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

What if there was a drug that could change a consequentialist into a deontologist? In other words, what if you gave this hypothetical drug to someone and he went from being a "needs of the many outweigh the needs of the few" sort of guy to a right v. wrong, rules sort of guy? Now what if that drug was prescribed based soley on the perfectly sound decision to relieve him of depression?

To grossly oversimplify, giving serotonin-boosting anti-depressants turned consequentialists (yes, I know there are more flavors of them than of ice cream at Baskin-Robbins but those flavors are just their common deontological side peeping through in different places) into right/wrong thinkers. Better (depending upon your perspective) yet, it made them more rational in "the greatest misfortune that may befall a man is great good fortune for his neighbor" sorts of experiments in which people are tested to see if they'd cut off their own noses to spite their neighbor's face. See: "Serotonin Selectively Influences Moral Judgment and Behavior Through Effects on Harm Aversion". ht: Marginal Revolution

Those are pretty big changes. They affect politics, friendships and so world views. I brought it up though not to discuss liability for making or prescribing such beneficial medicines but rather, I must admit, for a wholly different purpose - to very briefly discuss picking a jury. My number one rule of jury selection, from the defense perspective, is to identify and get rid of depressed veniremen. They tend not to care about rules and to be far too willing to cut off your client's ear and thereafter paint their masterpieces out of piles of her money.

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Without a randomized controlled trial we may never really know the answer to that question though maybe the complex systems / molecular biology people will get it worked out one of these days.

We will however get to find out if the data on which the RECORD trial (Rosiglitazone Evaluated for Cardiovascular Outcomes in Oral Agent Combination Therapy for Type 2 Diabetes - don't ask me how that works out to "RECORD") was based had been properly characterized before being analyzed. In "Regulatory Action on Rosiglitazone by the U.S. Food and Drug Administration", the announcement of new tighter restrictions on Avandia and the end of the TIDE trial, it was also disclosed that the FDA "is requiring an independent readjudication of end points at the patient level" of the RECORD trial's data. While the RECORD trial apparently established the noninferiority (NI) of Avandia versus the standard treatment, claims of design flaws that biased the results in favor of Avandia, data cherry-picking, and worse were subsequently raised (see "The Doctor Doth Protest Too Much, Methinks") .

What all this dredging and now reclassification-to-be-followed-by-redredging will reveal is anyone's guess and at best it will only lead to a posthumous vindication. The more important question is how will the battle between those who hold epidemiology to be a source of actionable knowledge and those who hold it to be a source of testable hypotheses play out. On one side of the debate, at least in the Avandia context, are idealistic academics. Their presentations to FDA were filled with lots of exclamation points, suspicions and worries about the rich and powerful exploiting the poor, sick and vulnerable. On the other side are the practitioners, pragmatists and industry scientists. They (to ruin my metaphor) played Spock to to the anti-Avandia group's Captain Kirk.

Will Avandia wind up with a pardon? If so, this episode may in hindsight turn out to have been the last stand for a methodology that for 40 years reliably generated the "knowledge" needed to support a particular world view; a methodology which has now gone decades without a big hit (e.g. asbestos). If not, and should Dr. Nissen's view prove to be the accepted one, the conclusion that the approval of Avandia was "one of the worst drug safety tragedies in our lifetime" resulting in up to 47,000 needless heart attacks could reignite a "science" that for three decades ushered in wave after wave of mass tort litigation. Whichever way it turns out I'm guessing it'll be Avandia's lasting legacy.

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To test the hypothesis that vitamin D plays a role in protecting people from cancer wouldn't it be sensible to monitor the serum levels of the vitamin in thousands of subjects and see if it's related to their risk of cancer? It's been done and the results are in.

"Serum Vitamin D and Cancer Mortality in the NHANES III Study (1988-2006)", the work of the NCI's Division of Cancer Epidemiology and Genetics, reports that whatever the levels, whatever the latitude and whatever the race among 16,819 participants across the Americas there was no evidence that vitamin D prevented cancer.

Of course, epidemiology being epidemiology, if you want good news on vitamin D and cancer all you have to do is open the next journal and find "Vitamin D in Health and Disease" and you can feel better about taking your vitamins as it reports, upon reviewing the literature, a protective effect not only from breast and GI cancers but heart disease, diabetes and more.

And so it goes.

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Workers exposed to trichloroethylene (TCE) who carry at least one copy of the GSTT1 allele are reported to have an 88% increase in risk of renal cancer in the new paper "Occupational Trichloroethylene Exposure and Renal Carcinoma Risk: Evidence of Genetic Susceptibility by Reductive Metabolism Gene Variants." Those workers without the polymorphism had a slight decrease in risk. Given that the allele occurs on a gene coding for cysteine β-lyase, which plays an important role in the metabolism of TCE among other molecules, the finding demonstrates biologic plausibility as well as increased risk.

So back to yesterday's post about risk : which risk, if any, would be relevant in a TCE toxic tort case? The risk given to all workers collectively; the risk at a particular range of exposure; the risk given to those carrying the polymorphism; or, the risk to those with the polymorphism exposed at high levels? And could it be the case that one risk is relevant to the question of whether a defendant's conduct was reasonable while another was relevant to the question of causation? How would that work?

However it works, as the causes of individual susceptibility are identified expect these sorts of challenges to multiply. 

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That's it for Avandia. The FDA has put the TIDE trial "on full clinical hold and the regulatory deadlines for its conduct are rescinded." The plan is to reassess the data from the RECORD trial to see if reliable "ischemic risk can be obtained from [] re-adjudication..." In Europe physicians have been directed to stop prescribing the drug. Meanwhile, in the U.S., patients will still be able to get the drug if they are already on it or have tried other drugs like pioglitazone without success.

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Glioblastoma multiforme is an aggressive and invariably fatal primary brain cancer. The cause(s) of glioblastoma is (are) unknown but one factor is strongly and consistently associated with a decreased risk of the cancer. That factor is the consumption of caffeinated tea and coffee; and the association is dose-dependent. Men were reported to have a 41% decrease in risk while women experienced a 26% decrease in "Coffee and Tea Intake and Risk of Brain Tumors in the European Prospective Investigation into Cancer and Nutrition Cohort Study" just published in The American Journal of Clinical Nutrition. Those numbers are consistent with the findings reported in "Coffee, Tea, Caffeine Intake, and Risk of Adult Glioma in Three Prospective Cohort Studies".

What's with all the good news about coffee and tea? It stands in stark contrast to the epidemiology published in the 1970s and early 1980s. Back then the literature was full of reports linking coffee in particular to pancreatic cancer, kidney cancer, colon cancer, diabetes, heart attack and bladder cancer. The difference perhaps is due to the fact that modern studies involve huge cohorts and assessment of exposure (dose) is much more rigorous. Yet what should be made of all the big studies of non-coffee drinking Seventh-Day Adventists and their decreased risk of all manner of maladies? Only that something besides skipping coffee is at work.

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Despite the fact that the Texas Supreme Court in Merrell Dow Pharmaceuticals, Inc. v. Havner wrote "[w]e do not hold, however, that a relative risk of more than 2.0 is a litmus test..." many lawyers and some courts believe that Havner (and even Daubert) require that plaintiff establish epidemiological evidence of a "doubling of the risk" before she can establish so-called specific causation. In my view all those two courts ever said was that if you wanted to play the game of epidemiological causal inference then you had to play by epidemiology's rules; and, furthermore, that if all you had was probabilistic evidence then that evidence had better show that defendant's product probably did it.

Whatever the interpretation, we mass tort lawyers often wind up fighting over whether there has been a doubling of the risk. One thing we're just beginning to fight over is "when do you measure the risk?" Take for instance the Women's Health Initiative and hormone replacement therapy (HRT).

Depending on when you decide to look HRT either caused an 80% increased risk (after one year of treatment) of coronary disease or a 30% decreased risk (after five years) of coronary disease. So how do you choose which risk is the "real" one?

In what promises to become an epidemiology blog posted for free at Epidemiology is a copy of "The Hazards of Hazard Ratios". In it the author makes the point that hazard ratios, an approximation of risk ratios, often vary over time and may be subject to biases, as when, hypothetically, over time the exquisitely sensitive, by virtue of suffering the malady earlier, manage to be deselected from subsequent years' calculations.

The phenomenon is well known to those doing benzene litigation. Had the study of the Pliofilm workers been done today the very same cohort would demonstrate a relative risk less than 2.0 quickly trending towards 1.0. The obvious retort is that "latency" somehow is responsible but that doesn't explain the fact that no member of the cohort has developed leukemia in decades. The most sensible answer is that those susceptible of getting it get it and those who aren't don't just fail to get it - they can't.

In other words, the distinction in toxic torts between "general causation" and "specific causation" is likely often (if not usually) a false one. Thanks to the laws of physics, bullets can reliably be said to be a general cause of bullet holes in people since all are susceptible to the effect. The same cannot, however, be said of benzene or HRT. Apparently they only increase the risk (perhaps to 1.0) in those people who, due to genetics, epigenetics, microbiota, environment or some other factor(s), are primed to produce the effect while simultaneously imposing an increase of 0.0 on everyone else.

So how, other than flawed post hoc "reasoning", do we determine whose injury was caused but for an exposure? Biomarkers have clearly failed of their promise. Now what? The way things have been going I bet it'll look something like this: "Discovering Graphical Granger Causality Using the Truncating Lasso Penalty" but maybe we'll get lucky and it'll look more like: "Causal Diagrams and Change Variable". In the meantime plaintiffs without biomarkers need to do a better job of demonstrating how they are like those in the time interval with the biggest risk.

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Remember "The Story of Cosmetics" - Sophistry At Its Finest? Well, there's a new epidemiological study of cosmetologists that throws cold water in the face of the cosmetics scare. In "Cancer Incidence in Female Cosmetologists and Manicurists in California, 1988 - 2005" researchers report a 16% decrease in the cancer incidence among 325,228 licensees. Even when sorted by cancer site no large increase for any cancer could be found though small increases were noted for thyroid and lung cancer.

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What does it mean to say that I've given someone a 1 in 1 million risk of death? Is he now just 99.9999% alive? Is he 0.0001% dead? Is either a "loss"? Must we await the verdict of the Fates to decide the reasonableness of my conduct? If so, why does some other agency decide whether an act in the past was good or bad?

What does it mean to say that I've given one million customers a 1 in 1 million risk of death? Is my conduct judged myopically on the basis of the one who died; or, shall we consider the 999,999 who wound up with a useful product and suffered no harm? And how is my conduct to be judged? Shall we add up all the good, subtract out the bad (consequence's books having been audited by the trial court), and have the jury decide whether my decision-making was, being Monday morning after all, "good" in light of the final tally?

If 1 in 1 million is too risky then so is getting out of bed in the morning. Yet 1 in 1 million is 300 American lives nonetheless. And if 1 in 1 million is a reasonable risk why isn't 1 in 100,000 or 1 in 1,000 or 1 in 10? Where do we draw the line, and why?

Does it, or should it, make any difference whether I actually knew the person on whom I imposed a risk? Does the answer change if the risk materializes? Does it, or should it, make any difference whether I actually estimated the risk before imposing it? Why do jurors punish the diligently knowledgeable while being far less wrathful towards the consciously ignorant? What, if anything, should the law do about it?

Ultimately, how should courts deal with the risks we impose on each other in this world of inevitable risks? A very good discussion can be found in "Statistical Knowledge Deconstructed".

I have one quibble and a few takes. First, the effort seems sometimes to be aimed at reconciling a Bayesian decision-making approach ("degress of belief" tending to sound rather appealingly deontological to me) with a consequentialist ex post assessment of the ultimate utility of an act. Consequentialism isn't generally thought to be informative on the ex ante side of decision-making - thus my objection to "... I mean to endorse an epistemic and (thusly) Bayesian conception of risk, not a frequentist conception". Second, his comments about cost/benefit analyses are dead on. Companies are abandoning the process and adopting "Nobody gets hurt, ever!" policies instead. One has to wonder about a legal system that advantages willful ignorance. Third, his suggestion that we let risk more openly inform determinations about where an act falls along the intentional - reckless - negligent - non-negligent spectrum would be especially helpful in mass tort cases in which risks are widely distributed.

Finally, we are in the midst of a scientific revolution in which the product of biological systems are being discovered to be unpredictable and invariably greater than the sum of their parts. Emergent phenomena arising out of vastly complex systems means that the balance sheets needed to make a consequentialist assessment of an act can never be closed nor the credits and debits ever intelligently summed. Perhaps then, like the earth's most ancient and successful organisms, we ought to have rules, or principles, as our guides rather than approaching every problem ad hoc. In that case, knowingly, or willfully ignorantly, imposing a significant risk on your fellow man that manifests might be such a rule for liability.

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The Avandia witch hunt saga just gets more and more absurd. Guess what just popped up from the FDA's Division of Drug Information? Notice of an ongoing safety review of pioglitazone (the "safer alternative" generic pushed by those urging Avandia be pulled from the market.). Apparently "an increased risk of bladder cancer was observed among patients with the longest exposure to Actos (pioglitazone) as well as in those exposed to the highest cumulative dose of Actos."

So does this mean that pioglitazone ought to be banned? Does this mean that the ongoing study of pioglitazone users needs to be discontinued because it's unethical? That's what the anti-Avandia activists argued re: Avandia and the TIDE trial; they wanted everyone off Avandia, on pioglitazone and the experiment halted - pronto.

No; it ought not mean any of those things. What it does mean is that it's foolish to let our decisions be bound by the results of a single data dredge.

For more on the Avandia issue see: "Avandia: Burn Her Anyway?" For more on the perils of data mining see "Lies, Damned Lies and P-Values". Here's the full text of today's FDA missive on pioglitazone:

The Division of Drug Information (DDI) is CDER's focal point for public inquiries. We serve the public by providing information on human drug products and drug product regulation by FDA.

The U.S. Food and Drug Administration (FDA) is reviewing data from an ongoing, ten-year epidemiological study designed to evaluate whether Actos (pioglitazone), is associated with an increased risk of bladder cancer. Findings from studies in animals and humans suggest this is a potential safety risk that needs further study.

Actos is used along with diet and exercise to control blood sugar or improve control of blood sugar in adults with type 2 diabetes mellitus.

Bladder cancer is estimated to occur in 20 per 100,000 persons per year in the United States and is thought to be higher in diabetics.

The drug manufacturer, Takeda, has conducted a planned analysis of the study data at the five-year mark, and submitted their results to FDA. Overall, there was no statistically significant association between Actos exposure and bladder cancer risk. However, further analyses were also performed looking at how long patients were on Actos and the total amount of the drug they received during that time. An increased risk of bladder cancer was observed among patients with the longest exposure to Actos, as well as in those exposed to the highest cumulative dose of Actos.

At this time, FDA has not concluded that Actos increases the risk of bladder cancer. Its review is ongoing, and the Agency will update the public when it has additional information.

For more information, please visit: Actos

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Not all of it is bad, of course. Dedicated health and science journalists often do a fine job of maintaining the necessary level of skepticism when probing the claims of new health research. The recent study of health care coverage "Does It Matter Who Writes Medical News Stories?" confirms as much.

Media though is a business and thus it should come as no surprise that a lot of what passes for journalism is simply the selling of the current product, the narrative that attracted customers in the first place, and the marketing of new and improved products fitting that narrative e.g. breathless reporting about miracle cures and health scares. It's therefore not surprising that TV human interest programs did the worst job of accurately reporting health news.

Takeaway: Stay skeptical, especially when it sounds too good, or too bad, to be true.

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A new study, reviewing and pooling results from prior studies in prostate cancer screening, shows that screening men for prostate cancer does not increase life expectancy.

While the PSA test is effective at predicting which men may eventually get prostate cancer, it is ineffective in increasing life expectancy. This is because most men with a high PSA will not get prostate cancer in their lifetimes and will eventually die from something else. Many men, some of whom I have debated the value of a PSA test with, get a high PSA test result and live in fear of cancer for decades, even though prostate cancer never develops. Further, prostate cancer treatments, including surgery or radiation, can lead to incontinence and erectile dysfunction in about a third of patients. Unfortunately, some men get the treatments after a high PSA from fear of cancer which may never reach them in their lifetime. Other men get the treatments when they contract prostate cancer, even though this slow-growing tumor will not hurt them in their lifetimes. It is a case where the cure is sometimes worse than the cause.

The study is part of an effort to streamline which medical tests are effective, not just in detecting disease or the potential for disease, but for actually increasing life expectancy and increasing quality of life. A similar effort was undertaken to critically and empirically view breast cancer screening. The breast cancer screening recommendations were met with a flurry of criticism. Hopefully, this recommendation will not meet the same result.

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In Wilcox v. Homestake Mining Company plaintiffs argued that in toxic tort cases involving an injury with multiple potential causes "causation in such cases may be proven through a substantial factor test, without regard to whether the injuries would likely have occurred in the absence of the defendant's actions." Plaintiffs further argued that a "but for" causation requirement would make recovery all but impossible in toxic tort cases. The court rejected those arguments.

All a plaintiff has to do to get to a jury is to develop testimony that that the putative cause (e.g. radiation) was more likely than not a necessary cause of her injury (e.g. bladder cancer) and if there are multiple tortious sources of that cause then she can avail herself of alternate causation approaches (e.g. Summers v. Tice)  to assert liability against a specific defendant. On the other hand, it's not enough merely to show that the defendant brought plaintiff into contact with one of the known causes of her injury and it's not enough to show that the putative cause is one of the more common causes of that such injuries.

That's helpful. "But for" goes with the first legal causation question: was it more likely than not that the exposure (e.g. 5 fiber/cc yrs amphibole asbestos) was a necessary cause of plaintiff's cancer (e.g. mesothelioma). So where does "substantial factor" go? The court doesn't say. Like most courts it doesn't even say what it is.

Where should "substantial factor" go? We think it makes sense for it to go with the second legal causation question which is "was the exposure (i.e. the risk imposed) unreasonable?" The ability to estimate the ex ante risk of cancer imposed by exposure to a carcinogen allows both qualitative and quantitative assessments of the reasonableness of the defendant's conduct and informs the question of whether a particular exposure was substantial (and thus a basis for liability) or merely de minimis (and so unable to support a liability claim).

As we argued in Borg-Warner and have argued since, in a toxic tort case the ex ante risk imposed is the best measure of the reasonableness of the man (or woman). And that's what "substantial factor" causation ought to be about - determining whether there's some notion of responsibility associated with the particular risk imparted.

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In Tamraz v. Lincoln Electric Company, et al the 6th Circuit held that an expert could not stack speculation about mechanisms upon unseen and undetected lesions in the plaintiff to get from manganese exposure to his Parkinson's disease. Furthermore, the court ruled that you can't reasonably arrive at a causation opinion using what's erroneously called a differential diagnosis (it's more properly called simply a process of elimination) when you've no sound basis for ruling anything either in or out.

On the other hand, there's growing evidence that vitamin D deficiency is strongly associated with Parkinson's. Best of all, it makes sense. It looks like the enteric nervous system is first to be degraded in Parkinson's and that system is exquisitely sensitive to the gut mediated immune system which in turn is adversely affected by vitamin D deficiency. See: "Parkinson Disease: Could Sunlight Offer Protection from Parkinson Disease?"

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Before answering the question let's see if mind control is even possible. By now you're probably aware of the fact that a fungus (Cordyceps unilateralis) can zombify an ant; making it leave the colony and move to the perfect spot for the fungus to sprout out of its head and complete its life cycle. For this and other examples of hijacked brains see 10 Fascinating Cases of Mind Control.

You'll notice on that list the case of Toxoplasma gondii. It's a nasty little microbe that infects the brains of rats and tells them to find cats. Once gobbled up by a cat the T. gondii in the rat infects the new host and completes its own life cycle. Now that's unsettling. It's one thing for ants to be zombified, but rats? We've unhappily shared microbes with them before. Is there any evidence that T. gondii alters human behavior? Yep.

Is it possible that T. gondii is the cause of some cases of neuroticism, schizophrenia, depression, bipolar disorder and obsessive compulsive disorder? Yep, yep, yep, yep and yep. See "Toxoplasmosis as a Cause for Behaviour Disorders - Overview of Evidence and Mechanisms". Neuroticism? What's the evidence? See "The Diagnosis of a Personality Disorder Increases the Likelihood for Seropositivity to Toxoplasma gondii in Psychiatric Patients" and "Manipulation of Host Behaviour by Toxoplasma gondii: What is the Minimun a Proposed Proximate Mechanism Should Explain?"

So, a new client walks into your office and she's a zombie. T. gondii infections come primarily from water or improperly cooked food and your client can be shown to have been wrongly exposed. The problem however, given the fact that 30% of all humans carry T. gondii, is that while 4 of your jurors are likely to be zombies themselves the other 8 aren't. In your jurisdiction you need 10 for a verdict. How do you convice the 4 that being a zombie is a bad thing while convincing the 8 that your client isn't a monster?

What a world.

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Martyn Smith et al have just had published "Formaldehyde and Leukemia: An Updated Meta-Analysis and Evaluation of Bias" in the Journal of Occupational and Environmental Medicine. They report a relative risk of 2.47 for myeloid leukemia for those with high occupational exposures to formaldehyde.

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All things in moderation. That wisdom applies profitably to meat consumption; including the processed variety. See "Meat, Poultry and Fish and Risk of Colorectal Cancer: Pooled Analysis of Data From the UK Dietary Cohort Consortium".

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Researchers at MD Anderson report that pesticide exposure in general was associated with a doubling of the risk of lung cancer among 212 Mexican-American lung cancer patients at the hospital. The exposure data was, however, troublingly anecdotal and unverified. See "Assessing Environmental and Occupational Risk Factors for Lung Cancer in Mexican-Americans".

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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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Tonight the NYTimes has an article on bisphenol A (BPA) headlined: "In Feast of Data on BPA Plastic, No Final Answer". It's a very good overview of the current status of the research on BPA; which is to say that despite the hyperbolic claims of some there's precious little evidence that BPA causes harm in humans.

Is there a tsunami of literature showing that on a molecular level cells sometimes adapt to BPA? Sure. Is there evidence that these changes lead to any harm? Not so much.

So what's going on? What's going on is a very public battle between theory, hatched from conventional thinking about what constitutes an endocrine and how it should work, and what we witness in the world - i.e. dramatically decreased morbidity and mortality among inhabitants of modern economies exposed to lots of BPA - and no evidence of an excess of morbidity or mortality for those exposed to more, rather than less, BPA.

Much is at stake in this contest. Will the effort to turn scientific research into a sort of blue collar affair in which statistical tools supplant genius be successful? Or will modern research efforts, bounded by old paradigms, be overcome by the simple collection of observations and the unanticipated spark of induction that leads us to a wholly new understanding? It's part of a larger political battle and this time everyone's pulling out all the stops. One side or the other will lose and lose big. Moneywise I'm long on the empiricists.

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Whenever epidemiological data is used to support a claim of causation in a toxic tort case a fight over causal inference invariably erupts and for the last twenty years or so that has meant an argument about whether Sir A. B. Hill's so-called causal criteria have been met. Long before Hill tried to prove that smoking causes lung cancer Robert Koch tried to find a defensible argument for the claim that microbes were the cause of anthrax. What he came up with are known as Koch's postulates and they've been around for well over one hundred years. Now, in an attempt to update them for a world in which often only bits of pathogens long gone remain an attempt to update the postulates has been published.

In "Microbe Hunting"  the author summarizes the problem of causal attribution when the responsible bacteria can't be cultured or even found and when their role in disease is the result of an incredibly complex interplay between host, uncounted trillions of microbes and the external environment. He discusses the methods for teasing out pathogens from dense webs of causation and proposes a refined set of causal criteria. It's well worth reading because if you do mass torts you'll be dealing with this issue for years to come.

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If a plaintiff's cancer was caused by one molecule or one fiber damaging a single cell's DNA causing it to become malignant, and plaintiff was exposed to billions of molecules or fibers from multiple sources, how could he possibly prove that ,"but for" any single source of exposure or subset of exposures, he would not have developed his cancer? As stated, this is the Summers v. Tice problem traditionally resulting in burden shifting rather than dismissal so long as the conduct of each defendant was tortious.

Similarly, if plaintiff's cancer was caused by the cumulative effect of any one of several subsets of exposures from multiple sources, e.g. if three widgets were sufficient to cause cancer and plaintiff was exposed to one widget from each of A, B, C and D, she could never prove that "but for" A's widget she wouldn't have gotten cancer since the widgets of B, C and D were sufficient to have caused it; and the same would be true if she sued B, C or D. Again, the traditional answer to plaintiff's problem, assuming each defendant's conduct was tortious, has been to shift the burden of proof on causation. See Landers v. Texas Salt Water Disposal Co.

Suddenly the 5th Court of Appeals has in essence held that Borg-Warner v. Flores puts the burden of proof of causation back on plaintiff; doing so in a case in which the defendant stipulated so-called "general causation". See Georgia-Pacific v. Bostic. There's essentially no discussion of the rationale for imposing a "but for" causation proof burden on a toxic tort plaintiff nor is the impact of this monumental shift in Texas law even discussed so maybe the court didn't intend such a result. Indeed it did proceed to discuss substantial factor causation even after concluding that a "but for" burden was borne by a mesothelioma plaintiff with the result being that plaintiff's evidence was held insufficient to "provide quantitative evidence of [plaintiff's] exposure to asbestos fibers from [defendant's product] or to establish [plaintiff's] exposure was in amounts sufficient to increase his risk of developing mesothelioma."

So if you establish an increase in risk you've established substantial factor causation and that's the same as"but for" causation?! This case has a lot of lawyers scratching their heads.

It's time for a clearly articulated definition of "substantial factor" and it's time to get rid of the confusing and, in cancer cases, nonsensical "general causation" v. "specific causation" dichotomy. More on that after I get home.

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The Texas Supreme Court has just muddied the waters of its causation jurisprudence. For the last twenty years the court moved in a straight line towards a modern theory of legal causation. The court recognized the problem of causality; put fault back at the heart of torts - even in product liability cases; reaffirmed the counterfactual account of causation holding that plaintiffs must prove that "but for" the defendant's act or omission they'd be uninjured today; and, put reasonableness, and its best measure, the risk imposed, at the center of the calculus of how to define the limits of liability. Suddenly, everything (may have) changed.

In Transcontinental Insurance Company v. Crump, a worker's compensation case, the court held that a jury must not only be queried as to whether a putative cause was a "but for" cause, they must also be asked whether the alleged cause was a "substantial factor". As the court recognized years ago, in the context of causation in tort there's generally to be found the concept of substantiality "in which there always lurks the idea of responsibility.." Ok, but workers' comp is a no-fault scheme. What is "substantial factor" doing in a comp case then?

Maybe, just maybe, the court has come to think of "a substantial factor" as being a "big cause" - this is the idea that one or more necessary causes are somehow (despite them each being necessary) more significant than other (logically equal) necessary causes. They could have adopted something like a proximate cause concept (the idea of circumscribing those causes upon which liability may be predicated) but didn't - likely because the act itself uses the term "producing cause" long understood to mean a "but for" cause wherever it's found along the causal chain. As a result they may well have stripped "the idea of responsibility" from Texas' conception of "substantial factor".

If that's the case it's time for Texas' mass tort plaintiff lawyers to shake off the blues. A substantial factor test shorn of concern about responsibility means that Borg-Warner's test of reasonableness - risk, is now simply a test of whether or not the putative cause was a big one. And when it comes to, say, mesothelioma, what "bigger" cause is there than asbestos? There's now a good argument to be made that Judge Davidson's requirement that any putative cause be a sufficient cause in order to survive Borg-Warner sets the bar too high and that plaintiffs need only show that among all exposures adding up to .1 fiber/cc/yr the ones of which they complain are relatively "big". Good grief.

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