Well, we're better off than in the '70s right?

Toxicology fascinates me, and I love passing that fascination on to students eager to learn about how chemical contaminants impact their environment, and what they can do about it. But it’s a difficult science to teach to undergraduates. It’s hard not to talk about environmental contaminants without the doom and gloom. Particularly this semester, when I’ve decided to run a new course, introducing students to emerging contaminants, by having them investigate and write - for this site and others - about what they’ve discovered.

Because really, there’s nothing “new” or “emerging” about these chemicals, except that we’re now aware of their existence in the environment, and in us. As most of my students now know, many of these contaminants have been around for decades. Some were never regulated; some were regulated, but ended up contaminating land and water across the country anyway; some, have taken environmental scientists and regulators by complete surprise.

“How do you not get depressed?” asked one student, head in hands, slouching into the desktop.

“Well,” I reply, “we’re a lot better off than we were back in the ‘70s.”

Whoa, did I really say that?! The ‘70s? Do I have to harken back to the 1970’s to make us look OK now? A time when many environmental regulations were new, and couldn’t help but improve the condition of air, water and land?

I can relate to my students' sense of loss. It’s like having the rug pulled out from under. We all want to believe that all the regulations and regulatory agencies that serve to protect us from harmful chemicals really are effective. And, for the most part they are, and we are better off for it. But these emerging chemicals are more insidious. For decades many of these chemicals have contaminated food, water, us – in part because they were beyond the reaches of the analytical chemist. No one knew they were there - although some might have been predicted to be a problem, others were thought to degrade, break apart into harmless products.

But now, with improved techniques we know that we are not only stardust, but we’re synthetic chemicals as well.

So I point out that there’s hope. I say that even though PFOA and PFOS, which belong to a class of perfluorinated contaminants, were a big regulatory “whoops,” they now are undergoing the appropriate scrutiny, and within a fairly short timeframe, scientists have begun to measure their decline in the environment.

Shortly after that discussion, I sent the students off to investigate their favorite “emerging contaminant.”

Now I’m depressed.

Of the seven different “emerging contaminants” they chose to investigate, four of them, Pthalates, Atrazine, PBDEs, and Nitro-musks are banned by the European Union. But here in the United States? All four are still legal. (OK, California recently banned pthalates and many states have issued bans on specific PBDEs .)

As Mark Schapiro, editorial director of the Center for Investigative Reporting, reveals in his book Exposed , the differences in chemical regulation between the U.S., once an environmental leader, and the EU the rapidly emerging new leader are vast, and like the universe, rapidly expanding.

“All this makes me want to move to Europe,” commented one student, or maybe California.

A nanometer of regulation: EPA, TSCA and nanomaterials

I just came across a little blurb in this week’s issue of Science, noting that the EPA has finally made some decisions about regulating nanomaterials. A quick read indicates that 1) the EPA has decided that for chemicals already registered under their TSCA Chemical Substance Inventory (TSCA is the law enacted to protect us humans and the environment from nasty chemicals – and the inventory is a listing of all those chemicals from which we’re being protected) – nano-formulations of those chemicals will not require new registration (or registration as a new chemical) and 2) they are asking for voluntary submission of health and toxicity data, by manufacturers and users of nanomatierals. Huh.

So what does this mean? I was confused when I first read it. After reading and writing about nanomaterials, I thought one of the advantages of producing these things were specifically (in some cases) because they act differently than their bigger, larger, brothers and sisters. For example compounds like titanium dioxide and zinc oxide were nanoized in the first place was to take advantage of the differences between the larger forms and the smaller. So, I though, maybe the EPA didn’t really mean that.

Fortunately, EPA has an easily readable paper that explains these things – like how they define a new chemical - in great detail. According to their TSCA Inventory Status of Nanoscale Substances – General Approach (2008) paper, EPA focuses on “molecular identity.” In this case, chemicals that have the same molecular formulas, the same crystal structures, the same spatial arrangement of atoms – are the same chemical. That means, according to the EPA, and to borrow from Dr. Suess, titanium dioxide is titatinium dioxide no matter how small.

Why is it important to distinguish a chemical as “new?”

Normally, when a company manufactures a “new chemical,” unless it’s exempt – the company must submit a Pre-manufacture Notice, which then triggers some basic testing. That little bit about “exempt” can be important. In fact, you’ve likely got some of those “exempt” chemicals floating around in you right now. Remember all the hubbub about PFOA and PFOS? Those chemicals in Gore-Tex and Teflon and other products? Well perfluorinated chemicals involved in the production of PFOA and PFOS were granted exemptions, in this case because they were in commerce before TSCA came along. But look what happened. Now we’ve got those chemicals contaminating wildlife around the world. To be fair, it’s possible that would have happened anyway – who knows. But here’s the catch, the exemption was granted with the understanding that under TSCA, should any manufacturer realize that there might be health and safety issues, such information “ [would] be submitted to the Agency…when companies learn of it.” In the case of these products this didn’t happen, and Dupont ended up settling that account for $10 million dollars.

A steep price to pay; and an example which hopefully demonstrates for manufacturers that honesty really is the least expensive policy.

There are various ways a chemical might be exempt. If it’s used only for research and development, it might be exempt. If it’s produced in low volume, it might be exempt. And, if there’s some indication that it would be released in only small concentrations or that there would only be small exposures, it might be exempt.

Bottom line? There will be nanomaterials that will not be required to undergo testing.

Ah but rest assured, EPA has considered that some of these exempt or untested chemicals may have adverse health or environmental effects. You see, they recently announced their Nanoscale Materials Stewardship Program, where according to the program description, “Participants are invited to voluntarily report available information on the engineered nanoscale materials they manufacture, import, process or use,” should they happen to observe anything funky happening with their materials.

Let’s hope they do.

For a good readable explanation of TSCA and how it may or may not apply to nanomaterials check out the article “TSCA and Engineered Nanoscale Subtances,” by Lynn L. Bergeson and Ira Dassa and published in Sustainable Development Law and Policy.

Virus farms or salmon farms? Wild salmon and IPNV

Here in the Valley, many of us love our local Atlantic salmon. We wait patiently watching as thousands of shad, and hundreds of eel pass by the murky fish ladder windows - where thick panes of glass separate us from the roiling Connecticut in spring - hoping to glimpse the rare silvery salmon. We scan the scoreboard, where FirstLight Power Resources, the local dam and fish ladder operators, records numbers of each species passing by the ladders. How many salmon, we wonder, will make it back to Holyoke where the majority of returning fish are captured and transported to the Richard Cronin National Salmon Station in Sunderland, for spawning?

Each winter and spring, school kids tend salmon eggs in their classrooms, watching as the large salmon embryos develop. They squeal with delight as the young salmon squirm from their translucent shells and begin to dart about the tank, their oversized yolk sacs sustaining them for the months to follow. Finally, as the salmon absorb the last of their maternal sustenance, developing into fry, the stage at which they’ll be released into the wild, they name them, and say their farewells, gently tipping cups of fry into local streams. In this valley, to paraphrase Monty Python, “every salmon is sacred.”

So when I awoke one Monday morning this past fall to Laurie Sanders’ familiar voice explain on Field Notes, her weekly show aired on WFCR, why most of this year’s 141 sea run returns – 121 salmon possibly raised and released by some hopeful school kids, fish that had spent the past two or so years at sea, dodging predators, seeking out food, and finding their way back home – were destined not for reproduction but for destruction, I turned to my own resident salmon expert, conveniently lounging in bed beside me: my husband Ben.

For the past ten years as an aquatic ecologist at the Silvio Conte Anadromous Fish Research Center in Turners Falls, Ben has led a team of scientists and resource managers who mix and match salmon mates, using genetic marker-assisted broodstock management techniques to better understand the factors limiting restoration and population growth of Atlantic salmon.

“What does she mean,” I asked, “that they have to destroy all those salmon?”

“Not just the salmon,” he said, regretfully, “but all their eggs too.” He’d just spent over a week at Cronin playing matchmaker for those 121 doomed salmon. Turns out, as Ms. Sanders explained, ovarian samples from two of those returning adult fish were infected with Infectious Pancreatic Necrosis Virus or IPNV, a potentially lethal disease in salmon. And so, as a precaution to prevent the possible spread of the disease, all of the adults, and over seven hundred thousand of their eggs were slated for destruction at the hands of the hatchery managers who had tended and cared for these precious wild fish.

As one who’d killed many a fish for research, but who towards the end of her career could barely kill a minnow, I couldn’t imagine how they must have felt.

“I was devastated,” said Mickey Novak, hatchery manager for the Cronin station, speaking of the drastic measures required to stay the spread of IPNV. “I’ve tested thousands of samples. I’ve never had to do this in my entire career.”

On the other hand, noted Novak, “had we missed those eggs, once they hatched [fertilized salmon eggs from Cronin are transported to the White River National Fish Hatchery in Bethel, VT] they could have contaminated the entire Connecticut River watershed with IPNV – and other susceptible species like bass and trout could easily have been wiped out.” Humans, notes Novak, are not susceptible.

Because of the threat that sea-run fish may bring to not only their own progeny but to the program as a whole, salmon that come into the hatchery are run through a battery of tests for viral, fungal and bacterial diseases. Some tests rely on blood samples, while others like IPNV require different bodily fluids. In this case, ovarian fluid from strip spawned females is collected and sent to the Lamar Fish Health Center, U.S. Fish Wildlife Service, in Lamar, PA, where it is cultured for IPNV.

According to Trish Barbash, assistant fish health biologist at Lamar who tested those samples, “IPNV is endemic to freshwater rivers and streams in the northeast and may actually have originated here in Brook Trout…. This is the first occurrence of IPNV in Northeastern wild Atlantic salmon since many of these restorations began.” That is, in the over 30 years since efforts to restore Atlantic salmon stocks began, this disease has never once been detected in Atlantic salmon returning to natal rivers along the northeast coastal United States. Additionally, as Barbash noted, though the disease is endemic in Pennsylvania and some other Northeastern states, it has not been detected in Massachusetts rivers and streams in any species.

Where did the strain infecting the Cronin salmon come from? Barbash's analysis reveals that the virus infecting the Cronin salmon is not a known North American strain, but is genetically more similar to a Canadian genotype. So, it is unlikely that the salmon were infected with IPN during their life stages in the waters of the U.S., but may have come in contact with Canadian or European fish carrying this virus strain during their migration in the ocean. As Novak explained, back in the dark ages of conservation, the late 1800s, IPNV was likely transported from the U.S.Europe along with native brook trout. Over the past 100 years all sorts of trout and their associated diseases have crossed the Pond, in tanks rather than under their own piscine power, thanks to our incessant meddling, and
over the years, IPNV has diversified into a whole range of different strains. These strains are geographically scattered across the world, but not necessarily out of reach of the Connecticut River Atlantic salmon when one considers their migratory trek.

Ironically, though this is the first appearance of IPNV in wild U.S. salmon stocks, IPNV is well known in Europe, particularly in (or perhaps thanks to) European fish farms in Norway, Scotland and Ireland. Because of its impact in Europe, it is currently considered the most important viral disease for salmon in the European Union. Several years ago, IPNV was estimated to cost Norwegian salmon farms upwards of 100 million krone. In case you haven’t traveled to Norway lately– that’s roughly 20 million dollars. And, IPNV is just one disease of many endemic to salmon farms.

When I’d first heard that the fate of the Cronin fish may have been in some way associated with European salmon farms, I felt that familiar surge of anger towards industrial tinkering with natural systems mixed with guilt as I looked forward to my morning coffee, toasted bagel, cream cheese and, you guessed it – salmon. Salmon that likely traveled from a farm in Norway, Scotland, Chile or maybe Canada to my breakfast plate. As we all know, viruses thrive when their hosts gather in high densities, be it a crowded airport, our kid’s classrooms, or a fish farm. So while scientists estimate the prevalence (or number of existing cases) of IPNV to be very low in wild fish populations – making this year’s finding of IPNV in wild North American stock all the more important – that is not the case in fish farms.

Fish farms may be, according to a recent report by the Norwegian Seafood Federation’s aquaculture division, “the most important reservoir of IPN virus in the aquatic environment,” as infected fish shed virus in feces, urine, dead and dying fish into surrounding waters. And, according to some reports, IPNV can survive up to twenty days in seawater. As wild salmon migrate past infected Norwegian or, say, Scottish fish farms, though they may flip a fin at their captive cousins, they may also swim away host to a deadly disease.

But wait, you say. What’s fish in farming Europe got to do with Connecticut River salmon? It’s a big ocean after all – hard to imagine our small fry out there mingling with the Euro crowd.

Yes there’s lots of wide-open space out there in the North Atlantic. But, in the ocean, as on land, migrating animals tend to follow the beaten path, so to speak, or in this case ocean currents. So after spending two to three years, half their lives, in freshwater rivers and streams around the Valley, the salmon that many of us gently tip from PVC buckets, increase in size and grow into sea-ready salmon smolts, and head on out into the big blue. There, according to Janice Rowen of the U.S. Fish and Wildlife Service Connecticut River coordinator’s office, “They migrate to the North Atlantic following ocean currents. They spend a couple of years off the west coast of Greenland feeding, and sometimes, rarely, they stray further east. European salmon may mix with North American salmon there. But, the majority of European salmon seem to migrate to an area closer to Europe, near the Faroe Islands.” Large quantities of capelin are apparently at least one attraction, as salmon from afar mix, mingle, gorge, and as with any crowd anywhere – share disease before heading back from whence they came.

For years, Mickey Novak has been sampling - looking out for what wasn’t there. Thanks to Mickey, Jan and Trish and others who patiently sample and test, year in, year out, it still isn’t.

This article was first published in the Montague Reporter, Montague, MA

Lead in toys: A year in review

The current Environews Focus published in Environmental Health Perspectives, Face to Face with Toy Safety by Charles W. Schmidt reviews in mind-boggling detail, the lead problem that blindsided both consumers and major toy manufacturers this past year. By now – who isn’t familiar with stories of exceedingly high concentrations of lead in the brightly colored glossy paint on Thomas the Tank Engine toys, or in the sparkling beads and baubles that little kids love?

Even though it’s an issue we’re all familiar with, the numbers reported in Schmidt’s review are startling. Here are a few: 42 toy recalls, 6 million toys (and these were just the one’s recalled), lead levels in some toys (primarily vinyl) upwards of 2,000 parts-per-million or ppm, that’s 2 part-per-thousand (concentrations of lead paint over 600 ppm trigger a recall. A movement is underway in Congress to reduce this number further.) Some of the highest concentrations are found in kid’s jewelry, which caused at least two cases of lead poisoning in children, one of which was fatal.

In addition to the lead threat, Schmidt also reviews the use of pthalates (certain pthalates are what makes plastic squeeze toys, bottles and other items squeezably soft) another ubiquitous yet less well understood class of chemical contaminants. Some pthalates are known reproductive toxicants, and there are concerns that such pthalates may act cumulatively, potentially additively – such that combined exposures to small potentially non-toxic amounts, may add up to biologically active and toxic concentrations.

It’s an interesting article also covering the Toy Industry’s and the Consumer Product Safety Commission’s response in addition to proposed solutions.

Cross-posted at Encyclopedia of Earth Forum