Wednesday, September 26, 2007

frogs, frogs and fewer frogs

Oh, the beleaguered frogs. You probably already know that amphibian species are declining around the world. You have probably seen the depressing photos of deformed frogs trying to get through life with too many (or too few) legs. You may even have seen Dr. Tyrone Hayes' breathtaking presentation on how the herbicide atrazine turns boy frogs in to hermaphrodite frogs.

This week the N & O ran a story about a new study that reinforces the theory that farm runoff is causing the deformed limbs. Excess nutrients in the water lead to lots more parasites in the water that turn normal tadpoles into sickly, deformed adult frogs.

One of the questions about this research is, how come the trematodes make frogs so sick? They're not a new pathogen - they've always been in the frogs' environments. It's just that lately the frogs can't seem to fight them off. Another stumper: if it's one disease deforming the frogs, why does it affect so many species? Leopard frogs, bullfrogs, wood frogs, and many others have shown up with the deformed limbs, in many different parts of the U.S. and Canada.

The answer may actually lie in the frogs' immune systems: one of Tyrone Hayes' experiments found that wild frogs who live in pristine waters are easily able to fight off common infections, while wild frogs who live in waters containing agricultural runoff die at astonishing rates from the same exposure to disease. Distinguished researchers around the world have pointed at all sorts of explanations for the frog decline, deformities and hermaphrodism: climate change, habitat destruction, parasites, pesticides, and more. The sad answer may be that there is no smoking gun, but that an alphabet soup of environmental changes have over-burdened the frogs' immune systems to the point of destruction. Parasites and infections that formerly posed little or no threat to amphibian populations become deadly.

Biologists like to call frogs a "sentinel species," because they are so sensitive to their environments and serve as indicators for problems that can grow to affect other species as well. I hope we're paying attention.

Thursday, September 6, 2007

Toxics: Adding it up

Have you ever kept a food journal? It goes something like this:

Monday

  • Breakfast: Glass of OJ, bowl of cheerios with soy milk, black coffee (X calories, X grams of fat).
  • Lunch: Microwave burrito (X calories, X grams of fat).
  • Afternoon snack: Half a box of Thin Mints Girl Scout cookies...

...you get the idea. I'm stopping before I get to the second afternoon snack. What if we kept toxics journals, that charted our various exposures all day long?

Monday

  • Overnight: polybrominated flame retardants (mattress), volatile organic compounds (carpeting).
  • 7:00 AM. Shower: Nitrosamines, triclosan (soap), fragrances, methylisothiazolinone, benzoate (shampoo), toxaphene, copper, trihalomethanes (water), 1,4-dioxane (deodorant).
  • 7:30 AM. Breakfast: Trisodium phosphate (cereal), plant-based phytoestrogens (soymilk), phthalates (milk container), ethion, carbaryl (orange juice), caffeine, chlorpyrifos (coffee).

...okay, let's stop right there, before we get out onto the highway and have to try to write down all the ingredients in diesel exhaust.

Everybody knows that we are not exposed to chemicals one-by-one, but in a chemical soup, all day long. Congress first tried to get their regulatory minds around this problem with the Food Quality Protection Act, in 1996. The FQPA suggests that kids don't just eat one apple with chlorpyrifos residue in it, but also carrots, peaches, strawberries... so when performing risk assessments for pesticides, EPA should have to consider that the residues might add up.

The problem with that is in the toxicity testing itself. Even though we know that we are exposed to mixtures, we don't test the mixtures for how their toxicity differs from the parent chemicals. We test single chemicals, one-by-one , and our chemical regulations are based on the results of isolated exposures to different levels of isolated chemicals. That's pretty unrealistic.

Here's what happened when Earl Gray, a toxicologist at the EPA's research labs in Research Triangle Park, started adding two fungicides together. Gray's research was featured in a recent article on chemical synergies in New Scientist magazine:

Gray... and his team also tried exposing pregnant rats to vinclozolin and procymidone. When they exposed the animals to the compounds individually, they too saw no effect. But when they combined the two, half of the males were born with hypospadia [a birth defect of the penis]. Gray calls this phenomenon "the new math - zero plus zero equals something".

Gray saw similar results when he mixed two kinds of plastics together - neither of them had any effect when given to pregnant rats on their own, but given together, all the male rat pups were deformed. Believe it or not, he got the same results when he mixed the unrelated plastic and fungicide compounds, which attack the developing organism through totally different mechanisms.

Okay, so we know that mixtures are a problem. So let's get some people together and study the effects. All we need to do is find a group of exposed people, and then an unexposed group, and compare... oh wait. There is no unexposed group. Again, from the New Scientist article:

"Everyone has exposure to chemicals, even people living in the Arctic," says John Sumpter, an ecotoxicologist at Brunel University in London. "We can't go to a group with a mixture of nasty chemicals and then go to another who have had no exposure and compare their rate of breast cancer risk or sperm count. We are doing a scientific experiment by letting these chemicals accumulate in our bodies, blood and wildlife."

So what do we do? Well, here in the U.S., we're mostly still taking the whack-a-mole approach, and regulating troublesome chemicals like flame retardants, lead, and individual pesticides one by one. In Europe, new legislation called REACH went into effect on June 1. REACH stands for registration, evaluation, authorisation and restriction of chemical substances.

The aim [of REACH] is to cut health risks associated with everyday chemicals by forcing chemical manufacturers and importers to register their compounds and provide safety information to the new European Chemicals Agency, based in Helsinki, Finland. This information must be provided before the chemicals are sold. The new law shifts the burden of responsibility for the health effects of chemicals from government to industry and is also intended to encourage the use of less harmful alternatives for the more toxic chemicals.

The REACH legislation is a whole new approach to chemicals regulation. Unlike the "innocent until proven guilty" approach that we use in the U.S., REACH makes manufacturers prove safety before letting these chemicals out the door. It's based on a concept called the Precautionary Principle. Look before you leap. Better safe than sorry. You get the idea.

REACH isn't the whole solution, but it's a powerful regulatory incentive for manufacturers to start phasing out the worst chemicals, and to find safer solutions. Many of us work hard to limit our own exposures to potentially harmful toxics in any way that we can - but we have to rely on government to control the toxics pouring out of smokestacks, tailpipes and products that we can't control.

It will take a tremendous amount of expensive research to understand exactly how all the toxics we're exposed to all day long affect us when they're mixed together, and who is most vulnerable to long-term harm. The regulators have a choice: they can sit back and wait until the results are in, or they can heed the red flags we see now and take precautionary action. The REACH legislation took option #2. It's up to us to decide how the U.S. will act.