Tuesday, April 12, 2016

Raisin Hell (and Dogs)

20150531_162658 (2)(Cross-posted from toxicevolution.)We were closing in on the end of a glorious spring weekend when my husband discovered the bag. “Any chance you left this lying around — empty?” he’d asked holding the remnants of a one pound bag of Trader Joe’s raisins I’d purchased just the day before with images of molasses filled hermit cookies in mind. I hadn’t, nor had I made the hermits, or chewed away the corners of the bag. Apparently Ella (pictured above) had consumed every last raisin, save the two handfuls my husband snacked on before leaving the bag on the living room floor.
“I bet she won’t be feeling too good later,” he’d said, eyeing the ever expectant dog sitting at our feet, tail wagging, hoping for a few more of the sweet treats. He had no idea. Nor had I. Not really. I’d had some inkling of a rumor that raisins and grapes were bad for dogs, but never paid too much attention. It’s one of those things you hear at the same time you hear of people treating their dogs to grapes. So, to be safe (and feeling a bit sheepish that, as a toxicologist I ought to have an answer to the raisin question) I suggested he call the vet. And that is when we fell into the raisin hell rabbit hole. Five minutes later dog and husband were on their way to the doggie ER, pushed ahead of the mixed breeds and the Golden and the sad-sack blood hound and their people waiting for service.
Meanwhile I took to Google. Was this really a life or death dog emergency? If so, why weren’t we more aware? I get it, that one species’ treat can be another’s poison. Differences in uptake, metabolism, excretion. Feeding Tylenol to cats is a very bad idea (as if you could feed a cat a Tylenol tablet). And pyrethrin-based pesticides in canine flea and tick preventions are verboten in felines. The inability to fully metabolize and detoxify these chemicals can kill a particularly curious cat. But raisins in dogs? Not so clear. Googling will either send you racing off to the vet or to bed. You may even toss your best friend a few grapes for a late night treat, smug in the knowledge that those who have bought into the hysteria are hemorrhaging dollars while paying off the vet school debt of a veterinarian who is gleefully inducing their dog to vomit, while you snooze.
Even Snopes the online mythbuster was confused (though they suggest erring on the side of caution.)20160412_115827
By the time I arrived at the clinic, uncertain enough to follow up on husband and dog, Ella’s raisin packed gut under the influence of an apomorphine injection (a morphine derivative which induces vomiting in seconds) had done its thing.  While Ben and I waited for Ella’s return in the treatment room, somewhat relieved, we played, “Guess how much?”  Treatment with a drug, time with the vet, multiplied by the “after hours factor” this being a Sunday evening after all, we’d settled on something in the $300-400 range.
“Ella did great,” said the vet tech who’d taken her from Ben and hour or so earlier.  “A pile of raisins came up. Some were even still wrinkled!” Phew. Potential disaster averted.  We’d accepted that it’d likely cost a few hundred – but we’d soon be heading home with Ella in the back seat. We had a good laugh about the revisit of the raisins. But the vet tech wasn’t finished. That was just the first step. “So now we’ll give her some activated charcoal,” she continued “and you can pick her up on Tuesday.” Total estimated low-end estimate? A bit over $1000. Paid up front (I have wondered what would have happened if we couldn’t pay – but that is a whole other issue). Apparently we had underestimated the price of a good vomit.
“We can’t be sure we’ve got all the raisins. So we treat with aggressive I.V. Two days is the standard minimum.” Noting our jaws dragging on the floor, or maybe my comment “that’s a plane ticket to Europe” she added, looking at us a bit less sympathetically. Adding “well, of course you can take her tomorrow, or even tonight….if that’s what you want. But that’s what we do. You can talk about it with the Vet.” Or, sure, go ahead take your chances. Poor dog.
Emetics like apomorphine, according to the literature, are only good for purging 40-60% of a dog’s stomach contents. So, even a good barf, will likely leave some raisins behind.
Two days though? With I.V? While waiting for the vet another bout of Googling confirmed the standard treatment. Induce vomiting, charcoal, two days of IV and kidney chemistry panel. Ouch.
But, here is the kicker: no one in the whole Google universe could tell me why we were doing this. Why the fruit we take for granted in our cookies can kill our dogs. The virtual gauntlet thrown, I took the challenge. Surely the scientific literature sitting behind a pay wall would provide the answer. But even in my go to database, the Web of Science a site that normally yields more far papers than I care to even skim their titles – there were a handful of articles. Yet there was evidence of poisonings: one article reported kidney failure in a Shih Zhu and a Yorkie in South Korea.  Another wrote of a Norwegian elkhound, lab, Border collie and a Dachshund all poisoned by raisins. The most popular article, published over ten years ago focused on 43 cases of renal failure following raisin consumption drawn from a decades’ worth of reports to the AnTox database (sponsored by the ASPCA).
That study confirms renal failure following raisin ingestion. Since all dogs in the study were already presenting with symptoms the authors couldn’t provide information on what proportion are sensitive.  Though they acknowledge that there are plenty of anecdotal dogs for whom grapes and raisins are a risk-free treat. They also suggests there is no correlation between amount of raisins ingested and degree of kidney toxicity. In other words there is no dose response. That alone is enough to confound a toxicologist (dose response is a basic tenet of toxicology, the dose makes the poison and all that), and spark controversy amongst dog owners. A dog can eat a few and die. Or eat a whole 16oz bag, and get by with or without treatment depending (albeit with the upset to be expected after eating a heap of dried fruit.) Not only that, but no one know why raisins cause kidney failure. There have been plenty of guesses: fungal toxins; pesticides; something intrinsic to a particular variety; or canine genetics. But there just isn’t enough consistency to identify a mechanism of toxicity. And so vets err on the side of caution.
One vet tells me her dog went into kidney failure after eating some grapes she discarded (she managed to save the dog). Another says she’s never seen a dog with raisin toxicity (of course absence of evidence isn’t evidence of absence – but those dogs who can eat grapes and not die, won’t show up on the vet’s doorstep either.)
“Sorry to hear about your dog’s experience with raisins,” writes veterinary toxicologist John Babish writes after I’ve emailed him about Ella’s ordeal (John was my advisor while in graduate school at Cornell University) asking: what’s up with the raisins?
“The same thing can occur with grapes – all kinds and colors. Canine responses to grapes and raisins are highly variable and some dogs are not affected at all – about 30% are sensitive to very sensitive and a clear majority do okay with no effects. A negative fallout of the inconsistency of response is that some bloggers maintain that grapes/raisins are not toxic to dogs.”  Which explains blogs and websites like the Dog Place posting Snopes and ASPCA Poison Control Urban Legend; Poisoned by Grapes, NOT; Grape/Raisin Debate; or No More Vet Bills,Grapes Toxic to Dogs?
We are not used to uncertainty. We live in a high-tech age of data. We can sequence the human genome and create disease resistant rice. We can measure toxic substances down to the parts per quadrillion (trust me, that’s a really small amount,) and tease apart the inner workings of our cells in detail unimagined even a decade ago. But sometimes you have to make a decision with the information you have. We weren’t willing to bet that Ella was in the majority.
Two days later we collected our pooch, happy as ever and oblivious to the whole ordeal. We won’t ever know (I hope) if she is in the minority of dogs who can’t handle their grapes and raisins; or if that $1000 worth of purging saved her life, or simply emptied our wallet. But, just in case – that replacement bag of raisins I bought? Those will remain on the top shelf hidden away until I get the urge to make some hermits.

Tuesday, April 21, 2015

You say tomato, I say blight!

From http://www.longislandhort.cornell.edu/vegpath/photos/lateblight_tomato.htm#images
The first inkling that things were really bad was the news that late blight had not only wilted and rotted my own tomatoes but Red Fire Farm’s (Montague, Massachusetts) as well. Farmer Ryan Voiland has been growing and selling tomatoes since middle school, setting up a road-side stand outside his parent's home. A decade or so later Voiland – a thirty-something soft-spoken organic farmer with a degree from Cornell – had become an award winning tomato grower. “That first year was remarkable,” recalled Voiland, cracking a shy smile, “we heard about the Massachusetts Tomato Contest …. had a good crop and managed to send in some specimens.” Red Fire's tomatoes won five out of twelve awards, more than any farm, organic or conventional, had ever won in a single year. Red Fire, now a successful Community Supported Agriculture farm or CSA, grows more than 150 different tomato varieties offering them up for tasting at their annual Tomato Festival. But in 2014, a fungus-like disease called Late Blight had made its way up the valley, jumping from one farm to another until it hit Red Fire. Tomato crops died within days. Rows of once lush plants resembled vegetative versions of Zombie armies; upright stalks studded with browned blight infested leaves. Large brown spots blossomed on the fruits turning them soft and unsellable.
late blight on leaf
From: http://www.longislandhort.cornell.edu/ vegpath/photos/lateblight_tomato.htm#images
That my kitchen garden, just a few miles away from Voiland's farm succumbed as well, was no surprise; I am not the most attentive farmer. When I can amble down to the Red Fire farm stand and purchase plump red Brandywines, Big Yellow Zebras or Sungolds, tending to tomatoes is not a make or break situation. But for independent farmers and CSAs, such large scale crop loss can be devastating. The 2014 outbreak left local tomato fields in tatters, but it wasn't the worst case of the blight to hit Red Fire. In 2009, writes Voiland in his farm blog, Late Blight “caused massive crop loss and severely impacted us financially.” Voiland had plenty of company that season as the blight ripped into tomato plants all along the east coast and mid-Atlantic. Chef and author Dan Barber penned a New York Times op-ed about the outbreak, “You Say Tomato, I say Agricultural Disaster.” The article was just one of hundreds published that year. “I, myself,” wrote Martha Stewart in a 2009 blog, “have lost seventy percent of the fifty different varieties in my garden. Even though I still have tomatoes on the vine, many of the beautiful heirloom varieties, which were planted, never had a chance.” Stewart's post was accompanied by an image of an ugly diseased tomato, a far cry from the doyenne's trademark perfection.
Diseased tomatoes are nothing new, whether grown by conventional or organic tomato farmers. Voiland and others are constantly on the lookout for early blight and black mold; cut worms and leaf miners; and all sorts of specks, spots and cankers.  But Late Blight, caused by the fungus-like Phytophtora infestans – a pathogen with an affinity not only for tomatoes but also for their botanical cousin the potato – was a new one for Northeast growers.  And, ever since it's 2009 debut, the blight that wipes out crops within days, has returned each growing season. For Voiland and many CSA farmers tomatoes are an essential crop. A classic summer vegetable. But ever since blight, tomatoes have become harder to bring to market.
That 2009 outbreak may have been the first to hit northeast tomatoes but it certainly was not the first time Phytophthora went pandemic. Nor were tomatoes the first vegetable (or, fruit) to be taken by blight. Over a century ago a mysterious potato disease spread across Europe like wild fire. Healthy plants died within days. Potatoes in the ground turned putrid. Tenant farmers in Ireland were hit particularly hard. Some one million Irish died and more than a million sailed for distant shores. Late blight had touched off the infamous Potato Famine, altering social structures, politics, and agricultural practices – its effects relevant even today. Since its emergence on potato fields blight has remained the bane of farmers around the globe. Even so, no one expected the 2009 outbreak.
“In our experience,” writes Cornell plant pathologist William Fry and colleagues of the outbreak in their recent article The 2009 Late Blight Epidemic in Eastern U.S., available online by the American Phytopathogical Society, “the scale of pathogen release was completely unexpected and unprecedented.” Fry has tracked the plant pathogen to its roots and teased apart its DNA. So what changed? How did this happen? Using an NCIS-like approach including DNA finger-printing, the group traced the 2009 outbreak to a single source and a single strain, subsequently named “US22” (there are dozens of late blight strains; but US22 was the bane of 2009 growers.)  While the scenario played out like an agro-terrorist attack with blight hitting just about everywhere in the east, the cause was disturbingly mundane.  Blight infected plants, traced back to big box distributors like Home Depot, Kmart, Lowes and others, which had purchased their plants from one national plant distributor.  News reports fingered Alabama-based distributor Bonnie Plants a charge the company vehemently denied though that summer, though they pulled their plants from a dozen states and took a financial hit. Since the outbreak, working with Cornell plant pathologists, the company has cleaned up their act.  Now, it seems as if blight is here to stay. Even so, no matter the source, the mere existence of the fungus-like blight isn't enough to cause disease.  For Blight to take wing, it requires moderate, wet conditions. When the temperatures hover around the 70s and the rains settle in – an apparently healthy crop can disintegrate within days.
Had 2009 been hot and dry, Voiland and others might have been hauling out the hoses and irrigation equipment, rather than contending with Blight. But along the east coast, conditions both in 2009 and 2014 have been more reminiscent of Ireland and England than Arizona.  Since that initial outbreak, the threat of late blight has loomed large. Before 2009 few tomato growers in the Northeast worried about losing whole crops to late blight; now even home gardeners are wondering how to tame it or better, avoid it altogether.
Should the weather turn cool and damp and the blight start flying this summer there are few options other than:
1) Consider choosing resistant varieties like the Iron Ladies, Defiants and others.
2) Track blight and prepare as best you can using  http://usablight.org/
4) Give your plants space, and watch them like a hawk.
Published in the Montague Reporter April 2015
Cross-posted from toxicevolution.wordpress.com

Happy to be back! And with new Book in tow!!

It has been quite a while (apologies to those who left comments over the past 3 years...when Google took over, I couldn't figure out how to get in!) Just tried again after getting on the forum and am happy to have control of my blog back.

Anyway, in the meantime, I have been continuing to think about evolution and toxicology and what that means for us. It's a big deal. Evolution is relevant in our everyday lives (just think about antibiotic resistance; pesticide and herbicide resistance which even if you don't use, you are impacted because it forces users to increase application rates.) And, though we tend to think of evolution as something that happens over billions or millions of years - we now know it can also happen rapidly. Depending on who's doing the evolving in days, weeks, months or a few years. Not only that but we humans can and do influence evolution of everything from bacteria to plants, bugs, fish, even mammals. This isn't a good thing. At least, not for us.

Any who, the upshot of all of this is a new book! Unnatural Selection: how we are changing life gene by gene is written for anyone interested in the too-often under appreciated downsides of using lots of chemicals. That is, evolution in the pests and pathogens we tend to insist on wiping out! Next up is a book about the solutions. Hopefully in a year or so.

I've posted some blogs at toxicevolution.wordpress.com and now have a site with updates about events and talks at emilymonosson.wordpress.com 

Wednesday, March 28, 2012

The Neighborhood Toxicologist is Evolving

When I started writing this blog, my goal was to explain why certain chemicals in consumer products were toxic, as well as discuss some of the uncertainties in toxicology. Over the years, all this writing about one chemical after another - many of them industrial age chemicals - got me thinking about all the defenses we have that protects us to some degree against toxics. Would these systems hold up to the onslaught of chemicals in the world today? Why do we handle some chemicals better than others? How can we better predict and prevent toxicity?

One thing led to another, which eventually led to a book! So I am happy to announce the publication of my first toxicology book, Evolution in a Toxic World, and another blog by the same name. Hope to see you there.

Monday, August 16, 2010

Peanut allergies in a nutshell

This summer I met a family from Australia who’d mentioned their daughter was highly allergic to peanuts. Wondering if all the concern about peanut allergies was yet another case of Americans overreacting to anything health-related I asked if they’d ever heard of schools in Australia banning peanuts.

“Our daughter’s school has been peanut-free for years,” they replied, as if it were an odd question. They added, “Lots of schools are.”

Like many people, I’ve also wondered if the seeming rise in prevalence of peanut allergies was real. After all, how many times have I heard someone say, “Well, we all grew up with peanut butter, and I didn’t know anyone who was allergic. What’s all the fuss about now?”

Turns out -- according to several studies published in medical and allergy journals over the past decade -- that peanut and tree nut related allergies, or hypersensitivity of the immune system to specific proteins in these nut families, truly is on the rise in Australia, the US and other Westernized countries. It is now estimated that over 1% of the US population has peanut or tree nut allergies, and one study reported a doubling of peanut allergies in children over a five year period.

So what’s going on? Has something changed in the way we are exposed to peanuts, tree nuts and other increasingly allergenic foods (sesame, and soy for example)? Or is it simply that our immune systems are going haywire?

The immune response is complex. While we’re all familiar with the role of antibodies, which confer immunity to anything from the common cold to polio, they are only one of five different types of immune proteins, or immunoglobulins. Other immune proteins protect vulnerable regions of the digestive and respiratory tract from pathogens, elicit our bodies to produce antimicrobials, and help us get a “jump” on our response once pathogens have breached other protections and entered our bloodstream.

Then there is immunoglobulin E (IgE). Although recent studies suggest that IgE may protect against certain parasitic worms (less of a problem these days in western countries compared with other regions of the globe), IgEs are most notorious for their role in causing allergic reactions, or an inappropriate immune response to a relatively harmless substance. Basically, once a body is sensitized by a potential allergen, a bit of basement mold perhaps, or a whiff of pollen from the old oak tree, IgEs are then distributed thoughout the body in association with immune cells like mast cells and basophils, which lay in wait for the next exposure.

When subsequent exposure occurs, these sensitized immune cells release a slew of potent chemicals including histamine, cytokines, and prostaglandins. These are all useful chemicals when released at the appropriate time and place, as during a normal immune response when the body is combating a pathogen or healing a wound (and even then they may cause some damage to healthy cells and tissues.) But as far as anyone knows, there is no appropriate time or place for an allergic response. Yet no matter the reason, when these chemicals are released the body responds.

The allergic responses many of us experience are caused by the increases in vascular permeability, constriction of smooth muscles (including those around the smallest passages of our lungs), and increased mucus production caused by histamine and other chemicals. The impacts on a body can range from mild to severe.

So, while I might suffer through a month or two of asthma, sneezing and itchy eyes (along with the more than 20% of the U.S. population affected by allergies), thankfully my IgEs seem to respond relatively mildly. But for some, an IgE response can cause anaphylaxis, a far more severe and systemic condition which may include vomiting, constricted breathing, and plunging blood pressure. The onset of these life-threatening responses can lead to anaphylactic shock and can occur within minutes of exposure.

A 2008 study published in the journal Current Opinion in Allergy and Clinical Immunology estimated that allergic anaphylaxis may occur in up to 2% of the U.S. population at some point in their life, with varying degrees of severity. And the risk of occurrence, particularly in children, is on the rise.

Which brings us to some of the top triggers for anaphylaxis - a list that includes many common substances like latex, insect venom (e.g. bee stings), medications (e.g. penicillin) and certain foods including shellfish, milk, tree nuts, and peanuts. Of these, food allergies are among the most common triggers of anaphylaxis requiring emergency room treatment. By some estimates, in the US food allergies account for roughly 30,000 visits to the emergency room and at least 100 fatalities a year, and several reviews of the medical literature including a 2009 review published in Clinical Pediatrics conclude that peanuts and tree nuts cause the majority of reported allergy-induced fatalities.

When a food is allergenic, the allergic reaction is usually caused by a specific type of protein contained in the food. In peanuts, eight different allergens have been identified. What differentiates allergenic proteins from other food proteins is that they resist acid, heat, and enzymatic breakdown in the gut. So they tend to be identified by the body’s immune system as an intruder rather than a nutrient, with potentially devastating consequences.

Efforts to understand why the US and other Westernized populations has a higher prevalence of peanut allergies than, say, China, where peanut consumption is also high, have identified the U.S. food industry’s practice of dry roasting peanuts rather than boiling or frying peanuts as one potentially relevant factor. The higher temperatures reached by the dry roasting process increases the allergenicity of peanut proteins. Other factors contributing to higher prevalence likely include differences in diet, routes (oral or dermal) and timing of nut exposures. Additionally, scientists have hypothesized that improved hygiene and reduced disease incidence in young children may also contribute to increased prevalence of allergies in general. Scientists and allergists have also speculated that increased use of peanuts in common consumer products, from soaps to shampoos and skin creams, may contribute to creating a more sensitized population.

Whatever the underlying cause, some people, once they are sensitized, need only ingest a very small amount (50 millgrams, approximately 100th of a teaspoon, down to as low as 2 mg) of peanut product to cause what could become a life-threatening reaction.

It is a mind-boggling response. Consider the tiniest oral exposure setting off a systemic response within minutes. How does this happen?

“What you think of as low dose might contain plenty of stable antigen [or allergenic protein],” explains Southeastern Louisiana University Immunologist Dr. Penny Shockett. “Also,” Shockett added, “once the system is sensitized it doesn't necessarily take a high dose for tripping the mast cell response. If you are highly sensitized (i.e. allergic) you have more sensitized mast cells in tissues (or basophils in the blood) sitting and waiting for the allergen, which can potentially detect it quickly and strongly.”

Studies indicate that not only has the prevalence of peanut allergies risen over the past few decades, but also the risk of anaphylaxis in general, at least in the United States and other Western countries. As we alter our diets based on the ever-changing suggestions of health and nutrition experts, cultures adopt one another’s diets, and diseases are reduced through changes in hygiene and vaccines, scientists are in a quandary as to the causes of increased peanut and tree-nut sensitivity. Hopefully both the underlying causes and solutions for those who are allergic will be identified sooner than later.

For those currently affected by severe allergies, the focus is on management. In addition to education of individuals with allergies, particularly children, this means a range of options for schools. First and foremost involves appropriate medical and treatment plans in schools, followed by education of the school community, and strategies to avoid exposures for allergic individuals. In the case of peanut allergies avoidance in schools ranges from peanut free buildings to peanut free classrooms or separate lunch tables. As to the most effective management practice, the jury is still out.

Emily Monosson, Ph.D. writes and blogs as the Neighborhood Toxicologist, is a member of the GMRSD school committee, and is a member of the district’s Wellness Committee. The information presented here is the product of her own research into the issue and does not represent the opinion or work of the GMRSD school district, or the Wellness Committee.

Wednesday, May 05, 2010

McElligott's Plastic

“Ask for a cone, save the environment!” proclaimed the sign at the local Creamee. The girls asked for cups anyway, to catch the drippings of the oversized soft-serve half-and-half cones they'd ordered. “Guess we’re not saving the environment today,” said one, dipping her plastic spoon into the Styrofoam cup.

Styrofoam is one incarnation of polystyrene plastic – more affectionately known as “#6” or, the plastic we can’t recycle. Polystyrene is also the black polystyrene casing of my computer, my bicycle helmet, the foamed polystyrene clamshell we were offered to carry home the remainders from a local restaurant and, the countless little white Styrofoam pellets degraded from sheets of weathered insulation I spent the weekend picking from the weeds at the local junk-yard turned conservation land along with a handful of diligent volunteers.

While collecting the little white bits from the earth, I imagine how each year some portion of those beads along with larger rafts of insulation are blown or washed into the bordering Sawmill River, some journeying only as far as the local swimming hole, while others carried by the Sawmill make their way to the Connecticut and beyond. I imagine their journey a perverse version of Dr.Seuss’s McElligot’s Pool, where you never know what exotic species might make their way from the deep ocean to a backyard pond, only these make their way to the deep ocean. This isn’t fanciful fiction. Just this year scientists confirmed the presence of a plastic “patch” of our own in the North Atlantic, the evil twin of the infamous North Pacific trash gyre – a region known for its accumulation of plastic from soccer balls to microscopic bits of Styrofoam and other assorted plastics. Looking around at all the Styrofoam I’ve missed, the scientist in me wants to radio-tag those naughty bits and send them on their way. Maybe in a few years we’d know for sure if pieces of Montague were swirling about the wide Sargasso Sea.

Captain Charles Moore, an adventurer, environmentalist and researcher, credited with discovering the North Pacific patch once commented on the return of plastic to the oceans and its consumption by marine life in an article for Natural History Magazine, “Ironically,” wrote Moore “the debris is re-entering the oceans whence it came; the ancient plankton that once floated on Earth's primordial sea gave rise to the petroleum now being transformed into plastic polymers. That exhumed life, our ‘civilized plankton,’ is, in effect, competing with its natural counterparts, as well as with those life-forms that directly or indirectly feed on them.” Research by Moore and others, now shows that plastics in the ocean can accumulate toxicants long banned like PCBs and DDTs, and there is some concern that once ingested, contaminated plastics might release these chemicals, along with others used for plastics production including colorants, fire retardants and plasticizers into their host. Someday there may be no need to shrink-wrap seafood.

Like other plastics, polystyrene – the base material for Styrofoam or foamed polystyrene clamshell food containers, microwavable cups (think cup-o-noodles), plastic plates and coffee cups – is a polymer, a chemical chain of repeating units, like beads on a string. In this case the beads or monomers are styrene. Produced naturally by plants and animals, styrene – like many chemicals - is relatively non-toxic in these small amounts. And, like many chemicals, natural production is dwarfed by human production (at least in localized concentrations,) which in the case of styrene tops 13 billion pounds a year in the US alone. The majority is used to produce polystyrene. While polystyrene might not appear on the top ten list for toxic chemicals, it is made from benzene. Over 50% of all benzene that is produced from oil is eventually turned into styrene. And sweet smelling benzene is nasty stuff. Just a whiff brings me back to organic chemistry lab in college. We used it without a care until the day it was officially deemed a carcinogen – and then we didn’t. At the risk of showing my age, that was in 1979. And in a strange case of collective heads- in-sand, benzene was known to cause cancer since the 1920s. (We can thank industry along with federal regulators to for that small lapse.) Benzene is now one of the few industrial chemicals officially listed as a known human carcinogen – causing leukemia in this case – and it is industry workers who are most at risk.

So what happens to all that polystyrene? The EPA estimated that in 2007, nearly 3 billion pounds of it was used in the production of disposable goods, including foamed polystyrene plastic plates, cups, egg cartons, and packaging peanuts. Aside from the packaging peanuts we might bring to a UPS store for reuse, with a recycling rate for all polystyrene estimated as a mere 0.8%, most will end up in a landfill. At worst it’ll end up our local streams, rivers and oceans.

And, when it does according to new research by Katsuhiko Saido and colleagues from the Nihon University, in Chiba, Japan, it will not only degrade more rapidly than it would on land (under certain marine conditions) but it will also release toxicants including a small amount of bisphenol A, notoriously linked with polycarbonate plastics, and styrene which brings us back to – d’oh!

The good news is that like most other plastics, technically, polystyrene foam is recyclable. In fact, it can be recycled back into many of the products from which it came – plates, clamshells, egg cartons and insulation, or into less desirable “dead end” products like light-weight concrete. The bad news is that the process isn’t cost effective, at least in the US – and so isn’t all that popular.

Then there are the more creative uses for this problem plastic. Some, like Cass Phillips, writer and co-owner of Kamuela Greenhouse/Specialty Orchids in Waimea, Hawaii have considered turning the environmental blight into beauty. With USDA grant funding, Phillips is currently testing the utility of various locally collected and processed recycled plastics as a growth medium additive with an eye to providing a durable low cost product for the Hawaii orchid industry. When asked about foamed polystyrene, she responded:

“I found that a certain type of orchid, miltoniopsis (aka the pansy orchid), grew fastest and largest in straight granulated polystyrene foam, in a trial that included three controls (cinder, coconut fiber and orchid bark)…... What truly stunned me is that the pansy orchids went into their bloom cycle 2-3 months before any other sample." There could be several reasons for the accelerated growth. One might suppose improved water retention could be a factor, but the ground polystyrene foam dried out almost instantly. That leaves us pondering other possibilities, including one that could be considered insidious: the release of growth-inducing chemicals. Sorting out the differences will require further analysis, but in the meantime Phillips has found herself wondering about the wisdom of schools using Styrofoam plates in their lunch programs, and the consequences of slurping down cups-o-soup from Styrofoam tubs.

Of course the best way to keep this ubiquitous plastic from polluting the oceans and clogging the landfills is to reduce use (according to the American Chemistry Council, the PS industry has been in decline for the past four years, though they give no reason), and close the recycling loop. More immediately, I’m sure there’ll be many more opportunities to pick Styrofoam from newly acquired conservation land, and for those rare occasions when I can’t clean my plate while dining at one of the local eateries, I’ve begun asking for foil or cardboard for the leftovers.

Monday, January 25, 2010

Yankee Swap: tritium contaminated water anyone?

First published in the Montague Reporter

First we hear about tens of thousands of picocuries* in the groundwater beneath Vermont Yankee Nuclear Power plant, next it’s over one hundred gallons of water contaminated with over 2 million picocuries in some sort of concrete trench. Oops. Besides sloppy practices, lax monitoring, shoddy construction, and obfuscation (what underground pipes?) what do these numbers mean? Should we worry about all that tritium? And what the heck is a picocurie anyway?

Tritium is a radioactive isotope of the element hydrogen. What sets apart the radioactive elements from the non-radioactive is their lack of stability. They can disintegrate spontaneously, sometimes changing into other elements over time. Uranium, for example, decays into lead (although it may take billions of years,) while it takes roughly a decade for tritium to decay into helium.

The difference between a radioactive element and a plain old element depends upon what’s in the nucleus. The nucleus of any atom consists of protons (positive elements), neutrons (neutral elements) and electrons (negative elements). While the chemical properties of an element mostly depend on the number of protons in the nucleus, the radioactive properties are determined by the number of neutrons and the balance amongst the protons, neutrons and electrons. An element like hydrogen and its radioactive twin, tritium, have the same number of protons (and so, the same chemical properties), but instead of a single neutron, tritium has three neutrons. Tritium occurs naturally in small amounts, in addition to being produced by man either purposefully for research and consumer products (ever wonder about that glowing watch dial or that luminous EXIT sign?), or as a by-product of the nuclear industry.

Because tritium is chemically similar to hydrogen it can and does take the place of hydrogen – when this happens in water tritiated water or radioactive water is formed.

The radiation released by tritium is referred to as a beta particle. Beta particles, or electrons, are a form of ionizing radiation capable stripping electrons from other atoms, causing a sort of chain reaction of destabilization, and breaking chemical bonds. Although the beta particles released by tritium are low energy, incapable of penetrating through barriers such as skin (unlike some other forms of radiation), should tritium enter the body through inhalation or umm…water, those emitted particles would then have full access to vulnerable tissues and molecules.

Tritiated water is particularly insidious. The tritiated water lurking below Vermont Yankee for example, could be absorbed by the root systems of nearby plants, or imbibed by unsuspecting animals. Once consumed, distributes rapidly throughout the body of plant or animal. Additionally, ingestion of tritiated water, can lead to incorporation of tritium into organic materials like DNA, proteins and amino acids. Only, unlike hydrogen, tritium will eventually decay, leaving behind an atom of helium and releasing a beta particle with enough energy to break nearby chemical bonds.

In the body, the making and breaking of the chemical bonds between atoms is a highly coordinated process, normal and essential to life. The “unscheduled” breaking of chemical bonds can cause permanent cell damage, damage to the cell’s DNA or cell death.

The human genome is contained within the DNA of our 46 chromosomes located in a cell’s nucleus. Replication of these chromosomes during cell division is a critical process, requiring a number of complex biochemical interactions including copying and construction of identical chromosomal pairs that are then split off into the newly divided cell. Because integrity of the genetic material is essential to life, not only are there biochemical systems involved in maintaining chromosomes during division, but there are also a number of mechanisms by which errors may be repaired.

Say a few molecules of tritium enter the cell and cozy up to nuclear DNA. At some point in their unstable life-time they will disintegrate, releasing their energized electrons. Should the cells’ chromosomes be in their pathway, the transfer of energy from electron to chromosome may be enough to break off a bit of chromosome. Sometimes, depending on conditions within the cell and location of the break, the broken pieces may rejoin the chromosome, leaving little or no evidence of damage; other times a broken piece remains separate, becoming a chromosomal deletion; or both the deleted piece and the damaged chromosome will be copied as if nothing happened, only it will be altered. Or, instead of direct interference with DNA, emitted electrons may interact with other molecules such as oxygen, causing “indirect” damage by creating highly reactive oxygen radicals.

Since DNA tends to be a target of ionizing radiation, tissues made up of cells that are rapidly dividing – such as blood forming organs constantly churning out cells – tend to be far more sensitive to radiation damage than say, brain cells. Similarly, embryos and fetal tissues are more susceptible to radiation damage than adult tissues.

There is some good news amidst all this havoc and destruction. That is, most if not all cells have some capacity for DNA repair. These include an array of enzymes and proteins that find and correct damaged DNA in addition to a number of antioxidants capable of disarming those reactive oxygen radicals. The presence of such repair mechanisms have led some to speculate that exposures to very low amounts of radiation may be a good thing, “priming” these repair systems and leading to greater protection with low levels of exposure – a phenomenon referred to as hormesis. However, a National Academy of Science report on The Health Effects of Low Level Ionizing Radiation, published in 2007, found no available evidence of radiation induced hormesis in mammals, and concluded that any single track of ionizing radiation (for example by a single ejected electron in the case of tritium) has the potential to cause cellular damage.

And, despite the capacity for repair, sometimes the system is overwhelmed, or sometimes the repair itself introduces a new error (think sloppy auto mechanic.) At this point the genetic damage has the potential to become permanent, or “fixed.” Permanent damage to DNA can result in the eventual development of cancerous cells, or a defect in an exposed fetus or as a mutation passed on to the next generation. While the evidence for carcinogenicity in human populations is strong for some radioactive isotopes like strontium-90, plutonium and radium, the health effects of tritium, a weak beta emitter are less clear.

Which brings us to concentration. How much is too much? What does it mean that the groundwater has over 200,000 picocuries of tritium per liter of water, or that there are “troughs” with over 2 million picocuries per liter? A curie (named in honor of radiation pioneers Pierre and Marie Curie) is a quantity of radionuclide in which there are 37 billion disintegrations a second. That’s a lot of disintegration and in the case of tritium would be a lot of beta particles whizzing about. But the amounts drawn from the ground water were measured in picocuries per liter – or one millionth of a millionth of a curie. So, every second, until all the tritium has disintegrated to helium (the half-life for tritium is 12.5 years) there would be roughly 7,400 electrons winging about in a liter of Vermont Yankee groundwater.

As a result of the current hypothesis that exposure to any amount of ionizing radiation carries with it some risk of cancer, the U.S. EPA’s Maximum Contaminant Level Goal for all radionuclides in drinking water, a goal which aims for “zero-risk” to public health, is zero picocuries per liter. Unfortunately, achieving “zero risk” is not only wishful thinking but currently unenforceable and, because there is some naturally occurring tritium impracticable. Instead, EPA has developed Maximum Contaminant Levels (MCL) for drinking water. While the MCLs are enforceable, they are calculated considering best available technology and economic feasibility. For tritium, the derived** MCL is 20,000 picocuries per liter, while the derived MCL for strontium 90, a more powerful beta emitter associated with bone cancer and leukemia, is 8 picocuries.

Here’s the thing. Right now we’re talking two wells and a trench (where, incidentally, a small amount of radioactive cobalt has turned up as well.) While current concentrations in the ground water (the trench is another story) may not present an immediate health risk, who knows what a more comprehensive analysis - currently underway - might reveal?

*As of Feb 10, 2010 over 2 million pCi was measured in test wells around the plant.

For more see: http://www.rutlandherald.com/article/20100205/NEWS04/2050349/1003/NEWS02

**The MCL for beta emitters is based on a dose of 4mrem/year to the total body and assumes ingestion of 2L a day – the picocurie concentrations are derived for each specific beta emitting isotope depending on their strength. Over the years, there has been discussing of using different calculations for tritium that would dramatically reduce the MCL.

Thursday, January 07, 2010

Evolution of the Toxic Response: In the beginning there were chemicals....

The following is what I intend to be the first in a series of essays on the Evolution of the Toxic Response – a topic which piqued my interest after what could either be called a disastrous flirtation with the publishing world, or an invaluable lesson in pursuing your passion. The disaster was allowing myself to be duped into thinking the content and style of this blog would actually make an engaging book (wrong,) the passion was in realizing that writing primarily about toxicants of interest to the consumer (and in the style that would be most appealing to mass market publishers) has caused me to lose my way as a toxicologist and a scientist.

There is no doubt that some toxicants are, well, toxic. But there is always the question of exposure, dose, and potency. Topics often lost in breezy articles meant to engage a reader – rather than inform about the complexities not only of toxicology but science in general. Unfortunately the publishing world seems to have no confidence in its mass readership. Readers are attracted by alarmism, so hype it up. They’ll doze if there is too much science, so keep it simple. They just want to be told what’s best for them, so just tell them. But after whipping off one light and fluffy page after another about dangerous toxicants hidden away our homes and gardens (along with a few good toxins in our ‘fridges) all in preparation for my failed Book Proposal, a request by the local news paper to write about bisphenol A or BPA resulted in a nearly visceral reaction at the thought of writing yet one more article for consumer consumption about chemicals consumed by consumers.

But after the storm, and the lull where I could barely bring myself to write another word about chemicals, came the passion. I was attracted to toxicology because I was fascinated by chemicals that screwed up the normal processes of life. But that was back in a time long long ago when toxicology meant PCBs, lead, mercury, dioxin, and assorted pesticides. These were obvious chemicals in concentrations that couldn’t hide within the peaks and valleys of the chemists’ printout. But science has come a long way since then. Now, we know far more about the minute amounts of a myriad of chemicals contaminating our water, air and food than we do about the way they might interact with our lung cells, or livers, or brains. We know that our bodies sequester the smallest amounts of these chemicals in our bones, brains, and fat cells.

Many of these chemicals will stick around on earth at least for our lifetimes, and those of our children. What will be the consequences of these chemical exposures – if any? What do we really mean when we say that these chemicals are toxic? At what point does a contaminant become a toxicant? Given all the synthetic and naturally occurring chemicals entering and exiting our bodies with virtually every breath – some of which by now are unavoidable, others we might choose to inhale and ingest, and still others have been with us for eons, how can I, as toxicologist better understand the collective impact?

This was when I remembered I’ve inherited more than my big ears, hazel eyes and dry skin from my ancestors. I’ve inherited a whole system of toxic defense mechanisms, because really, well before the first animal ventured onto land, well before the first single-celled organism respired oxygen, life on earth relied upon chemical defense mechanisms of one sort or another.

And to some extent, we owe our lives -- as do all life forms -- from bacteria, to plants and all animals -- to these toxic detoxification processes.

Yet are they enough to protect life from the steady rain of natural and synthetic chemicals experienced by life on earth today?

That is the question I intend to explore in this upcoming series of essays, so stay tuned if you dare.

Also if you are a toxicologist, chemist, geologist etc. and would like to discuss the topic further please don't hesitate to contact me at emonosson@verizon.net I'd love to begin a virtual journal group on this topic.