At the same time that the Food and Drug Administration
announced a significant shift in its view on the potential health risks posed by Bisphenol A, the Department of Health and Human Services said that it is investing $30 million in human and animal studies over the next two years to yield further information about BPA's health effects. BPA is a chemical used in the linings of most food and beverage cans as well as in many clear plastic containers.
Shepherding this crucial research effort is Linda Birnbaum, director of the National Institute of Environmental Health Sciences
(NIEHS), a federal research center based in North Carolina. The center's mission, as defined on its Web site, is "… understanding how the environment influences the development and progression of human disease." Birnbaum, an award-winning microbiologist and toxicologist, has served as a federal scientist for nearly three decades. During that time, her research has focused on the health effects of environmental pollutants such as dioxin, which like BPA is thought to be an endocrine-disrupting chemical.
I interviewed Dr. Birnbaum just a few days before the FDA's policy change was announced. Excerpts from that interview in the Q&A below address the challenges that lie ahead in assessing the safety of one of the highest-volume chemicals in the world: At least 7 billion pounds of BPA are produced annually for use in products ranging from dental sealants to medical equipment to coatings on cash-register receipts, as well as food containers and packaging. —Andrea Rock
Q: What do you think the most important unanswered questions are? In this $30 million of research what would be at the top of your list?
A: I think there are a couple that are really important. We really have to understand the severity of effects that can be caused. How important really are the effects that are being reported at very low levels of BPA? And there's a multitude of effects. Some of the analyses or the evaluations have focused, for example, on the effects on the developing reproductive system or the developing nervous system. Well, there's evidence that it also affects the immune system . There is evidence that it affects the cardiovascular system . And I think it's very important that we have a better understanding of the overall nature of the effects.
The other thing we really have to understand is how much of the BPA is needed to cause these effects? And what are the critical times of exposure in people? Are the critical windows in utereo? Are the critical windows in infants? What about puberty? There are now several new studies that have come out showing effects in adults. When you do cross-sectional studies, which are what these new studies are, and you look at a single point of time in people, you don't really know if the effects you are seeing are caused by the current exposure to BPA or whether it was the history of exposure that led to that effect. Those are still some major questions
Major issues that I think other groups are looking at are trying to get a better handle on where is BPA in our environment. It's not just in linings of cans, it's not just in the polycarbonate bottles. Many of those sources are now being removed from the market. Industry has responded very responsibly and said we're looking for alternatives. But where else is the BPA and how are we really being exposed? Is some of the BPA in the indoor air, is some of the BPA in dust, where it's coming out of different consumer products? So we don't understand. You really need to understand how we're really being exposed eventually if we want to prevent exposure from happening. Q: Do you believe there is enough uncertainty about BPA's safety to caution people to avoid it in all food contact items?
I think we don't really know where it is in many cases. Your study, Concern over canned foods
, very clearly showed that in two cans of the same brand, some had a lot of BPA and some had very little. Q: But I'd read that you did say that was your belief, that there was enough uncertainty to caution consumers to avoid BPA in food contact items?
I think people have to do what makes sense to them and follow their own conscience and what they think and if people find that there's something that they have concerns about and they have alternatives, then it's their decision to choose. Q: In your personal life have you made those kind of decisions?
Let's just say I'm a pragmatist and I do things that make sense to me. Q: Like cutting back on canned food use and not microwaving in plastic containers?
I've never been a canned food user. I buy fresh vegetables as much as possible and I've done that for years. And I will say I stopped microwaving in plastic about 15 years ago, not because of concerns for BPA but just because of the lack of necessity to do that. Q: Do you advocate our government following the precautionary principle?
I'm a believer in the precautionary principle. It doesn't say that you act when you have no information, but you act in the presence of concerning information even if you don't have certainty. Science is rarely 100 percent certain. So if you follow the precautionary principle, you look at all the evidence and you say maybe we don't know everything, but there's enough to suggest that we might want to be cautious. That's the appropriate use of the precautionary principle. Q: And with BPA and some of the other endocrine disruptors, do you think that applies at this point?
I think that there's a wealth of information, not all in agreement, but there is information that suggests that there may be a concern and that's why we're continuing to investigate to try to answer that question with more certainty. This will allow the regulators to make the appropriate decisions. Q: What would you like to see FDA recommend with regard to its reassessment of BPA?
I think the FDA is working very hard on coming out with their decisions. What we are doing right now is conducting $30 million of research to address some of the questions about the potential adverse effects of BPA. And the studies that we are doing are not only going to help us understand BPA, but they're really going to help us understand endocrine-disrupting chemicals in general. Other chemicals that are like BPA, other estrogenic kind of chemicals as well as others. Our mission is not regulatory. Our job is to try to understand what the health effects of things may be and if we can understand the effects, maybe we can understand how to prevent them. Q: What products and/or exposures are you most concerned about when considering the risks of endocrine disrupting chemicals?
There are many compounds which have wide-spread exposure and little toxicity information at low doses. I would like to see more emphasis on studying compounds with lots of exposure to people, especially to children. And I would like to start trying to look at the totality of the exposure, instead of one chemical at a time. Q: Testing at high doses doesn't always reveal risks that may occur at low doses for endocrine-disrupting chemicals, so do we need to re-evaluate how we assess risks of BPA and other endocrine disruptors?
A: It seems to me that science has moved in the last 30 or so years and we know a lot more than we did 30 years ago. We're understanding that the way chemicals can interact with the body is much more complicated than we originally thought. The real issue is that different things can happen at different levels of exposure. It's not that for example, a certain effect that occurs at a high dose may not occur at a low dose--that may be true--but other things may occur at a lower dose.
Take something like body weight as a simple example. People can weigh more for a number of reasons. If they exercise real hard and build up muscle mass, they will actually weigh more from that. Or maybe they're really sick and are having a lot of fluid accumulation, their heart isn't working right and they're in heart failure and they've got all this fluid accumulation, they weigh a lot more. Maybe they weigh a lot because they eat too much. Three completely different mechanisms leading to the same weight change.
So we have to be very careful when we're looking at effects of chemicals or the other kinds of exposures in trying to understand that different things may cause the same phenotype but they may have totally different causes. So that's been one of the things that endocrine disruptors have really made us think about. At very, very, very low doses we may be perturbing hormone systems in one way, and if we get to a much higher dose we may be causing toxicity in a totally different mechanism.
Q: You've said that exposures don't occur singly, the way they are usually tested in the lab. All of us are exposed to various chemicals at the same time. How can we assess the risks of combined product exposures to low levels of BPA and other endocrine disruptors, and is anyone doing that kind of research?
A: The answer is both yes and no, and let's just start off by saying it's a very difficult problem. There have been approaches people have tried to use. For example, they've said I'm going to take all of the chemicals that have an estrogen-like activity and I am going to assign each of them some relative potency, that they are 1/10 as effective or 1/100th and then I'm going to basically weigh that effect and I'm going to add it up, so kind of an added effect of all these different chemicals.
That's one approach, but that may only look at the specific estrogen activity. Many chemicals don't just have estrogenic activity. They might also, for example, affect the androgen receptor. Or they might affect the thyroid system or they might affect the progesterone system or they might affect something else. So it's very difficult.
We've successfully used this kind of additive approach, for example, for dioxin-like chemicals where you can take a complex mixture and ask the question well how much dioxin-like activity is there? It doesn't account for all the non-dioxin like activity that might also be present in the mixture.
The Canadians have tried to make a mixture that kind of looks like what's in human breast milk. So they've analyzed the major chemicals present in human breast milk and they've synthetically made a mix that looks like that and they've exposed experimental animals to varying amounts of that . And when they do that, they do see some effects.
I think we know how to do the simple addition of chemicals that have the same mechanism of action, so we know that if chemicals are all estrogen-like, there's kind of a mathematical way that we can add them up and if we have all the chemicals that may be anti-androgens we can add them up and we can add up the chemicals that may be dioxin-like and we can add the chemicals, for example, the pesticides that are organophosphate inhibitors and add them up. But we really don't know what happens when we put them all together. It's a big question and it's something that a number of different groups are starting to work on and I think it's going to take a while to understand it.
I think a more tractable understanding at this point is the fact that we used to talking about control animals and control people and treat them as if they were a tabla rosa, but it doesn't exist. We all have exposures. We all eat, and guess what, foods are chemicals. They may not be synthetic, at least hopefully, but you know that gives us a baseline. If you have a different diet, that's going to affect how you respond to different chemicals.
So we now have studies—and again there aren't that many of them—but they're starting to come out in the literature, showing that people who eat a fatty diet respond very differently to certain chemicals than people who eat a lean diet. So you've got to consider all of these background factors, never mind your past history, never mind whether you're male or female, never mind what you were exposed to in the past. All of those can have an impact on how you respond.