What recent research funded by NIEHS shows the most promise for disease prevention in the near term?
We have developed sensors to measure exposures. If we know what people are exposed to, then we can prevent the exposures. With bisphenol A, where is it all coming from? It’s not just baby bottles. It’s not just cans. How is it getting into us? Is it getting into our food, in our drinking water, in our house dust? Let’s identify the major sources of exposure, and work to control those. The very minor sources may not be an issue. NIEHS identified the BRCA1 and BRCA2 genes, which has furthered breast cancer research. There is also the “sister study” of 51,000 women followed for 10 years looking at nutrition, lifestyle, exposure to environmental chemicals and biological markers.
What are we doing to answer the big questions: Are chemicals in the environment increasing breast cancer, reproductive diseases and neurodevelopmental/behavioral problems?
We’re addressing it at this point very much on a one-chemical-at-a-time basis. We need to begin to develop strategies to look more broadly because no one’s exposed to one chemical at a time. And we need a better understanding of whether the whole suite of chemicals in our bodies is associated with the problems. Nobody’s trying to look at the sum total. A study I’m trying to encourage is where you’d make a mix of what’s in the American population and expose animals to that mix. Maybe I would start in by looking at the high-end of the population. If we saw something in our animals, that would certainly be a concern. Now if we didn’t see anything, that doesn’t mean things aren’t happening. But I think it would be a study worth doing.
Do you still have concerns about people’s exposures to the brominated flame retardants, PBDEs?
Yes. There is no convincing evidence that PBDEs are declining in people or wildlife in the United States. It’s too soon. Manufacturers stopped production of penta and octa in 2004. The chemicals are still getting into the environment from existing products. Deca continues to be produced. Until recently, scientists didn’t measure deca in people. Deca rapidly metabolizes in people and wildlife but is very stable in the environment. PBDEs look as though they are on the decline in Europe where they were never used as widely as in North America. The European Union banned them in 2004. Germany banned them in the 1980s, and Sweden stopped use in the early 1990s. The peak levels in Swedish women occurred around 1997, and have since declined.
Many experts talk about the “data gap” when it comes to our knowledge of the risks of chemicals. How substantial are these gaps and how can we fill them? What new testing should be required?
Some [gaps] we can fill by testing, and some by doing specific studies. We have to prioritize the data gaps of the greatest concern. As the first toxicologist heading NIEHS, I will bring in exposure science. Toxicology is a hybrid science that examines the safety of different exposures using all the tools of molecular biology, analytical chemistry, biochemistry, physiology and pathology. Today’s toxicology is not our grandparents’ toxicology. It’s not the old-fashioned “dose ‘em and count ‘em.” I would like to see any study done on animals get a measure of the internal dose so we can compare the animal results to humans. We need to know if the levels in experimental animals that are associated with effects are similar to the levels that we’re finding in people. If the levels where we see effects in the animals are similar, or within a factor of 10 or more than we see in people, then I think we should be concerned. The standard tagline was “the dose makes the poison.” But it’s the dose and the timing that’s critical. Different things happen at different doses.
You have said, “Animals may not be people. But people are animals.” Can you explain what you mean by that?
Nature is inherently conservative. So many of the basic processes that govern development and physiology in fish, for example, are the same processes that occur in human beings. Some people are concerned whether rats or mice, or in some cases, cats or dogs or non-human primates, are good models for humans. If we have chemicals that cause a multiplicity of effects in several species, why would we think that some people are not going to be susceptible to the effects?
This article originally ran at Environmental Health News, a news source published by Environmental Health Sciences, a nonprofit media company.



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