Monday, April 27, 2009

Chemicals we love to hate, Body Toxic book review

A while back I was invited by American Scientist to write my first ever book review. After having just edited a book that was reviewed (mostly favorably), I was nervous. What if I didn't like it? When reading books about toxics, especially books written by non-toxicologists, my sci-dar is on full blast. Most authors seem to have an agenda whether it's chemicals=bad, or the opposite (although those tend to be written by scientists.) Over the years, I've encountered a few written by toxicologists who seem to have forgotten the "oath" of objectivity, or rather, taken the "better living through chemicals" oath. Although those books are great for teaching (so... who checked out the author's affiliation, the funding source or the publisher?), and readers tend to be self-selecting.

Controversy sells. Wishy washy, we don't fully understand doesn't. It's a problem.

So with some trepidation that my first (and possibly only) book review might be negative, I cracked open Body Toxic, written by journalist Nena Baker. What follows is the uncut version of the review recently published in AmSci:

Teaching toxicology to college seniors and juniors was never easier than this past year. Each week students easily and eagerly fulfilled their “current events” assignment with links and clippings of articles revealing widespread contamination of wildlife or humans, with PFOA and PFOS, PBDEs, PBBs, phthalates, BPA, and atrazine.
No longer did I have to rely on stories from the “old days” of legacy contaminants like PCBs, DDT and dioxins - not when there all these great so-called “emerging contaminants.”

Although these chemicals have been around for decades they’ve “emerged” into our collective consciousness thanks to much improved chemical detection methodologies and technologies. As chemists extracted and detected smaller concentrations of chemicals from smaller and smaller tissue and urine samples, chemicals like PCBs, and dioxins were detected not only in parts-per-million or parts-per-billion, and but also parts-per-trillion. Many of those emerging chemicals were there, we just didn’t know it. But it wasn’t simply the improved chemistry that helped raised awareness. As analytic methodology improved, many, including toxicologists were stumped by the “so what?” question. So what does it mean when a fish is contaminated with parts-per-trillion concentrations of dioxin?

Now with improvements and some maturation of toxicological testing, toxicologists are now able to evaluate the subtle effects of smaller and often more environmentally relevant concentrations of potentially toxic chemicals.More importantly over the past couple of decades, toxicologists have expanded the definition of “adverse effect” to include impacts on subtle reproductive and developmental processes which may respond to very small concentrations of foreign chemicals.

The outcome of all this new and improved sensitivity? A greater awareness of all the new and improved products that are in all of us, thanks in part to the Center for Disease Control’s (CDC) 2003 National Report on Human Exposure to Environmental Chemicals. And this is where Nena Baker begins The Body Toxic.

Back then, CDC reported concentrations of 250 chemicals including stain repellents, flame retardants and phthalates along with the old standbys, including mercury lead, and DDT in human blood and urine (data from their subsequent analysis will be released this year.)The report piqued Baker’s interest to the extent that she eventually dropped her day job as a journalist to chase down the answers to three basic questions that we all ought to be asking: 1) Should we be worried about the effects of these pollutants on our health? 2) Can everyday items be responsible for the chemicals inside of us? 3) Don’t regulators already make sure we’re safe from daily doses of hazardous chemicals?

We’ll save the first question for last. The answer to the second question, as everyone knows by now, is a resounding yes, of course. We are all contaminated by bits of everyday items from our kitchens, living rooms, bedrooms, offices, even our hospitals.Is this a surprise? Well, yes and no.We know from the history of fat-loving chemicals like the organochlorines (many now banned nationally and internationally) that we can indeed be “incidentally” exposed to environmental contaminants. No one ever purposefully ingested PCBs (at least not that I know of,) yet we’ve all got them in us. And, more importantly, no was ever asked if they minded being exposed to PCBs, DDT, dioxin or any other of these chemicals. It simply wasn’t and unfortunately still isn’t, a choice.But hey, that was back in the day, before Silent Spring and before the birth of the Environmental Protection Agency, when those chemicals were freely released as pesticides or into the environment both legally and illegally.

To address Baker’s third question, no one can deny that over the past 30 years chemical releases into the environment, food, and water have been greatly reduced thanks to expanded federal regulation. But, as Baker reveals in both the Introduction and in her first chapter, A Chemical Stew, what we are dealing with now is more insidious.These chemicals have flown “under the radar” and into our bodies.Some like bisphenol A were never expected to be released from their chemical matrix or become “available”, others including PFOA and PFOS were thought to break down more rapidly than they did, and still others like certain phthalates managed to be absorbed, apparently unexpectedly, into the body. These are chemicals that many of us never thought would end up circulating our bodies, or worse, those of our children. The second chapter, Chemicals We’ve Loved, explores how we got here from there beginning with the post World War II chemical frenzy, and ending with the myriad of chemicals currently registered by the EPA. In the best of all worlds the book would end here. If they’re registered, then surely EPA must have adequate information to protect the public from exposure to toxic concentrations?

Au contraire. As Baker writes, “under our regulatory structure, ignorance is rewarded: manufacturers have no obligation to test for the safety of substances they sell. [p51]. And we, the public, are ill-informed as to whatever chemicals we may ingest, absorb or inhale. The regulatory structure to which Baker refers is EPA’s Toxic Substances Control Act of 1976. When first enacted, TSCA was a big deal. Writes Mark Schapiro in his book Exposed: the toxic chemistry of Everyday Products and What’s at Stake for American Power, “TSCA was the first effort by any government to assert some level of oversight over the vast amount of chemicals that had been introduced into the marketplace since the end of World War II.
With TSCA, the EPA was a world leader in chemical regulation.” [p 132.]

It was a hopeful time. It was a hopeful time. According to an October 1976 EPA press release, EPA’s Administrator Russell E. Train, declared TSCA to be "one of the most important pieces of 'preventive medicine' legislation…..its basic aim is to give public health far more of the weight that it deserves in the decisions by which chemicals are commercially made and marketed, by which they enter and spread throughout the human environment."

Sadly, 30 years later as Baker writes, TSCA is “notoriously weak and ineffectual” [p.7]. A conclusion shared by many others including the General Accountability Office, which concluded according to Baker, that “the EPA has given up trying to regulate chemicals and instead relies upon the chemical industry to act voluntarily when problems arise.” [p.16]

One notorious example of the naivety of such a voluntary program was when DuPont apparently forgot to report that not only was PFOA persistent, but also possibly toxic to humans and wildlife. Subsequently in 2005, DuPont paid over $10 million in fines and EPA initiated a voluntary phase-out of the chemical by 2015 (a program in which DuPont along with several other manufacturers, is a participant.)

And, although not discussed by Baker (perhaps because there isn’t enough to discuss just yet,) is the fate of nanomaterials under TSCA. Nanomaterials encompass a broad category of chemicals with one thing in common they’re small. Really small. One of the advantages of certain nanomaterials is that they act differently than their larger chemical counterparts. But this very quality concerns some toxicologists who fear that nanoized chemicals may be different enough that they may behave differently in traditional toxicology tests. Yet under TSCA, nano-formulations of existing chemicals will not require new registration (or registration as a new chemical). Further, EPA is asking for voluntary submission of health and toxicity data, by manufacturers and users of nanomatierals. At this point, feel free to ask, “when will we learn?”

What went wrong with TSCA and other federal regulations and the consequences of regulatory “misses,” make up the bulk of The Body Toxic’s chapters beginning with the pesticide Atrazine, followed by chapters on phthalates, polybrominated biphenyls, bisphenol A, PFOA and PFOS. And Baker presents a thorough case study of each through a combination of primary literature, anecdotes, interviews, and popular news articles, all cited in the Notes section. As I am often leery of books on toxics, having perused a few too many alarmist articles and books I was pleasantly surprised to find that, beyond Baker’s Introduction where at times words like “ghastly” and images of bathroom shelves “brimming with chemical-laden personal care products” (of course they’re chemical laden – what isn’t?!), the bulk of her writing kept to the science and the policy.

Returning to Baker’s first question, what does it mean to be exposed to all these toxicants at low concentrations, she doesn’t take the easy route and proclaim they’re the route of all evil. “While biomonitoring studies provide a much more accurate picture of our chemical body burden,” she writes, “limitations remain. The studies don’t tell researchers the source of an exposure, how long a substance has been in the body or, most important, what effects, if any a substance is having on human health.” [p.23] She continues with quote from Linda Birmbaum, then director of experimental toxicology at EPA, who acknowledged that “We really need more research to understand whether the levels we’re finding could be associated with adverse health effects.” [p.23] Fortunately Birnbaum, now director of the National Institute of Environmental Health Sciences, should be in a good position to do just that.

The final chapter Reaching Ahead is devoted to the European Union’s new approach to toxics, REACH. The approach is essentially a mirror image of TSCA. Where TSCA requires the EPA to demonstrate that a chemical is a risk to human or environmental health, REACH requires that the manufacturers test and ensure that chemicals do not pose a risk. Where the US was once a leader in chemical control, we can only hope it will become at the very least a follower.

Overall, The Body Toxic makes for informative reading that is not too technical- a plus in this case. Although I would have liked to some synthesis, (for example a discussion of all contaminants discussed which share a common target,) by providing some insight into the complexities of regulation and the workings of scientists Baker’s book opens many avenues for discussion.
It’s a good book for a “non-majors” introduction to toxicology.


[1] [EPA press release - October 21, 1976] http://www.epa.gov/history/topics/tsca/03.htm

Wednesday, March 11, 2009

We do have a choice: VOC in paint

Our white wall to wall bookcases, blackened from over a decade of “dog” rubbing against the corners, kids whose little shoes marred the window seat, and woodstove particles that had settled into the cracks and crevices, were looking dingy. They’d become a shade of off-white no paint store would dare market, and were in need of some attention.

A good scrubbing helped. But there’s nothing like a new coat of paint to brighten things up, especially after a long winter. With my hired hand in tow (whose little shoes are now size 11) we trudged into Dakor Center and plunked down a can of old paint.

Filler up with the same, I requested. But no such luck. Apparently Deerfield Academy just cleaned Dakor out of the Benjamin Moore Regal I’d used before. But, suggested Richard from behind the counter, I might try the Benjamin Moore Eco-spec™, the virtually no (or very low) VOC paint they use over at the Franklin Medical Center.

VOC means volatile organic compounds, a family of chemicals that paint companies have been trying to phase out or reduce for years – with a little push from state and federal environmental regulations.

The term VOC encompasses a broad category of chemicals with at least two things in common: they are easily volatilized and many are not soluble in water. VOCs are everywhere, from the chlorinated cleaning fluids of olden days which now contaminate drinking water around the country to the ingredients of the Purell Hand Sanitizer that kills 99.99% germs. They are also released from home furnishings, household cleaning products, air fresheners and cigarette smoke. VOCs are produced when coal and oil are burned, when chlorine combines with organic material in water resulting in chloroform, and when cows fart. Recall the flap about cow farts and global warming? That was methane, a VOC. You know that “fresh-cut” grass smell? That’s the VOCs released when the blades are damaged, though they pale in comparison to all the VOCs released by the very act of mowing the lawn (unless of course, you’re using a push mower, then it’s just your own gas that counts.)

Outdoors, VOCs contribute to the formation ground-level ozone or smog, when they combine with other air pollutants like the nitrogen oxides released by burning fossil fuel. The EPA estimates that the nearly 600 million gallons of latex paint (which contains far less VOC than some other paints) sold each year in the US, accounts for nearly 120 million pounds of VOCs released to the atmosphere. Indoors, VOCs can occur at concentrations as much as five-times higher than outdoors, and as much as 1000-times higher after stripping paint.

Some of the worst VOCs are really nasty, causing a range of effects from liver and neurological damage to cancer - though some of the worst offenders are no longer used in consumer products or are present only in very small concentrations. But that doesn’t mean that indoor or home exposure to VOC is harmless. Particularly for those who are sensitive to certain chemicals, who have asthma, or are very old or very young.

Knowing all of this, and as low toxic as I try to be, I wasn’t sure I wanted to pony up more cash for the low VOC paint, the Benjamin Moore Regal was pricy enough. Sensing my hesitation, I was quickly informed that the two paints cost the same.
I could have kicked myself right then and there. How long had this stuff been around, I asked? Since 1999.

Ah, but was it really any better in terms of indoor air pollution than regular latex? Hadn’t latex gotten much safer over the years anyway? The answer to that question took some digging.

“Ingredients that are in conventional latex paints that are not in our Zero VOC paints would be, ammonia and coalescing agents, biocides that are formaldehyde releasers such as Nuosept 95, propylene or ethylene glycol, mineral spirits such as Isopar L, and pigments that contain any free crystalline silica,” emailed Mark Lamborn from Benjamin Moore, when I’d asked about the difference between semi-gloss latex and Eco-Spec.

What did all that mean? Aside from the biocides, which are highly toxic and release formaldehyde, but tend to be used in relatively small amounts – and no-VOC paint still has biocides - the other major difference is the VOC Isopar L, (other paint companies may use something called Texanol.) As listed, the VOC for Regal latex paints ranges from 50-149 grams per liter of paint. Roughly, that’s a bit less than a cup for the lower end, to two cups of VOC for the higher end, per gallon. When painted on gypsum board or drywall, according to an EPA study, those VOCs will volatilize slowly over a period of 3 years.

Mark also explained that the “recently reformulated Waterborne version of Eco Spec (WB) are formulated with raw materials that do not volatize during the drying/curing process. Any trace amounts of VOC [Eco-Spec still has 0.96 gram per liter of VOC] stay within the paint film.” Which, I suppose is why it can be sold as no VOC.
So, no-VOC paint, verses a few cups volatilizing over a few years? Although we’ve got plenty of other indoor pollutants circulating around our home (particularly after a good burrito dinner) why add more in a home where the asthma inhaler often makes the rounds. I went with the low-VOC paint and so far, have been pleased with the results.

A few considerations if you’re in the market for paint:
•There are now many different brands of low or no VOC paint – some rated better in terms of coverage and durability than others, so shop around.

•Watch out for tints. Tints tend to have high VOC so if you’re looking for little or no VOC ask about the type of tints. Some companies now produce Zero VOC tints.

•I focused on latex paint, which uses very little VOC containing solvent, it’s noteworthy that paints for tougher situations (the alkyd paints) can contain upwards of 400grams/L of VOC, now we’re talking VOC. That’s over four cups and, it’s worth noting much of that is released from a painted wall within the first ten hours after application.

Wednesday, February 04, 2009

Get Your Peanuts Here....or not

First published in the Montague Reporter, Montague, MA

Lately, I’ve been craving peanut butter. Maybe it’s because my husband finished off the jar a week or so ago, and didn’t put it on the list (grrrr,) or maybe it’s because I can’t pick up a newspaper without reading about the great peanut butter recall. Although you’d think that hearing it linked with Salmonella as it so often is these days would be enough to scare me away, who’s to reason with a craving?

Plunking a jar of Teddy All Natural peanut butter onto the check-out belt at Stop & Shop, I felt a little sheepish. Was anyone wondering if I’d been in a news blackout for the past few weeks? Who in their right mind would be buying peanut butter when peanut products are the stars of the Federal Food and Drug Administration’s (FDA) largest food recall ever? Certainly not Robert Humphrey, the retired insurance executive from Georgia, who according to the Atlanta-Journal Constitution has given up all peanut products (normally a mainstay of his diet.) And Humphrey isn’t alone. In Houston schools pulled all peanutty products from vending machines and menus, as did school districts in Michigan, Connecticut and California among others. While I couldn’t find any evidence of Baystate districts jumping on the ban-wagon, according to Jim Loynd, Food Service Director for Gill-Montague district, “All of our elementary schools are peanut free. At the middle school and high school building we’ve checked to make sure we don’t have products affected by recall. The only peanut butter products we have are from the USDA commodities program,” which, according to their web site did not purchase any recalled peanut butter. Amidst all the furor, the FDA asserts that “major national brands of jarred peanut butter found in grocery stores are not affected by the [Peanut Corporation of America] recall,” though they caution that some “boutique brands” of peanut butter may be subject to recall.

Salmonella typhimurium isn’t a bug to be trifled with. The Centers for Disease Control and Prevention have reported over five hundred cases of illness from 43 states since September, with a 22% hospitalization rate. Eight deaths have tentatively been linked to the outbreak. Like most bacteria that live or infect our guts, Salmonella typhimurium, are facultative anaerobic bacteria. That means that they grow and thrive with or without oxygen. They’re versatile, unlike one of my favorites, Clostridium botulinum, a strict anaerobe for which oxygen is toxic. When present in an airtight can, for example, Clostridium may produce botulinum toxin, one of the most potent toxins known. Fortunately for us, it not only produces toxin but also gaseous metabolic byproducts – enough to cause bulging lids in canned goods, cluing us in to its deadly presence. Last year at Stop&Shop I picked up a nice toxic can of tuna.

Salmonella infections, caused by ingesting contaminated foods like undercooked chicken, eggs, and more recently tomatoes are the most frequently reported food-related infections in the U.S. While some studies indicate upwards of 1 million little buggers are required for one to experience acute onset of fever and chills, nausea and vomiting, abdominal cramping, and diarrhea, some outbreaks may be caused by just a few hundred bugs. This “infectious dose” varies based on a number of factors including age and immunity of the host, and the food matrix. According to the USDA, foods high in fat, (like peanut butter,) may protect the bacteria from harsh conditions in our guts. In this ongoing FDA case, contaminated peanut products have been linked to a single peanut processing plant owned by the Peanut Corporation of America’s (PCA) Blakely, Georgia plant, now the focus of a criminal investigation.

In the largest food recall to date, over 400 items and 31 million pounds of peanut product have been removed from store and institution shelves. The recall ranges from Cliff Bars and Luna bars that contain peanut butter to Trader Ming's (AKA Trader Joe’s) Spicy Kung Pao Chicken, Big Y Sundae Cones and Famous Amos Soft Batch Peanut Butter cookies. But so far, the only tubs of actual peanut butter recalled is King Nut, a brand distributed only through food services.

Wondering about my Teddy peanut butter, I found the American Peanut Council’s web page which lists links to dozens of company sites whose products have not (yet) been recalled, including the Leavitt Corporation of Everett, MA, who produces Teddy brand. Teddy, they say, is clean. According to Leavitt’s site, they’ve never used PCA products, and don’t use peanut products from outside the company. While Teddy was clean, cruising the FDA recall site I found reason to pitch the Keebler Toast & Peanut Butter Sandwich Crackers that had been sitting in the pantry since last spring.

If you’ve got peanut products in your house, I’d suggest taking a gander at the FDA site. Of course if you’re in doubt you’d do best to throw it out, especially when President Obama has just promised a complete review of FDA itself.

Oh, and just in case you’re wondering, it’s been a week since we got the Teddy, and so far so good.

Friday, January 16, 2009

Musings of an obsolete toxicologist: nanotoxicology is a whole new world

This morning while walking across town to the Lady Killigrew , a small hipster café located just around the corner from home, I was thinking about a report I’d just begun to draft. The focus was how to evaluate the toxicity of nanoparticles. I was wondering if I’d been too strong in my dismal assessment of toxicology and had hoped that a good slap of cold air (the thermometer outside our kitchen window read -25C) would weed out the dramatic, and clarify the reality.

I’ve pasted some key points below, and while the topic and eventual report are confidential – there’s nothing confidential about the sentiment – I, and many others have been writing about it for a while:

1) The field of nanotoxicology is in its infancy, yet is ever expanding as newly created nanomaterials require assessment of potential health and environmental impacts. I’ve never before had the experience where I’ve considered research from 2006 as “old,” and where, the majority of literature cited is 2008 and 2009. Yet development of a new field within toxicology provides opportunity, and at the same time demands that toxicologists use both hindsight and foresight as they develop the methodology appropriate for these new materials.

2) Hindsight provides us with a glimpse of toxicology as a field, in large part, focused on application as a science catering to the need for rapid assessment and cost-effective regulation. Standardized toxicity testing methodology was developed and implemented as a result, quickly becoming a rigid set of test procedures, a good deal of which, over the years have become obsolete.

3) In part, because of the difficulties with changing test methodologies associated with a regulatory framework (check out the timeline for reproductive and developmental testing – “in development” for what, at least 10 years?) - standardized toxicity testing, useful for screening out the obvious is insufficient for detecting more subtle adverse effects or revealing the impacts of the complex mixtures of contaminants, drugs and naturally occurring chemicals to which we are all exposed.

4) We have an opportunity to consider the history of toxicology as we move forward. Many have expressed concern that “business as usual” may result in failure to adequately evaluate toxicity of nanomaterials. Oberdorster et al., (2005) representing the International Life Sciences Institute Research Foundation/Risk Science Institute (ILSI/RSI) writes “There is a strong likelihood that biological activity of nanoparticles will depend on physicochemical parameters not routinely considered in toxicity screening studies.” Additionally different physicochemical parameters may also affect behavior of particles in media typically used in preparing for traditional toxicity testing, the ability of researchers to adequately evaluate exposure concentrations, and particle behavior in the body. Problems only occasionally encountered in the past.

5) When it comes to some nanomaterials, such as quantum dots and functionalized particles we’re potentially dealing with multiple organic and inorganic materials that may, or may not, be released over a period of time. How do we assess that?

Well, as I wondered if I was getting a bit too dramatic, after grabbing a cup of decaf and ordering a breadboard with mustard I settled in and checked my emails. Bingo. There in the inbox was a link to Peter Montague’s recent article entitled "Can Chemicals be Regulated?" published in Rachel’s Democracy and Health News. Read it and weep.

Or, read it and be hopeful. I really do think that we’re at the proverbial crossroads. We’ve seen the consequences of becoming too rigid, of constrained linear thinking. But this is a new multitasking interconnected networked “wisdom of the masses” kind of world, not just for me and my Lady K compatriots (the majority of whom – to the dismay of the management - are more attentive to their electronics than to their stomachs) but also for those laboring away in research laboratories around the globe.

Maybe I need another slap of cold air, but if we can embrace this new fluidity in information, knowledge, and thinking, perhaps we can embrace a new way of not only evaluating health and environmental impacts of new chemical products, but a new way of using that information wisely.


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.