The Neighborhood Toxicologist has evolved!

Please join me at my new site, Evolution in a Toxic World.  (I will no longer be checking or posting content to this site.)

Model Kay Heffernon with a soda and hot dog on Jones Beach, 

NY 1948. Photo by George Silk, LIFE photos. 

Dear Mr. Pruitt, let's talk about lead

Dear Mr. Pruitt,

Last week I wrote to you about DDT. This week let’s consider lead. Like DDT, another jaw-dropper for my environmental toxicology undergrads. You may not remember leaded gasoline. It was phasing out just as you were probably hitting the road. But I do, and I remember feeling good about asking for “unleaded” at the pump. Those were the days when the tetra-ethyl lead added to gas was called just “ethyl.” The manufactures, a combination of Dupont, Standard Oil and General Motors, branded their new company and their product with a young woman’s name, leaving out the second half – the lead — that literally drove men crazy if not to their death. The chemical helped gas burn more efficiently; a good thing. And it helped the oil industry dominate the automobile industry by pushing aside other possible fuels or fuel additives, like ethanol.

Lead is another opportunity to discuss the  struggle between those who tried to protect Americans and the nation’s workers and an industry that values profit over all. A struggle that is now something you must face almost daily. In this case Alice Hamilton, a tireless and pioneering advocate for worker health who, along with others, tried to get the lead out as early as 1925. This was just a year after workers at the so-called House of Butterflies died; one of them in a straitjacket, his brain poisoned by the additive. There is also the story of how tetra-ethyl, a product of American Industry, helped launch the Nazi Luftwaffe (leaded fuel was a necessity for their airplanes). And the story of how the industry, when asked by the surgeon general if public health impacts of the new additive had been considered, apparently assured him, sans any data, that the streets would be “…so free from lead that it will be impossible to detect..”*

Industry assurances and oil politics aside, I don’t need to exaggerate, advocate or hammer home the benefits of chemical regulation when it comes to lead.

Despite Hamilton and colleagues’ best efforts, the industry went on to use, at its peak in 1970, some 250,000 tons of lead in gasoline. That is hundreds of thousands of tons of lead pried from the earth’s crust and spewed into our air, water and soil. The sheer magnitude of lead used in gasoline was another shocker for students alerted to the problem of lead more recently via the recent news from Flint, Michigan and elsewhere. A generation who now equates lead with old pipes and drinking water. Those were the days when there was an average of 2-3 gramsof lead in every gallon of gasoline. My mother’s Country Squire, the old wood paneled station wagon, much like today’s Escalades, Land Cruisers and Suburbans (which have only slightly improved mileage) burned through about a gallon of gasoline every twelve miles. Living in the suburbs our family contributed plenty of lead to our neighborhood, the back streets of Boston and points north and south. (Back of the envelope: 10,000 miles of travel per year, 833 gallons of gas meant roughly 2000 grams, or 70 ounces of lead, a year.) Over the courses of my childhood, my mother’s car added a little less than my own body weight at the time, ninety pounds of lead,  to our environment. And that was just one car — my dad’s black VW bug (roughly 20 MPG) contributed it own fair share. I don’t think these  are numbers anyone could be proud of. No matter who you are, where you live or what political party you belong to.

By the 1960’s the national average for lead in blood rose to somewhere around 600 parts per billion (we can’t blame this all on ethyl, our homes – inside and out – were coated in the stuff as well.) It’s likely that my sisters and I carried in our blood, lead levels that would now be considered high  – although most likely,  we were better off than kids living in the city. Today, we worry about children with blood lead over 50 parts per billion. We also know that aside from the more immediate poisonous effects, even in small amounts lead can lower children’s I.Qs and alter their behavior.

That my students were clueless about leaded gasoline, is, in large part thanks to the EPA. When your agency ordered manufacturers to phase-out lead and find a replacement, it was not only an EPA victory, but a victory for all Americans. Here is Carol Browner as the final nails hit the lead coffin in 1996:

The elimination of lead from gas is one of the great environmental achievements of all time. Thousands of tons of lead have been removed from the air, and blood levels of lead in our children are down 70 percent. This means that millions of children will be spared the painful consequences of lead poisoning, such as permanent nerve damage, anemia or mental retardation.

Why even talk about leaded gasoline? Because like DDT, this was another triumph of your agency. Another victory over powerful industries that put profits over human health. Lead is clearly still a problem – particularly for municipalities and homes with aging pipes and in too many cases lead paint – legacies from our earlier generations, that sadly keep on giving. But we all still use gasoline. And, both the automobile industry and the oil industry have retained if not grown in power over the decades. I would love to provide my students with current examples of good Corporate Citizens. I’d like to say, “That was then, this is now.” There is plenty of opportunity for the corporations that impact the quality of the air we breath and must hold  responsibility for our health and for our changing climate (I understand you disagree here – so I won’t belabor this point). With nearly a century of exposure to oil combustion products – the health-science is indisputable.  As you advocate for a smaller EPA, and consider the current CAFE (fuel economy) standards, I would very much appreciate some examples to share with my public health students, so that they can rest assured that they won’t be telling their students jaw-dropping stories from the time that EPA handed its authority over to big oil and the auto industry.

Featured Image: Sign on an antique gasoline pump, advertising gasoline additive (tetraethyl lead) by the Ethyl Corporation. Photo taken at the highway rest stop on I-94 westbound, east of Bismarck, North Dakota, USA. Plazak, 2010.

*Midgley, T. Jr., 1922, Letter to Cumming, National Archives Record Group 90, 30 December 1922

Dear Mr. Pruitt, today we talked about DDT

Dear Mr. Pruitt,

I teach an introductory environmental toxicology class to undergraduate public health majors. Each week we talk about different issues from mercury to DDT and nanomaterials. And each week, inevitably, we talk about the EPA. I am a child of the 1960s, the age when it finally dawned on us that for all the benefits of modern industrial chemicals – from plastics to mosquito-free evenings — maybe there was a dark side to welcoming these new products into our homes and releasing billions of tons of new chemicals into our environment. We talk about what happened, or didn’t, before the EPA reined in pesticides, air pollutants, water pollutants. This week’s topic was DDT and the beginning of pesticide regulation.

Life Magazine ad, meant to show safety of DDT

First I need to tell you, I am not someone who eats all organic all the time. I realize that until we have better solutions, some growers will use pesticides to save their crops. And not everyone can grow (or buy,) organic. I know that not all pesticides are problematic, and more often it is over-reliance or over-use that is the problem. But I can also say this with some level of comfort because these pesticides are registered and regulated by our federal agencies, most importantly the EPA. Though, I have add that there is plenty of room for improvement! I’ve seen only a couple of applications for pesticide registration and I think even you would be surprised by the amount of missing information.

As the new administrator, I am sure you know the history of DDT, Silent Springand the emergence of the EPA. But did you know that some of the first pesticide regulations (pre-EPA) focused on “immediate” harm rather than long-term? Then the EPA began to require consideration of other “adverse” effects and environmental effects. Eventually DDT and similar pesticides were banned. Even so, we still live with their legacy. A recent study has linked DDE exposure at a young age (or even possibly in utero) with an increased incidence of breast cancer in women.

While it would be nice to be able to say “of course, we know so much more now, that can’t happen again.” That there won’t be another DDT. My students know that some day in their life-time there will be another DDT. Maybe it won’t be a pesticide. Maybe it won’t accumulate in the environment. But, some new miracle chemical or maybe even gene product will have effects that could — without pressure by agencies like yours – cause the next generation to look back with disbelief, asking how could this happen?

Making new pesticides, safer pesticides is costly with all the hoops and testing that must be done. And we’ve learned so much from past mistakes. I haven’t read much about what your intentions are towards pesticide regulation and enforcement – but the cuts proposed in EPA’s budget and some of your past efforts seem like you might lean towards deregulation. If that is the case do you really honestly believe, that this current generation and their kids, will be better off without federal regulation of pesticides? I would love to believe that industry would regulate itself – but they haven’t a good track record for self-regulation.We can learn from past mistakes, but then we have to apply what we learn. If you have some examples that show otherwise, I would love to share them with my class.

By their very nature, there will always be things we don’t know about new products. The qualities that make them useful is often their novel activity (nanochemicals are a great example of that.) Look, in the beginning, no one knew DDT would hang around for decades. Or that humans would end up with more DDT in their bodies than was permitted in the food they ate. Or that it might cause breast cancer decades later. But had producers been pushed to ask some of these questions – we might be free of these chemicals today, rather than having molecules produced over half a century ago still jiggling around in  our love handles and muffin tops.

Your family as well as mine and this current generation of college kids are all better off today than in the days before the EPA. This is thanks in large part, to your predecessors and all those who now work for you. Let’s move forward together, rather than backwards.

Best, Emily

About Twelve Percent

Ok, I’ve had it. Too many times on the news, I’ve heard something like this, “after all, 53% of white women voted for Donald Trump.” Or, "42% of women voted for Trump."  WRONG. What they mean of course is the percentage of those who actually voted. But too often that part is dropped. Like here in the New York Times "About 53 percent of white women voted for Mr. Trump, according to exit polls." As my husband says, that's asking a reader to do some work to realize that doesn't mean 53% of all white women who are eligible to vote. 

Consider that only 59% of total eligible voters in our country voted. And assume that also means roughly 59% of women  (more women than men voted so could be a little more) for which we match up woman to man almost 1:1 if not a bit more, depending on the state. And OF THOSE 42% voted Trump. Which means, about 12% or so (like I said, a little more if there are more women than men) of all women who can vote in our country voted Trump.

Or approximately: 0.59*0.5*0.42=0.123. (This also means that, roughly, only 16% of women in our country who could vote, voted for Clinton.)

One friend suggests that maybe the media is trying to hold us voters accountable when they throw around figures (for so few voting in general). Which may be the case. But with all the fake news today, it's more important than ever to be accurate with our numbers. Let's not take the percentages out of context.

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.

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.)

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.) 

Raisin Hell (and Dogs)

(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.)

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.

You say tomato, I say blight!

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.

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/

3) Read up on blight http://www.extension.org/pages/18361/organic-management-of-late-blight-of-potato-and-tomato-phytophthora-infestans#.VS1fw_nF-Uk

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 

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.

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 100^th 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.

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.