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Partial transcript of Dr. John Peterson Myers’ speech on endocrine disruptors, 15 years after co-writing Our Stolen Future:

We’re actually living in a midst of a scientific revolution based on these findings. And they’re changing how we think about the relationships between contamination and health, particularly — and perhaps surprisingly because the initial focus was on fetal exposures — how those fetal exposures contribute to chronic diseases of adulthood.

Some of the discoveries in this science have been completely unexpected, including signaling that some of the materials we have embraced and included within our households, some that we thought were safe actually are not. For me the most exciting thing is out of this science have come many opportunities for prevention of disease.

I’m going to walk you through what I would regard as the six essential themes of this revolution in science:

The first one is that — and this is the most profound — contaminants interact with genes in ways that not only don’t reflect current health standards, but also in ways that traditional scientific tools used to assess toxicity didn’t acknowledge.

Second, these interactions can take place at extremely low levels.

Third, exposures in the womb — this will be a central theme — exposures in the womb can set in motion things that play out over a lifetime.

Fourth, these exposures are ubiquitous — everyone experiences them — and they take place in mixtures that can interact in unexpected ways.

Fifth, the tools that we have used in toxicology to assess risk are blind to some of these impacts, and especially several that I will focus on.

And sixth, there is now emerging a science called green chemistry that’s using this science to guide new chemical syntheses, to create a wave of new materials that offer opportunities for innovation — both material innovation and economic innovation — based on materials that are inherently safe.

[… 7:30 on full version:]

When we heard that a disease was linked to a gene, we used to think that by definition that meant it was inherited, and therefore not preventable. Now, when I hear the Human Genome Project has discovered yet another disease is linked to a gene, I don’t ask about the source of mutation, I ask what contaminants might be altering that gene’s expression. It turns out that happens a lot.

[…]

[Myers shows a photo of two mice, one much fatter than the other.]

It’s the same strain of mouse. They monitored caloric intake over the lifetime of the mouse, up to this age, and they monitored the activities [sic] level, and they were basically not statistically distinguishable — same activity, same caloric intake. But obviously two very different mice.

What’s the difference: The fat mouse was exposed to one part per billion of a potent endocrine disrupting chemical right at birth. We now know a lot about the science that makes this happen. What’s in essence happening is DES, and other endocrine disruptors, can increase the rate of conversion from stem cells to fat cells, so the mouse grows up with a lot more fat cells than it normally would have, and those absorb more lipids, more fat.

The second part of this message, this lesson from these mice is if the animal had been exposed to a thousand parts per billion, a thousand times what it takes to make a mouse fat, it would’ve been scrawnier than the control. So a high dose experiment doesn’t predict what happens at low doses. That’s vital when you’re considering endocrine-disrupting compounds.

Third, back to that theme of developmental exposure, developmental exposure led to obesity in adulthood, which gradually developed over the life of the animal.

So, three key issues there:

  1. Low levels matter.
  2. High dose testing don’t [sic] predict low dose results.
  3. Early life exposures can impair adult health.

[…]

Another key element of this revolution, which I touch on briefly, is we used to think only high levels mattered, because you’d need a high level to mutate something, you need a high level to kill something overtly. But when you’re dealing with changes in gene expression, things happen at low levels — levels that people commonly experience, levels that couldn’t even be measured twenty years ago.

[…]

If you look at the animal studies, there are links to animal versions of each of these endpoints. [5:45]

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