What’s in Your Fav Five? Five top contaminants

I’d been blabbing away for the past hour or so about chemical contaminants, imparting my imperfect knowledge upon my seven brilliant college students.

“So, what do you think are the five most important contaminants?” asked Beth, my student who has been investigating atrazine, one of the most ubiquitous pesticides in this country.

I was speechless. “Um..” I wavered, “well….” I pondered, before finally copping-out with “that’s a really good question.”

“I guess that’ll be my assignment,” I grimaced, “but I’m not sure I’d be able to come up with just one list.” Although it seemed a fair if not daunting assignment, since I’d been asking them to stretch their brains all semester, I’m guessing if you asked ten toxicologists for their “Fav-Five” they’d come up with at least twenty different lists.

As with anything in toxicology, there are some basic questions about exposure, toxicity, how the stuff behaves in the environment, and who’s most at greatest risk? For example, we might use some pretty nasty stuff to clean our ovens, paint our toenails or kill rats but we might not expose ourselves to concentrations that are of concern (though that might be debatable), unless we drink them.

Then there’s toxicity. Does it cause cancer? Impair reproduction? Contribute to the development of asthma? Which is worse? Or maybe it’s more insidious, as one of my students, Liz, revealed about a group of fragrances, used in more consumer products that I can name, called synthetic musks. Some of these compounds impair the ability of our cells to spit out foreign chemicals. Finally, there’s the question of how the chemical behaves in the environment, and in us. Does it accumulate? Do we metabolize it? Does it seep into water? Is it spewed into the air? And this is just considering human toxicity. Finally there’s the ‘at risk’ question. Are we talking most problematic for humans? The Environment? Wildlife?

My brain was off in all directions. There are just too many variables. Even David Letterman hasn’t attempted at top-ten list for chemical contaminants I checked.

But I already copped-out once. I couldn’t do it again. So I did some academic soul-searching (A.K.A: A Google Search).

Maybe there are some existing lists that hordes of experts, policy makers and regulators have already developed? But no such luck (although please correct me if I’m wrong. I’d love to see one.) Then I dared write to representatives from USGS and EPA’s Office of Water, but got no response other than a boiler plate answer from the EPA's press office assuring me that in addition to protecting us from acute problems like pathogens, "EPA is concerned that water systems protect their sources of drinking water, address replacement of aging infrastructure, have properly trained operators, and charge sufficient rates to ensure that they have the revenue needed to provide access to safe drinking water."

So for better or worse it seems I’m on my own (with help from the universe of information available on the web – and these are in no particular order – they are about as random as my selection process,) though I’d love to see a poll of those in various fields to see what they’d come up with, here goes – not in any particular order:

1) Arsenic is linked to many different types of cancer, and occurs naturally in soil and water (and may occur in drinking water). It's a chemical once used widely as a pesticide. As a result it may be found in the neighborhood playground (arsenic is one of a triumvirate of metals in CCA or chromated copper arsenate,) or contaminate the soil of old fruit orchards (and elsewhere) thanks to its effectiveness as a pesticide. In terms of large scale environmental release, mining industries – like the Newmont Mining Corporation, in Nevada which describes itself as one of the leading gold companies in the world - may be most important. According to Scorecard a site originally created by Environmental Defense (and now "owned" by Green Media) that digests and synthesizes EPA’s Toxic Resource Inventory into a more readable format, arsenic is the number one cancer concern, and Newmont releases almost 300 millions pounds of arsenic a year into the surrounding environment.

Arsenic also tops the Agency for Toxic Substances Disease Registry Top 20 List which is based on contaminants most commonly found at National Priority List or Superfund sites and which are considered most important in terms of potential for exposure and potential for causing adverse health effects.

Finally, in 2002, the EPA dropped the drinking water standard from 50 part-per-billion (ppb) down to 10 ppb, after considering even lower standards of 3 and 5 ppb.

2) Lead. This is not only important as a neurotoxic contaminant now because it exists in old house paint and other paint (e.g. on old peeling highway bridges), courtesy of the lead industry who once encouraged Americans to paint their houses with white lead, and advertised, yes actually advertised that “Lead Takes Part in Many Games,” (see Deceit and Denial for some fascinating reading,) but it’s also in our water having been used for pipes and solder. The EPA estimates that twenty percent of human lead exposure is the result of contaminated drinking water. Lead also tops NRDC’s Scorecard for number one, non-carcinogenic contaminant, this time thanks in part to Red Dog Ops in Alaska, another mining company.

Several years back, as a pregnant mother of a toddler, I dutifully tested the window sills of our new 1860’s home for lead paint – when the hardware store lead-test stick turned a shade of hot-pink I hadn’t seen since the psychedelic ‘70s. I immediately (and maybe not so wisely) purchased some gel non-toxic stripper and scraped away. Sometimes we do dumb things. And sometimes we just don’t learn. Maybe we will this time around.

Here’s a little ditty I found on EPA’s site:

Hence gout and stone afflict the human race;
Hence lazy jaundice with her saffron face;
Palsy, with shaking head and tott'ring knees.
And bloated dropsy, the staunch sot's disease;
Consumption, pale, with keen but hollow eye,
And sharpened feature, shew'd that death was nigh.
The feeble offspring curse their crazy sires,
And, tainted from his birth, the youth expires.
(Description of lead poisoning by an anonymous Roman hermit,
Translated by Humelbergius Secundus, 1829)

3) Priority Air Pollutants. Air is not my field, but no top-five list can be complete without at least a few air pollutants. These include particulate matter - released by power plants, motor vehicles, (especially older diesel vehicles), and some factories; ground-level ozone (primarily from motor vehicles and industry), carbon monoxide (from burning fossil fuel), sulfur oxides (fuel again, particularly coal burning plants), nitrogen oxides (yup, burning fuel again) and finally lead (again – so now you see it’s a double assault.)

We’ve all heard how asthma rates are going up. At least a few of those pollutants listed above aggravate asthma, and are known to cause or aggravate other respiratory conditions (for a historical perspective on the killing smog of Donora Pennsylvania, When Smoke Ran Like Water is a sobering read)

Although thanks to the Clean Air Act, smoke no longer runs like water, it’s still a pervasive pollutant, as anyone with a respiratory condition will tell you. As a parent who watched her asthmatic toddler’s every breath, and then watched as he bounced off the walls following massive doses of Ventolin (he’s thankfully grown out of it), I cannot imagine living in fear of the air. But people do, every day, and it’s criminal. Unfortunately, unlike water, until the sources clean up their act, there is no choice when faced with contaminated air (except perhaps, to visit one of those oxygen bars.)

4) Trichloroethylene, the “miracle” solvent of the twentieth century. I don’t know of too many contaminants that have their own blog, except for TCE (there’s also a very active TCE list serve run by Lenny Siegel, director for Center for Public Environmental Oversight). Though it may or may not reflect the importance of this developmental immuno - , neuro – (basically you name it) toxic and potentially carcinogenic contaminant, it does reveal the importance of this chemical. According to the EPA, TCE is present in 60% of their National Priority (NPL) or Superfund sites around the country, not to mention all the tens of thousands non-NPL sites contaminated with TCE as a result of past industrial, military, small business, or legal and illegal dumping. TCE not only contaminates water – including drinking water, but, depending on the depth of the water table and soil conditions, TCE vapors from contaminated ground water can and have intruded into homes, businesses and schools. Several years back, a class of mine worked with residents in North Adams, MA – a town where seventeen houses were bought-out and razed because of concerns about TCE vapor intrusion.

5) Bisphenol-A. Actually, I don’t know that anyone might consider this one a top-five, though it’s certainly among the top-five in “Buzz.” Bisphenol A is one of those seemingly all too-common estrogenic plasticizers. As we’ve all heard by now, this is the stuff that leaches from polycarbonate bottles – including those colorful Nalgene bottles that college students carry around (to make a statement about their environmental mindfulness) baby bottles, metal can linings, and even tooth sealants. Way back when, in the dark ages of 1993, when the realization that very small amounts of chemicals could really tweak developing reproductive systems was just dawning, the EPA’s Integrated Risk Information System (IRIS) stated, “The developmental toxicity of bisphenol A has been adequately investigated. Confidence in the RfD, therefore, is high.” Consequently the EPA set the “Reference Dose,” an amount considered as safe, at 50 parts per billion per day. Recent studies now suggest concentrations nearing this reference dose may cause reproductive and developmental toxicity. Bisphenol A now contaminates rivers, streams, with unknown impacts on wildlife, and because of its use in consumer products, its in us as well, at concentrations nearing the EPA reference dose.

Phew. That about does it for me, I now submit to class for grading. Comments, corrections, additions and subtractions are welcome.

EU to the Rescue? Regulating Toxic Chemicals

Throughout my professional life, I have, for the most part buried my head in research. That’s what it’s all about - the science - right? Wrong. Not when it comes to toxic chemicals. Back when I was in graduate school, there were some hints that other things, like regulation and risk assessment were important – but I couldn’t be bothered. Even as Sheila Jasanoff, who boggled me with her intelligence and eloquence, led us graduate students through the morass of legalese in her Toxic Torts class, I just didn’t get it. Why laws were written so unintelligibly I could never understand, except maybe to help employ more lawyers.

So twenty years later – maybe even to the semester that I earned the only “C” in my post-secondary career (well – I also pulled off a C in History of the World a well known “gut,” freshman year of college), I am struggling to understand why our country’s Toxic Substances Control Act, the legislation designed to protect us from harmful effects of toxics does not; and why Europe’s new chemical control policy promises so much more.

Thankfully I’m not the only one trying to figure this out. This summer the General Accountability Office or GAO released a report comparing TSCA with Europe’s new Registration, Evaluation, and Authorization of Chemicals (REACH) legislation. Noting one primary difference between the two, the GAO states:

“TSCA places the burden of proof on EPA to demonstrate that a chemical poses a risk to human health or the environment before EPA can regulate its production or use, while REACH generally places a burden on chemical companies to ensure that chemicals do not pose such risks …….” (emphasis added)

You don’t have to be a toxicologist to know how difficult it is to determine that any one particular chemical poses a risk, you just have to read the papers. He says this, she says that, and meanwhile, polybrominated fire-retardants contaminate the dust in our homes, bisphenol-A leaches from baby bottles, and we’re wondering how the gasoline additive MTBE, which now contaminates groundwater across the country could ever have been allowed. But now the EU is requesting that industry take the lead ensuring (as best they can) that a chemical poses little risk to human health and the environment before setting it loose.

Then there are the tens of thousands of chemicals that were on the market prior to the 1980 enactment of TSCA. Unless there was reason for suspicion, those were grandfathered into chemical complacency. And into our food, clothing, air and water.

Unlike TSCA, REACH does not distinguish between new chemicals or old chemicals, according to a recent article in Environmental Health Perspectives REACH will require safety and exposure data on something like 30,000 chemicals currently sold in Europe. Those chemicals that are “carcinogenic, mutagenic, persistent or bioaccumulative or toxic to reproduction” will receive special attention. I just hope the EU has armies of toxicologists lined up to review this stuff!

Many times I’ve harped on how we seem to make the same mistakes over and over again. But it seems the EU has finally looked back before moving forward. When in class, I try to make it clear that being toxic isn’t enough to raise the reputation of a chemical to celebrity status. Exposure matters. How and how much we are exposed to certain chemicals is key. Sometimes exposure takes us by surprise. Who knew that polybrominated fire-retardents would shake free from their products (although one would think that their similarity to PCBs and dioxins might have raised some concern early on about their tendency to bioaccumulate), or that bisphenol-A would leach into water and food to the extent that it does, or that MBTE would wend its way around soil particles into our water, leaving other fuel components behind to be degraded? To address exposure – the EU proposes to consider all uses of a chemical – and to inform all “downstream uses,” clothing, cosmetic, packaging manufacturers for example, of not only the chemical’s properties but also how it behaves in humans and in the environment.

This kind of information, according to Joel Tickner, from the Lowell Center for Sustainable Development, (as reported by EHP), may drive innovation towards less toxic, safer products. According to EHP, “[Tickner] says there is a clear interest of downstream users of chemicals who want the functionality of the chemical but not their toxicity. Companies in sectors such as health care, footwear, electronics, and cleaning chemicals have already started to demand these products from suppliers.”

Amen. And with some trickle down – U.S. companies wishing to supply E.U. with chemicals will have to comply with REACH – there’s hope that we can clean up our act here at home.

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

High-tech trashed again

High tech trash is a problem that just won’t go away, and a problem which all of us help (if you're reading this you're included) generate. Whether it’s moving on to a more powerful and streamlined computer or buying the latest and greatest cell phone (and even if you don’t keep up with colorful cell phone trends, most only last a couple of years,) we all generate high tech trash or e-waste.

Though I wrote about this earlier (e-waste impacts in China) the January, 2008 National Geographic has an excellent article about the impact of High Tech Trash, by Chris Carroll, this time focusing on the impacts in Africa.

Here are a few sobering numbers from the article based on 2005 data:

• Of the roughly 760 tons of discarded TV sets only 13.4% are recycled. Just think of what will happen here in the U.S. when digital TV rules. Though a converter will get those of us with decades old sets tuned in, my guess is the changeover will be at the very least a good excuse for many to make the switch to a newer, slimmer tube (so to speak.)
• The proportion of discarded computer monitors fared better with 24.5% of the almost 390 tons that were discarded.
  
• The “frit” that connects the glass panel to the CRT funnel is 70% lead
• Pre-1990’s glass panels are 2.5% lead

As usual, at least on the environmental front, the European Union is steps ahead, with mandatory take-back programs and restrictions on the amounts of certain toxic substances incorporated into new electronics.

From the EU’s Removal of Hazardous Substances site: “The RoHS Directive stands for "the restriction of the use of certain hazardous substances in electrical and electronic equipment". This Directive bans the placing on the EU market of new electrical and electronic equipment containing more than agreed levels of lead, cadmium, mercury, hexavalent chromium, polybrominated biphenyl (PBB) and polybrominated diphenyl ether (PBDE) flame retardants.”

In the EU manufacturers are required to literally take-back electronic goods when consumers are done with them (and with a long history of planned obsolescence – that can be quite frequently with some goods) and manufacturers must ensure that electronics are either responsibly recycled or disposed. The U.S. requires no such thing.

From High Tech Trash:“In the United States, electronic waste has been less of a legislative priority. One of only three countries to sign but not ratify the Basel Convention (the other two are Haiti and Afghanistan), it does not require green design or take-back programs of manufacturers, though a few states have stepped in with their own laws. The U.S. approach, says Matthew Hale, EPA solid waste program director, is instead to encourage responsible recycling by working with industry—for instance, with a ratings system that rewards environmentally sound products with a seal of approval. "We're definitely trying to channel market forces, and look for cooperative approaches and consensus standards," Hale says.

The result of the federal hands-off policy is that the greater part of e-waste sent to domestic recyclers is shunted overseas."

Now, if I could just get my kid, who's been lobbying for a new flat screened TV to read this!

Story of Stuff - now showing on a computer near you!

My friend Cal recently sent around a link to the online video The Story Stuff. After a bit of inter-e-mail discussion by those receiving the email Cal asked if I'd post something about the Story so the discussion could go online. The following is my own experience with the video. We'd be interested in hearing yours - so we hope you'll share your thoughts in the comment section (you don't even have to read through my babble - you can skip right to the comments!) -Emily

Who doesn't use stuff?

Over the past couple of weeks I’ve been bombarded by well meaning friends and colleagues with emails about the new 20-minute online video, The Story of Stuff. At the time I was in the middle of teaching a six-week high school workshop on “The Environmental Impact of Your Clothing.” Bingo, I thought, there's one class I wouldn’t have to prepare. Just download, turn off the lights and click.

The Story provides an overview of consumption from raw materials to disposal using clear and engaging cartoon graphics, narrated by Annie Leonard, whom I found equally clear and engaging.

“So what’d you think?” I asked my high school seniors.

“Oversimplified,” said one.

“Yeah, and biased,” said another.

I was surprised - though in some ways impressed. I’d worked with these kids for a couple of weeks and we’re a pretty small class. I knew they cared about environmental issues and that they were aware of the consequences of consumerism. They weren’t very impressed with this clip. Were they too old?

I didn’t think so – while the clip uses simple graphics, it covers a range of ideas that are complex and that really are aimed at adults, not just children. Had they ironically seen to much of this kind of stuff? Or too little?

Well, I thought, so much for that. Guess it’s not so useful after all. I had planned on showing it next semester to my college students but was having second thoughts.

Then one student asked, “What’s up with all that dioxin coming out of the stacks? Does that really happen? And is it really, like, the most toxic chemical?"

Aha. While I had honed my skill as a graduate student when dioxin was “hot stuff,” so to speak – these kids have barely heard of it. And what they have heard, sometimes came from clips like this – or as the prime example of a toxic disaster.

As with many environmental contaminants that have now become just buzz-words, they had no clue as to what dioxin was, how it can be formed, how it enters the environment and what happens when it does. We spent the remainder of the class talking about disposal of toxics, and the current problems caused when dioxins are released by villagers “cooking” e-waste. This issue of e-waste is one that they can all relate to. In fact - in some ways - I'd wished the Story of Stuff had focused a little on e-waste (though I understand the universal approach -we use and toss lots of stuff.)

"Who hasn't," I asked, "bought or tossed or hopefully recycled - something electronic in the past couple of months?"

Reluctant shrugs and sheepish grins all around.

Over-simplified as The Story may be, we're all participants.

It's definitely on the agenda for my Mount Holyoke class this spring - at the very least to spark lively discussion.

Fishing for disease

Just a brief note as I prepare a longer (and more depressing article) on farmed fish - salmon in particular. Hearing how local wild caught Connecticut River brood stock salmon, and their offspring, had to be killed off this month after Infectious Pancreatic Necrosis (IPN) virus was detected in a few returning fish, I decided to take a closer look at the relationship between farmed fish and disease in wild fish.

It’s not a pretty picture, and although the link between IPN in our few and very precious local salmon is unclear, there’s plenty of evidence indicating that fish farming has increased disease in wild fish populations. Additionally there are a multitude of other problems that require attention – before farmed fish in a safe (and by this, I mean environmentally sound) manner.

For a quick read on the topic check out “Farming the deep blue sea,” an article about moving fish farming from near shore or coastal areas to offshore, published last spring in Environmental Science and Technology or more recently, Parasites from fish farms driving wild salmon to extinction in the news section of the journal Science.

So - enjoy your salmon in ignorant bliss over the holidays while you can. I'll be posting more on this, particularly the impacts of coastal and near-shore salmon farming in excruciating disease ridden detail later, after the new year.

Bisphenol A in the news again

For those interested in reading more about the estrogenic plasticizer bisphenol A (BPA), the Milwaukee Journal Sentinel just published its own review of BPA literature in response to the recently released National Toxicology Program (NTP) report, which according to the Sentinel, found "bisphenol A to be of some concern for fetuses and small children. It found that adults have almost nothing to worry about."

The article discusses conflicting conclusions by two different panels one convened by the NTP the other by National Institutes of Environmental Health and Safety) and NTP's recently released BPA report.

The Sentinel analyzed 258 studies, although a search of the links provided along with the article didn't lead to a list of those articles, nor the depth of their analysis, and who actually did the analysis, they do provide a graphic summarizing general conclusions of each study (found an effect, vs. did not find effect or were not looking); the dose range (low verses high); and the funding agency for each study (industry, nonindustry.)

If you want to read more about the scientific reports (those produced by government panels rather than the Sentinel), check out what J.Lowe has to say over at Impact Analysis in his blog about the "Tangled story of bisphenol A."

Cross posted from the earthportal forum

Greenpeace Guides the Way for e-waste

What to buy if you’re compelled towards holiday consumerism, yet feel just a twinge of guilt when you pick out the latest hot-pink cell phone or the must-have computer game-console?

Fear not, dear consumer. Greenpeace just released its “Guide to Greener Electronics.” Although the truly greener thing would be to hang on to the old phone or out-dated uncool game device until the bitter end, and then choose not to replace - that's a bit idealistic these days. At the very least, you can now figure out how to recycle the thing, and perhaps replace it with a more environmentally friendly model.

Ratings are based on reduction of hazardous materials (and intent to reduce hazardous chemicals in the future) in production and ease of recycling. Criteria include elimination or phase-out of persistent organic flame-retardants such as polybrominated biphenyls, producer take-back programs and transparent information on amounts of recycled product. What’s not clear is if recycling practices (what happens once they collect the stuff) are evaluated as well.

One particularly useful feature of the report are the links to recycling programs for each brand. So, by following the links I could finally print out a Waybill for that Dell computer I threatened to send back to Michael Dell several years back - but then decided it wasn't worth spending another dollar on that lemon. Every major component had to be replaced before its second birthday. It has spent the last two years hiding under our futon couch just waiting for this moment. Though I’d never again buy a Dell, they ranked pretty high with a 7.3 on the 10-point scale. That places them in a tie, for fourth highest score. The loser was Nintendo with an astounding ZERO points!

Even more on grapefruit juice

Ok, this is it. One last word on grapefruit juice. As both JLowe at Impact Analysis and my sister who actually reads the Wall Street Journal just informed me, grapefruit juice is now being pharmacueticalized if there is such a word. That is, someone's finally decided to capitalize the inhibitory potential of grapefruit juice extracts.

You can read a more detailed analysis at Terra Sigillata who suggests that trying to boost drug activity (and minimize dose) may be asking for trouble. But then, as the WSJ article suggests there are some cases where boosting the efficacy of a poorly absorbed drug might be advantageous.

My take - after all this discussion of drug interactions - is why add yet another drug (unless absolutely necessary) when it's clear as Terra suggests that we're not only looking at combining drugs but also interindividual differences in how each body handles drugs - which depends on many factors including genetics, nutrition, gender, age, etc.

More on grapefruit juice and drugs

A few weeks back, I wrote about drug interactions. On the recommendation of my editor (it was originally for the local paper,) I'd removed the details of how certain drugs are metabolized - the part I found most interesting, and the part he thought would most likely lead to bored and frustrated readers.

At the time I'd agreed with him and cut. But then, over the Thanksgiving Holiday, when I'd jokingly commented on the cranberry juice cocktail my friend was about to finish off, she said,

"...but I only take the Lipitor at night. Drinking a glass of cranberry juice during the day shouldn't matter."

Maybe, maybe not. I don't know much about the combination of Lipitor (atorvastatin calcium) and cranberry juice but the comment reminded me of why I'd written about the details of drug metabolism in the first place.

While the science of drug metabolism is complicated enough, when one adds the potential for drug-drug or drug-food interactions the level of complexity can skyrocket.

First, a quick introduction to drug metabolism. Lipitor is a drug metabolized primarily by enzymes belonging the CYP detoxification or drug metabolizing system. Years ago the CYP system was one of the few recognized detoxification systems in the body. That is, a collection of enzymes working together to metabolize toxic chemicals and send them on their way before they can cause any damage. Back then we knew of only a couple of enzymes, now there are dozens and dozens grouped into "families" of CYP enzymes. In the case of Lipitor, CYP3A4 is key for proper metabolism and eventual excretion of the drug.

For chemicals that require metabolism by CYP enzymes prior to excretion, the CYPs play an important role in determining the half-life of a drug or chemical.

Half-life refers to the length of time required for a drug or chemical to be reduced to one-half the initial concentration. Knowing the half-life is necessary to determing dosage ensuring that 1) there is sufficient levels of drug in the system and 2) concentrations don't get too high that they become toxic.

Anything that screws with the half-life of a chemical is potentially very dangerous. For chemicals that must be metabolized in order to be excreted, an increase in CYP metabolism would reduce half-life, resulting in drug concentrations that may no longer effective. Conversely, a reduction of CYP metabolism, or inhibition of metabolism can increase half-life, causing drugs to accumulate to toxic, possibly even lethal concentrations.

And even asking "what's the half-life" of a drug under normal conditions isn't so simple. Take the example of Lipitor. While the parent compound Lipitor (the actual drug that you ingest) may have a half-life of only fourteen hours, the metabolites of the drug - which in this case are most active - have a much longer half-life of twenty to thirty hours. That means that it can take up to thirty hours for half the initial concentration of active metabolites to exit your body.

Now lets consider the interaction between grapefruit juice (really certain chemicals in grapefruit juice) which act as inhibitors of CYP3A4. In this case, those CYP enzymes responsible for metabolic breakdown of Lipitor would be inhibited, essentially extending the half-life of the drug possibly leading to potentially toxic concentration of the drug.

And, what makes this all really complicated is that depending on how an inhibitor like grapefruit juice does it's dirty-work, the inhibitory effects may either very short-term or can last for days. In the case of grapefruit, according to one article in Pharmacy Times drinking grapefruit juice not only has immediate (within 30 minutes) impacts on metabolism, but, depending on how long and how much one has been drinking, inhibitory effects can last up to three days. This is because the chemicals responsible for inhibition by grapefruit juice, essentially combine irreversibly to CYP3A4, taking them out of action for good, necessitating synthesis of new enzyme.

Phew - maybe my editor was right! Well, you get the point I hope.

When taking new drugs or adding new food and beverages to your diet, it's well worth the little extra effort to inform your doctor or your pharmacist of the changes.

Environmental Impact of Clothing Revealed

It's not easy finding information on the waste products, the energy used, or the carbon dioxide produced by your favorite shoe manufacturer or clothing company, but that's exactly what Patagonia (you know, the expensive but generally well-made and stylish outdoor adventure clothing company) does on their site, called the "Footprint Chronicles^TM ."

Of course not many of us really want to know. But this winter I'll be working with students at a local high school building a website that focuses on the environmental impacts of their favorite outfits. When I came across the Patagonia site, I knew I had my model.

They highlight a few key products (an organic cotton t-shirt, a waterproof shell, a wool sweater and a leather shoe,) covering the major categories of textiles, and provide details on the carbon dioxide production, energy use, and waste production.

For example according to the site, fiber for the cotton T originated in Izmir Turkey, traveled to Bangkok for spinning and sewing and then on to Reno, Nevada for distribution, traveling 14,100 miles, and generating 27 pounds of CO2 (remember this is a gas!), ten ounces of waste, and using enough electricity to power an 18w compact fluorescent bulb for 72 days.

After trying in vain to gather information on the ubiquitous Crocs ( a couple of emails to Tia Mattson their public relations manager asking questions about recycling and the chemistry of crosslite (PCCR) the primary material - only left me waiting by the phone for her call which never came), the apparent openness of Patagonia was a welcome find.

Of course, ever the skeptic I tried to find the holes. What about tanning? What about other toxics surely used in dying processes? Well, I couldn't find much on dying, but on their discussion page, readers did raise questions about tanning, and, the "localcrew" responded to reader's comments with seemingly honest and useful information. Patagonia also notes that although they still use PFOA in their "Eco-Rain Shell" they are seeking alternatives to the persistent environmental contaminant. Finally, a closer look at endpoints like "waste generated" reveals that this includes only solid waste, and not liquid or hazardous waste.

At the very least, it'll be a great place for students to begin, for in addition to maps and videos of manufacturing locations, they also provide detailed references which include several websites on Life-cycle analysis for various materials, energy use, and CO2 emissions.

Check it out, and thank you Patagonia for doing (at least part of) my howework!

Bindeez and Aqua Dots

As many are aware by now, there's been a lot of interest in Bindeez beads, the toy beads that can turn toxic if or when ingested. I first read about this in the New York Times, which reported how doctors treating a comatose child in Australia, first discovered that a solvent used in production of the beads, once ingested, can be metabolized into the infamous date-rape drug, GHB.

According to news reports, ingestion of these beads have led to additional hospitalizations, both in Austrailia and here in the U.S. where the beads were sold as Aqua-beads.

Both countries have issued recalls or bans for the products.

That industrial solvent, 1,4-butanediol according to an article by Rueters was apparently used by some manufacturers in China, in place of the less potentially toxic solvent 1,5-pentanediol. The intense news coverage has led Science blogs to name 1,4-butanediol "Molecule of the Day."

Scienceblogs provides brief description of how our alcohol-metabolizing enzymes convert the industrial solvent 1,4-butanediol into GHB. There's also an interesting educational site about the conversion of 1,4-butanediol at Neuroscience for Kids.

Drug Interactions: more common than you might think

Many years ago, my father suffered a TIA or transient ischemic attack – a sort of mini-stroke. This episode occurred in association with a very common type of cardiac irregularity called atrial fibrillation. And what should have been a relatively short hospital stay turned into an all too real example of the adverse effects resulting from multi-drug interactions.

Following the TIA, thanks to a quick response by the local ambulance company, by the time my father reached the hospital he was relatively symptom free. A fact apparent to all but the admitting doctor who, upon checking for impaired mental capacity, asked him to recite the months backwards, beginning with the current month.

He said, “Enuj.”

It was the month of June, and that was my dad.

But as doctors struggled to find a safe and effective dosage of Coumadin (known generically as warfarin), a common blood thinner used to prevent future and more severe blood clots that can cause TIAs and worse, my dad’s blood levels of Coumadin bounced around, predictably unpredictable, thanks in part to his well developed drug metabolism system. You see, in his early twenties, following a bout of spinal meningitis, my father was diagnosed with epilepsy. For the rest of his life, he relied upon a combination of Meberal and Tegretol, two powerful medications to keep the seizures at bay.

Meberal is a derivative of phenobarbital, a drug that I’d been using in the toxicology laboratory at that time to increase the amounts of specific drug metabolizing enzymes. Tegretol will do the same. These enzymes belong to a system of detoxification enzymes that essentially alter toxic chemicals into more excretable compounds sending them on their way out of the body before they can cause any damage. Most likely, it was those same enzymes, induced by years of Meberal and Tegretol, which wreaked havoc with my father’s early Coumadin levels, measured then as “pro-time”, or anticoagulant activity.

To be fair, Coumadin is one of the most difficult drugs to manage, in part, because it is so susceptible to interactions with other drugs and nutrients (more on that later). Says Ed Tessier Pharm.D, and clinical pharmacist at Baystate Franklin Medical Center in Greenfield, MA, “It’s a life saving drug, but it’s known nationally as one of the most difficult to manage, not only because of drug interactions but genetics as well.” As with most biological systems, there is a strong genetic component of the detoxification system. Some of us are rapid metabolizers, some of us are not.

But here’s the thing. Although many of us don’t think we’re prime candidates for Who Wants to Host a Complex Drug Interaction, many of us do occasionally ingest potentially toxic combinations of drugs and chemicals in our food and drink without a second thought. Sometimes one of these combinations render drugs ineffective, sometimes it turns them toxic.

Take caffeine and Tylenol (or acetaminophen) for example. Acetaminophen is one of those drugs metabolized by the liver enzymes mentioned above and according to an article published online by eMedicine by Dr. Susan Farrell, assistant professor in the Department of Emergency Medicine at Harvard Medical School, “Acetaminophen is the most widely used pharmaceutical analgesic and antipyretic agent in the United States and the world….. As such, acetaminophen is one of the most common pharmaceuticals associated with both intentional and accidental poisoning.”

Most of the time, most of the acetaminophen we ingest is metabolized by specific detoxification enzymes to nontoxic by-products or metabolites, which we excrete without a problem. But sometimes, depending on the amount ingested, or, since we are talking about drug interactions, whatever else we may have ingested prior to, or along with the acetaminophen, some of it takes the toxic route, resulting in highly toxic metabolites. If you’re a cat owner, this may sound familiar. Acetaminophen and cats are a potentially lethal combination because in cats, unlike in humans, most acetaminophen is routinely metabolized via this toxic route.

Since most of this drug metabolizing drama takes place in the liver, it is the liver that is most susceptible to toxic metabolites. Notes Farrell, “In the United States, acetaminophen toxicity has replaced viral hepatitis as the most common cause of acute hepatic failure, and it is the second most common cause of liver failure requiring transplantation in the United States.”

Now say we drink a few too many Starbucks Grandes in addition to ingesting a hefty dose of Tylenol. According to Dr. Sidney Nelson, Professor of Medicinal Chemistry at the University of Washington, and lead author of a recent article in Chemical Research and Toxicology on the interaction between APAP and caffeine, “…very high concentrations of caffeine (the amounts individuals might achieve by drinking approximately 20 cups of coffee) can triple the amount of a liver toxic metabolite of acetaminophen.”

Twenty cups? That seems like an awful lot, although these days between high-test coffee and higher-test energy drinks, it would be wise for those heavy drinkers to take note. Not only that, but if one were to add a night of excessive drinking (this time I mean alcohol), followed by a morning requiring Tylenol and caffeine, it may not take twenty cups before your liver begins to suffer the consequences.

Says Dr. Nelson “…There is a period of 12-36 hours [after acute alcohol consumption] during which more acetaminophen toxic metabolite will be formed because of increased amounts of the metabolizing enzyme.”

You see alcohol, like my dad’s anti-seizure drugs also increases specific enzymes involved in certain detoxification (sometimes toxification) systems. And unfortunately, it’s not just “recreational drugs” like caffeine and alcohol that can interact with other drugs in potentially devastating ways. For a few years following my father’s TIA, after doctors figured out the correct Coumadin dosage, his blood levels of the drug remained relatively stable. He was an extremely attentive patient, interested in tracking levels of the drug as the doctors made them available, well aware of potential interactions of drugs and diet.

Then one day his Coumadin level shot up. This time, his medications weren’t to blame, nor was his overactive liver. Something was inhibiting the metabolism. The culprit, doctors eventually discovered, was his latest favorite beverage, grapefruit juice. Once again, my father’s real-life experience reflected what I had learned in toxicology. To inhibit detoxification enzymes in some of our experiments, we had used quercitin, one of the active substances in grapefruit.

According to Ed Tessier, for most Coumadin patients grapefruit juice may not be as important as other food and drug interactions, however, “grapefruit does affect metabolism of a great number of other drugs, including most of the “statin” drugs to lower cholesterol (such as atorvastatin – Lipitor®) and can lead to rhabdomyolysis - a life threatening condition which results in muscle tissue injury and possible kidney failure.”

As we add new foods to our diet, and new pharmaceuticals and herbal remedies to our medicine cabinets the potential for interaction is never-ending. One more product I am compelled to mention is St. John’s Wort, the herbal remedy commonly used to treat depression, also induces detoxification enzymes.

According to Nelson, “Chronic ingestion of St. John’s Wort….may increase the formation of the toxic metabolite of acetaminophen. If acetaminophen is taken in therapeutic doses, it is very unlikely that there would be any problem. However, if the individual taking these drugs takes larger doses of acetaminophen and drinks large amounts of caffeinated beverages (say 8 cups or more of strong coffee) or takes large amounts of caffeine-containing drugs, they would form significantly more of the toxic metabolite that could put them at risk of liver damage.”

And, among the many medications that may fall prey to enzymes induced by St. John’s Wort are most antidepressants, as well as many migraine medications, HIV medications, and birth control pills. Only in the case of some of these drugs -- including birth control pills -- the result of increased metabolism isn’t increased toxicity, but reduced efficacy.

Should this brief lesson in drug interaction scare you off your meds, fear not. These days, doctors like Kathleen McGraw MD, Medical Director of Hospital Medicine at Baystate Franklin Medical Center are blessed with instant access to reams of information on drug interactions through the web some of which can be downloaded onto hand held computing devices.

Within minutes of my mentioning St. John’s Wort, McGraw was on her PDA running the Epocrates program, scrolling through lists of drugs known to be adversely impacted by St. John’s Wort. Just as quickly she rattled off drugs affected by grapefruit juice.

To avoid problems caused by the potent chemicals in grapefruit juice, says McGraw, “I tell patients they need to give it up totally (same with cranberry juice) unless it is something they can't live without in which case they have to commit to having the same amount every single day. Given that choice, everyone says they'll quit.”

Adds McGraw, “I encourage every patient on Coumadin to remind any physician giving them a prescription for a new medication (especially antibiotics) about the Coumadin and ask if it will be affected.”

Thankfully, since the days of my dad’s TIA, the science and the awareness of drug-drug and drug-food interactions have come a long way. But it’s a two-way proposition. For pharmacists and doctors to do their part, we have to do ours, whether it’s disclosing that we’re on Coumadin, Viagra, birth control pills, herbal medications, Starbucks Grandes or the newest favorite, pomegranate juice.

UPDATE March 2010: it is well known that individual metabolic differences can dramatically impact drug metabolism. Particularly important for drugs like warfarin (coumadin.) A recent study shows that by tailoring doses based on genetic testing may help reduce hospitalizations due to drug imbalance. Read more here: http://www.businessweek.com/lifestyle/content/healthday/637031.html

Reprinted from the Montague Reporter, please feel free to quote using proper attribution.

Back to the Tap

The following article about Nestle's interest in our local water isn't my usual entry, but after noticing that the moderate sized tanker truck I was following down Route 2 in Massachusetts, was carrying none other than "Water," my stomach turned as a I imagined a future of similar "Water" trucks, removing water from one town, selling it to another, all for corporate profit.

So, I am posting this, with hopes that it will encourage citizens around the country to keep close tabs on their own water - before it's sold off - and to consider getting their drinking water (whenever possible) the "old fashioned way" - from the tap.

(Reprinted from The Montague Reporter)

This week, Nestle Water North America announced it was suspending its plan to explore the aquifir below the Montague Plains as the source for a potential water bottling plant in our community. So it seems Montague residents won’t be paying $2 a bottle to purchase our own pure Montague Plains water, at least not from Nestle, and at least not in the near future.

But that’s no reason to let down our guard. That was the message from Tuesday evening’s meeting held by the Montague Alliance to Protect our Water. Following a detailed “tour” of water flow in the plains, and the aquifer below, hydrogeologist Nancy Caffall (formerly with the state Department of Environmental Protection,) noted that “this kind of formation is particularly attractive for bottling companies.”

That’s one reason to keep on guard. Although Nestle’s may have found drilling on State land too “complicated,” because of the nature of the aquifer, and the profitability of a good water source, there’s always the potential for Nestle or another corporate bottler to pursue access through private land abutting the state owned plains.

“A municipal official from the town of Montague should ask if Nestle is talking to other property owners in the area,” suggested Russ Cohen, of the Department.of Fish and Game Riverways Program, prompting discussion of how best to inform nearby property owners of the larger impact, and potential risks of opening the door to a Nestle representative.

What would it take to discourage or deny drilling permits in the state of Massachusetts? In addition various MA DEP regulations, says Nancy Caffall, there is also the Massachusetts Water Management Act which requires that water withdrawals not stress the host river basin. That is, all withdrawals to a particular basin are considered rather than a more piecemeal approach, or one that considers only the impact on nearby surface waters.

Ironically, what makes spring water Spring Water is that it must be withdrawn from a location that is hydrogeologically connected to a surface stream. In other words, sites that are often more ecologically sensitive – with nearby habitat, freshwater fish streams etc.

And, says Kirt Mayland, Director of the New England Office of the Eastern Water Project of Trout Unlimited, the water industry wants to keep it this way – rather than going to sites where there’d be less impact. For example in Wisconsin, bottlers have drilled wells near some of the best trout streams in the region.

The case of Montague verses Nestles didn’t get as far as evaluation of impacts on nearby streams, or host river basins, in part thanks to the now famous Article 97. In addition to guaranteeing the people’s right to public resources, Article 97 also grants that removal of natural resources from public lands must be in the best interest for wildlife and wildlife habitat. So, unless like us, critters living on the plains have turned to bottled water, it’s hard to envision how corporate withdrawal would be of benefit to them, or to the public.

But as one meeting participant pointed out, “While Article 97 seemed like a real silver bullet, and although it has the most wonderful language for resource protection, there are a lot of terrible plans that happen – in this case the state may have been sensitive to all the opposition because it’s on state land.” Since most legislation regulating and protecting water was passed in the old days, when we drank water from the kitchen sink, or the bubbler down the hall, and before the rise of the multi-billion dollar bottled water industry, there are plenty of loopholes that corporations with deep pockets can ferret out. In short, there’s plenty of work to be done identifying and filling in the loopholes of state water legislation.

Not only is the extraction of a common trust resource, one that should be as free and accessible as the air we breath an issue, but between the trucking and the bottling there are plenty of other environmental impacts of the bottled water industry.

“There’s a whole lot of trucking,” impressed Mayland who noted that because the industry is so reliant on trucking, and because fuel prices are soaring, and because we here in the Northeast are major consumers of bottled water, the Route 91 corridor is of particular interest to bottled water developers, as are other locations in the Northeast that combine access to good water with access to good roads.

There is no doubt we have, in part, brought this upon ourselves by becoming a culture reliant upon bottled water. According to the group Corporate Accountability International “One of the most visible examples of corporate control of water is bottled water. It is the fastest growing sector of the US beverage market and just three corporations – Coke, Pepsi and Nestlé – make up over half of the US bottled water market. These corporations are privatizing our water, bottling it and selling it back to us at prices hundreds, even thousands of times what tap water costs. They have turned a shared common resource into a $100 billion global market – and one of the world’s fastest growing branded beverages.”

But if corporate greed isn’t enough to make you think twice about purchasing that next bottle of Aquafina, Poland Springs, or Evian, then think locally. We all know what happens to bottles that aren’t recycled, they’re tossed into garbage, flattened along the road side, or floating down the river. Then there is the toxic side of plastic bottles, and the potential for bottles, depending on the plastic to leach small amounts of toxicants into drinking water.

It’s time to turn back to the tap, relinquishing the bottle, and protect our municipal waters.

Polycarbonate plastics: if only toxicology could be that clear

An ongoing debate about the health impacts of bisphenol A (BPA), the ubiquitous chemical used in production of polycarbonate - that hard clear plastic we use for eating, drinking, and storing food – continues, according to a recent article by Janet Raloff published in the September 29 issue of Science News. Her analysis provides good insight into why we often hear conflicting reports when it comes to environmental and health impacts of chemicals.

Raloff reports on the conflicting results of two different panels recruited by the National Toxicology Program (NTP) and charged with reviewing and evaluating the potential developmental and reproductive impacts of BPA. While one panel “labeled ‘as confident’ its assessment that BPA at low doses has had negative effects on experimental animals,” and that such findings were suggestive of impacts in humans, the other panel “concluded that current BPA exposures appear to pose little risk to humans.”

According to Raloff, one of the differences cited in this analysis, leading to conclusions ranging from don’t use the stuff if you don’t have to, to it’s a non-issue, were concerns about the basic experimental design used by scientists evaluating BPA. When laboratory animals are exposed to experimental chemicals there is often a trade-off between ensuring exposure to the chemical, verses exposing the animal in a realistic manner. Way back when, when I was interested in the effects of PCBs in fish populations, I’d load up syringe and inject. Now unless fish were mainlining PCBs (and concentrations in some wild fish were certainly suggestive of that!) clearly this wasn’t realistic. But, what it did provide us with was an exposure where we were sure that PCBs got to where we wanted them to go. Confident of our exposures (we’d also do some chemical analysis – which was the most costly part of the study back then, and so something toxicologists would like to avoid if at all possible), we could more efficiently get down to our intended business, evaluating the effects. Our option would have been to develop food with amounts of PCBs that fish would eat in amounts that we could somehow measure (you ever watch fish eat? Biting off pieces of food, letting the rest drift to the bottom, possibly snatched up by less aggressive fishes), that wouldn’t leave us with gallons of toxic water to cleanse in the end. The fact is there are often good reasons to use the needle, although as pointed out by the panels, there are limitations to these kinds of unrealistic exposures, one of them is interpreting experimental results to a broader range of more realistic exposure scenarios.

Raloff outlines other differences in the panels, for example, she writes that the panel which concluded impacts are likely, had either worked with the chemical or similar chemicals, while the panel that came to nearly an opposite conclusion “were selected precisely because they had no direct BPA experience and, therefore, no obvious vested interest in judging the quality of the data on the chemical.” Fair enough, I suppose. You’d hope scientists can see past their own interests, although I’ve always thought it’d be interesting to see a study correlating the evaluation of experimental data with sustained funding for a particular subject over a period of time.

For more details on the subject, the article is available on the Science News site, and, according to Raloff, “ultimately, NTP will issue a single report that integrates conclusions from both panels, along with any new information on BPA that comes to light during the next few months.” Now that ought to be an interesting read.