Wednesday, December 10, 2008

This isn't your mother's melamine - or is it?

Melamine is yet another cool ‘50s invention that failed to enter my mother’s kitchen. While friends and neighbors stocked up on the nifty new light, durable and colorful plastic dishware, my mother filled her kitchen with white, pure white, simple, elegant, breakable ceramic. Her cupboards are still filled with the stuff – white, white, white. Not so at my in-laws, where the everyday dinner ware is red, blue and yellow melamine, pleasingly smooth, tough and virtually unbreakable.

Just a couple of years ago, Crate and Barrel in an effort to appeal to boomers who recall dining off the colorful plastic, offered melamine in colors that harkened back to the fifties and sixties – bright orange, acid green and red (far better on plates than on the cabinets and counters) and, being deprived of the plastic as a child, I pounced, buying a cute set of eight orange, green and red oval-shaped melamine dishes.

This is all to say that until a year or so ago any thoughts I had about melamine were pleasant and nostalgic. Now when I think melamine, I hear the rattle-snake sound of the old westerns, the sound that happens just before something bad is about to happen. Just before the good guy is about to drink the tainted water, or the heroine is about to drink the poisoned wine.

Chemically, melamine is a pleasingly round molecule made up of hydrogen, carbon and nitrogen, and is used in the preparation and production of a range of items including house wares, flame retardants, and fabrics. When combined with formaldehyde and heated up – melamine is transformed into the dinnerware. Which by the way, when heated together with your favorite acidic food, (reheated tomato sauce anyone?) can release upwards of 2.5 milligrams of melamine per 100 cm2 according to the National Toxicology Program, that’s roughly 2.5 mg per one big round plate – but that’s a separate issue.

By itself, melamine’s acute toxicity is comparable with that of table salt (i.e. not very toxic) although recall that toxicity is often a moving target depending on the sensitivity of the endpoint, exposure duration, age of test subject and other considerations. That melamine causes kidney toxicity following longer exposures to high concentrations in test animals (say 2 – 4 parts per thousand in feed,) is well known and until now, not considered highly relevant, because those concentrations were considered unrealistically high. Here I’d emphasize were, but we’ll get back to that later.

What first brought melamine to our attention here in the states, is the toxic transformation that occurs when it combines with cyanuric acid, an FDA approved feed additive, also used to produce dyes, herbicides, antimicrobials and pool water disinfectant. That's when the "watch out" snake start rattling. Cyanuric acid, a derivative of melamine is also a ringed nitrogen containing structure, and like melamine it is considered not acutely toxic. But when these two chemicals get together, like the Witches of Eastwick, the mayhem begins. Following ingestion, the chemicals make their way to the kidney destined for simple excretion. Unfortunately should they meet up, melamine and cyanuric acid join together to forming melamine cyanurate crystals, a toxic combination capable of lodging in kidney tubules and causing acute renal failure and death.

A year ago contaminated pet food from China was implicated in the deaths of dozens of cats and sickened thousands of dogs and cats. The culprit was subsequently traced to melamine tainted gluten. Gluten, derived from wheat or rice, is a common source of protein. Protein is sometimes estimated by measuring gluten nitrogen content. Given the high amount of nitrogen groups in both melamine and cyanuric acid (available as “scrap residue” from the melamine industry) it isn’t hard to imagine unscrupulous processers adding the stuff to their products to dupe purchasers or regulators into thinking they were selling a higher protein product.
After the massive recall of over 150 brands of pet food one would think that the incident alone would deter anyone from trying the same thing again, at least anyone with a conscience. But sadly, like the string of corrupt Illinois politicians, there’s always someone next in line no matter the consequences.

This past fall over 50,000 infants became ill, and at least four died of kidney failure after drinking melamine laced formula in China. The scandal soon spread beyond formula to candy, milk, and other diary containing products produced by dozens of companies. To date, only melamine has been implicated – leaving scientists to wonder about the mechanism of toxicity – recall with the pet foods melamine was mixed with its evil twin, cyanuric acid.

According to the World Health Organization upwards of 6196.61 mg/kg have been measured in dairy products including infant formula. That’s 6 grams in one kilogram of product, or, 6 parts-per-thousand. While that may be the high end, recall the sub-acute toxicity tests mentioned above and those screamingly high concentrations now seem more relevant. Additionally, chemicals are most often tested in weaned animals – not nursing animals – so concentrations that might be OK for adults may not be OK for the very young.

The Sanlu Group one of China’s major diary and infant formula producers whose products were fist shown to contain the chemical quickly blamed the dairy farmers – suggesting that they were the ones who added melamine to fool protein tests.
More recently, according a news article in the journal Science, investigators concluded that the adulterated infant formula was “nothing short of a whole-sale re-engineering of milk,” a skill likely out of reach for dairy farmers, but perhaps not for milk-collecting companies or corporations higher up the milk-chain.

China’s response to the tragedy, according to Science, is to pledge greater transparency and vigilance. In addition, China plans to open Food and Drug Administration offices here in the U.S. and the US FDA recently opened three offices in China. But old habits die hard and according to Chen Junshi a risk assessment specialist at China’s Center for Disease Control and Prevention, and quoted in Science, it’s likely that food adulterers will only become cleverer. Those willing to make money at the expense of their fellow citizens, will seek alternative methods challenging both Chinese agencies and the newly opened US Food and Drug Administration offices in China.

Now, about those colorful plates...

Tuesday, November 04, 2008

Wrapped in Plastic

First Printed in the Montague Reporter Nov 2008

I pull a gallon sized Ziploc bag from its sunny yellow box, one of several boxes my mother, who shops at Costco, sent home with me last weekend, and swallow the guilt as I add yet another virginal plastic bag to the relatively permanent archive of plastic things in the world.

Just to be clear, I don’t buy plastic bags. Well, not unless it’s for a good cause like packing away the twenty pounds of wild low-spray blueberries we raked last summer. I tell myself I’ll reuse them, and I do, from storing bagels, to blueberry muffins, to banana bread before tossing them in for a spin in the wash whenever a greasy film builds up. But then the inevitable happens. The plastic zipper tab breaks off, or the blue and yellow tracks warped by warm water and dryer heat no longer join. For a while the bag limps through still storing food, closed up with a rubber band, or rolled up tight and tucked away. But that only puts off its fate for so long – eventually the plastic shows its age, as small cracks and holes begin to let in air or let out drips of last night’s soup.

That’s when it’s pitched into the trash. I’d add them to the Stop&Shop recycling (or down cycling) pile – which allows shopping bags, dry cleaning bags and newspaper bags - but wary of “contaminating” plastic batches with Ziplocs I refrain, and make a note to ask Stop&Shop about this.

As frugal as I am about Ziplocs and Saran wrap, my mother is not. But it wasn’t always that way. I can still recall my envy over the little plastic sandwich baggies Amy Ellis, my best friend in grade school, pulled from her lunch box each day. Her mother, a decade younger than my 42 year old mom, was far more “with-it,” or so I thought. If there was a new product, Amy had it. While her sandwiches were moist and soft, good material for a lunch-time trade, mine, in its wax-paper sandwich bag, couldn’t compare. Now the shoes are on my slightly older feet and I refuse to pack my kids’ lunch in plastic baggies. Just check out the garbage pail in any school room around the country and you’ll find plenty. Their total useful life-time? About three hours.

According to the history of plastic bags, those little baggies, thin sheets of blown polyethylene film sealed along three sides first came into being around 1957, roughly twenty-four years after the discovery of the stuff, and ten years before the ubiquitous and larger, produce bag.

Plastic produce bags, primarily LDPE or low density polyethylene, now fill the cotton shopping bags of the most plastic-wary consumer whether they’re shopping the farmer’s market, the local co-op, Whole Foods or Big Y. So I was heartened last week when I loaded my bagels into a recycled plastic produce bag at Whole Foods. If only the darn thing didn’t break open and spill six bagels onto the floor! I’m sure in time they’ll get it right.

Like sandwich baggies, by some estimates the useful lifetime of produce bags is measured in minutes, or however long it takes to stuff some string beans into the bag, hit the check-out counter and dump them into the colander for dinner. Though the most fastidious of us might reuse them or cart them back to Stop&Shop for recycling, plenty still end up in the trash.

Like all plastics, plastic baggies flow from the crude oil tap which is refined and distilled before cradling our organic broccoli. Crude oil is a complex mixture of hydrocarbons – carbon and hydrogen containing molecules. Some are long, some are short. They are straight, or branched – but all have a carbon “back-bone,” or a chain of carbons C-C-C-C. For years I had a small vial of crude oil in my office, rescued from the Valdez Oil spill, the label thanked me for helping to remove some ridiculously small percentage of the original spill (it now sits somewhere on my son’s science teacher’s desk – beseeching impressionable minds to think more deeply about the consequences of using oil.) This particular crude is the darkest of browns, a thick balled up tar-like substance floating atop the Prince William Sound water captured along with it. It is hard to imagine the link between the transparent filmy Ziplocs in my pantry and a vat of crude oil.

During distillation successively lighter fractions are boiled off and collected, the shorter carbon chain the lighter the fraction. Gasoline for example is “light,” and one of the first fractions collected, while the heating oil that warms our house is thicker, heavier and consists of longer carbon chains. Carbon chains can also be “cracked” into shorter chains, like ethylene, a simple two-carbon molecule. Ethylene is a highly versatile molecule used in hospitals and medical offices for sterilization, fruit ripening (it is also a naturally produced fruit hormone which initiates fruit ripening – try storing some apples next to an overripe banana and see what happens), antifreeze, a one-time gasoline additive, and plastics.

It is one of the highest volume organic (carbon containing) chemicals in production. According to a recent report by
SRI consulting in 2006 “…global ethylene production amounted to about 110 million metric tons, with an estimated value of $122 billion.” 110 million metric tons, and guess what? Over half of that goes right into the production of polyethylene plastics including bags and plastic wrap.

“Everyone’s asking about plastic wrap in the microwave,” says my mother one afternoon. Apparently some of her friends had read or heard about the email promising death and destruction by dioxins and other “toxins dripping into your food.” For years she’s been using plastic wrap when reheating. Her reheated food is moist and her oven clean. I don’t cover, and my oven is encrusted with splatter and my food dry. Turns out the email was a hoax, but – according to both the American Chemistry’s Plastic’s Info site (Better Living with Plastics), and the FDA (for what it’s worth these days), consumers should be wary of combining their wrap with their food when microwaving. According to the Plastic’s Info, site, “..most manufacturers recommend leaving at least an inch between the food and the wrap covering the dish. This is to prevent the plastic wrap from melting, which could result from contact with extremely hot foods.” Not to mention allowing chemical additives present in some of the clear cling wraps to leach other chemicals into your food.

Plastic wraps are made from LDPE or polyvinyl chloride (PVC). Concern about toxics leaching from PVC wrap started the rumors flying. Although plastics are incredibly versatile materials, sometimes they are tweaked with chemical additives to get just the right clinginess, or color or flexibility. That meant diethylhexyl adipate (DEHA) in the case of chlorine containing cling wraps. Problem was under the right circumstances, like heating in a microwave, particularly heating things with high fat content, like cheese or meat, DEHA, a reproductive and developmental toxicant (although so far as we know just at relatively high doses) migrated from the plastic wrap resting on top of last night’s Buffalo Chicken Wings into the wings.
While the FDA acknowledges that substances like DEHA can and do transfer from plastic to foods during reheating, the controversy is over how much leaches and how toxic. While FDA maintains whatever leaches out is safe, some countries have banned the additive, while S.C. Johnson, producer of the granddaddy of all cling-wrap, Saran, switched from PVC to LDPE, winning an EPA “Designing Greener Chemistry Award” in the process.

Now, if we just can figure out how to consistently recycle all that wrap and all those LDPE baggies – we’ll all be a little bit greener.

Monday, October 27, 2008

More questions about BPA regulation

Though I am not in the habit of citing newspaper articles – after receiving the Center for Science in the Public Interest’s weekly Integrity in Science Watch, I linked to over the Milwaukee Journal Sentinel, which over the past year or so has done quite a bit of digging around on the issue of BPA.

Here’s the latest from Milwaukee: last week, the Sentinel accused the FDA of relying a bit too heavily on chemical and plastics industry citing 1) an FDA subcommittee chair whose institution accepted millions of dollars from a donor who had repeatedly expressed his views that the chemical was “perfectly safe;” and 2) using the consulting firm ICF, currently under investigation by the Committee on Energy and Commerce, which according to a letter sent to FDA commissioner Dr. Andrew von Eschenbach “…has done prior work for BPA manufacturers, and whose board members have ties to BPA manufacturers.”

Writes the Sentinel, “…Columbia University professor David Rosner, who researches the relationship of industry and government regulators of toxic substances, has compared the controversy over bisphenol A to tobacco and asbestos.” A few years back, Rosner, together with colleague Gerald Markowitz, authored Deceit and Denial: the deadly politics of industrial pollution, one of the better books I’ve read about the role of the chemical industry on regulation.

Coming from Rosner, as far as health scandals go, that’s a pretty serious comparison.

Friday, September 26, 2008

Just another brick in the wall: more on bisphenol A

My neighbor, the “real” doctor, called the other day, asking for “The Neighborhood Toxicologist.”

“So, what are you doing about your bicycle bottles,” she asked.

She’d just read the latest study and related commentary on the potential dangers of bisphenol A in the
Journal of the American Medical Association. It’s rare that I get to advise Katta, most often it’s me calling her – how does Sophie’s staph infection look? What do you think of this little black spot on my arm? I just called an ambulance for Ben, do you think you could come take a look at him while we wait?

I leaned into my expertise. “Well,” I said, “you know those aren’t
polycarbonate. It’s just the polycarb that has bisphenol A. Those bicycle bottles are polyethylene,” I said with some authority – impressing myself with my own recall. “As far as I know no-one’s found anything bad about those,” I pause, “not yet anyway.” Not unless you consider the filmy black crude (I’m guessing something biological rather than chemical) that inevitably coats the insides of those bicycle bottles – even if all you’ve ever had in them is water.

What’s confusing about the polycarbonate issue is that it provides s a perfect (or maybe imperfect) opportunity for the public to crab about the wishy-washyness of scientists. Most folks just want an answer – yea or nay, good or bad. But with bisphenol A you get two conflicting answers from two federal organizations, the FDA and the National Toxicology Program.

While the National Toxicology Program (under the National Institute of Environmental Health Sciences) concludes, as far as anyone can conclude, that bisphenol A “is of “some concern” for effects on development of the prostate gland and brain and for behavioral effects in fetuses, infants and children” (for details check out their final report, NTP-CERHR Monograph on the Potential Human Reproductive and Developmental Effects of Bisphenol A ,
) the FDA gives the A-okay all-clear for the chemical. According to their recently issued draft report, “…FDA concludes that an adequate margin of safety exists for BPA at current levels of exposure from food contact uses for infants and adults .”

So what gives? The FDA’s overall findings suggest that the available studies are “inadequate” (problems with dosing, species, timing – you name it.) It’s true that all of these can impact the outcome and that even the very best study on a particular contaminant can be rendered relatively irrelevant because the concentrations say, were screamingly high (for example beyond those anyone would ever be exposed to unless they ate their pretty blue bottles); or that the method of exposure is irrelevant (say, injecting a chemical – essentially mainlining it – rather than feeding it to experimental animals); or the so-called mechanism of action – how a chemical causes toxicity – is unique to a particular test species (though this one goes both ways – the sedative thalidomide offers a tragic example of why chemicals need to be tested in several different species.)

Unfortunatley, sometimes we just have to do the best with what we’ve got when it comes to data. Sometimes knowing what’s lacking informs experimental design, so studies that are “most appropriate” can be done. While I won’t review the review that reviewed the review (FDA’s most recent
draft) I would like to point out that there are no conflicts about BPA’s femininity. The chemical is indeed estrogenic – scientists knew that long before it ever became a part of those polycarbonate bottles. Estrogen, as we all know is a pretty powerful hormone.
And estrogenic chemicals can bind with, and activate estrogen receptors (referred to below as ERα and ERβ) which means that, like estrogen, they can also elicit all or some of the biological outcomes triggered by estrogen.

But contaminants like BPA must compete with both estrogen in the body and other ingested estrogens, here’s
FDA again, “In fact, BPA has an approximately 1000 - 10,000 fold lower affinity for ERα and ERβ as compared to E2, whereas genistein, a phytoestrogen, has a much higher affinity than BPA for ERα and ERβ. Accordingly, if equal concentrations were available, the assumed order of binding to the ERs would be E2, genistein, and then BPA.”

Here’s where even I’m a little confuzuled as my daughter used to say. Though I hesitate to reveal my ignorance – and I do pledge to take this on and fully understand the implications one day – are they saying that it doesn’t matter that BPA binds a powerful receptor because there are several other more “natural” chemicals that will beat it out? When we know that too much estrogen, or estrogen exposure at the “wrong time” could be bad (what I mean by “wrong time” is that there are times during say, development – particularly development in the male when natural concentrations of estrogen may be very low)? Why not take the cautious approach that adding another estrogen to the mix could also be bad – particularly one that is apparently easy to avoid – stop using BPA containing bottles (although that still leaves can linings.)

What follows is an excerpt from a
review by Alex Vidaeff and Lowell Server explaining why just knowing the relative potency of estrogens isn’t necessarily enough:
“It has been said that xenoestrogens and phytoestrogens, being weak estrogens with a low level of environmental contamination, are not sufficient to produce adverse effects. The opinions were mainly based on the observations derived from DES-exposed cohorts where only “sufficient” doses of DES generated adverse effects
[71] . Such considerations, based on an estrogen potency threshold, or dose-response effects, may underestimate environmental estrogens activity. Hazard identification and assessment in this area cannot rely solely on linear measurements of estrogen activity. Undoubtedly, the xenoestrogens are weaker estrogens than estradiol or even estriol, but studies focusing on binding activity may overlook the complexity of ER action as described above, and the fact that factors other than the binding affinity of the ligand for the receptor may affect gene expression…... When vom Saal et al. [70] observed an increase in prostate size after prenatal exposure to estrogens in mice, the dose-response curve was an U-shaped curve, whereby lower doses also resulted in larger effects. This supports the possibility that even low doses of estrogen in fetal life may affect the expression of genes involved in the morphogenesis of the prostate gland and possibly other genital tissues.”

And then there’s that JAMA article. What alarmed Dr. Katta wasn’t the squabbling over laboratory studies or the reproductive and developmental impacts in rats – but the more recent finding that very real concentrations of bisphenol A in human urine samples (yes we drink the stuff in and pee it out in small but measurable amounts) was positively associated with heart-disease and type 2 diabetes in adult humans in addition to the prostate and brain effects which are of concern to the National Toxicology Program.

But remember, an association is just that – the two things tend to travel together. In this case those with more BPA in their urine tended to have a higher incidence of disease but that doesn’t mean disease was caused by BPA – maybe those with more disease just eat more canned food compared with fresh potentially healthier food (can lining is another source of BPA.) It will take further laboratory studies to confirm any cause and effect linkages. But what’s notable about the study was that there are already rat data linking the chemical to insulin resistance – which in turn is key in the development of type 2 diabetes.

If you’ve read to this point – you must, by now get the idea of how complicated it can be to figure these things out. Oh only if we could just sit a bunch of infants down and have them chug warm milk from polycarb bottles – and then wait and see what happens.
Oops we’ve already done that.

Thursday, August 14, 2008

Silencing Spring: WWRD

First Pulished September 2008 in the Montague Reporter

In her 1962 publication, Silent Spring, Rachel Carson wrote about a spring in the near future potentially silenced by “indiscriminate use of pesticides,” with names like DDT, lindane, aldrin and mirex. What she didn’t write about back then, are the now infamous perfluorinated chemicals used in nonstick and waterproof surfaces, the polybrominated flame retardants that are infused into textiles and plastics, or the triclosan and triclocarban antibacterials in soaps, toothpastes and a range of consumer goods. Back then, no one knew that these chemicals used primarily in consumer products, would eventually find their way into not only you, but also your neighbor, and your neighbor’s neighbor, and, depending on the chemical possibly their uncle in Alaska and definitely the polar bear that just roamed through your neighbor’s neighbor’s uncle’s town.

Instead, Carson chronicled what in retrospect seems obvious now, but clearly wasn't back then. That spraying long-lasting (and by long - I mean decades) chlorinated chemicals like DDT, which accumulate in the fat and are designed to be toxic, on farms, suburbs, even cities just wasn’t smart. But if her expose seems obvious now, then why almost fifty years later are scientists finding, in addition to the remnants of chlorinated pesticides banned years ago, industrial fluorinated and brominated chemicals in water, sediments, wildlife and in humans? And why is one of the “next generation,” shorter lived, barely-bioaccumulative pesticides, atrazine, turning up in surface and groundwater supplies across the nation?

There is no doubt that the publication of Silent Spring wakened the American public to the very real consequences of “better living through chemistry.”

“I was in 8th or 9th grade,” recalls my neighbor Jeff, “and learned about it from the mainstream media. It had a pretty big impact – it started to frame the way you looked at things. I remember kayaking down the Connecticut. It was disgusting. But,” he conceded, “none of us were really sure what to do about these things.”

Barely a year old at the time of publication, and not cognizant of books except maybe as suitable teething material, I don’t recall its publication or the impact it had on my suburban life, although I do recall tanker trucks trundling along our road, spraying for mosquitoes and gypsy moths; the shelf in the garage full of bottles and spray cans that my father used to combat whatever ailed his beloved trees and shrubs; and, befitting my current occupation, I recall mixing up my own toxic potions – from cleaning materials stashed under the sink or in the laundry room, and testing them out on the earwigs and carpenter ants that raced along our swing set. Unlike Jeff, I was clueless.

Thankfully, there were plenty of folks who were neither clueless, nor baffled about what could be done to avert the impending environmental disaster described so elegantly by Ms. Carson. Eight years after Silent Spring, the US Environmental Protection Agency, the primary body responsible for registration, release and management of chemicals was born.

Of the December 2, 1970 launch of the agency Jack Lewis, writing for EPA Journal noted, “…Surely no factor was more pivotal in the birth of EPA than decades of rampant and highly visible pollution. But pollution alone does not an agency make. Ideas are needed--better yet a whole world view--and many environmental ideas first crystallized in 1962. That year saw the publication of Rachel Carson's Silent Spring….In fact, EPA today may be said without exaggeration to be the extended shadow of Rachel Carson. The influence of her book has brought together over 14,000 scientists, lawyers, managers, and other employees across the country to fight the good fight for "environmental protection."”

That’s an impressive legacy. But sometimes, I wonder what Ms. Carson would think of her legacy today?

Reading Silent Spring for the first time (I am ashamed to admit), it’s unsettling that nearly fifty years later, albeit on a different scale, Carson’s writing is still relevant. I don’t mean the the details – I think for anyone who didn’t live through those times – or who doesn’t live near farms where aerial spaying is still used – the events Carson described are hard to imagine. It’s been over thirty years since DDT fell from the sky like snow, and “housewives” swept pellets from their front steps or washed the stuff out of their kids’ hair, and the death of so many songbirds suggested a bleak future.

No doubt, we are all better off thanks to the EPA’s slew of chemical regulations and policies, but on a different scale, pesticides and industrial chemicals continue to contaminate water, consumer products, wildlife and us. And scientists, rather than focusing on lethality and reproductive success are now measuring more subtle changes in wildlife like altered reproductive function and development. The perfluorinated and polybrominated chemicals provide examples of history repeating itself – even with regulations in place. Sometimes chemicals slip by because scientists haven’t figured out how to measure them in the environment. Sometimes they slip by because no one expected them to be there, and sometimes they slip by because the industry that produced and released them didn’t provide all the relevant data. But thanks to greater collective environmental awareness ( by consumers, activists, scientists, policy makers and even industry), unlike DDT, it won’t take over a decade to phase-out fluorinated and brominated chemicals – phase-outs for these chemicals are already in progress.

But then there’s Atrazine. The top selling herbicide in the United States, banned by the European Union in 2003, atrazine is an example of a “new and improved” pesticide gone awry. Applied primarily to corn, with minor uses including lawns and golf courses, the EPA estimates that roughly 73 million of pounds of atrazine are applied to crops each year. Compared with the longevity of the chlorinated pesticides like DDT atrazine lasts for merely a blink in time with a half-life 146 days or so (although in these more enlightened days even that’s considered long-lived.) Unfortunately once Atrazine works its way into ground water it may last for years. The result? In the midwest, Atrazine is one of the most commonly detected contaminants in surface and groundwater, additionally it’s been detected although to a lesser extent in groundwater in the Northeast, including Massachusetts. Though detected concentrations often fall well below EPA’s 3 part-per-billion drinking water standards, there are a growing number of studies suggesting that other species, particularly amphibians may be susceptible to much lower concentrations.

University of California, Berkely researcher Tyrone Hayes reported back in 2003 that exquisitely low concentrations of atrazine, as low as 0.1 ppb, altered the steroid hormone balance in frogs, feminizing male frogs and resulting in hermaphrodism and demasculization of the vocal cords. And just recently, Krista McCoy and others, publishing in Environmental Health Perspectives, reported a link between hectares of farmland and feminization in local frogs. Although the authors didn’t measure specific pesticides, among the suspects is atrazine. All this got me wondering – where’s our EPA? Atrazine was recently up for reregistration, an opportunity for EPA to review data accrued over the years since a pesticide is first registered. For atrazine that was 1958. This was well before scientists were clued in to subtle reproductive and developmental impacts caused by small concentrations of chemicals. Nor was consideration given back then, and only rarely now, to the reality that seldom are individuals or wildlife exposed to single chemicals. We are all exposed to complex mixtures of contaminants released by industry, agriculture and from consumer products like soaps, sunscreens and pharmaceuticals.

Surely, I thought, given the pervasive groundwater contamination and the recent data on frogs, atrazine’s registration if not revoked would at least be restricted. At the very least maybe the allowable environmental concentrations (the “chronic criterion”) would be reduced below those found to impact amphibians? Unable to find the appropriate numbers on EPA’s website, I emailed EPA. “We anticipate this chronic criterion, when finalized later next year, will fall within the range of 10 to 20 ug/l [ppb]” wrote Frank Gostomski of EPA’s Health and Ecological Criteria Division. I asked if Hayes’ studies had been included. Yes, was the answer. But if Hayes’ studies hold up to scientific scrutiny –and there seems to be a growing body of literature that suggests that they do - then EPA’s concentrations are way higher than those found to feminize male frogs.

Though hard to imagine in our own backyard where spring peepers and cluckers keep us awake, is it possible that some day thanks once again to “indiscriminate use of pesticides” spring could still be silenced?

Thursday, July 24, 2008

Anti antimicrobials - time to get serious about triclosan and triclocarban

I thought I was “antibacterial” savvy. For years I’ve read labels on antiperspirants and soaps before tossing them into the shopping cart. It wasn’t until I joined a consumer products working group, whose current focus is the dynamic duo of antibacterials, triclosan and triclocarbon, that I found I should also be checking my toothpaste. That’s right, listed right there on the ingredients for Colgate toothpaste was triclosan.

So why the outrage, what’s so bad about these products? Most experts including physicians groups and an FDA panel agree that these antibacterials, originally used in hospitals, aren’t really necessary for the average consumer. Unless there’s a reason to be ultra-clean, there’s nothing like a good hand washing with plain old soap.

Then there are the environmental implications of washing this stuff down the drain. As discussed a while back on this site, these chemicals tend to make their way through sewage treatment plants, persisting in soil and water. But that’s not all folks. Back when I wrote about antimicrobials I focused on the release and impact of these things into the environment. But now I read that triclosan is detectable in breast milk. And although the author concludes that concentrations are below those that might be cause for concern, here we have a chemical that 1) doesn’t seem to do much good 2) gets into the environment and stays there and 3) gets into breast milk. Hmmm.

The breast milk study, by A.D. Dayan, found “No triclosan was detected in 2 samples, it was barely detectable in 9 and the concentration ranged from about 100 to about 2100 μg/kg lipid in the other 51 milk samples.” With the majority of samples testing positive it’s curious that Dayan ponders the results, adding the following “caveats” for how and why these samples might contain the antibacterial:

"Possible contamination at the time of collection.• For example, might the mother have used a triclosan-containing soap to wash her breasts shortly before donating the milk? When did she last use a medicated deodorant, dentifrice or dusting powder?• Was the milk sample collected early or late in lactation after parturition because the body’s fat stores change with time, possibly affecting systemic exposure to any lipophilic material stored in fat?• When was the sample collected in each episode of lactation, i.e. was it ‘fore-milk’, which is more watery, or a later, hind-milk sample with a higher fat content?• Was the sample collected after a period during which the mother had not breast fed or expressed milk? Even a necessarily brief period without milk expression may make the first sample of milk then obtained more concentrated than usual.”

Skepticism is fine – what would science be without some healthy skepticism. But in this case I can’t help but be skeptical in the opposite direction – if there’s no clear benefit of the stuff – why risk exposing the most vulnerable population? Besides none of these caveats lessen the implication that breast fed infants of these women would likely be exposed at some point.

Now, a study by Bruce Hammock (from the University of California, Davis) and others, published in Environmental Health Perspectives suggest that use of these products may in fact, do more harm than good. Reporting that while triclocarban enhanced activation of steroid hormone dependent genes, triclosan was found to be antagonistic in assays designed to evaluate interaction with steroid hormone dependent activity, the authors suggest caution when it comes to triclosan and triclocarbon concluding:

“These observations have potentially significant implications with regard to human and animal health since exposure may be directly through dermal contact or indirectly through the food chain. These screening studies revealed that further investigations into the biological and toxicological effects of TCC [triclocarban], its cabanilide analogs, and TCS [triclosan] are urgently needed."

Perhaps one route, rather than relying on the consumer to read, read, read is to encourage producers to remove the stuff - or to encourage the EPA to cancel all non-medical uses - which is exactly what several environmental and public health organizations are suggesting according to an article in Water and Wastewater News.

But for now, until their campaigns are successful, it’s time to take cleanliness into our own hands and keep reading those labels.

Wednesday, July 23, 2008

Who's screening sunscreens?

A while back I wrote about sunscreens here and here. But that was already over a year ago - and as anyone who is confused by he says and she says in science knows - the reports just keep on rolling. Just yesterday the New York Times Science Section published an article by Tara Parker-Pope calling sunscreen safety into question, and based in large part on an Environmental Working Group (EWG) report on the stuff. In short, it seems that the EWG is concerned about chemicals like oxybenzone (or BP-3 )which are absorbed by the blood and can be detected in urine - the problem is - health impacts are unknown (although a recent news article in Environmental Health Perspectives reports that in animal studies BP-3 " effects in liver, kidney, and reproductive organs, and studies by other groups have shown endocrine-disrupting effects,") and some claim EWG's rating system for sunscreens lacks scientific rigor. Either way, there just aren't enough studies - though one would wonder maybe why consumers are allowed to slather products on themselves and their young ones when "there aren't enough data."

According to Parker-Pope, "Of nearly 1,000 sunscreens reviewed, the group recommends only 143 brands. Most are lesser-known brands with titanium and zinc, which are effective blockers of ultraviolet radiation. But they are less popular with consumers because they can leave a white residue." But many of the titanium and zinc sunscreens don't leave a residue, and the reason they don't is that titanium and or zinc in "micronized." In other words - really small - sometimes nanosized.

Those who remember smearing the white stuff on their noses in the summer - most likely were using zinc that scattered not only the undesirable UV light but also visible light (hence the clown effect.) Today's micro or nano zinc
allow visible light to pass through them and so appear clear, while still scattering the sun’s shorter and harmful ultraviolet rays. Cool right?

Maybe. My friend Cal Baier-Anderson, blogging over at Environmental Defense just posted about a study initiated following an "...observation that installers of metal roofs who used these sunscreens inadvertently transferred the product onto the roofs. In places where the workers’ skin had touched the painted metal surfaces, the paint showed accelerated weathering. Why? Because the particular type of nanoscale TiO2 in the sunscreen (the anatase crystal form) is photoactive – when it absorbs UV light, it releases free radicals that speed up the oxidation of the underlying paint."

Cal wondered if the same might happen to our skin - inadvertently accelerating the weathering of our skin just as we are trying to stop any further damage. For more on the topic check out Cal's entry Nano on a Hot Tin Roof (rusted!) and her other entry on nanoproducts and sunscreen Burning Questions.

Friday, June 20, 2008

Will Nanoregulators avoid the Woulda, Coulda, Shoulda syndrome?

Before heading into nanotoxicology over the next few weeks (the bit that there is), I wanted to add the following tidbits both of which I think reiterate the need for sincere action – in the spirit of avoiding the inevitable shoulda, coulda, woulda, or maybe worse inertia:

1) The U.K. Council for Science and Technology, cautions that unlike in the past government “must cease to rely primarily on responsive mode of funding to fill the knowledge gaps.”

2) In their history of nanotoxicology, Oberdorster, Stone and Donaldson (2007) referring to abundance of national and international meetings producing and associated reports, “…these reports are not followed by appropriate action, thus creating the impression that there may be just too many of these meetings without serious follow-up.”

So as development and production of NP steams ahead of health effects research, for what it’s worth, national and international governments and regulators are wary and eager to track progress related to analysis and evaluation of the health impacts of nanoparticles (NP).

The result is an international consensus on some key issues that should guide future research and regulatory efforts:

1) There are potential differences of NP behavior in both the environment and in biological systems compared with their larger (or smaller) counterparts, and the potential inadequacy of traditional toxicity exposure and testing currently employed to evaluate NP toxicity. (And if you really read this – you note the overuse of potential. Of course there are plenty of synonyms, possible, probable, likely, impending – but the point is, we just don’t know enough to know right now – and so it’s all possible, probable and maybe even likely.)

2) These potential differences include differences in dose metrics, absorption and distribution as a result of size and/or external modifications, mechanisms of toxicity as a result of increased access to cell matrices or generation of reactive oxygen species because of new characteristics such as increased surface area (in addition to many as yet characterized differences.)

3) Many traditional testing and detection methodology may be inappropriately applied to NP. Further, beyond the current understanding of the impacts of natural and combustion-related NP on the lung, and the toxicity of fibers related to occupational exposures (both areas of research which currently lay the foundation for NP toxicology – appropriately or not), there is consensus that data on the impacts of NP (either naturally derived or engineered) in humans and on environmental receptors is insufficient or worse, altogether lacking.

And, on that note, have a nice weekend.

Thursday, June 12, 2008


A while back I posted a few items about nanotoxicology. Back then, I must confess I didn’t know much beyond those few articles. Now that I’ve had some time to really review the nanotoxicology literature here are a few thoughts about the rapidly developing field.

The potential toxicity of nanomaterials or nanoparticles in either human or ecosystems is of concern to researchers, government, non-governmental organizations (NGOs), industry and consumers around the globe. However, even with all of the past experiences with developing and regulating chemicals – even with the knowledge that before new chemicals (or new formulations of old chemicals) blanket the earth we ought to understand their potential impacts – the health and environmental impacts of specific nanoparticles lags far behind nanoparticle technology.

I’ve also learned that although government agencies, research collaboratives and others are working to remedy this situation, the funding available for research on health and environmental effects of nanoparticles, or nanotoxicology, compared with money spent on R&D, is in the millions verses billions spent on development.

But before we despair that once again, the nanokitties have left the residents of Whoville holding the bag, nanotoxicology does have several advantages over other “ancestral” fields of toxicology including:

  • Hindsight revealing flawed strategies of the past which led to inadequate prevention and protection (though this one is quickly slipping away.)
  • The more global economy, where regulations in one country for example may impact development of a product in another (the newer EU requirements under REACH for example) in addition to greater potential for international collaboration may stretch resources beyond those that any one government might be able to contribute alone.
  • Industries wishing to convince us that in addition to the “bottom line,” they really do care about health and the environment have shown some interest, and in some cases taken leadership in the field of nanotoxicology research – or entering partnerships with environmental NGOs (for example Dupont and Environmental Defense).
  • These days, the internet provides a powerful mechanism for rapid distribution of government, NGO and academic reports, providing all stakeholders – even us peons who sit at home, our computers our only source of information - access to emerging data, technology, and publications. It will be interesting to monitor the impact of public oversight of the field as it develops.

Yet despite all of this potential, the “state of the science” on environmental and health effects research today is something of a hodgepodge. But more on that later!

Monday, June 02, 2008

Flush with drugs: a new database for common pharmaceuticals provides insight into surface water contaminantion

A while back I wrote about the “drugs down the drain” program, targeted primarily at those with unused drugs who might decide to tip those bottles of old aspirin, or unused antibiotics. Yes, yes, I know – there should be no such thing since we’re all told to complete the course. But – there have been times when amoxicillin just didn’t cut it. Those times when the kids’ ears still screamed with pain and a visit to the docs office leads to a mid-course correction - a stronger antibiotic– leaving a half-full bottle of the pink stuff in our fridge.

In these cases it’s important to dispose of the stuff properly – so they don’t end up medicating everything downstream. But what about the pain-killers, heart drugs, antidepressants, antibiotics, gastrointestinal aids that we (and here I’m using the royal WE) take daily? What happens to them when we, pardon the expression, pee?

According to a recent review (introducing a new database) by Emily Cooper and others, just published in Science of the Total Environment, “…between 30 and 90% of an administered dose of many pharmaceuticals ingested by humans is excreted in the urine as the active substance…” and “…up to 90% of drug residues may remain in effluent after [sewage] treatment…”

Although the fact that flushed drugs end up in local streams, rivers and estuaries isn’t new to me – these numbers are astounding. Just imagine if we could reclaim all those drugs. Why - in our school district that might just pull us out of the fiscal hell we've been experiencing for the past decade! And aside from all that waste (though it makes you wonder if pharmaceutical companies design them that way,) once they're in the water - they're no longer beneficial, but rather, environmental contaminants.

But wait – the astute reader (perhaps one of my astute students) might say. What about dose? Certainly the stuff gets diluted, certainly the local trout are not exposed to therapeutic doses of valium or Tylenol? Certainly not. But as the authors point out, several studies now show that chronic exposures to low concentrations can adversely impact aquatic organisms. And, don’t forget – that the Tylenol that I might send over to the local treatment plant will mix with my neighbor’s kid’s antibiotics, and the psychotherapeutics of another neighbor and …you get the picture. There’s a little bit of a whole lot of stuff going down all of our drains collectively.

So what to do with a problem so pervasive? Prioritize, prioritize, prioritize. Fortunately Cooper and co-authors introduce a new, fairly user-friendly database called “Pharmaceuticals in the Environment, Information for Assessing Risk” or PEIAR that will allow researchers and others to do just this.

After a quick tour, I found the site easy to navigate, and easy to track back to original sources, and full of useful information. However, since I’ve made a career of avoiding risk assessment I can’t comment on its utility to risk assessors. I’ll leave that to the pros.

Check it out at

Tuesday, May 20, 2008

Great Future in Plastics

First published in the Montague Reporter, May 2008

It was a simple enough design. Pink and white tampon applicators separated by blue milk bottle caps and strung into a necklace. Those treasures washed by the sea onto our beach, and collected by my father over the course of a few hours one Sunday morning, provided the perfect accessory to the orange fishnet cape adorned with fading coke bottles, pieces of old lobster trap and other assorted beach waste items. Twenty years later, the image of my father, in his faded blue oxford shirt, dungarees and size 12 Jack Purcells sterilizing a pot of tampon applicators in my mother’s kitchen and in my mother’s soup pot, reminds me of a rare moment of father-daughter complicity.

That year as I attended the annual Society of Toxicology and Chemistry Halloween Dance dressed as “Beach waste,” I was naïve about the dangers of plastics. At the time those tampon applicators and milk bottle caps simply signaled failures of waste handling and sewage treatment – an issue George Bush the first used disingenuously to his advantage while campaigning against Massachusetts’ Michael Dukakis.

What I didn’t know back then was that the plastic army of tampon applicators, bottle tops, fishing nets, coffee cups and Barbie dolls (an occasional head, arm or leg had been know to wash ashore) wasn’t just gathering on the shores of my beloved Nantasket beach. These insidious soldiers of the chemical revolution were infiltrating oceans world-wide – and worse, over the years bits of plastic have literally become a part of life. In their relatively short time on earth (in 2007, synthetic plastics celebrated centennial birthday) plastic now contaminants marine mammals, seabirds and most of us – kids and pets included.

I’m sure John Wesley Hyatt hadn’t intended to promote such a legacy when in an effort replace the ivory used for billiard balls he invented one of the first known plastic back in 1863. Although, it’s not clear that his intention was to save the thousands of elephants slaughtered for their tusks, but rather to collect a $10,000 award offered for suitable ivory replacements. Nor should he have been concerned, since his process used natural substances including cellulose, a compound more prone to biological degradation than its synthetic followers, (and 140 years later, a compound that is back in style.)

Probably Leo Baekeland, hadn’t envisioned the reach of his invention either, when, in 1909 he developed Bakelite the world’s first synthetic plastic and wonder material. As a thermoset plastic, a magical resin that could assume any shape as a liquid resin, and then once hardened remain resistant to heat and solvents – Bakelite quickly found its way into the American dream – from telephones to electrical devices, automobiles and jewelry.

But it’s not Bakelite that scientists are finding in North Pacific albatrosses, or in us. It’s the next generation of polymer plastics which have invaded our lives for better or worse. In 2007, the American Chemistry Council reported upwards of 13 billions pounds of plastic resin produced by U.S. industries a year. This is 13 billion pounds of substances resistant to degradation and substances which we are now just beginning to understand can impact the development and function of reproductive systems in subtle yet potentially very important ways.

By now, unless you live radio-free and newsprint free you’ve likely heard about bisphenol-A which leaches from those colorful polycarbonate Nalgene bottles we all bought to avoid buying bottled water, and hard plastic baby bottles and some food-can linings. If not, you must have heard about phthalates – the plastic additive used to soften poly-vinyl chloride (or PVC) and which leaches from items like IV bags, those cute yellow rubber duckies my kids used to mouth during bath-time, teethers and soft plastic books. (Phthalates are also ubiquitous in personal care products including shampoos and lotions –another route of exposure for infants.)

Bisphenol A, and some forms of phthalates act like the potent sex hormone estrogen. For decades scientists have known that exposure to unnatural levels of sex hormones (either too much or too little), particularly during key periods of sexual development can result in tragic outcomes for both sexes. Estrogen is a naturally occurring hormone, which acts by binding with an estrogen receptor. Any other chemical that binds with this receptor and turns it on is an estrogen mimic. Some chemicals may bind with the estrogen receptor but instead of acting like estrogen, block the receptor from any further action – these substances are referred to as antiestrogens. The same is true of other hormones like the male sex hormone testosterone – there are mimics and inhibitors. Collectively these substances are called endocrine disruptors.

The impacts of synthetic estrogen exposure are best illustrated by diethylstilbesterol or DES. For those who don’t recall, DES was a synthetic estrogen prescribed to women from the 1950s through the 1970s to stem complications during pregnancy. Although eventually found ineffective, it continued to be prescribed until the consequence of extraneous estrogen exposure reared its ugly head in the form of clear cell adenocarcinoma in daughters exposed in utero. Later, structural differences in the reproductive tract and infertility were identified in both DES sons and daughters.

That bisphenol A acts as an estrogen is no surprise. Back in the 1930’s the chemical was almost developed as a synthetic estrogen, until DES stole the show. So seventy years later how does this stuff – a known estrogen - end up in plastic drinking bottles and plastic can liners?

Plastics are polymers – that is, they’re made up of many repeating units, strung together like a paper chain. The broad range of plastics we’re familiar with today results from the diversity of repeating units and chain formations discovered and developed at a feverish pace over the past century: vinyl, polyurethane, polystyrene, Teflon, Nylon, neoprene, polyethylene, polypropylene, and in 1953, researchers resurrected bisphenol A in the form of polycarbonate. That’s right. A key link in the polycarbonate chain is bisphenol A. Only back then, we can only hope, no one figured their grandchildren would be sucking down mom’s milk, lovingly pumped so that she could continue to work, from polycarbonate plastic bottles, or that food cans would be lined with the stuff. Or maybe no one figured that individual units of plastic could actually break loose.

But the fact is they do. And the more scientists look, the more they seem to find – whether it’s bisphenol A leaching from polycarbonate bottles, or phthalates leaching from IV bags. And as with many toxicants like mercury and lead, it’s our precious next generation that bears the brunt of our collective ignorance.

“So what would you do?” asked my neighbor, mother of two young boys. “Do you still drink out of plastic?”

Her mother had just given her the “You’re intelligent, how can you feed your children that stuff,” lecture – but she hadn’t yet tossed the sippy cups, rubber duckies and baby bottles.

I nodded sheepishly. I do love those colorful polycarbonate drinking glasses I purchased at Stop&Shop several years ago. And yes, last hiking trip we all sipped from the bright red Chaco Canyon polycarbonate liter bottle.

“I figure the water’s not sitting there all day,” I said, explaining that the greatest leaching of bisphenol A was reported after liquids were heated, or in very “well-used” or distressed polycarbonate. We didn’t even get into the phthalate issue, which extends beyond the use and leaching of phthalates from plastics, to personal care products

“But,” I conceded, “I did just buy some new water bottles, made from polyethylene, for the kids.” Unlike polycarbonate, polyethylene doesn’t leach any thing toxic, at least not that we know.

As I said this, I am sure that the little enviro-region of my brain, the one that lights up every time I do something hypocritical, began flashing away. Did I say I replaced one plastic with another? And did I say that while wearing my favorite purple polyester fleece and polyvinylchloride-bottomed Dansko clogs? Did I say that after dumping a box of broken plastic toys – nonrecyclables – into our 40 gallon plastic barrel?

Even more concerning than the plastic and related compounds in our food and beverage containers – substances which can eventually be manufactured out of these products, or avoided by the careful consumer, are the reports that millions of tons of plastic, from fishing nets to bits of what might once have been tampon applicators and polyester clothing, now circulating in the regions of the Central North Pacific Ocean (gyres). By some estimates, these trash or plastic gyres cover an area equivalent to the size of Texas. And although plastics may not degrade they can break into bits – some as small as 20 microns, creating a plastic soup served up to unsuspecting wildlife.

Writes Charles Moore founder of Algalita, a marine research foundation focused on the protection of marine environments, “I now believe plastic debris to be the most common surface feature of the world's oceans. Because 40 percent of the oceans are classified as subtropical gyres, a fourth of the planet's surface area has become an accumulator of floating plastic debris.”

Further, scientists suspect that some of that plastic may be circulating around for hundreds of years to come. For better or worse – plastics are part of our lives. But they don’t have to be part of us and they don’t have to be part of all creatures on earth. Improved production practices, and products that are easily recycled back into the same products, rather than dead ends like lawn furniture and plastic lumber, and improved public awareness might not rid the North Pacific of its trash right now – but maybe generations from now.

In the ‘60’s movie The Graduate, when Mr. McGuire, a family friend of young Benjamin Braddock advised “Plastics…..There’s a great future in plastics,” he had no idea.

Wednesday, May 14, 2008

Motherhood the Elephant in the Laboratory: time to speak up

This is, and isn't, a little off topic but as editor of Motherhood the Elephant in the Laboratory: women scientists speak out, I'm happy to announce that this book of 34 personal essays is now in print thanks to Cornell University Press, and many bold women who wrote about how motherhood influenced their science careers and vice-verse.

Writing and teaching about toxicology (to undergrads and sometimes to highschoolers) is one of the indirect impacts becoming a mother has had on my own career. Because I made the choice to work part-time, which is not an easy thing to do in the sciences, I've kept my own scientist alive through all sorts of interesting people and projects over the years. All of this fueled my desire to reach a broader audience through writing, beginning with articles in our local paper, the esteemed but very small Montague Reporter (hence the Neighborhood Toxicologist) and now through this blog.

As I write on the blog created for the book, Sciencemoms, those who take alternative routes through science ought not be considered failures, or second-class scientists - but apprecaited for their role as communicators, educators, and synthesizers. For more on this see the sciencemoms blog about the two recent editorials in the journal Science. The editorials, written by Bruce Alberts, highlight and support development of programs encouraging scientists to seek alternatives to academia.

Any thoughts on this topic are welcome either here, or at sciencemoms (and you don't have to be a mom - or a women to speak up!)

Tuesday, May 13, 2008

Tetrodotoxin 101

A good way to hook students into the wonderful world of toxicology is tetrodotoxin. Sound familiar? It’s what makes fugu, or puffer fish, what it is - a potentially deadly Japanese delicacy. Or does it? Would the delicacy be so appealing if the consumer didn't risk death or paralysis?

For those unfamiliar with fugu or tetrodotoxin, note that a mere “taste” of the stuff can and does kill. Although not the most potent toxin in the toolbox (recall that we’re talking toxin - or naturally produced poison) that honor most likely goes to either C. botulinum toxin (the toxin whose presence may be indicated by those puffed up cans – like the tuna can I once pulled from a grocery shelf,) or ricin – most recently of Las Vegas fame – and produced by the lowly castor bean.

Although non-toxic preparation of fugu has been raised to an art by highly skilled Japanese chefs, and although not all wild puffer fish contain enough toxin to kill, one article estimates that upwards of 50 mortalities may occur each year in Japan following puffer fish ingestion.

But now there’s good news for those who just must nibble – yet who’d prefer to avoid death or illness (tetrodotoxin inhibits muscle contraction causing paralysis). A recent article in the New York Times by Norimitsu Onishi reveals not only some interesting fugu history, but also describes the current trend towards raising tetrodotoxin free fugu.

For years, scientists seeking out the source of fugu (and many other marine species) tetrodotoxin had been baffled – where did it come from? Was it produced by the fish themselves or was it in the food they ate? And why didn’t it kill puffer fish and other tetrodotoxin laden marine animals?

Recent studies now suggest that, like many other potent toxins, tetrodotoxin is produced by the smallest of small, bacteria. By providing a home for bacteria, the boxy puffer is offered protection (and fortunately for the puffer fish, they’re at an advantage thanks to a genetic mutation, which makes them immune to its toxicity.)

As you might guess, here’s where the non-toxic fugu come in. By knowing the source, fish farmers can now feed fugu tetrodotoxin-free food (say that ten times fast) producing a risk free meal.

Although, for some the thrill of fugu may be in the risk – for others writes Onishi,, fugu liver is just plain tasty – like foie gras but without the guilt.

Wednesday, April 16, 2008

Polycarbonate redux

I am listening to NPR’s All Things Considered – it’s a story about bisphenol A, a common chemical that many of us have heard about by now. You know the estrogenic chemical that’s in those colorful polycarbonate clear plastic bottles that we all bought when we didn’t want to use bottled water, as well as in the linings of food tins and clear plastic baby bottles – that yes, I’m sure I used with my kids. And I’m thinking maybe we all ought to drink a little bisphenol A if it’s true that a little estrogen is good for improving memory.

Here’s why.

There is no question that exposure to estrogenic contaminants is problematic – particularly when exposure occurs during fetal development and in young children. There are reams of data that demonstrate adverse impacts on the development of reproductive organs, timing of puberty, and other effects on both male and female offspring of test animals exposed in utero and during lactation. Then there is the unfortunate example of diethylstilbesterol or DES, the synthetic estrogen prescribed to women back in the twentieth century to stem complications during pregnancy. It was found to be ineffective in the 1950’s but prescribed until the ‘70s (go figure) when the consequences of exposure to extraneous estrogenic chemicals during development first reared its ugly head in the form of clear cell adenocarcinoma in the daughters exposed in utero.

But did you know that at one time, back in the 1930’s scientists seeking synthetic estrogens like DES found that bisphenol A also behaved as a weak estrogen? That’s right. Back in the 30s this was known. Then some genius discovered that it could be linked together to make plastic. And voila – perimenopausal women like me just have to drink from our polycarbonate bottles to replenish our estrogen. Apparently back then no one figured anyone would be drinking from the plastic, or storing food in it, or sealing children’s teeth – and then when they did discover these uses of the plastic they must have forgotten that it was a known estrogen.

Seriously, we could all use a memory boost. Here’s a Science News article from back in 1999 by Janet Raloff which, besides being so last century, is so similar to recent reports about leaching of bisphenol A from polycarbonate that I did a double take when I came across it on the web (actually I probably read it back then, being a fan of Ms. Raloff, but have since forgotten.) It’s uncanny. Right down to reports that bisphenol A is more likely to leach from well-used polycarbonate and when liquids are heated in polycarbonate.

If that was then, why has it taken us ten years to toss our bottles? Maybe it’s because as Raloff pointed out, the jury was out. Well, almost ten years later it has returned in the form of a report by the National Toxicology Program’s Expert Panel evaluation of bisphenol A, here’s what they conclude (their emphasis):

“The NTP concurs with the conclusion of the CERHR Expert Panel on Bisphenol A that there is some concern for neural and behavioral effects in fetuses, infants and children, at current human exposures. The NTP also has some concern for bisphenol A exposure in these populations based on effects in the prostate gland, mammary gland and an earlier age for puberty in females.”

“The NTP has negligible concern that exposure of pregnant women to bisphenol A will result in fetal or neonatal mortality, birth defects, or reduced birth weight and growth in their offspring.”

Although I’ve confiscated my kids bottles I might keep them around for a few years in case I’m needing a little extra estrogen – if I can remember where I’ve stashed them!

Saturday, April 12, 2008

It’s TOXICANTS stupid

Whenever I have the opportunity to teach, I quickly learn how little I know. Maybe that’s what draws me towards the classroom. Besides the opportunity for human contact – especially contact with students who are so eager to learn about how we’ve managed to muck things up and what we can do about it.

A few months ago, I took on two challenges 1) introducing students at Mount Holyoke College to the fascinating world of toxicants, which, as they all now know– it’s toxi-c-a-n-t-s – unless of course it's a biologically produced toxin (and each time I reminded them of this, I was reminded of my graduate school advisor, the one we called “the pedant,” and shudder,) and 2) asking them to write about toxicants (and in one case, a toxin) for publication in the very public Encyclopedia of Earth or EOE ( (And write they did - articles ranging from PBDEs to Atrazine to Synthetic musks - something I hadn't know even existed!)

For some it was a slog. As one student wrote, and I’m sure more than a few students thought, “I never realized writing for the EOE would be so tedious.” For others it seemed a breeze. For me it was nerve-wracking. Particularly after I had the brilliant idea that each student should send her article out for review to whatever expert on her topic she felt most appropriate.
When they sent their work out for expert review, writing letters of introduction, attaching their articles and sending a small part of themselves out into the unknown – I warned them,

“Don’t be surprised if you don’t hear back.”

But then something amazing happened. Scientists wrote back. Scientists - many who are respected in their field, who are pressed for time, who let reviews for prestigious journals sit on their desk until pinged for the tenth time by the journal editor - these scientists took the time to review articles written by undergraduates struggling to comprehend and communicate their research.

It was frightening.

“I didn’t open the response for a day,” said one student about her “expert review.” Another found a sea of red marks – comments, corrections, and No! Wrong! Wrong again – followed by helpful suggestions and further reading.
I wondered if I’d thrown my students to the wolves. Though I’d commented, edited and corrected as best I could before review, the fact is – I could never claim expertise on the breadth of topics covered by this group of young women. This was the lesson I'd learned. I hadn't planned for that level of expert review - but when the drafts came rolling in, I knew I was over my head. Without reading each and every reference - there was no way I could truly comment on the accuracy of what they'd written.

So was it worth the ego-bruising effort? (And I'm not referring just to the students here.) I had asked my students to write not only for the highest level of review, but also in the end, to put themselves out there in a way that many scientists haven’t dared, communicating a highly technical topic - one which they'd just learned about virtually on their own, to the public and in plain language. 

It’s something that I never felt comfortable with until I was out of the lab. Until I felt I had nothing to lose. But these days it is often necessary for scientists to communicate not just with each other but with the public, and it is my hope that that’s the lesson that sticks.

Maybe the difference between “toxicant” and “toxin” is pedantic. But sometimes you’ve just got to get it right. I think they did.
Check out their articles on the Encyclopedia of Earth:

Tuesday, April 01, 2008

Toxicant Inspired Poetry: Happy April Fools!

I’d like to share a poem written by a student who is no April’s Fool.

Last week I'd asked my students to respond to an Earth Forum posting by Sidney Draggan about the detection of a range of chemicals from personal care products to pharmaceuticals to detergents (all considered indicators of municipal waste) measured in earth worms by scientists from U.S. Geological Survey’s Toxic Substances Hydrology Program and reported in Environmental Science and Technology.

Sidney asked if anyone was surprised.

This was one student's response:

When you have a disgruntling ache,
Ibuprofen’s the thing to take.
If you’re feeling a little blue,
Pop an antidepressant or two.
Your kid’s attention span is shorter than that of a fly?
Stimulant medication is the thing to try.
You see, we’ll cook up a cure for whatever ails you,
And maybe a smattering of things you never knew
We're problems with chemical solutions;
We assure you all your kinks have easy resolutions.
Pharmaceuticals are the way to go
When you get an infection in your big toe
If plaque has clogged your blood’s flow
If your hair refuses to grow
If your insulin has fallen a little low.
And a bazillion other things, you know.

With this present in your mind,
It may not be such a surprising find
That even our worms are taking drugs!
Yes these naughty little bugs
Load up all day long!
But before you begin to think them wrong,
And go about accusing,
You might consider it is not their choosing
To ingest this vile mix of stuff.
You see, oddly enough
We are the ones to blame.

We may nobly aim
With pills to eliminate our daily pain
But it all ends up going down the drain.
Everything we get down with a drink,
Everything we throw down the sink-
Be it detergent or anti-bacterial soap
(It would take ages to enumerate the scope)-
Goes right on to a waste treatment facility.
I hope it does not affect your mind’s tranquility
To hear this is not where they stay,
Some into our drinking water stray!
Others catch a ride on our own waste-
Or “biosolids” if you want to show some taste-
And are applied freely to agricultural fields
So they will have record-breaking yields.
Their life sentence may sound tragic,
But worms are the ones that work the magic-
Turning dung into beautiful soil,
And what do they get for all their toil?
A mouthful of our chemical excess.
I think this is something we should address.
There is simply no good to gain,
When these things enter the food chain.
Against our wishes,
Some find their way into our dishes.
You can imagine this creates
Some concern over the toxicity of what’s in our plates
Maybe the effects of these chemicals are not so bad,

Or maybe we’ll be driven raving mad.
But the truth is it’ll take years to unveil
The effects these multiple low-level exposures entail.
If we one day find
That deeply entwined
Are the causes of our health woes
And our daily chemical dose

I can assure you of this:
There is guaranteed eternal bliss
For the one who finds an antidote
Clarity Guerra

If you'd like to pass this around, please remember to credit Clarity!

Monday, March 24, 2008

Making Lists: Dr. Cal's thoughts on priortizing chemicals

Guest blogger, Dr. Cal Baier-Anderson, a toxicologist at the University of Maryland, Baltimore; and Environmental Defense, adds her own thoughts about prioritizing chemicals (also check out the list created by J. Lowe from Impact Analysis in the comments section of Fav Five.)

A few years ago at a professional meeting I participated in a panel on the chemical perchlorate, which was receiving a lot of attention as an emerging drinking water contaminant. Perchlorate, an oxidizing agent that is used in rocket fuel, can block the uptake of iodide in the thyroid. One member of the audience suggested that focusing attention on perchlorate was a waste of time and money, that there are other chemicals that are more important. Make a list, I challenged the group; professional organizations and industry should step up to the plate and identify the top 10 chemicals of concern, from an industry perspective. It is certainly not an easy task, as Emily pointed out, many different lists can be made, depending on what features are most important.

With tens of thousands of chemicals in commerce, chemical prioritization is a hot topic. The traditional risk assessment process focusing on one chemical at a time requires a lot of data collection: the identification of the most important hazard endpoints (a prioritization process in and of itself); determination of dose-response for the priority endpoint, the characterization of exposure; and the assessment of risks. Chemical prioritization can be based on hazard, it can be based on likelihood of exposure, or it could be based on risk, incorporating both hazard and exposure. Many environmental groups argue that there is so much uncertainty in the risk assessment process that it is better to focus on hazard, emphasizing carcinogens, mutagens, reproductive toxicants, and endocrine disruptors. This has lead to the creation of lists, such as California’s Proposition 65 list of carcinogens, mutagens and reproductive toxicants (CMR), which requires that products containing a chemical on this label their products with a special notice.

Chemicals that can be classified as persistent, bioaccumulative and toxic (PBT) are also considered to be high priority chemicals. EPA initially devised a list of PBT chemicals, but then developed a computer program that evaluates individual chemicals to score them as to PBT properties. Persistence and bioaccumulation are determined by basic chemical properties, whereas toxicity is based on aquatic toxicity data.

With public attention focused on chemicals in consumer products, many companies are critically evaluating their products’ ingredients to determine if they are made with chemicals of concern. But how can we define chemicals of concern? Based on hazard, or based on risk? Some companies have developed their own restricted substances list that contains chemicals that the companies believe to pose some unacceptable risk to their workers and/or consumers. REI has a list, but a simple Google search of “restricted substance list” will uncover many more.

At the recent SOT meeting in Seattle, there was a session on hazard vs. risk-based approaches. Many state governments and large companies are defaulting to hazard-based approaches as a simpler approach to removing chemicals of concern from consumer products. Several prominent toxicologists opined that focusing on hazard without considering exposure will result in time and money wasted on chemicals posing very little risk. But as my colleague noted during the discussion, there are many folks in the environmental community that are wary of our capacity to predict exposure, citing numerous examples where it was initially predicted that there would be no exposure, and the experts were wrong: PCBs, Bisphenol A, phthalates, PFOA, PBDEs…If we can’t correctly predict exposure, then confidence in the risk assessment plummets, shifting focus to hazard.

A new approach is being promoted by some very smart people: alternatives assessment. Rather than making simple restricted substances lists, focus on what are the alternatives and compare using a suite of criteria. These assessments can be used to drive continual improvement in materials safety – protecting workers, the environment and consumers. Makes sense to me!