Tuesday, January 10, 2017

Trump's war on science, a shot over the bow

I was hoping that maybe Trumps anti-vax statements would be one of those things he backtracked on (I have in my head the little tune from Scrubs, Wrong, wrong, wrong, wrong,); but his recent ask, this one to Robert Kennedy Jr, a well-know anti-vaxxer who  maintains that the MMR vaccine causes autism (despite the overwhelming science), to chair "a commission on vaccination safety and efficacy," suggests otherwise. I don't know why I'm surprised. Says Kennedy, "We ought to be reading the science and debating the science." 
I've been writing about vaccines for a few years in different contexts. Below is an excerpt from my upcoming book. The book is about how we can reduce our dependence on drugs and chemicals like pesticides, by relying on natural allies. One of those allies is our own immune response, this excerpt from a chapter about tech advances in vaccine development includes a bit about Maurice Hilleman, the virologist who developed the vaccine anti-vaxxers love to hate (along with many other vaccines):
The concept of a vaccination is simple enough: vaccines provoke immunity by exposing individuals either to pathogens that have been weakened or killed so that they can no longer cause full-on disease, or to bits of pathogens. But pathogens are wildly diverse, and a vaccine strategy that works for one disease may not work for others. Some are fairly straightforward—for example, injecting weakened or killed polio virus provides lasting protection. (Since 2000, the United States has used only killed polio virus.) When I was vaccinated as a kid, I likely received the next best thing to a natural infection: live but weakened versions of polio, mumps, and measles. A generation later, most of my children’s shots were filled with inactivated or killed viruses, or bits of microbes.[i] Kids today do still receive some attenuated (weakened) virus vaccines, notably against mumps, measles, and rubella.
Many of these twentieth-century vaccines began with Maurice Hilleman, a virologist and vaccine developer who spent most of his career at Merck Pharmaceutical. The mumps vaccine my kids received may even be traced back to the 1963 mumps virus that once infected Hilleman’s own daughter, Jeryl Lynn. As he tells the story, one night she woke complaining of a sore throat. “Oh my god,” said Hilleman, pointing to the glands under his chin and holding out his hands, “her throat was like this.” Though rare, a mumps infection can have serious complications, from permanent hearing loss to life-threatening brain swelling. There was no vaccine. So Hilleman raced to the lab and grabbed some swabs. Three years later, he treated his one-year-old daughter Kirsten with a vaccine he had developed from Jeryl Lynn’s virus. “Here was a baby being protected by a virus from her sister, and this has been unique in the history of medicine. . . . It was a big human-interest story.”[ii] Hilleman, who passed away in 2005, is credited not only with developing dozens of vaccines but also saving more lives than any scientist before him. But, as the authors of an article in Science about twenty-first-century vaccine development pointed out in 2013, “By the latter part of the twentieth century, most of the vaccines that could be developed by direct mimicry of natural infection with live or killed/inactivated vaccines had been developed.”[iii] In other words, the most manageable pathogens, like mumps, were under control. What’s left for vaccine makers are the problem pathogens.... They are also confronted with a growing trend of distrust in vaccines. Ironically, vaccination critics are part of a population that has benefited greatly from vaccines, largely avoiding the raft of infectious diseases that plagued earlier generations.
Yet no matter how many lives vaccines save, there is no skirting the issue. Vaccination is a medical intervention. We inject newborns and toddlers—the most vulnerable members of society, who cannot decide for themselves. Some parents worry about their kids receiving too many vaccines at once. Others are concerned by the small amounts of toxic chemicals like formaldehyde and ethyl mercury used to kill or to preserve vaccines. Some believe conspiracy theories about vaccines spreading disease. And many have been frightened by a now-discredited study accusing the MMR vaccine (also developed by Hilleman) of causing autism. Some of these concerns contain an unsettling kernel of truth. A portion of the polio vaccines that my generation—millions of children—received were contaminated with the monkey virus, SV40. Until the 1960s, polio vaccine was grown and isolated from green monkey cells. Hilleman and a colleague discovered the virus; a couple of years later, another researcher showed that the virus caused cancerous tumors in hamsters. By the time vaccine makers had replaced monkey-cell cultures with human cell cultures, an estimated 100 million of us baby boomers had been vaccinated. Fifty years later, despite much suspicion and study, the virus has not yet been shown to cause cancer in humans.[iv]...
While there may always be unintended consequences of vaccines, the role they have played (and continue to play) in saving lives over the past century has been huge. Now vaccine makers have the tools to develop increasingly safer vaccines, effective against some of the most obstinate pathogens—and they can do so more rapidly.
Adapted from  Natural Defense: enlisting bugs and germs to protect food and health (Island Press, Spring 2017)

[i]. Centers for Disease Control and Prevention, “U.S. Vaccines,” Appendix B-2, April 2015, http://www.cdc.gov/vaccines/pubs/pinkbook/downloads/appendices/B/us-vaccines.pdf, accessed August 9, 2016.
[ii]. For a video story by Maurice Hilleman, see: The College of Physicians of Philadelphia, “Mumps: Jeryl Lynn Story,” The History of Vaccines, October 29, 2004, http://www.historyofvaccines.org/content/mumps-jeryl-lynn-story, accessed August 9, 2016.
[iii]. Wayne C Koff et al., “Accelerating Next Generation Vaccine Development for Global Disease Prevention,” Science 340 (2013) doi:10.1126/science.1232910, accessed August 9, 2016, 2.
[iv]. Vicent Rancaniello, Virology (blog), http://www.virology.ws/2010/04/13/poliovirus-vaccine-sv40-and-human-cancer/, accessed October 2016.
[v]. Polio Global Eradication Initiative, “Vaccine-Derived Polio Viruses,” http://www.polioeradication.org/polioandprevention/thevirus/vaccinederivedpolioviruses.aspx, accessed August 9, 2016.

Monday, December 19, 2016

Toxic Textiles: Book review of Fake Silk

Book Review. Below is an excerpt from my recent review of:Fake Silk The Lethal History of Viscose Rayon Paul David Blanc, Yale University Press. The review first appeared in Science, 25 Nov 2016:Vol. 354, Issue 6315, pp. 977
In this slim, action-packed book, Paul David Blanc takes the reader on a historical tour that touches on chemistry, occupational health, and the maneuverings of multinational corporations. Our guide is a small, “elegant” molecule called carbon disulfide—a compound that is a key ingredient in the making of viscose (better known as rayon) and is also insidiously toxic, having devastated the minds and bodies of factory workers for more than a centuryFake Silk: The Lethal History of Viscose Rayon unveils a story that, in Blanc’s words, “deserves to be every bit as familiar as the cautionary tale of asbestos insulation, leaded paint, or the mercury-tainted seafood in Minimata Bay.” Who knew that the fabric that has had its turn on the highfashion runway, as a pop-culture joke (remember leisure suits?), and more recently as a “green” textile had such a dark side?
Rayon is a cellulose-based textile in which fibers from tree trunks and plant stalks are spun together into a soft and absorbent fabric. First patented in England in 1892, viscose-rayon production was firmly established by the American Viscose Company in the United States in 1911. Ten years later, the factory was buzzing with thousands of workers. “Every man, woman, and child who had to be clothed” were once considered potential consumers by ambitious manufacturers.
However, once the silken fibers are formed, carbon disulfide—a highly volatile chemical— is released, filling factory workrooms with fumes that can drive workers insane. Combining accounts from factory records, occupational physician’s reports, journal articles, and interviews with retired workers, Blanc reveals the misery behind the making of this material: depression, weeks in the insane asylum, and in some cases, suicide. Those who were not stricken with neurological symptoms might still succumb to blindness, impotency, and malfunctions of the vascular system and other organs. For each reported case, I could not help but wonder how many others retreated quietly into their disabilities or graves.
Yet, “[a]s their nerves and vessels weakened, the industry they worked for became stronger,” writes Blanc.  In Fake Silk, he exposes an industry that played hardball: implementing duopolies and price-fixing and influencing federal health standards. For more see here. (Though you may need a subscription or library to access the rest.)

Thursday, December 15, 2016

An antibiotic alternative? Hope through science.

Antibiotic resistance test. Image: Dr. Graham Beards
A toddler suddenly becomes deathly ill. In the ER she is diagnosed with dysentery, caused by a rare but particularly aggressive form of Salmonella. One antibiotic after another fails because the strain, picked up when her family was traveling across parts of Asia, resists multiple antibiotics; but there is an alternative new drug. Like a guided missile, the drug targets only the disease causing Salmonella. Not only that, but as long as Salmonella remains, the drug particles replicate, increasing in number until the infection subsides. Despite the carnage, the toddler’s gut microbiome remains unharmed – no need for probiotics or fear of complications like C. diff.  If Salmonella responds by evolving resistance, the drug may respond in turn engaging an ages old evolutionary dance. By the next morning the color returns to her cheeks. By evening, she is cured.
While still a fantasy here is the U.S., the scenario has been playing out in Eastern European hospitals and clinics for nearly a century. The “new” drug is a virus called a bacteriophage (or simply “phage”), that attacks bacteria. It is a cure nearly as old as life; at least as old as bacteria. Microbiologists have suggested that for every strain of bacteria on earth from the oceans to those populating our own microbiomes– there is at least one, if not multiple bacteriophages.
Viral phages infecting a bacterium. Image: Dr. Graham Beards
As diseases like TB, gonorrhea, E.coli, staph and other common infections increasingly evolve to resist our antibiotics, health care workers are fast becoming desperate for new antimicrobials that are both effective and cause minimal damage to our own microbiomes. Bacteriophages are potent antimicrobials. Once disparaged here in the U.S. and in western medicine in general, these bacteria infecting viruses are making their way back into academic and biotech laboratories. If all goes well, they may be coming to a pharmacy near you.
We now know that throughout our existence viruses have woven in and out of life – leaving their stamp on most if not all living things. By some accounts up to eight percent of our genetic material came to us by way of viruses. Yet for all the fear and harm we associate with viruses many (if not most) are phages, infecting bacteria, like those in our microbiome. Genomics is just beginning to reveal the diversity and representations of these entities in nature and within our bodies. But the role that phages can serve as potent antimicrobials is no mystery. As infectious agents of bacteria they are a normal and pervasive component of earth’s flora, and they have already saved countless lives. One day they just might save us or our loved ones.
This is only one solution. There are plenty of others in the works. Lets just hope they get the funding they need in the coming years.
Adapted from  Natural Defense: enlisting bugs and germs to protect food and health (Island Press, Spring 2017.) 

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.