Is there bias in bi(a)sphenol A?

Over the past two years the debate about bisphenol A (BPA) has become a quagmire where highly regarded scientists who once worked side by side, now sit across the fence virtually flinging insults at one another. You wouldn’t know this reading the Sunday paper or countless mainstream press articles, blogs and even academic journals which have successfully vilified this ubiquitous chemical. Like many Americans, you’re probably tossing away your polycarbonate bottles and looking askance at the stash of cans in your pantry.

Yet two summary panel reports on BPA prepared by the National Toxicology Program (NTP) and by the Food and Drug Association (FDA)* downplayed the risks of BPA, while at the same time, NTP highlighted the need for more research - and as of January 2010 the FDA indicated they too have concluded there is some cause for concern, particularly in infants and children. As a writer I find this disconnect fascinating. As a mother who replaced the polycarbonate bottles shortly after the first round of BPA press, I wonder if the chemical is deserving of its reputation as the evil twin of estrogen. As a toxicologist, I am dismayed by the apparent bias found on both sides of the fence.

Years ago, while interviewing for a job, I was asked if science was objective. I quickly answered in the affirmative. My future employer’s brow wrinkled, but she remained silent – giving me time to think. While science is objective, it is carried out by mere humans. And we all have our biases. I wouldn’t have been interviewing with a group whose mission was to support communities affected by industrial contaminants and who could only offer a pittance in salary if I didn’t lean towards the affected. Yet, I pondered, when reviewing the literature in support of their mission would I be biased? Here’s the truth – when reading studies funded by either the military or industry my sci-dar is on full alert. Likewise, I’m just as wary when reading studies conducted by environmental activist organizations, yet I am more trusting of studies produced by academics, particularly those funded by sources that tend not to have a stake in the outcome. Really, my sci-dar should be on full alert at all times, and in the end, I am careful not to cherry-pick studies from any one source, just to support a position.

Are there concerns about bias in the bisphenol A analysis? As a recent memoirist who shall not be named, likes to say, “You Betcha.” Just Google “BPA bias” and you’ll find over one million pages.

One need only read Environmental Health Perspectives, published by the National Institute of Environmental Health Sciences (NIEHS), where the most recent BPA battle is playing out. But the stakes are higher than simply resolving BPA’s toxicity. Bisphenol A has brought to the fore the very nature of toxicity testing and regulation, questioning the role or (or lack of) basic research in chemical testing and regulation.

That toxicity testing, particularly of endocrine disrupting chemicals like BPA is in dire need of overhaul is not in question. Says Dr. L. Earl Gray**, Research Biologist and Team Leader of the Reproductive Toxicology Division at the US EPA, about updating routine chemical testing:

“There is a lot more awareness of the issues with endocrine disrupting chemicals and thoughts about screening….they are also trying to shorten the multigenerational protocol [one of the standard toxicity tests required of industry]…hopefully and likely the new assays will be able to replace the old ones fairly quickly.”

Problem is, it took a decade to develop and validate those new assays. A snail’s pace, and a significant chunk of time for those at greatest risk, the very young. Even so, when it comes to BPA, there are those who suggest reviewers and regulators stick with studies based on regulatory testing protocols, because those methods have been rigorously validated, even if they don’t incorporate the latest science.

Of the hundreds of scientific articles on BPA many could be classified as basic science, while only a fraction use regulatory testing protocols. Studies in rodents report that BPA causes diabetes, weight gain, mammary gland cancer, early onset puberty, infertility and behavioral changes. Some of these findings cannot be repeated (reproducibility is a central tenet of science). Meanwhile studies in human populations report associations (which are not cause and effect linkages) between BPA and heart disease, diabetes, infertility in industry workers, and behavioral changes in toddlers born to mothers whose urine concentrations during pregnancy mirror those in the general population.

Despite the uncertainties, aren’t all of these studies enough to require that industry remove the chemical from our food and drink? While I am skeptical of studies produced by industries whose bottom line depends upon a particular chemical and in sticking with decades old testing procedures, I also know that a chemical posing an imminent danger is good for academic business, generating more grant money, more publications, and more consulting. It’s not an ideal system, but given time the scientific method prevails – and in the interim we have guidance from the expert panels. In the case of BPA both panels had the freedom to consider any and all relevant and valid studies.

While the NTP panel concluded there was cause of “some concern,” noting the need for more research, the FDA concluded that current exposures to BPA do not present a health risk. So began the fireworks. Critics charged the panels were biased omitting too many basic studies from their final analysis. In his congressional testimony, Gray who was a member of the NTP panel disagrees. Testifying before congress about BPA, Gray noted, that “the criteria [for inclusion in the review] provided minimum standards for experimental design and statistical analysis. Many studies failed to meet these minimal criteria – these studies came from industry, government and academic laboratories.

“The controversy,” says Gray “resides over the fact that standard and enhanced multigenerational studies are negative for low dose effects and many academic studies were positive…. several of the multigenerational studies have added low dose groups, estrogen sensitive endpoints and tried to replicate the low dose effects to no avail... These differences are due in part to differences in how a chemical is administered in a study.” Differences which also include the use of live animals versus test tube studies (which preclude metabolism and excretion of a chemical), the timing of exposure and the range of doses tested.

Yet based on accounts by the popular press, enviro-blogs and magazines – if you still drink from a polycarbonate bottles or serve your kids canned foods then you must be an irresponsible parent. When I replaced our reusable bottles with BPA free – but didn’t toss the canned goods, my inner toxicologist reasoned that we are exposed to a myriad of natural estrogenic chemicals in foods like soy, plants, and milk – was BPA any worse? Meanwhile the environmentalist in my brain reminds me that we don’t choose to consume industrial chemicals like BPA. Shouldn’t we have that choice? But since BPA does not accumulate in humans (a quality that may trigger a chemical ban), “that choice” depends primarily upon the amount and frequency of BPA exposure, how it’s metabolized and its potency.

So is it or isn’t it? Maybe the nearly 30 million dollars recently committed by NIEHS for BPA research will solve the question, and maybe BPA will be one more example for the scientific flip-flopper pile along with fiber, mammograms, and therapeutic estrogens. For now, there’s FDA’s final report due at the end of the month, and Consumer Report’s recent investigation of BPA in canned goods – both of which will surely add a few feet to the fence separating some very good scientists.

*This report is the 2008 draft, a final report was just published you can find FDA's current position on BPA here.

Here is a recent article on the relationship between BPA in urine and heart disease

CHECK OUT the US DEPT Health and Human Services site for the latest on BPA (added Jan 16 2010)

AND a Jan 28 2010 interview with Dr. Linda Birnbaum of NIEHS

**In the spirit of disclosure, I worked for Earl back in the early nineties, he was not only a great guy to work for, but I also respect his science and opinions.

Get your BPA FREE with each new bottle!

Roughly a year ago one of the first studies showing that BPA, the known estrognic plastic used to make polycarbonate bottles, leached into liquids under extreme conditions of heating and rigorous washing was published to much fanfare. The study raised a serious issue, although it seemed that unless you were routinely heating your liquids in a well washed bottle (huh? wash my water bottle? In the dishwater?) – a problem clearly relevant to new parents, but not so to folks like me who were done reproducing – ridding the household of all polycarbonate wasn’t a high priority. While I did replace the kid's bottles with the now suspect PET bottles (more on that one later) the old polycarbs still went to the tennis courts and up Mount Toby with me. I just couldn’t justify adding more plastic so the recycle or waste cycle so as long as I had it, I used it. Same with the gem-colored polycarb juice glasses we’ve used for years.

Well, as usual with chemicals we’re just getting to know more intimately than we’d like, there's always one more study that makes us wonder if "we've" really done our best when it comes to using chemicals wisely. This time it's a new study published in Environmental Health Perspectives by researchers at the Harvard School of Public Health which reports that BPA molecules really don’t need all that much coaxing to be released from bottle to water. In fact, just regular use, filling them up with cold liquids and drinking was enough to raise concentrations of BPA in the urine of polycarb bottle using Harvard students.

After one week of drinking all their cold beverages from Nalgene Lexan bottles (could you fill this bottle rather than that beer stein please?), and peeing into a cup during the designated hours of 5-8PM, students increased their pre-polycarb urine concentrations by 69%. In other words – you get a little BPA with your water even if you don’t heat it up and abuse the bottle.

Given that the very young (newborns and infants) tend to retain their BPA a bit longer (because their metabolic system which clears chemicals like BPA is less active than adults) this study, one of the first to show that normal use of polycarb means exposure to BPA, should give pause to any parent still using the old polycarb baby bottles. It’s certainly enough to push me to take those pretty gem-colored juice glasses and relegate them to the craft cabinet.

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.

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.

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.

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!

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.

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.