Mass Torts: State of the Art : Mass Torts Lawyer & Attorney : Vorys, Sater, Seymour & Pease Law Firm : Toxic Torts & Wrongful Death

Plaintiff's expert Martyn Smith has proposed a mechanism whereby benzene produces leukemia.

Night shift work modestly increases women's risk of obesity and thus their risk of diabetes.

Soy milk may make your baby girl grow up to be considerably less feminine.

I keep coming up with reasons to pass on my father-in-law's venison stew/boudin/sausage/etc.

It's not clear whether acetaminophen causes asthma or whether the flu is to blame.

Aspirin really does reduce the risk of colon cancer in those predisposed to it.

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Yesterday our energy partners reported on the EPA's claim of water contamination in Wyoming due to hydraulic fracturing fluids used in natural gas production. Today The New York Times is wondering whether earthquakes can be blamed on fracing. Thus it sounds like a good time to provide you some links to recent studies of the process that you may find of interest. Here goes:

Scientific American has the truth about "fracking" and thinks that engineering science has gotten ahead of safety

The comment period for New York's Supplemental Generic Environmental Impact Statement just ended and some public health advocates don't like it

Two miles underground amidst the shale and gas, where the pressures and temperatures are extreme lives a fascinating community

And some of its members traveled there via drilling muds

Finally, some public health advocates and journals tend to overlook one important aspect of the energy business - that it provides lots of high paying jobs and benefits from free laundry service to transportation to health care and often excellent pension benefits; not to mention an interesting and disciplined work environment - a big boost to socioeconomic status which bestows dramatic economic, physical and even mental health benefits that echo through succeeding generations. So let's not forget when balancing risks and benefits of fracing to add the profound public health benefits that flow from good jobs to the benefit side of the ledger.

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Illinois' "consumer expectation test" does not excuse a plaintiff from proving causation.

Chinese chrysotile asbestos workers have more than a threefold increase in lung cancer risk.

What doesn't kill you makes you live longer.

Toxicology is rethinking recent dogma and its gaze is turning towards Goldilocks and hormesis.

Market economics explain otherwise inexplicable plant-fungi interactions.

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There's little evidence that parental exposure to solvents is associated with their children's ALL.

Hospitals and clinics have take-home exposure issues too.

The endocrine disruption hypothesis: good science has its boots on and is beating back a good, but unsound, narrative

Mesothelioma does run in families.

Colon cancer is probably also caused by a disrupted gut microbiome.

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Formaldehyde has been known to be a cause of nasopharnygeal cancer for a long time but the NTP's determination that it likely causes leukemia and other lymphohematopoetic cancers is a big deal. The inclusion of styrene on the list of things "reasonably anticipated to be a human carcinogen"is the real shocker though. Back in the late 80s when the butadiene litigation was beginning to unfold there was considerable worry about whether the other big component of styrene-butadiene rubber might be a carcinogen. Numerous studies settled the question and the litigation never went anywhere (well, they sued the butadiene people instead of the styrene people). Expect styrene litigation.

Finally, the glass fiber determination brings with it a fair share of irony. For years asbestos plaintiff lawyers claimed that glass wool was a safe, non-carcinogenic substitute fiber (and I'd bet it is, actually). For more see: "12th Report on Carcinogens" or the report itself in .pdf.

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Today's scare du jour was just launched by the Center for Science in the Public Interest. They claim that the caramel coloring in Coke (and in dark beer and lots of other good stuff) is carcinogenic and ought to be banned. See "FDA Urged to Prohibit Carcinogenic 'Caramel Coloring'".

The claim can be summed up as follows: industrial caramel is unnatural and the product of scary-sounding processes involving scary-sounding chemicals; one of the resulting constitutive chemicals, 4-methylimidazole, has been found "in significant levels" of five brands of cola; 4-methylimidazole causes cancer in lab rodents; therefore, my Cherry Coke is a cancer hazard. Is there anything to it?

Well, sure enough there's a study of lab rats and mice that found small increases in the risk of lung cancer and leukemia that increased as doses (the rodents got the equivalent of thousands of cans of cola per day worth of 4-methylimidazole) increased. See "Toxicity and Carcinogenicity Studies of 4-Methylimidazole in F344/N Rats and B6C3F1 Mice". But something else very interesting happened along the way to a good health scare - something not mentioned by the CSPI.

It turns out that while there were small and at best equivocal indications that 4-methylimidazole might be associated with one or two rodent cancers there were big, statistically significant and dose-dependent associations between cancer prevention and 4-methylimidazole consumption. For example, compared to the rodents not given 4-methylimidazole the female rodents drinking cola by the barrel were essentially completely protected from mammary tumors as well as a host of other cancers. Overall, rodents on a cola binge experienced a greatly reduced risk of many cancers and saw some tumor rates reduced by orders of magnitudes compared to their cousin rats and mice not given 4-methylimidazole.

There was no call for research into the protective effects of caramel coloring. The great big silver lining wasn't even disclosed. Instead, the two insignificant bits of data showing a small risk of tumors in rodents were cherry picked from the forest of data and the big effect, a cancer-protective effect, was completely ignored.

I'll go out on a limb and predict that this scare, like the CSPI acrylamide in bread, chips and roasted coffee is going to give everybody cancer scare, is also headed for the dustbin of history.

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When it comes to cholesterol the thing to worry about is too little HDL. Your total cholesterol level can be high and your LDL can be high but if your HDL is up there you're swimming in the shallow end of the risk pool. That's what makes "Acute Decrease in HDL Cholesterol Associated With Exposure to Welding Fumes" so interesting.

The finding of a large decrease in HDL without effect upon other lipids following exposure to pm2.5 in welding fumes provides, if replicated, a biological mechanism for some of the maladies laid at the feet of pm2.5. Low levels of HDL lead to inflammation and chronic inflammation leads to a variety of illnesses like hardening of the arteries.

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The idea that a known cause of cancer, e.g. ionizing radiation, poses a risk of cancer at any dose, no matter how small, is a central thesis informing modern environmental and occupational regulations and modern, which is to say low dose, toxic tort cancer litigation. In the toxic tort context plaintiffs regularly employ the logical fallacy of the appeal to ignorance (argumentum ad ignorantiam) to prove that even the slightest exposure was risky. They say that because defendants cannot establish a safe level of exposure it follows that every exposure is necessarily unsafe. The formal name for the idea that risk doesn't drop to zero until exposure drops to zero is the linear no-threshold dose theory or LNT. The LNT theory, always longer on theory and politics than evidence is increasingly under attack. Now even NIOSH has had to concede that at least in some circumstances there is indeed a safe dose for a carcinogen.

In "Checking the Foundation: Recent Radiobiology and the Linear No-Threshold Theory" the author states "a large and rapidly growing body of radiobiological evidence indicates that cell and tissue level responses to [radiation damage], particularly at low doses and/or dose-rates, are nonlinear and may exhibit thresholds ... this evidence directly contradicts the assumptions upon which the microdosimetric [LNT] argument is based". The idea that a substance that is harmful at high levels can be harmless or better yet beneficial or protective (the idea of hormesis) at low levels is discussed at length in this month's issue of Human & Experimental Toxicology.

The claim that "if it takes an ounce to kill ten men then a drop will thousands" was itself just a theory based on the idea that carcinogenesis was a stochastic process. Getting cancer was sort of like hitting the anti-lottery and the more tickets you bought (exposures you sustained) the more likely you were to lose yet if you were unlucky enough just one ticket could do it. Like black box epidemiology LNT was simply a way to ignore the formerly incomprehensible molecular biological mechanisms responsible for cancer. Now that those mechanisms are being uncovered and understood they can no longer be ignored as they shatter one paradigm after another.

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Since it's detected at low levels in 95% of us and since Americans have been exposed to it for more than 50 years you'd think someone would have noticed if exposure to bisphenol A (BPA) were responsible for widespread illness, deformity and death. Apparently not, at least not if the findings from a recent wave of BPA studies are to be believed.

The new findings are, in no particular order, that BPA: (a) damages sperm (b) inhibits the normal development of ovaries (c) alters brain development (d) causes premature birth (e) may be a carcinogen like DES (f) damages blood cells (g) activates breast cancer cells (h) impairs the body's defenses against colon cancer especially in women; and, (i) makes offspring anti-social and neurotic. And those are just a few of the "findings" published in the last two months. Obviously the world that existed before 1950 or so, before  BPA was everywhere used to seal bacteria out of food and dental cavities, had to have been a much healthier and more peaceful one. Alas.

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Why are mice so much more susceptible to butadiene? Apparently it's because they metabolize it into potent mutagens at 200 times the rate of humans. As a result, while mice exposed to butadiene at current occupational levels promptly yield evidence of genotoxicity there's no evidence of genotoxicity in humans at current workplace exposure levels. See: "1,3-Butadiene: Biomarkers and Application to Risk Assessment".

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In vitro testing has been proposed as a way to clear out the backlog of toxicity testing on thousands of chemicals currently in use. It's quicker and cheaper and lab animals needn't be "sacrificed". The plan is to use the results to estimate the dose response curve in humans so that regulatory agencies can regulate accordingly. Too bad it won't be that easy.

In this month's Environmental Health Perspectives, Kenny Crump et al discuss the daunting task of using data from in vitro testing to set reasonably safe exposure limits. See (free): "The Future Use of In Vitro Data in Risk Assessment to Set Human Exposure Standards".

The problem of course is that it's not a matter of exposing some cells in a petri dish to the chemical of interesting and watching what happens. There are multiple pathways and multiple feedback mechanisms involving multiple types of cells that define the pathways to toxicity, not to mention any that work to offset and fix the ill effects. How many might there be and in how many ways might they interact? A model of how E. coli protects against heat shock "consists of a set of 31 differential-algebraic equations with 27 kinetic parameters, data for many of which are not yet available." Just finding these pathways will be a huge undertaking and billions of dollars in funding are being sought over the next decade to find and elucidate them.

Nevertheless, the authors conclude: "Use of in vitro data in risk assessment has great promise toward allowing chemicals to be tested more quickly and cheaply and for reducing or eliminating the need for subjecting animals to toxic insults. It is our hope that the bar for accepting approaches based on in vitro data will not be set too high. In view of the numerous serious limitations of current approaches, results from these methods based on whole-animal data should not be held up as gold standards. This point is particularly important considering that almost all whole-animal data are obtained from high doses that may operate through different sets of [toxicity pathways] than do low doses."

That last sentence is the key. We're entering a whole new world of toxic torts. One in which many heretofore innocuous chemicals will be claimed to be toxic at very low doses.

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Apparently, whether you get them or not depends on the microbes that live in your gut.

It may not make sense intuitively (undoubtedly a common problem in times of crumbling paradigms) but the bacteria in your intestines may decide whether your skin responds to UV damage with wrinkles or is instead rejuvenated. See "Probiotics for Photoprotection".

Interested in how the right gut microbes suppress central nervous system inflammation and how the wrong ones cause just the sort of chronic brain and spinal cord inflammation thought to be responsible for MS? Read: "Proinflammatory T-Cell Responses to Gut Microbiota Promote Experimental Autoimmune Encephalomyelitis". Here's one of many interesting takeaways: "... mammals are colonized for life with extraordinary multitudes of indigenous bacteria, and the contributions of this enormous and diverse ecosystem to human health remain poorly understood. Recent studies have launched a revolution in biology aimed at understanding how (and more importantly, why) mammals harbor symbiotic bacteria."

Take a mouse predisposed to rheumatoid arthritis and make it germ free. No rheumatoid arthritis. Then expose it to a single microbe, the segmented filamentous bacteria, "and arthritis rapidly ensued." That was the finding of "Gut-Residing Segmented Filamentous Bacteria Drive Autoimmune Arthritis via T Helper 17 Cells". And for a real eye opener read "Segmented Filamentous Bacteria Shape Intestinal Immunity". How could two genetically identical mice have dramatically different immune systems? By having different microbes in their guts - as in the case of B6 mice from two different vendors.

Memo to self: look into whether different sources of B6 mice might correlate with different results re: butadiene's carcinogenic potential.

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There's a remarkable but necessary admission in this month's Environmental Health Perspectives.  It is that that a new (some would say old) paradigm has emerged; that pathogens, sometimes in concert with what for 40 years have been known as toxicants, are responsible for a very large portion of human suffering. Unable to deny any longer that diseases of nature inflict a staggering toll on humanity the "NIEHS Office of the Director will be working with division leaders to develop an initiative on infectious disease and environmental health—to incorporate infectious disease into the toxicological paradigm."

The editorial points to "A Niche for Infectious Disease in Environmental Health: Rethinking the Toxicological Paradigm" just published in the same journal. It's a call for the study of infectious diseases in environmental health research. Ultimately it's a recognition that the simple (and simplistic) models of many diseases are collapsing under the weight of modern microbiology. It's an admission that "the complexity of real-world exposures and multifactorial health outcomes" cannot be captured by the simple one-to-one associations that ruled environmental health research for the past four decades.

Years ago real insight, real genius (at least when it came to environmental illness) was replaced by a sort of blue collar approach to science in which grotesquely simplified statistical data dredges could be automated so that a never ending stream of putative causes of human suffering could be manufactured, studies and regulated. Some of the techniques were so malleable that clever researchers could not only manufacture causes, they could also decide in advance what the causes would be. Now, the real causes are uncovered and it often turns out that our ancient enemies, pathogens, were to blame all along.

The long war continues, but now the scales that covered environmental science's eyes for decades are falling.

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