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

We had another jury trial and thus were offline for a few weeks but it didn't take long to dig up something I hope you'll find of interest. I ran across it in a recent opinion by the district court in the In Re Fosamax Product Liability Litigation. What is it? It's a duty to actively mine the FDA's data for a signal, a hint, that your approved pharmaceutical product might be associated with an adverse event.

As an initial matter I almost didn't get to the interesting part of In Re Fosamax Product Liability Litigation thanks to this eye-roller: "In applying the nine Bradford Hill factors, he [Dr. Cornell] reviewed Plaintiff's medical records from 1996 to present, the office notes and depositions of her treating physicians, and 'past and current medical literature on the topics of osteopenia, osteoporosis and their prevention and treatment with bisphosphonate drugs including alendronate'". Which was followed by: "The methodology Dr. Cornell used is sufficiently reliable because the Bradford Hill criteria are 'broadly accepted' in the scientific community 'for evaluating causation, and 'are so well established in epidemiological research". This business of giving expert witnesses a pass for doing nothing more than invoking the great epidemiologist's name and saying that their method consisted of peering at the evidence through the supposed lens of Hill's "criteria" is utterly appalling but it would take several paragraphs to explain and we've done it before so I'll leave it at that.

The portion worth pondering is found further down in the discussion of defendant's motion to exclude a different expert witness, Dr. Madigan. Madigan is a statistician from Columbia with an impressive resume. He was tasked with assessing "whether a signal of problematic oversuppression of bone turnover and associated [atypical femur fractures (AFF)] . . . existed for Fosamax, using industry standard pharmacovigilance techniques and data sources, and the adverse event terms selected by Merck to internally evaluate the same" and whether "the strength of that signal, if any, in comparison to the signal, if any, for such events in other products indicated for the prevention and treatment of osteoporosis". To identify and evaluate such a signal Madigan took several medical terms considered by the defendant to be possible indicators of "oversuppression of bone turnover" and/or AFF and, using a program called Qscan, ran them through FDA's Adverse Event Reporting System ("AERS") database looking for associations with Fosamax use.

The data revealed "the presence of a clear signal for oversuppression of bone turnover and associated atypical femur fracture events utilizing the terms selected by Merck for such analysis. By standard metrics of 'signal' detection, the signal is strong, consistent, and not ambiguous. Of perhaps greater concern, the signal was striking in comparison to that for other drugs indicated for the prevention and treatment of osteoporosis. As early as 2001-2002, the spontaneous report data for Fosamax provide signals for a number of indicators of suppression of bone turnover. For the comparator drugs, such signals either never appear or appear years later." As Qscan (or similar software) data mining is widely used (and often mandated in the pharmaceutical industry) and as peer-reviewed papers arising out of data generated by the software had been published the court concluded that "data mining in pharmacovigilance" is a reliable method. Fair enough.

The excitement comes in the next paragraph in which the court concludes that Madigan's testimony "fits", and so is relevant to, an issue in the case because it informs the question of whether the defendant should have warned of the later-perceived risk of AFF. The court thereby implicitly held, I think, that the defendant had a duty to mine the FDA's data as early as 2001-2002. In other words, the existence of powerful data mining tools capable of uncovering an early signal of a possible harm associated with defendant's product created a duty to use such a tool. Ultimately, that's a duty to discover any statistical association between your product and some harm in the FDA's (admittedly accessible) that might be causal and to thereafter warn about it; and it's a duty to mine not only your data but any data that might shed light on your product.

It's hard to know what to make of a duty to mine big data. Obviously it's a potential problem for defendants. "Should have known" is no longer what was reasonably knowable (by humans). Instead it's what was knowable given a duty to use "powerful data mining and signal detection capabilities" including "a powerful query-by-example module that allows users to mine and visualize data through inquiries utilizing multiple case data elements." We're already in the middle of something similar; a case in which the plaintiff is demanding to see all of the death certificates collected by our client's benefits department claiming that we had, or had assumed, a duty to look for mortality patterns among our workers that might suggest a work-related etiology - the idea being that the plaintiff's decedent had succumbed to one such workplace illness and we either knew or should have known from looking at the death certificates that danger had been lurking.

And of course there's the problem of experts coming in after the fact and running term after term after modified term in varying combinations until an association emerges. Working backwards they'll then construct a narrative about why the set of terms eventually founded to produce the association would have been the obvious choice at the time the data mining ought to have been done; and the failure to look for such an obvious potential association will thereafter be cast as willful ignorance.

Then there's the bane of defendants in all latent disease cases - the hindsight bias. It's the "knew it all along" fallacy that emerges when a jury is shown the picture on the box before they see the puzzle pieces inside. They can't thereafter imagine that the few anecdotes and case reports that constitute a handful of the pieces that make up the picture on the box could ever have suggested mere randomness. That means the ability to mine huge amounts of data will make signals easier to find while making it harder to mount a successful state-of-the-art defense any time Qscan can tease a signal from the data.

Data mining has led, and will lead to startling discoveries in the sciences. In the law it may well lead to startling liabilities - especially if defendants are made to pay for harms foreseeable only by the most powerful software available. Ponder that.

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In fact, it is so favorable that the post hoc ergo propter hoc fallacy is enough to carry the day. Consider Clements v. Norfolk Southern.

Plaintiff, an employee of a railroad, either slipped off or fell off a tire. How he came to be on it is not made clear but the tire was four feet in diameter and off it he went. At trial he testified that prior to the accident he had been free of back pain but was afflicted by pain, and a herniated disk, thereafter. Though he had no expert willing to opine that his fall was the cause of his sore back the court held "[i]t is not beyond the province of an ordinary person that falling off a four foot high tire could cause a herniated disk."

While it has long been the case that "experts" can be found who are willing to testify that tying one's work boots will readily cause a herniated disk or that falling off the roof of a two story building can't possibly cause a herniated disk - and one side or the other of every scenario in between - courts ought not give up on the quest for sound science in such cases. That's because science, at long last, is starting to test various theories concerning the causes and appropriate treatment for herniated disks. So far, evidence-based assessments are giving the "province of an ordinary person" a thrashing.

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One of the longstanding disputes in toxic tort litigation revolves around whether or not animal models are good (i.e. predictive) models for assessing the likely outcome of exposures to the chemical in question. As we've written previously the 1,3 butadiene question hangs crucially upon the question of whether or not workers in SBR (styrene-butadiene rubber) plants are likely to metabolize butadiene the same way as B6C3F1mice. However, isn't there an assumption here that goes unexcavated?

Aren't we assuming that all people metabolize things like butadiene the same way? Undoubtedly. But guess what? Thanks to differences in the bacteria in their gut, their diets and likely other yet undiscovered factors, people metabolize things differently. Read all about it at: Human Breath Analysis May Support the Existence of Individual Metabolic Phenotypes

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Back to the Burks problem from the last post.

Is there something wrong with shifting one element of plaintiff's burden of proof (defendant-specific "but for" causation in the case of alternative liability) to the defendants when nature may well have been, but probably wasn't, the cause of plaintiff's injury? The trial court in Burks didn't think so. After all, the rationale behind the decision in Summers v. Tice to engage in such burden shifting was that as between a defendant who committed a wrong, and an innocent and wronged plaintiff, the risk of loss ought to be borne by the wrongdoer. So why would it be necessary that all of those potentially responsible for the harm be present? After all, thanks to Summers the wrong (breach of a duty) has been decoupled from causation in the "wrong + 'but for' causation = legal causation" calculus.

Thus, if the defendants each breached a duty, and collectively the probability exceeded 50% that they, as opposed to nature, were responsible for the plaintiff's C. sakazakii infection, you have everything you need for legal causation and alternative causation ought to apply since plaintiff can't possibly prove where the bacteria came from, right? I don't think so.

Let's go back to David Hume and causation. Remember his quote: "We may define a cause to be an object, followed by another, and where all the objects, similar to the first, are followed by objects similar to the second. Or, in other words, where, if the first object had not been, the second had never existed." This is what we all today recognize as causation, or counterfactual causation; if "x" hadn't happened "y" wouldn't have followed. Easy enough.

Now think about causation in the case of Summers - in which the burden of proof was shifted from plaintiff to the two hunters, each of whom had failed to handle his firearm responsibly and had discharged his weapon in plaintiff's direction. What happens if the second hunter "had never existed"? It doesn't change anything. Causation falls on one defendant instead of two. The cause of plaintiff's harm would have been the act of the first hunter and liability would have been imposed on defendant by his own hand as he'd be the only cause left. But what happens in the Burks scenario if a defendant goes missing?

The Burks plaintiff sued two suppliers of a product potentially contaminated with C. sakazakii, a common environmental pathogen, and the probabilities are such that it's slightly more likely (51%) that plaintiff's infection was due to the contamination of one of defendants' products. Let's say the probabilities were 26% that it came from the first defendant, 25% from the second and 49% from Mother Nature who sprinkles the bacteria around many homes. The district court in Burks thought alternative liability would apply in such a case because the source of the pathogen was, collectively, more likely than not the defendants. But what if one of the defendants' breach of a duty "had never existed"? Suddenly the remaining defendant is not liable. What was determinative of liability?

If I've got this right then the rule in Burks is as follows: Whether or not you are liable for plaintiff's injury hangs on the conduct of third parties over whom you had no control. Right? And that can't be the law. Or is liability independent of likelihood such that it goes all the way down? More on that tomorrow (or the next day...)

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Two yellow pads are full of notes, diagrams, thoughts and arguments and still the answer eludes me. So, rather than continue not to post anything about all the interesting stuff going on in mass torts while I try to figure it out I'll just throw out what I've got so far over a series of posts and move on to something less difficult (and likely more interesting). On then to the question that's been bugging me for a month.

Should alternative liability, in the form of burden of proof shifting, apply in the following case: (1) a neonate contracted a Cronobacter sakazakii infection and was seriously injured; (2)  C. sakazakii is a ubiquitous pathogen and readily forms biofilms on stainless steel, inside household water pipes and upon other surfaces (3) C. sakazakii infections in neonates have also been repeatedly traced to PIFs; (4) plaintiff's experts opined that it's more likely than not that the source of C. sakazakii was the powdered infant formula (PIF) fed to the neonate; (5) PIFs are not sterile since the process of sterilization would destroy the nutritional value of the PIF; (6)  there were two or more suppliers of PIF whose product was prepared for the neonate; (7) none of the remaining PIF fed to the newborn, nor any of the lots from which they were drawn, were found to contain C. sakazakii; and, (7) the wrong complained of was a failure to warn that full term neonates, like the plaintiff, were at risk of C. sakazakii infections.

Alternate liability analysis often begins with Summers v. Tice. In that case both hunters who had fired their weapons in plaintiff's direction had been sued and both could be shown to have breached their duty to safely handle those weapons. Because it was impossible for the plaintiff to show whose buckshot was responsible for his injury, and because it was deemed just that the consequence of that impossibility fall on the culpable defendants rather than the innocent and injured plaintiff, the court held that the defendants, rather than the plaintiff, should bear the burden of proving from which shotgun the pellets had originated. Fair enough.

Here, in Burks v. Abbott Laboratories, both of the manufacturers of PIF consumed by the plaintiff had also been sued. Furthermore, neither's product bore a warning about the hazard which plaintiff claimed they had a duty to disclose. However, not all the possible sources of C. sakazakii (Mother Nature being judgment-proof) were before the court. Nevertheless, the court held, though it "located very little authority on this specific question" that  the determination of whether it was more likely than not  that the source of plaintiff's C. sakazakii infection was the defendants' PIF should be applied to the defendants collectively.

Ponder the consequences. Let's say that 51% of all C. sakazakii infections in neonates are due to PIFs even when C. sakazakii can't be isolated from the product or the lot from which it was drawn, and that 49% of all C. sakazakii infections in neonates are due to C. sakazakii found in the household water used to reconstitute the PIF or on kitchen surfaces. Also, assume the warning could fairly be said to be lacking (which in this case is not at all a given and in fact raises as many questions as stacking defendants to get to the 51% threshold - but that'll be addressed in subsequent posts).

If there's only one supplier of PIF there's no need for alternative liability so assume there are at least two. But what happens when you start dividing up the 51% among the defendants? Unless one of them was responsible for ~99% of the product the result is that you've stacked two defendants who might, but probably didn't, have something to do with plaintiff's infection and handed them all of the liability for it. Is that fair? What if there were 100 suppliers? And what's the justification for stacking defendants? Is it because they're in the same business? If so, how similar must their businesses be to permit such stacking? If in order to get to a 51% likelihood as to the source of the infection you had to stack PIF manufacturers with stainless steel kitchen appliance manufacturers (because C. sakazakii happily lives on stainless steel and creates biofilms that makes it nearly impossible to remove with household cleaning products) could you justify handing them the burden of proof by saying they were all in the food business? 

Or what about reducing defendants' liability by Mother Nature's share? Would that solve the "overdeterrence" problem? What follows from the fact that the potential for these sorts of infections, due to the nature of pathogens, is essentially binary (you get it or you don't) and not of the dose-response variety seen in typical mass tort cases?  These are the sorts of questions that have led to a lot of head scratching but so far few answers.Over the next couple of days I'll type up more of these questions and the paths down which they lead (at least the ones I've thought of and followed).

How a fact pattern like the one in Burks gets resolved is I think a very big deal. That's because an awful lot of diseases laid over the last forty years at the feet of man-made substances and bad habits turn out to have been due to pathogens all along. It also appears we're entering an era in which old scourges reemerge thanks to having evolved antibiotic resistance and new ones arise thanks to globalization.  The resulting morbidity and mortality will makesevery other mass tort pale in comparison and so far juries aren't having much trouble blaming defendants for the depredations of Mother Nature's tiniest critters. We think there's a wave of litigation coming in which plaintiffs will assert liability for facilitating the transmission of pathogenic agents. The answers to questions like those posed by Burks will be critical in determining how it all plays out. 

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Here's some good news.

Though at first they decided not to hear plaintiff's appeal, the Texas Supreme Court has reconsidered. Hopefully that means there'll be an argument about the Dallas Court of Appeals' interpretation of Borg-Warner v. Flores in its Bostic opinion wherein it held that every putative cause to which liability may legally attach must be a "but for" cause.

The problem with Bostic, for asbestos claimants or any other claimant asserting a cause of action against multiple defendants each responsible for an act which was potentially sufficient to have caused plaintiff's injury, is that it created a rule whereby a plaintiff could not recover from any defendant so long as more than one defendant put in motion a series of events that could have lead to plaintiff's injuries. As we've been saying for months, the idea that if three defendants each negligently and separately start a fire capable of burning down the plaintiff's house she can't recover from any of them for the destruction of her house because she can't prove which one was the "real" cause is not only unfair, it hasn't been the law in Texas for a very long time. Anyway, we'll report on the briefs, the arguments and the result as the case proceeds.

In the meantime, we've been speculating about why the Court decided to give Bostic a second look. My pet theory is that someone dug into Dow v. Abutahoun, an opinion just a week or so old (and also from the Dallas Court of Appeals) and decided that for the first time since Havner a philosophical discussion about causation is in order. In Abutahoun the appellate court held that our Chapter 95 (triggering a requirement that plaintiff prove control over the contractor employee's work and actual conscious knowledge of the risk created) applies to a case in which employees of the premises owner create, or contribute to, the hazard of which plaintiff complains; so long as it was the same improvement to real property on which both contractor's and premises owner's employees were working. The idea seems to be, again, that when a defendant creates a risk of harm indistinguishable once manifest from those created by others, then the plaintiff bears the burden of proving that the putative harm was the "real" harm. That hasn't been the law and we doubt that the legislature intended such a result when it enacted Chapter 95. We'll see.

Finally, lest you think we've gone in the tank for plaintiffs, we'd note for the record that in both cases we'd hold for the defendant if we got to wear the robes - but we'd do it on different grounds. While it's impossible to say which fiber or group of fibers caused any given case of mesothelioma, it's easy for all sides to calculate the risk posed by any given exposure. And nowadays the exposures we're fighting over are typically minuscule and the risk associated with them are literally about the same as having a large meteorite explode 25 miles above your head. Which is to say that they've fallen to the point of simply being among those "ordinary risks of life" that make this life so interesting and so terrifying.

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In the run up to the trial of a case in which we're arguing that the B6C3F1 mouse ain't a man and 1,3 butadiene ain't a human carcinogen just because it causes cancer in the B6C3F1 mouse, out comes "Mice Fall Short as Test Subjects for Humans’ Deadly Ills" by Gina Kolata of the NYTimes. And it's a bombshell. Kolata reports on the paper "Genomic responses in mouse models poorly mimic human inflammatory diseases" and its central finding that immune responses in the mouse, including those related to heart disease and cancer, are no more closely correlated with human responses to the same stimuli than the roll of a pair of dice. It's the long-sought explanation as to why e.g.

"every one of nearly 150 drugs tested at a huge expense in patients with sepsis has failed. The drug tests all were based on studies in mice. And mice, it turns out, can have something that looks like sepsis in humans, but is very different from the condition in humans."

Good stuff, though not all that surprising if you've been following the sad tale of the development of drugs that cure cancer in mice yet have no effect in humans. And it doesn't mean that all scientific studies done on mice are worthless. Far from it. The ability to produce for example so-called knockout mice, rodents lacking a particular gene required to make a particular protein, allows an otherwise forbidden glimpse into the workings of the tiny chemical factories that we call cells. Nevertheless, the study does shatter the assumption that those little factories in mice run just like their counterparts in humans.

However, that's not the end of the story. If you read the whole thing you'll find this:

The study’s investigators tried for more than a year to publish their paper, which showed that there was no relationship between the genetic responses of mice and those of humans. They submitted it to the publications Science and Nature, hoping to reach a wide audience. It was rejected from both.

... reviewers did not point out scientific errors. Instead, [one of the authors] said, “the most common response was, ‘It has to be wrong. I don’t know why it is wrong, but it has to be wrong’ ”

which leads to our final point. Daubert's peer review factor was intended to serve as an independent indicator of reliability. The Court assumed that disinterested scientists on the lookout for bad science served as gatekeepers of the journals through which "scientific knowledge" was disseminated. Perhaps when there were far fewer journals and far fewer academics desperate to be published peer reviewers served such a function. Nowadays they too often serve the status quo - barring from publication the sort of disruptive findings that would discomfit the guild they serve. Thus, if we're not careful, does Daubert risk being effectively transmuted, at least in part, into Frye - i.e. a test of general acceptance rather than a test of sound science.

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The publication of "Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis" in the British Medical Journal should be sobering news for twenty-first century public health advocates. The results of the biggest and most thorough study thus far to investigate what happens when people switch from animal fats to vegetable oils couldn't be more clear. Those who heeded the advice to switch from saturated fats to polyunsaturated vegetable oils dramatically reduced their odds of living to see 2013.

What happened? Fifty years ago the medical community did an about-face (it had previously thought the evidence equivocal at best and so cautioned against jumping to conclusions) and instead went all in on polyunsaturated fats. It reasoned that since (a) cholesterol is associated with cardiovascular disease and (b) polyunsaturated fats reduce serum cholesterol levels, it inescapably followed that (c) changing people's diet from saturated fats to polyunsaturated fats would save a lot of lives. In 1984 Uncle Sam got involved - Time magazine reported on it in "Hold the Eggs and Butter" - and he made a big push for citizens to swap out animal fat in their diet for the vegetable variety and a great experiment on the American people was begun.

Assuming the inferences drawn from the Sydney Diet Heart Study (~60% increase in risk of death by switching from animal fats to vegetable oils) apply to Americans and considering the population at risk of death from cardiovascular disease (~37% given recent NHANES data) we can't think of any mass tort, or combination of mass torts, that has produced as much harm as the advice to change to a plant oil-based diet. Maybe some clever lawyer will find a way to use the tort system to quell the fervor of those armed only with a desire to do good and evidence of an association between something they don't like and something else they don't like. We won't be holding our breath. But we will be hoping that those seeking to impose lean body styles and low salt diets on their fellow countrymen take a good long look at the polyunsaturated vegetable oil data before they order their riders to sally forth on the next crusade.

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Getting the causation arrow pointed in the right direction: obesity leads to vitamin D deficiency and not the other way 'round.

Happy TRAIL to Pharma - homeruns are still possible with small molecule drugs.

Whew, no cases of rabies, plague, polio or hemorrhagic fever this week. Then again, only 1 person died in all of Miami last week?

Hormone replacement therapy for chronic illnesses gets a "D" from the USPSTF; and that included so-called "bioidenticals".

H. pylori infection more than doubles the risk of colon adenocarcinomas.

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