve T, Gallipeau S. Atrazine induces complete feminization and chemical castration in male African clawed frogs (Xenopus laevis). Proc Natl Acad Sci U S A. 2010 Mar 9;107(10):4612-7.
-Past Research articles to support main paper (please look at and potentially use for question generation):
-Hayes TB, Stuart AA, Mendoza M, Collins A, Noriega N, Vonk A, Johnston G, Liu R, Kpodzo D. Characterization of atrazine-induced gonadal malformations in African clawed frogs (Xenopus laevis) and comparisons with effects of an androgen antagonist (cyproterone acetate) and exogenous estrogen (17beta-estradiol):
Support for the demasculinization/feminization hypothesis. Environ Health Perspect. 2006 Apr;114 Suppl1:134-41.
-Hayes TB, Case P, Chui S, Chung D, Haeffele C, Haston K, Lee M, Mai VP, Marjuoa Y, Parker J, Tsui M. Pesticide mixtures, endocrine disruption, and amphibian declines: are we underestimating the impact? Environ Health Perspect. 2006 Apr;114 Suppl 1:40-50.
-Hayes T, Haston K, Tsui M, Hoang A, Haeffele C, Vonk A. Herbicides: feminization of male frogs in the wild. Nature. 2002 Oct 31;419(6910):895-6.
– 00:00 My interest in amphibians and all the kind of stuff I do now starts way, way back. I grew up in South Carolina in an area where amphibians and reptiles and well, animals in general were just abundant. And in particular I’ve been interested in amphibians because of their dual lifestyle. That they depend on the water and then they have this terrestrial component to their life. But I think most importantly, the fact that they have no egg shells, and that the eggs are just there in the water and as a child I could watch them develop and turn into tadpoles and turn into frogs and that whole developmental process simply fascinated me since the time I was a child. Long story short, I went from South Carolina to Harvard with very little, oh how can I say, it wasn’t a strategic decision so I only applied to one school, I was a first generation high school graduate on my father’s side of the family and the whole process was foreign to me. And Harvard did some good recruiting and I’d heard of the place and so that’s where I ended up. And I went into Harvard knowing that I was interested in science, knowing that I was interested in experiments and animals and amphibians, but had no idea what career path one took when you enjoyed doing those kinds of things. Luckily I ended up as a freshman with a professor, Bruce Waldmen? Actually in a summer REU, in an NSF REU program. And I got involved in research as a freshman and then continued in that laboratory until graduation. And in college my interests were also in amphibians and also in amphibian development and metamorphosis and growth, but I was particularly interested in how the environment influenced development and growth and reproduction. Towards the end of my career I became interested in how temperature potentially affected sex differentiation and reproductive development in frogs. And right in my senior year for my honors thesis became interested in whether or not temperature had this effect by influencing hormone levels which in turn influenced things like time to metamorphosis and size of metamorphosis and whether or not you’re a male, whether or not you’re a female. So with my graduate work I came to Berkeley to learn more endocrinology, so to learn about hormone metabolism and hormone production and hormone function and activity, mostly steroid hormones. And then towards the end of my graduate work, for my graduate work I studied how the role of hormones in reproductive development metamorphosis, but with more of a physiological organismal approach, a lot less field work. And then towards the end of my graduate work, got more interested in molecular mechanisms of hormone action, and then did a short post-doc at the NIH to learn some molecular techniques and then as a professor, I was hired shortly after I graduated, shortly after I got the post-doc, I’ve really desired to put everything all together, to look at animals in the field, to look at ecology, evolution, populations and how they’re affected by the environment. And in turn, the mechanisms by which the environment induces those effects by altering hormones and how the hormones work. Somewhere in there it became clear to me that some of the biggest environmental influences on development through affecting hormones were chemicals in the environment that could either mimic or alter hormone production or degradation or through any number of mechanisms. And that led me to atrazine which has occupied most of my career for the last decade.
– 03:32 2006 paper on pesticide mixtures, you mentioned a lot of studies that used pesticide concentrations around 10,000 times. The low concentrations used in your studies. Now your low concentrations are relevant because they are what in the environment. So why do these other studies use such high concentrations? Because it seems like it’s obvious that if you use a very potent dose of a chemical you will get some effect but that won’t really help you understand what’s going on in the environment.
– Well I think some of it’s a cultural shift if you will. So lots of people, so let’s back up I guess. The high levels are the result of people who are doing what I would say, classic toxicology. Historically the interest was, what is the safety level of which we can use this chemical. And that safety level was defined by things like mortality, like LD50 the lethal dose at which 50% of the animals die. Or growth deformities or things like that. And so what people typically did is they’d start with a relatively high dose, and then you’d go lower and lower and lower until you saw no effect, until you got to the so-called no observable effect level. The reality is though, that hormones, sorry that chemicals that interfere with hormones are active at much lower doses than they would be considered toxic. So for example, what I referred to as a culture shift is that the levels that I work at from my point of view, are actually not low levels at all. They’re actually fairly high levels. Because hormones are active at levels that are even 1,000 times lower than I’m using. So from a toxicologist perspective, I’m looking at levels of a pesticide that aren’t toxic, you’re not gonna die, you’re not gonna be grossly deformed or outwardly deformed, and so they generally have been considered safe, so for example atrazine’s active at 0.1 micrograms per liter. So that’s 100 nanograms per liter, or 100 picograms per mill, estrogen itself is active at 100 to 1,000 times lower than that. So it’s a low level to a toxicologist, to me it’s not a low level at all.
– 05:38 Then why is an atrazine exposure dose kind of, where as like you said, for frogs a lower dosage of atrazine has a certain specific effect?
– I don’t have that paper in front of me, but I believe I know what you’re talking about. So the difference is, I think many of these curves are sort of bell shaped or inverted U shape, if you will. So for example, birth control pill. Estrogen works exactly that way. You would be infertile without estrogen, right? You need low levels of estrogen for the effects on the uterus and for ovulation and egg development. And so there’s a range as you get more and more estrogen. You would increase your fertility, correct? Whereas at high doses, because of negative feedback on the pituitary, estrogens actually will inhibit fertility. So with some range of doses, you get an increase in fertility and then as you get to the high doses you start to get a decline of fertility. So I think what you’re looking at when you compare the fish to the frog paper it’s just different parts of the curve. So we’ve shown some similar effects in frogs, where as you give more and more estrogen, you induce Vitellogenin, Vitellogenin is the egg yolk, the gene for egg yolk protein that’s produced in the liver. As you give more and more estrogen, you increase that effect, so if you look at just the bottom part of the curve, you’d see a dose dependency, but if you go to higher levels you can actually start to see the effect decline. And I think that’s in general true of hormones as well as hormone mimics and other endocrine destructors.
– 07:02 In individuals with delayed metamorphosis due to pesticide exposure, I was wondering if there was one stage during which development was arrested or prolonged, or if it was more like a uniform lengthening of development? And I was wondering if, depending on that answer why that would be the case?
– Ah that’s a good question. I can tell you with hormones that inhibit metamorphosis or certain compounds like thiourea that inhibit metamorphosis, they do inhibit specific stages or they are more potent at certain stages for example. And some of them have to do with which aspects of an amphibian’s development are thyroid hormone dependent. So a compound that blocks thyroid hormone production might not inhibit the very early stages such as the hind limb development. But would have a really big negative impact or inhibitory impact on the later stages which are thyroid hormone dependent. So that would be the explanation for why. In the case of the pesticides, or I can give you another example, stress hormones, like corticosterone, early in development, they are inhibitory because they’re inhibiting thyroid hormone production. Later in development, they actually accelerate metamorphosis because they enhance thyroid hormone activity, so once you’re already making the thyroid hormone, then you get the synergism, but prior to that you get inhibition for hormones, for the pesticide mixtures, I can’t answer the question. Because all we know is their time to metamorphosis was delayed, so we didn’t measure developmental stages along the way, we just know overall it took them longer, so the specific stages that were inhibited, we don’t know.
– 08:33 What do you think causes the deviation between the SSD frogs and the hermaphrodism treated with the same dose of atrazine? So why do some develop ovarian tissues while others produce only testes even though there’s multiple in both cases?
– There’s a young woman in my laboratory named Susan Long, and if we knew the answer to that question, she’d have her PhD. So I have someone working on that question. So what we think happens, if you look at develop of the gonads from an undifferentiated or a gonad to whether you become male or female, the gonads start out long and then if you’re a testis, you shrink and you eliminate the pigment. I don’t know the relevance of the pigment, but testis in Xenopus, in African clawed frogs don’t have pigment, if you’re an ovary you don’t shrink and you are clear like a testis but then you start to develop this pigment, so we think what happens is those are different stages of sex reversal if you will. So if you get multiple testis, those are parts of the gonad that should have gone away, that should have dissolved but they are retained. And then they don’t quite get feminized yet. So the first step, we think, is this sort of multi testis or the long testis. But it’s still testicular, at least histologically. The next step is that you develop an unpigmented ovary, so we believe that’s the next stage of gonadal development. And then when you’re completely sex reversed, you develop a full ovary with the pigmentation. So I think what you’re looking at is different individuals having a different sensitivity to atrazine or to estrogen. We see the same thing with estrogen. And I think the answers to those questions are similar to why if I give a carcinogen to 100 people, some people get full blown cancer, some people start to develop the, you know there are just different sensitivities. So some of the things we’re looking at are whether or not different individuals, and we also get differences between populations, which we haven’t published yet. Whether or not different more sensitive individuals differ in their estrogen uptake or their estrogen metabolism, whether or not there’s a difference in receptor binding or receptor number, or whether or not they simply metabolize the hormone or in this case, atrazine faster. So it just reflects different stages of the sex reversal and the different stages reflect different sensitivities between individuals.
– 10:55 So just to followup on the non pigmentation in the ovaries, and I was just wondering what exactly does the lack of pigmentation do, is it in ovary function or just an indicator that something’s wrong?
– No idea. All I can tell you is that males in Xenopus laevis, the tests don’t have melanin, and the ovary is characterized by this melanin throughout the gonad. These melanin, this pigmentation. I have no idea what the function is. There’s some species of frogs that actually have a melanin coat around the testis even, where the testis is completely black. And I’ve heard in a lot of desert amphibians for example also have a black tissue layer lining around their gonads. And I’ve heard speculation that some of what the pigmentation does is block out UV light which could damage the germ cells. But I have no idea how UV light would get inside the animal and affect the gonads. So I think it’s all just speculation. And I’ve never heard of any functional significance.
– 11:53 The research that we’ve been reading shows the impact of that on one generation. Have you conducted or any of your clients conducted research on trans-generational effects of atrazine?
– Yes, so we have numbers studies that are ongoing right now, I believe we’re approaching third generation, many of those studies are using estrogen in parallel with atrazine. And the idea is to look at, for example, when we select for the more sensitive individuals, so for example in some of the estrogen studies we treat a whole bunch of populations with estrogen. Some populations, 100% of the animals transform at a given dose into females, other populations at 10,000 times higher dose, we get no response. So there’s an incredible different range of sensitivity across these populations. And so we’ve been doing studies where we actually breed sensitive individuals with insensitive individuals to look at the heritability of the sensitivity, and what I can tell you so far, just based on one generation, is that the sensitivity follows the female, in other words if I take a sex reversed male, a male that’s been exposed to estrogen that turned into a female at a low dose from one population and cross breed it with a male that would have been exposed to estrogen but showed no response to estrogen, the offspring all have the sensitivity of the mother. So you select for sensitivity not resistance. And the same student is looking at what mechanisms might underlay that, whether it’s they’re inheriting a really sensitive receptor or, I mean I can tell you what the answers aren’t. It’s not a difference in estrogen uptake. Because we’ve measured that, it’s not a difference in how much estrogen circulates in their body. Because we’ve measured that, and it’s not a difference in receptor, estrogen receptor expression. So in other words the genes are expressed at the same level. So it’s something post receptor expression. And we’re looking to look at this across three or four generations, but as you can imagine, the frogs take three or four years to mature.
– 13:47 How much of the atrazine from the runoff do you think the frogs actually come into contact with and is it possible that women who are pregnant will then see their unborn child’s androgens and estrogens be disrupted if they do come into contact with that?
– So how much do you come into contact with agriculture runoff, I’m sure as most of you know, atrazine is the most commonly detected chemical contaminant that pesticide and rain water, surface water, drinking water, you name it, so the likelihood of coming into contact with atrazine is very high. Studies have shown, not my studies, but studies have shown that the unborn fetus in humans is exposed to over 300 chemicals before it’s born, and atrazine is one of those, being the most common pesticide contaminant of drinking water, et cetera, et cetera, et cetera. The people who are most at risk are farm workers, agricultural workers, and factory workers. Atrazine in the urine of people who work with atrazine can be 24,000 times higher than we know to be biologically active. So we get sex reversals in frogs and things at 0.1 micrograms per liter and the urine levels in somebody working with atrazine can be 2,400 micrograms per liter. So that’s the big potential, and my biggest concern would be in pregnant women being exposed and the unborn fetus. Now, it’s hard to extrapolate from frogs. It’s maybe less hard to extrapolate from rats to humans. So there are studies in rats that show that rats exposed to atrazine when they’re pregnant suffer from a testosterone, estrogen, progesterone imbalance that often leads to chemically induced abortion. That’s an EPA laboratory published those studies. A second EPA laboratory showed that rats exposed to atrazine, the offspring are born with prostate disease. So they’re already born with the prostate of an old man, so to speak, and a third EPA laboratory published and showed that rats that are exposed that don’t abort, the daughters are born with impaired mammary development, so impaired breast development, and as a result, those exposed daughters aren’t able to feed their offspring. So the grandmothers of the exposed rats suffer from retarded growth and development. So a number of other studies that look at neural damage and birth defects in rats that are exposed to atrazine and other chemicals. Now humans, of course there’s no experimental evidence, but there are a number of studies done by the Center of Disease Control for example, that’s looked at things like pre-term labor in humans exposed to atrazine, low birth weight, exposed to atrazine and other chemicals. There’s a very strong correlation, and it leads to birth defects, one that involves the digestive tract being on the outside of the fetus when it’s born, and another one that involves called coital atresia in complete development of the nasal and oral cavities. And both of those have been highly correlated with atrazine exposure. So in humans you’re only gonna have correlative or epidemiological evidence, you’re not gonna have experimental evidence, but that’s backed up by experimental evidence in rats. The other thing that’s difficult in extrapolating to humans is trying to figure out what dose to a frog is the equivalent dose in a human. Part of that’s because of a lack of available data. So in frogs and fish, what we measure is how much atrazine in the water, so we know exactly what they’re exposed to. And in most rat studies, they measure what’s put into food. Nobody has any idea what circulates in the blood of a rat or what comes out in the urine in terms of atrazine. And in humans, what people measure is what comes out in the urine. So you’re trying to extrapolate one, what dose it takes to have an effect on a frog to how that relates to a dose that’s found in the urine of a person who’s been exposed. And then you have to translate that to the equivalent biochemical doses. Humans have a higher metabolism, but we’re also large, or I’m sorry, humans have a lower metabolism but we’re also larger. So how do you extrapolate those doses and have an equivalent frog to human dose extrapolation? That I don’t know how to do, I don’t know that anybody knows how to do.
– 18:00 In your 2002 nature article, you suggest the possibility that continuously exposed populations undergo adaptive resistance to atrazine, and if this is true, how would the frogs initiate this adaptation, what mechanisms would be responsible, and could other vertebrate groups exhibit the same pattern of adaptive resistance?
– Sure, so if you’re exposed continuously, we already know for example plants, the targets organisms for atrazine. There are over 80 atrazine resistant plants. There’s at least three mechanisms by which that resistance have evolved, if you will. Some of them involved a change in the protein that atrazine binds to, so that the plant doesn’t respond, and some of them involved, the plants evolving enzymes to metabolize the atrazine and some of them involved plants evolving the ability to bind the atrazine with something called glutathione and essentially detoxify. And glutathione’s also present as you may know in animals as a mechanism for detoxifying, so mechanisms of resistance could involve everything from decreased uptake to increased metabolism, to decreased binding in the cell where atrazine binds to phosphodiesterase. And that adaptation would involve, well we could be talking about a couple things. One there could be physiological adaptation, and we see that even with estrogen in frogs. So if you give an adult frog estrogen, you’ll get a response whether it’s induction of Vitellogenin or inhibition of behavior. And over time what happens is that frog will stop responding to that dose. And that’s because the frog will start metabolizing much, much, much, more quickly. So initially when you’re exposed to estrogen you’ll get an effect, two weeks later you’ll get exposed to the same dose of estrogen and you won’t see an effect, that probably involves the up regulation of enzymes that are there to metabolize toxins and hormones. So that would be a physiological adaptation. There’s the possibility of an evolutionary adaptation where animals might, through any one of those mechanisms, decreased uptake, increased metabolism, decreased binding to the target protein, any one of those. What we do know, as I already said is we do know that different populations or different strains of frogs, differ in their sensitivity. They vary in their sensitivity to atrazine or to estrogen, and that’s without the physiological adaptation.
– 20:19 Different voices say that there has been adaptive resistance to atrazine. I was wondering is there a possible small cospeciation for this population, that do share adaptive resistance?
– I could answer that question, but it would be complete speculation. I could imagine how that can happen, right? I mean I can imagine that, sure, you can drive individual populations as they’re selected for atrazine resistance, or maybe even select for atrazine sensitivity, right? Because you have the choice between either being a male that’s not functional or completely sex reversing and being a functional female. So I could make up all kinds of scenarios how that might lead to isolation and speciation. But I don’t know of any evidence for that at this time.
– 21:05 In your 2010 paper that you coauthored, if an atrazine treated male ended up copulating with a female, would that be viable?
– Oh, except that they don’t. So in that section of the paper, there was only two, I think we ran four trials. So everybody was only tested once so we didn’t have to worry about experience and all this, they were all virgins so to speak. There were only two atrazine treated males that ever copulated, then if you look at that paper, there’s a second set of experiments using a completely different set of animals where we paired either the controls and females or atrazine treated males and females, so no competition. The males that are alone have such low sperm production that the fertility’s, if they copulated at all, the fertility’s like 15%, or something like that. So those males usually don’t even show the behavior. But when they do they tend to have a very low fertility. And there’s sections of the testis, in that paper that show you that there’s an absence of sperm in those males’ testis, now subsequent to that in a paper that we’re submitting this summer, we now know that a number of those males that don’t copulate actually do copulate but they behave like females, so if you put them in a scenario where there are other males available, other males will copulate with them but they’re nonfunctional, that part’s not in the paper yet.
– 22:25 What is your opinion on the studies that have contradicted your findings on the effects of atrazine on frogs? Your opinion on the EPA’s response to your studies and how do you think the interests of companies like Syngenta affect the scientific studies conducted on their products? How do you think they influence the results?
– My most straightforward answer is, there have been no studies that have contradicted my studies, period. So if you look at the first studies that Syngenta commissioned, which I was there for, they actually show hermaphrodites, they have p-values of like point zero, zero, zero something, showing inhibition of development, inhibition of growth, edema, erratic swimming, and those things are all in the paper. So they actually show more adverse affects than we do in their first paper, but they claim that I don’t know, I don’t recall how they actually worded it, but if you actually look in the paper, the effects were all there, including hermaphrodites that look exactly like the hermaphrodites we produced, including a dose response to atrazine, which we didn’t even show, so if you look at an original Carr et al paper you’ll see that. The other papers, and even in their paper there were some issues, like contaminated controls and things but let’s leave that aside. The other papers aren’t even really worth discussing so much. So in one of them where they claim that there are hermaphrodites in controls and in atrazine treated ones, and you can see this, I published a paper that actually addressed these issues. In one of those, the controls had as much atrazine as their atrazine treatments and if you read in the paper, the frogs jump from tank to tank and they didn’t keep track of where the frogs were. So there were no controls essentially. In another one of those papers that came out of Michigan, if you look at the mortality data, 80% of the frogs died, right, so you have 90 animals that are treated with atrazine, 80% of those died. Which means that you’re looking for, and I’d say of those that survive, whatever the number is, eight frogs or so, half are gonna be females, so you’re looking for hermaphrodite in four animals that were dying, you know, so it’s not even really worth the discussion, I’m not even sure how those things got published. There’s another paper, for example where they compared, these Syngenta funded people, frogs from corn growing areas, and frogs from non corn growing areas. But if you look at the atrazine levels in the water, they didn’t differ. So there was really no comparison. There’s another one where they reported differences in hormone levels between frogs from non corn growing areas that looked just like the levels that I’ve published. There’s a final paper by Kloas Verner that again, was an EPA panel member that then became a Syngenta funded guy, and it’s interesting what you say. So what the EPA panel review said is different from what the EPA said. So what the EPA panel review, when they reviewed his work, they one, were, they questioned why the EPA was only looking at the industry funded study. And they also questioned why the Syngenta funded study looked at a resistant strain of frogs. And what the EPA concluded for that was that the question was done, no more work needed to be done. But that’s not what the panel recommended. So that last particular study by Kloas Verner, their frogs didn’t even respond to estrogen properly. So how could you expect them to respond to the atrazine? The other thing is, in terms of when you say “contradict”, it would be a contradiction if my work, our work, was repeated. And in fact there are so many differences in every one of their studies that there’s no contradiction. It was simply a different study. So they use a flow through system, they use different doses, they use different temperatures. They use different populations, they use different feeding regimes, you know. Anybody can design a study that shows nothing.
– 26:05 So I know that EU has now banned atrazine. So what do you think is preventing other countries like U.S. from initiating the ban? Do you think it’s the influence of the companies producing it or do you think it’s other factors? And is there a movement going on in the U.S. to try to ban it?
– How much time do you have? So the EU has a strategy whereby if anything’s found in the water, they used a precautionary principle. If anything’s found in the water that is potentially hazardous to human health or environmental health it’s gone. Unless the company can prove or provide evidence that that danger is minimal, in other words you’re guilty until proven innocent. The U.S. has a different policy. You’re innocent until proven guilty. And several people asked me, well, how did these chemicals get in the market anyway? But most of the chemicals like atrazine, which has been here since 1958, there was no EPA, EPA didn’t exist in 1972. So most of the pesticides that we use now, there was nothing there to regulate them. They’re on the market, and it’s an innocent til proven guilty kind of, you know. So the company’s charged to prove that their compounds are environmentally hazardous or hazardous to human health, otherwise it’s left on the market. Now, why is it so difficult for the U.S. to do anything? In my opinion, it has very little to do with atrazine, with atrazine’s biological effects. In fact at the last EPA hearing, they all but said “okay yeah, there are biological effects. But they’re not adverse” and you weigh that against the economic importance of the compound. Atrazine is, to sum it up, atrazine is the number one, or I’m sorry, right now, the number two pesticide used on the number one crop in the U.S., corn. We eat less than 2% of the corn we grow. Most of that corn now goes to the ethanol production. You see, now you’re talking about a whole different political question, right, the head of the EPA is appointed by the president, and the first presidential caucus is where, in Iowa. So you’re not gonna go to Iowa talking about regulating a chemical that’s used on a crop in Iowa, or that you’re gonna appoint a head of the EPA that’s gonna regulate the number one chemical, number two chemical sorry, used on the number one crop in Iowa. Then you got all the ethanol industry, and all the biofuels and renewable energy, politics and lobby tied up in that. So there’s a big, big reason why atrazine not being regulated, now the other question you asked, is there’s an incredible influence by industry. And the lobbyists for example, you asked if it was, if there were attempts to ban it. There’s a bill to ban all triazenes right now in U.S. Congress, I doubt it’s gonna go anywhere. There’s a bill, Illinois tried to ban atrazine. New York State was trying to ban atrazine. Tasmania’s tried to ban atrazine. Minnesota’s spent a huge amount of time trying to ban atrazine, and then the companies then spent a huge amount of time, Hawaii was trying to ban atrazine. The companies then spent a huge amount of time with lobbyists working with the politicians who would drop those bills, who would put those bills in for example, the other question you asked is a little more, even concerning. So the EPA Scientific Advisory Panel, when atrazine went up for review, the head guy, Ron Kendall, who was working for the manufacturer at the time, so he was the head of a company working for for Novartis Syngenta, he was also the chair of the Scientific Advisory Panel for the EPA at the exact same time, right. Even now there was a guy on the EPA Scientific Advisory Panel named Kloas Verner, he was working for the EPA, he then got paid by Syngenta to do many of the studies that they claim refute my studies. So you had an EPA panelist that was then paid by Syngenta, then returned back, presenting to the same panel that he was a member of and he’s still a member the Scientific Advisory Panel even those he’s publishing with the manufacturer now. So it’s complicated.
– 30:08 Has the EU experienced decrease of common related cancers in humans since banning atrazine? Have their amphibian populations rebounded, and are they still using other potentially harmful endocrine destructive chemicals, which I think you’ve probably already answered.
– With the human population stuff, there’s not enough time to tell. So it’s been less than 10 years or so. And if anybody’s doing those studies, which I don’t know if they are, it will take more than 10 years before you can really get a big enough trend. Especially when you consider how cancer develops and the time it takes in the detection, and then trying to correlate it with changes other than the ban of atrazine. So it’d be some time before you’d see that. There are studies though, for example, I forget the chemical now, there was a chemical used as a roach spray in New York where in a low income, minority community, they banned two of those chemicals. And their names escape me now, and immediately, infant birth weight and preterm changed for the better. Like immediately you could see that effect. But something like cancer, you won’t see that effect. But cancer oftentimes takes years to develop, even post exposure, right, so you wouldn’t see it. Have frogs rebounded, I don’t know that there’s any evidence, and I don’t know that anybody looked at frogs in Europe, I don’t, I don’t know of any study that looked at atrazine in frogs in Europe. I’m pretty sure there’s not one out there. So the data from before and after would not exist. What they’re using now is a chemical called terbuthylazine, which is very similar to atrazine. It differs by about a methyl group.
– That seems an interesting choice.
– Well I think what these companies do, is they have a bank of chemicals that if something happens the next one’s ready to go. So terbuthylazine is not registered here. It’s not used here in the U.S. But I would guess that if atrazine went away, it would be registered pretty quickly.
– 31:58 Is there a safe way to filter out atrazine once it contaminates our water systems? Or will our water systems remain contaminated for some time once exposed to atrazine?
– Here’s first why I don’t like your question. If I had a dime for every time I sold a Brita filter by giving a talk, I’d be a rich man by now. So yes, any carbon filter will take atrazine and probably most of the chemicals, the pesticides that you worry about out of the water. It doesn’t solve the environmental health risk and it also doesn’t solve the problem for the people who are most at risk. So the people who are factory workers or farm workers, those really high levels they get are from inhalation and absorption across the skin. So even if those who are most at risk had access to the information and access to the finances to provide the filtration, they would still be at very high risk. The other reason that I commented on your question that way is sort of a philosophical one. That if a company sells a chemical to a farmer and that farmer uses the chemical and it ends up in your water, why should you be financially responsible for taking it out, and right now the way the laws are, is that the water company would ultimately be responsible. So you could sue your water company. And in fact, that’s what happened recently.. Is people came together in a mass action lawsuit, sued the water company, the water companies then turned around and sued Syngenta to have filters put on, and they just settled that out of court for $105 million. And the idea of the original court case was that it would be so expensive to remove atrazine from everybody’s water that Syngenta would just stop selling it, but that tells you how big the cost is to you as an individual. That this huge corporation doesn’t want to pay the money to take it out, then they’re passing that cost on to you.
– 33:43 What amount of responsibility do industrial scientists, corporations, and regulatory agency have towards maintaining health for the public and the environment?
– I think we all should take personal responsibility. For me personally, I’ll give you an anecdote. I was just in Hawaii in a town called Waimea. So if you go on Google Earth and look at Waimea Bay, you’ll see exactly what I’m talking about. That the Pioneer, and a number of other seed companies which are owned by chemical companies are working there on the island of Hawaii, there’s a little town there. And they’re surrounded by these GMO fields that are using lots of pesticides. What you can see in the Google Earth thing is that one, the whole town’s covered in this red dust, the topsoil from all the agricultural stuff. And then you can actually see the silt running off into the Pacific Ocean don the Waimea river, down the valley. And my point is that, even if it weren’t for the high use of pesticides in direct exposure to that town, if I were a worker, if I were an individual, how could I look at how we’ve destroyed this beautiful landscape, and how could I tell my child, yeah that’s my job I’m doing that, right there, so I think we all have to take personal responsibility. And I think some of us, if we’re regulators, if we’re working for the industry, if we’re industrial scientists or academic scientists, then I think we have a personal and social responsibility, and that’s one of the things that I’ve come to note in my own career. Where as I thought as a scientist my job was just to produce the data, but how can I do that knowing what I know, how could I not take some responsibility to educate the public, to educate my neighbor, to educate my mom, right, whereas most scientists will tell you, oh you’re supposed to be objective and just publish, and in fact, most of the places that were published are inaccessible to the public. Which has just occurred to me, it’s ironic that you call it publishing when you put it in a journal that 99.9% of the world doesn’t have access to. Sort of an interesting language I guess. But I think they all have some responsibility. I think you have a bigger responsibility if you have the information, if you have access to the science.
– Do you think they’re cherry picking what they release out of industrial research?
– Sure, absolutely, remember that I was, for three or four years a consultant with those guys. I know exactly what they do, and they knew long before me or anybody else that’s now been published, who’s working on atrazine, they knew exactly what the problems were. I know that for a fact.
– 36:04 Although it’s been shown to be a pretty potent teratogen and atrazine is still a hallmark chemical of the agricultural industry, so I was wondering how do you balance the need to get rid of this toxic chemical while still preserving the integrity of a system that’s already kind of financially under distress?
– I don’t know that I can answer that question. My response would be that there is no cost that I’m willing to pay to risk environmental health and public health, I look at it this way, knowing what I know, would I let my daughter drink it? Knowing what I know, would I spray it on my corn in my backyard, which I do have corn in my backyard. And I don’t understand economics enough to know why we’ve been reliant on a chemical that only increases corn yield by 1.2%. It’s a very little margin, but that’s a lot of money. To me that money’s not worth, it’s just not worth it. So I don’t know how, when you say how do “you”, I don’t know how we as a government, and how we as a regulatory panel balance those kinds of things, but for me, the answer is very clear, it’s gone. Figure out something else, the European economy didn’t collapse when they got rid of atrazine. They didn’t stop growing corn, and I suspect that if they got rid of terbuthylazine they would still continue as well.
– 37:20 What influenced things censored by policy, i.e. the Data Quality Act? And furthermore, looking toward the future what will be necessary to make environmental health issues a priority in society?
– Okay, that’s an interesting question. So you mentioned the Data Quality Act. So the atrazine regulation was the first time the Data Quality Act was used, it was written by a guy whose name escapes me now, but he’s a paid industry person who also worked for the tobacco industry. His name will come to me in a minute. And the Data Quality Act was really written to actually stand in the way of regulation, such as atrazine or smoking, so it as not written to actually, I mean it sounds good, right? But it was specifically written, Jim Tozzi’s his name, so you can look him up. So it was specifically written, and it was slipped into another bill. And that’s how it was passed, so it was specifically written to actually prevent regulation not to actually foster regulation and public awareness. The difficulty’s I think, and you can turn to climate scientists to address this. I think there’s a difficulty in the public having access to primary scientific information. And then even when they do, one of the things that the industry or people like the climate doubters do, is that they are intentionally trying to confuse the public, right, because you want on the one hand, the public says, or my mom for example, says things like “well scientists say” or “doctors have shown”. So you want a certain level of trust, but then you have other people with those same letters, with those same titles specifically coming in to generate problems so that there’s a mistrust by the public. And I think climate change is equally probably better example of the climate science of what we’re thinking about, and I think the difficulty will become for example when they say well the work was not reproducible, or there’s this other thing they throw out all the time, well Hayes refuses to share his data. My data are published, but if you were in the public and you hear that, you think oh well he has something to hide. Or in one of my studies like we were just talking about, whether males turned into females, they said something like, well he’s only used 90 animals. Well so what, what if I used 900? What if I used 9,000, the point is, males turned into females, right? Even if it was only one, males turned into females. But when you put things out there like that, right, to generate the doubt, then that stalls things. That stops things from happening. That stops the public from knowing, should I use my cell phone or not? Is climate changing or not, are we running out of oil or not, is atrazine bad or not? So I think that’s the job of the Data Quality Act, and that is to really make things confused. To generate confusion so that nothing happens.
– Looking towards the future, what can we do to raise awareness in the public?
– I think more scientists have to become publicly active. I think we have to lobby for more funding for science education in public schools. Most people don’t go to fancy colleges like us and all those kinds of access. I think we as scientists need to spend, once you become an academic, what we really really wanna do is teach the upper division, really challenging science classes. I’ve started teaching a freshman class six years ago, exactly for the reason that you asked now that these are the people who are voting on stem cell research and whether or not we can do it. But ask the average person, what is a stem cell. Ask the average college student, who’s not a science major, right, what is a stem cell, but these are the, you know scientists aren’t usually politically active. Climate change policy, renewable fuels, nanotechnology, evolution versus creationism in schools, most of those decisions aren’t gonna be made by us scientists. They’re gonna be made by people who at most might have high school biology, maybe. And so I think we as academics as scientists ourselves have to make more efforts reaching out to the high schools and reaching out to non majors because those are the people who are gonna make these decisions. My mom, right, not the guy in the lab next door to me, so I think we have to take that responsibility.
– So my question is, to what extent do you believe the public understanding of anthropogenic degradation