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

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.

• Email This
• Print
• Share Link

The Texas Supreme Court just withdrew its previous opinion in Marks v. St Luke's and substituted a new one - or rather several new ones. At issue was the question of whether an improperly assembled hospital bed that caused an injury was a premises defect or an integral part of the patient's care and treatment such that the claim necessarily falls under the Medical Liability and Insurance Improvement Act (MLIIA). The second opinion, a plurality, determined that the claim, however pled, is really a health care claim subject to tort reform.

What has caused all the consternation, as far as I can discern, is that the court previously held in Diversicare v. Rubio that premises liability claims that don't have something to do with the provision of health care may still be pursued against health care providers. The problem is that no one seems to be able to figure out what set of facts could constitute such a claim. If a bed is an inextricable part of the health care provided by a hospital what isn't? Apparently something in a hospital isn't inextricably tied to the provision of care as otherwise the simpler rule would be to say that since a hospital is built from the ground up with provision of medical services in mind then everything in it is subject to to the MLIIA.

Until something's found in a hospital that has no connection to health care it's best to plead your claim as a health care claim and timely file your expert report.

• Email This
• Print
• Share Link

What has initially appeared to be a long litigation road to the answer of whether individuals have a private right of action to sue for climate change damages, may not be such a long road after all. Obama Admin Urges Supreme Court to Vacate Greenhouse Gas 'Nuisance' Ruling.  For some time, there appeared to be a 2-1 lead for advocates of a private right of action for climate change damages in light of the Second Circuit’s decision in AEP v. Connecticut and the Fifth Circuit decision in Comer v. Murphy to allow such claims against the Ninth Circuit district court decision in Native Village of Kivalina v. Exxon Mobil to dismiss such actions. But how quickly things can change. After granting a rehearing en banc, which automatically vacated the panel decision allowing the private right of action, the Fifth Circuit dismissed the district court appeal after it lost quorum due to a disqualified judge. Thus, only the AEP v. Connecticut Second Circuit decision remains in favor of a private right of action.

Yesterday, in a brief filed on behalf of the Tennessee Valley Authority, the acting United States Solicitor General agreed with the defendants in AEP v. Connecticut, stating that the U.S. EPA's newly finalized regulations on greenhouse gases have displaced that type of common-law claim.  This position clearly supports allowing the EPA, and the lawsuits against the EPA, to set the tone and pace of climate change regulation, but also brings the preemption, or displacement as some are calling it, versus tort claims debate experienced in other areas of mass torts to the environmental field. It is hoped that the Supreme Court will take up this issue once again sooner (as in this Fall) rather than later.

It is interesting to note that one of the administration’s recent Supreme Court appointee’s, Sonia Sotomayor, served on the panel but did not sign the decision issued by the Second Circuit in AEP. Interesting indeed.

• Email This
• Print
• Trackbacks
• Share Link

The oil spilled into the Gulf of Mexico is being degraded more rapidly than expected and without a precipitous decrease in oxygen levels. Those are among the fascinating findings in "Deep-Sea Oil Plume Enriches Indigenous Oil-Degrading Bacteria " just published in Science. An excellent write up can be found at the Berkeley Lab press center under "Study Shows Deepwater Oil Plume in Gulf Degraded by Microbes".

The essence of the findings are summarized in the release as follows:

"Hazen and his colleagues attribute the faster than expected rates of oil biodegradation at the 5 degrees Celsius temperature in part to the nature of Gulf light crude, which contains a large volatile component that is more biodegradable. The use of the COREXIT dispersant may have also accelerated biodegradation because of the small size of the oil particles and the low overall concentrations of oil in the plume. In addition, frequent episodic oil leaks from natural seeps in the Gulf seabed may have led to adaptations over long periods of time by the deep-sea microbial community that speed up hydrocarbon degradation rates.

One of the concerns raised about microbial degradation of the oil in a deepwater plume is that the microbes would also be consuming large portions of oxygen in the plume, creating so-called “dead-zones” in the water column where life cannot be sustained. In their study, the Berkeley Lab researchers found that oxygen saturation outside the plume was 67-percent while within the plume it was 59-percent"

• Email This
• Print
• Share Link

In "Risk of Cardiovascular Events and All-Cause Mortality in Patients Treated With Thiazolidinediones in a Managed-Care Population" the authors report on the health outcomes of over 36,000 patients with type II diabetes taking either Avandia or pioglitazone. Over five years 4.16% of the patients on Avandia suffered heart attack, heart failure or death while 4.14% of those on pioglitazone suffered similar outcomes. The difference was obviously insignificant.

Well aware of the controversy into which the journal has waded and the shrill ad hominem attacks launched against anyone suggesting that the drug doesn't increase the risk of heart attacks, heart failure or death a free editorial accompanies the study. It confesses that the evidence against Avandia is equivocal at best, frets about the find it and bind it approach to supposed biomarkers and then limply concludes "[t]hus, the simplest message might suggest the avoidance of [Avandia] until more reassuring evidence for the drug becomes available." What that evidence might be, or how much of it there ought to be, isn't discussed. I'm guessing that the hope here is that the TIDE trial is halted so that embarrassing questions don't ever have to be answered.

• Email This
• Print
• Trackbacks
• Share Link

In Lance v. Wyeth the plaintiff alleged, among other things, that defendant had somehow negligently designed the molecule dexfenfluramine and that such negligent design was the proximate cause of her daughter's death. The defendant however prevailed on its motion for summary judgment having demonstrated to the trial court that plaintiff did not have any cognizable product liability claims under Pennsylvania product liability law as it applies to prescription drug cases. On appeal the trial court's rulings were affirmed one by one until the appellate court came to the negligent design claim.

The court held "that notwithstanding comment k in section 402A Restatement (Second) of Torts, this claim is actionable under Pennsylvania law." Noting that "a strict liability design defect claim is distinct from a negligence design defect claim" the court examined section 395 (negligent design of products) and found no exemption for unavoidably unsafe products like the one for things like pharmaceuticals found in comment k of 402A. Accordingly, the appellate court determined that "Appellant's negligent design claim is not precluded by comment k, and is a valid cause of action upon which relief may be granted. The trial court thus erred in entering summary judgment in favor of Wyeth on Appellant's negligent design defect claim."

In arriving at its conclusion the court relied on just three cases. For the proposition that plaintiff can lose on a strict liability design defect claim yet prevail on a negligent design defect claim the court cites Phillips v. Cricket Lighters. In that case though the court held that on the strict liability side the question went to whether the lighter was safe for the intended user, in that case an adult, whereas on the negligence side the question was whether the lighter's lack of a safety feature was a design defect given the fact that an unintended but foreseeable user, a child, started the fatal fire. In Lance, of course, the person for whom the drug was intended and its user were one and the same so I don't see the point.

For the proposition that their reasoning applies to pharmaceuticals the court pointed to Toner v. Lederle Labs. In Toner though the question wasn't whether a molecule like dexfenfluramine was defectively designed; the question was whether making a vaccine out of a whole library of bacterial molecules, most, necessarily, of unknown nature and function could have been done more safely by using just a few bits of B. pertussis rather than the whole cell. Ok, but that's mixing apples and sangria.

Finally, for further support for the proposition that you can lose a strict liability design defect claim and yet win on a negligent design defect claim for the same product the court points to Artiglio v. Superior Court. Artiglio was a petition for writ action seeking a reversal of a summary judgment in favor of defendant on plaintiff's strict liability claim in a breast implant case. Plaintiff's petition for writ was denied; the appellate court finding that "the entire category of medical implants available only by resort to the services of a physician are immune from design defect strict liability." The problem with Artiglio and of the case to which it points, Brown v. Superior Court, is that they appear to stand for the proposition that in a prescription drug case there's really no such thing, at least under California law as strict liability defective design case - not that it's somehow different and so equally actionable.

Putting all that aside for the moment, what would it mean to defectively design the small organic molecule that is the essence of any modern medicine?

Surely it doesn't mean that the molecule ought to have been made up of different atoms. If that were the case then it necessarily wouldn't have been the same drug - we're not talking alternate design; we're talking alternate universe. Even in Beaumont twenty years ago the judges tossed out plaintiffs' claim that benzene ought to have been designed with all of its useful properties but with a methyl group in place of one of its hydrogens. 

Maybe the claim could have to do with how the atoms are arranged in the molecule. It's true that some organic molecules can be made in two forms akin to our right and left hands and that each form may have different biological properties. Thus if say, to use a trivial example, D-glucose (right handed) was safe and effective and L-glucose (left handed) was unsafe though effective you might have something to talk about if you'd taken the L- variety. Such a circumstance is mainly hypothetical and the typical finding is that one form is ineffective so that it's never consciously made in the first place leaving at best a manufacturing defect claim, if anything.

Perhaps the claim goes to the design process itself. Drug design has gone from trial-and-error to a find it and bind it approach to mindbogglingly complex efforts involving huge numbers of simulations run on supercomputers. But if something's wrong with the approach then the complaint, again, is not with the product consumed but with the failure to discover a different and better product. Something akin to a loss of chance claim perhaps. Surely the courts won't impose a duty of scientific discovery on companies. If they do they could at least solve the problem of induction first.

All in all it's hard to see how this new negligent design defect claim changes things. Really, what can it possibly mean to say that someone defectively designed something she didn't design, or to say that she defectively designed one thing because she didn't design it like something completely different? Can a car be found defectively designed because it's not an airplane? I hope not.

• Email This
• Print
• Share Link

It has generally been assumed that bacteria evolve to overcome host defenses at a rate much slower than that of viruses. That assumption appears to be wrong. Helicobacter pylori, a cause of multiple cancers in humans, mutates at a rate similar to many viruses. See: "Microevolution of Helicobacter pylori During Prolonged Infection of Single Hosts and Within Families".

Just how fast can bacteria evolve? Would you be surprised to learn that within the lifetime of mice, bred to be free of gastrointestinal bacteria, bacteria from drinking water cannot only set up shop and colonize their hosts' guts but evolve into whole new species? If you are surprised, read: "Bacteria From Drinking Water Supply and Their Fate in Gastrointestinal Tracts of Germ-Free Mice: A Phylogenetic Comparison Study".

The long war continues, of course; and while we've been basking in our assumed victory over them for the last forty years our ancient enemies, descended from a long line of brilliant sappers, have been hard at work.

• Email This
• Print
• Share Link

We've previously reported on the finding that when it comes to causal associations experts typically get it wrong. From the mass torts' perspective the problem seems to be that courts tend to confuse frequentist data with Bayesian degrees of belief - and thus did I get to see the late and truly very great trial lawyer John O'Quinn once convince a judge that any study showing an association that had a p-value less than .5 ought to be admissible and supportive of a verdict under Texas' "more likely than not" civil evidentiary standard. Armed with such a lax rule plaintiffs' experts ran wild. Heck, even today with a .05 threshold they are free to opine about causal associations that almost certainly do not exist.

The ability to manufacture health scares clearly serves a variety of political and economic interests but what to do about it? Doesn't peer review help? Not really. As long as the standard for statistical significance is low the odds are that even the most rigorous journals will publish more junk than science.

What about getting rid of peer review altogether? It's coming. In the future papers will be dipped in the acid bath of online skepticism and their ultimate worth will be determined by whether they survive the test. No longer will partisans, skirmishing behind the scenes, determine what gets published and what doesn't. See: "Scholars Test Web Alternative to Peer Review".

• Email This
• Print
• Trackbacks
• Share Link

Out of thousands that I've handled, in only one toxic tort case did I think my client actually had done anything wrong. The demand was the same as usual, of course; cancer cases are valued on the basis of type and damages and, and to a lesser extent, causation - not fault. So what happened at the mediation of that case was completely unexpected.

After the usual presentations by the lawyers my client representative asked to address the widow directly. She rose and, as best as I can recall, said that the company had failed to fulfill its promise to one who worked for it,  said we're better than that, and then said "on behalf of those who founded this company and those who work there today I apologize to you and promise this will not happen again". The widow and my representative, both crying, then hugged.

The mediator suggested a break and that we retire to our separate rooms. Shortly thereafter the mediator knocked on our door and upon entering announced that he had a demand we couldn't refuse. The demand was indeed within our authority though at the high end. We accepted on the spot, my representative saying that to negotiate further would be faithless. Plaintiff's counsel was furious and said that day, and has said several times since, that he'd never bring his client to a mediation with that defendant again.

I'm not sure exactly why the apology worked so well. I've seen other apologies. Most did nothing to alter the parties' positions and a couple produced fireworks that made the cases impossible to settle. So if an apology is in order something about its content and how it's delivered will determine its success. But what?

Apparently you cannot craft a good apology unless you understand the plaintiff's own narrative of the story of her life. Once the "components" of your apology fit the apology predicted by that narrative you have a chance at forgiveness. Otherwise, apparently you're wasting your breath. See "When Apologies Work: How Matching Apology Components to Victims' Self-Construals Facilitates Forgiveness". Hat tip: Mind Hacks

• Email This
• Print
• Share Link

For years a controversy has raged over whether simian virus 40 (SV40) causes mesothelioma in humans. While the evidence that SV40 causes mesothelioma, brain cancer and lymphoma in some animals is very strong it's a different story when it comes to humans. Evidence of prior SV40 infection in patients with e.g. mesothelioma has been equivocal at best. Just this month, in "SV40 Associated miRNAs Are Not Detectable in Mesotheliomas", researchers again failed to find the genetic fingerprints of SV40 in mesothelioma samples taken from victims of the disease.

Not every viral perpetrator of cancer leaves genetic evidence at the scene of the crime though. That's the finding in today's "Vaccination Against a Hit-And-Run Viral Cancer" (free). For the first time the scientists have been able to demonstrate an experimental animal model for sarcoma in which "virus-triggered oncogenesis" generated cancer cells that lacked viral genomes.

In their dicussion of findings the authors make the following four points: 1) "Most analyses of human cancers have focused on examples of genome retention". 2) The fact that some virus-induced cancers retain viral genomes doesn't prove that all or even most do so. 3) "Relying on viral genome detection to establish aetiology" may dramatically underestimate the role of viruses in cancer. 4) Vaccinations against viruses previously thought to be of little benefit may do far more good than expected.

Does any of this prove that SV40 is a hit-and-run cause of mesothelioma in humans? No, but it does raise the question of whether viruses have played a role in some of the biggest latent cancer toxic torts of all time. To this day the discoverer of one of the most studied cancer clusters wonders whether it was more than a coincidence that almost half of the stricken workers lived in the same boarding house and that three roomed together. More on that another day.

• Email This
• Print
• Share Link

Back in March we reported on the finding that beta amyloid, which accumulates in the brains of Alzheimer's patients, is a potent antibiotic; thereby generating the hypothesis that its presence wasn't the result of a malfunction but rather was an effect of an immune response to a chronic brain infection. If that's really the case, getting rid of it might not be the way to go.

Today Gina Kolata of the NYTimes is reporting on the dramatic failure of a drug designed to reduce the amount of beta amyloid in the brain. It's not that it didn't reduce beta amyloid; it did. The problem is that it made the subjects' Alzheimer's worse; and the more they took the more their conditions worsened.

None of this proves that the real killer is a chronic fungal infection which is slowed down by beta amyloid but it does prove that when it comes to biomarkers the "which is cause and which effect" trap can ensnare the brightest and the savviest.

• Email This
• Print
• Share Link

According to a new meta-analysis of studies of painters there's a small but consistent increase in the risk of bladder cancer among painters. What it is about painting that accounts for the risk is unknown. See: "Bladder Cancer Risk in Painters: a Meta-Analysis".

• Email This
• Print
• Share Link

What does it mean, in the law of torts, for one to have caused another's injury? The standard legal account of causality has been that of the counterfactual put forward by David Hume as follows: "where, if the first object had not been, the second never had existed." (1748, Section VII). In the law it's the "but for" test and for our purposes then the courts tend to attach legal liability (assuming the existence of a duty and its breach) only upon the following: had Defendant done otherwise, Plaintiff would today be uninjured. 

Generally speaking the "but for" test is easy to use and produces a nice clean binary answer of the sort favored by courts trying to resolve disputes. (e.g.  "But for" Defendant having run the red light Plaintiff would have passed through the intersection without incident and would not have suffered the broken leg of which she complains.) Of course there are innumerable "but for" causes of the accident, including the Defendant's mother having given birth to him and the rudeness of the fellow with a cart full of groceries in the "10 items or less" line who slowed Plaintiff down so that she wound up in the intersection at the same moment as Defendant. Nevertheless, and almost invariably without much analysis, the parties settle on just one among the countless posibilities as the sine qua non act (or omission) to be subjected to the "but for" test.

However, when deployed in a case in which plaintiff's injury was caused by only one of several identical and indistinguishable acts (see e.g.  Summers v. Tice) or by the cumulative effect of some subset of several identical and indistinguishable acts (see e.g. Landers v. East Texas Salt Water Disposal Co.) the "but for" test would, without some other rule, produce the jarring judgment that none of the defendants, considered individually, were more likely than not the sine qua non cause of the plaintiff's injury. In those cases, finding that the acts (divorced from the inquiry of whether they were actually causative) were tortious, the courts held that the defendants should bear the burden of proof that theirs was not the act that caused the plaintiff's injury. The instances in which such a rule would apply were surely few and even a century ago the idea of treating the defendants collectively and shifting the burden on to them was not unheard of. See 2 J. Wigmore, Select Cases on the Law of Torts Section 153, p. 865 (1912) ("When two or more persons by their acts are possibly the sole cause of a harm, or when two or more acts of the same person are possibly the sole cause, and the plaintiff has introduced evidence that one of the two persons, or one of the same person's two acts, is culpable, then the defendant has the burden of proving that the other person, or his other act, was the sole cause of the harm.")

An effort to distill all judicial reasoning about causation down to its essence and to make a rule of it has been underway for some time. Probably the most cited rule, a form of which is incorporated into the Restatement (Third) of Torts, is the NESS test. NESS stands for "necessary element of a sufficient set". The NESS test is itself a restatement of an older test in which a singular putative cause is said to indeed be causative if it, though insufficient, is nevertheless a necessary element of a precipitating event which event, though perhaps itself unnecessary, would nevertheless have been sufficient to have produced the outcome under investigation (see "Causes and Conditions" by J.L. Mackie). What in the world does any of that mean? In Mackie's example investigators of a fire are satisfied that a short-circuit was the cause of a house fire when conditions were such that the short circuit existed, flammable rags were nearby and those rags once ignited were sufficient to cause a conflagration that would burn down the house. The short-circuit alone was insufficient to burn down the house but it was necessary (other causes having been ruled out) to catch nearby flammable rags on fire. Lots of things can ignite and so burn down a house (so burning rags are not necessary to have a burning house) but burning rags are sufficient to torch the place. Whew.

"But for", causal analysis seems then to be about ruling things out and settling on what's left (the short-circuit). On the other hand, the investigation of the product of the remaining thing(s) (sufficient set) seems aimed towards the propensity of one condition (burning rags) to lead to another (burning house). It is out of this second analysis, of the propensity for one thing to lead to another, that queries about reasonableness and foreseeability and risk arise. More on that later though when I get to risk.

Anyway, the reductionist effort itself precipitated a debate about whether the NESS test accounts for all judicial causal reasoning that continues to this day. Take for instance the hypothetical case of the desert traveler. The desert traveler set off to hike across the desert with just enough water to make it to the other side. Unbeknownst to the desert traveler, defendant "A" had poisoned his water such once that he'd consumed all of it he would surely die. Along his way across the desert however, defendant "B" stole the desert traveler's water bottle. The desert traveler was found dead in the desert. If defendant "A's" conduct was not the cause of his death, why not?

Such conundrums would normally make for nothing more than an obscure niche in the law in which a few academics could regularly generate tedious and unread papers. Then forty one years ago Clarence Borel, dying of mesothelioma, filed a products liability claim in Beaumont, TX culminating in an opinion that would usher in the age of mass torts. Concluding that as it was impossible "to determine with absolute certainty which particular exposure to asbestos dust resulted in injury" and because "each exposure may result in an additional and separate injury" the 5th Circuit held in Borel v. Fibreboard that a jury could reasonably conclude "that each defendant was the cause in fact" of Borel's injury.

Twenty seven years after Johns Manville sank under the wave of litigation unleashed by Borel the practical effect of the ruling continues to drive companies into bankruptcy. The Restatement (Third) of Torts was awkwardly silent on the issue of "the mother of all mass torts" but recent musings by its Reporters and others suggest that they thought rather a lot about it and that its impact on the restatement effort was in fact profound. The shame of it is that they almost got it exactly right. All that was needed was to distinguish between risk and causation and to embrace Palsgraf's true meaning: that the risk imparted is the measure of the reasonableness of the man.

Next time: Risk.

• Email This
• Print
• Trackbacks
• Share Link

Every day 20 to 25 tons of crude oil seeps up out of the naturally occurring Coal Oil Point off the coast of  Ventura, CA. The amount of petroleum in surrounding sediment remains constant at about 800% to 8000% more than that in sediment at the site of the Exxon Valdez accident and there's a persistent slick and steady plume of hydrocarbons along the continental shelf from the 24/7/365 seepage. Accordingly it presents an opportunity to study the fate of the petroleum, the impact of currents and weather on dispersion, the natural biodegredation by microbes and the differences in habitats inside and outside the zone of weathered petroleum. For a primer see: "Weathering and the Fallout Plume of Heavy Oil From Strong Petroleum Seeps Near Coal Oil Point, CA."

For a discussion of the amazing diversity of life that lives in and on crude oil see (for free): "Microbial Diversity in Natural Asphalts of the Rancho La Brea Tar Pits".

Finally, if you want some reassurance about Corexit, you might want to read "Analysis of Eight Oil Spill Dispersants Using Rapid, In Vitro Tests for Endocrine and Other Biological Activity". A free version looks to be available at the EPA. Long story short: in vitro testing shows no evidence "that any of the dispersants will display biologically significant endocrine activity via the androgen or estrogen signalling pathways."

• Email This
• Print
• Share Link

Six hours a day, for five days, rats were exposed either to amosite or to joint compound with chrysotile. Over the course of a year subsets were sacrificed and their lungs examined. The rats exposed to amosite sustained an inflammatory response and by the end of four weeks had developed evidence of interstitial fibrosis and inflammation in the parietal pleura. Those rats exposed to chrysotile-containing joint compound never showed evidence of fibrosis and their bodies cleared the chrysotile fibers quickly. By the end of the year there was still no evidence of inflammation or migration.

See: "The Pathological Response and Fate in the Lung and Pleura of Chrysotile in Combination with Fine Particles Compared to Amosite Asbestos Following Short-Term Inhalation Exposure: Interim Results"

• Email This
• Print
• Share Link

Would you believe that an act that was neither sufficient nor even necessary to produce an injury could still be considered a legal cause of it simply because it had exposed an injured plaintiff to risk? You need to read Restatement (Third) of Torts: Liability for Physical Harm. Wherever adopted it will expand liability in asbestos cases against those that almost certainly had nothing to do with plaintiffs' injuries; it will extend asbestos litigation's special rules to any claim for a cumulative or indivisible injury due to toxic exposure; and, it will do it by standing modern thinking about causality and risk on its head.
 

To understand why Restatement 3rd will change everything you need to read "The Insubstantially of the 'Substantial Factor' Test for Causation". Among the authors are the Reporters for the Restatement (Third) of Torts and they specifically examine the problem of causation in asbestos cases. They survey the landscape of modern attempts to deal with the issue and settle on Lohrmann, Rutherford, Gregg and Flores as representative.
 

Concluding that Rutherford stands for the rule that "[p]laintiff need only prove that defendant contributed to the risk of disease by exposing the plaintiff to asbestos" the authors conclude: "[g]iven the reality of causal uncertainty, we believe the Rutherford solution to the problem is the best yet devised. The Rutherford approach of imposing liability for risk contribution is self correcting in the case of small doses, at least in jurisdictions with several liability. The defendant who contributes .05% of the dose to which the plaintiff was exposed will be liable for that same percentage of the plaintiff's damages."
 

What’s wrong with that? Well they've conflated risk and causation. They're defining cause as risk and risk as cause and imposing liability without regard to cause or even the degree of risk imparted. How so? By saying that dose, which is only an aspect of risk, is the measure of cause; and by saying that cause is simply the set of all proven doses (which is to say risks)- thus: 0.05% dose (risk) = 0.05% of the causation.
 

The authors make it clear that there is no lower limit above zero that could not be the basis for liability. Either each fiber was a necessary cause under the “straw that broke the camel’s back” view or each fiber was a member of some sufficient group or set of fibers thus satisfying the Restatements’ version of the NESS (Necessary Element of a Sufficient Set) test for causation. How do we know this? There is a “trivial-contribution exemption” that applies in situations where there are multiple sufficient causal sets but the authors state that this exemption does not apply in the asbestos context. How could that be so? They must have determined that asbestos doses are fungible and the disease the result of the dose such that the sufficient set of causes of say mesothelioma necessarily includes all asbestos exposures; and thus by extension, each fiber “a factual cause subject to liability”. Otherwise, calculating the answer to the "how many sufficient sets can we make out of the total dose" question would lead to the logical conclusion that it is impossible to say that any given defendant's contribution to dose was causative. To be sure that can't happen there's Section 27.  

If you doubt that each fiber can be a legal cause or still doubt that that there's no lower limit of liability read section 27, especially comment f. 

"Section 27. Multiple Sufficient Causes

If multiple acts occur, each of which alone would have been a factual cause under section 26 (what the Reporters say is the essence of causation, the "but for" test) of the physical harm at the same time in the absence of the other act(s), each act is regarded as a factual cause of the harm.

... comment f. The fact that an actor's conduct requires other conduct to be sufficient to cause another's harm does not obviate the applicability of this Section. Moreover, the fact that the other person's conduct is sufficient to cause the harm does not prevent the actor's conduct from being a factual cause of harm pursuant to this Section, if the actor's conduct is necessary to at least one causal set."

Basically, this is just the old game of "How do you know asbestos caused his mesothelioma? Because he was exposed to a sufficient dose. But how do you know he had a sufficient dose? Because he got mesothelioma. How do you know that every exposure contributed? Because otherwise he wouldn’t have had a sufficient dose. But how much was needed for a sufficient dose? Enough to cause his mesothelioma.”

If courts adopt such a rule it'll be a happy day indeed for plaintiffs' lawyers. Their refrain, and that of their experts, that "every dose is causative because the risk doesn't become zero until dose is zero" - the logical fallacy behind conflating risk and causation and behind the "one fiber" theory - will have become law; and the law will be deeply biased against defendants.

Next up, we'll discuss causation and risk and why the reasoning in Borg-Warner v. Flores best captures the essence of American tort jurisprudence. Hint: "the risk reasonably perceived defines the duty to be obeyed" is best understood as being about risk and the reasonable man, and not about foreseeability.

• Email This
• Print
• Trackbacks
• Share Link

Before the paper was even pre-published online the lead author of "Pubertal Assessment Method and Baseline Characteristics in a Mixed Longitudinal Study of Girls",  Dr. Frank M. Biro, was giving interviews. The measured write up in The New York Times reported that "[s]ome researchers also suspect that environmental chemicals that mimic the effects of estrogen may be speeding up the clock on puberty, but that idea is unproved." Later however it quotes Dr. Brio, whose new project involves an attempt at correlating the subjects' hormone levels and chemical exposures, as saying "I think we need to think about the stuff we're exposing our bodies to and the bodies of our kids. This is a wake-up call, and I think we need to pay attention to it." From what I can see of the article it doesn't even purport to examine such an association and nothing about the data other than a crude sort of - our use of more and different chemicals may be going up (an assumption which is not assessed in the article) and onset of one prepubertal sign is going down - would even suggest such a hypothesis.

MSNBC took a far less measured approach. Whereas the NYTimes correctly reported that the study actually found no change in the onset of menses, MSNBC reported that "American girls are maturing earlier and earlier." Then it went on to write about all the possible perils of those who "go through puberty early" without disclosing that the 7 and 8 year old subjects had not in fact "gone through puberty" at all. And while MSNBC discusses the putative link between obesity and early puberty they quickly move on to a comment from Dr. Stanley Korenman (not one of the authors) who "says environmental exposure to estrogens in plastics, chemicals and foods has been going up" adding "and estrogens do stimulate breast development". All of this then prompts Dr. Biro to conclude "[u]ntil we know what the cause is, the best way to slow puberty may be to 'start living green'.

What's behind this belief that there's a simple answer to something like trends in the onset of puberty? Well, there's that whole third age of epidemiology business whereby many came to believe that changed and chronic conditions just had to be man-made. And there's also risk factor epidemiology which, if done often enough, is essentially guaranteed by the laws of probability to produce a study showing a statistically significant association between condition and chemical. Of course, as we've written before, that now 40 year old paradigm and the tool used to support it have been crumbling under the weight of erroneous predictions for the last 20 years. The problem was that causation was far more complex than most people expected and many of the tools needed to model causal networks had yet to be developed.

Enter eco-epidemiology. For a discussion of this new field you'll not find a better primer than "The Eco- in Eco-Epidemiology" and if you're really really interested and want to watch some lectures on the topic try The Yale Center for Eco-Epidemiology. For those beginning to doubt that nature is benign try the talks from "Zoonoses: Diseases from Nature". Finally, for those wanting the short version suffice it to say that causation, even for something like AIDS, is very very hard. A host of impacts from genes to culture determine who and how many will be infected. And genes shape cultures and culture may well shape genes . (h/t GNXP) Eco-epidemiology aims to deal with all of these multilayered causes.

Finally, back to the puberty panic. Our culture has changed in many ways over the last fifty years. For example resources have become more abundant. Elsewhere in nature when that happens critters exploit the opportunity by breeding sooner and more often. Why should we assume that we don't, albeit unconsciously, do the same? Eco-epidemiology aims to find all the contributors to the human condition and let the chips fall where they may.

• Email This
• Print
• Share Link

Coffee, especially caffeinated coffee, has been the subject of numerous epidemiological investigations; and the endless cycles of "this week scientists said it causes cancer, last week they said it doesn't and next week they'll probably say it prevents it" did as much as anything to make even epidemiologists ask whether it was time for the science of black box epidemiology "to call it a day". Of course they didn't call it a day and many continue to try to discover whether everyday "stuff" like coffee and tea are in fact deadly carcinogens. They do it by attempting to discern an association between exposure and disease beyond what chance would predict. Here's the newest one on coffee: "Coffee and Tea Intake and Risk of Head and Neck Cancer: Pooled Analysis in the International Head and Neck Cancer Epidemiology Consortium".

The study is large and looks to be very well done. Overall, neither coffee nor tea seems to be associated with head and neck cancers but what's interesting is the unexpected and dose dependent decrease in cancer associated with drinking lots of caffeinated coffee each day. Those downing three or four cups each day reduced their risk by 30% and those drinking more than four cups per day lowered their risk by almost 40%. What to make of it?

Well, as we regularly argue here, it's pretty much impossible to know what to make of it. We could jump to the conclusion that coffee battles cancer but we'd be ignoring, among a host of other factors, the fact that a lot of head and neck cancers are caused by human papillomavirus (HPV). The authors write that "there is no reason to think that coffee intake is associated with human papillomavirus infection" but just because they can't think of a reason doesn't mean there isn't one. Maybe heavy coffee drinkers have fewer partners (all work and no play ... etc.). Maybe some people have a rare gene that simultaneously protects against head and neck cancer and makes them crave caffeinated coffee. Who knows?

None of which is to say that these sorts of studies are useless. In fact they're often invaluable. The point is that such studies ought to be put in perspective. They aren't valuable because they answer the question of causation. They can't. They're valuable because they generate insightful clues that can be shaped into testable hypotheses that if borne out lead to real answers about causation and from there to further clues about prevention and treatment.

• Email This
• Print
• Share Link

The New York Times has an excellent write up of the new article "Human Milk Glycobiome and its Impact on the Infant Gastrointestinal Microbiota" in today's Science section. Two profoundly important points are made both by the write up and the article; they are (1) that we are each individually a "we", an emergent organism dependent upon billions of organisms within us to promote and to maintain good health; and, (2) just because we don't know what something does that doesn't mean it does nothing - it just means we haven't thought about it hard enough.

It turns out that mother's milk nourishes not only her baby it also selectively recruits and thereafter employs (with payment made in special milk sugars that baby can't digest) billions of tiny bacteria which earn their keep by aiding digestion, protecting epithelial cells and assisting the immune system in its never ending war against pathogens. And what of the other forms of milk sugars whose purposes have yet to be elucidated? The search for whatever they're feeding is now on in earnest.

As for the now refuted claim that the indigestible (at least by baby) milk sugars serve no purpose it's important to recognize just how many such claims are falling these days. It was a big deal three years ago when the ENCODE researchers announced "You know those non-coding DNA segments? You know, the flotsam and jetsam of millions of years of evolution that doesn't really do anything? Well, guess what?" These days stories about aspects of our selves once thought to be vestigial shadows of distant ancestors turning out instead to be critical determinants of health are common. As a result, we live in a time of great promise but also of great uncertainty.

So what does this have to do with mass torts? First, there's the issue of causality. The task of unraveling causation becomes fantastically complex once we understand the role that genetics, epigenetics, diet and social interactions, including swapping bacteria, play in disease. Second, there's the matter of what bacteria we host unconsciously due to the food that we eat and the impact on our health of the bacteria we will consciously choose to populate our bodies when we consume probiotics. So far the news on probiotics is quite promising but it must always be borne in mind that we are at the beginning of a great revolution whereby we come to understand ourselves as superorganisms and the complex interactions of genetics, epigenetics, diet, social networks and environment (and all that entails, known, unknown and unknown unknowns) that make us what we are. As with most revolutions, because of the uncertainty they bring, it's best to expect the unexpected.

• Email This
• Print
• Share Link

Etc indeed. The list of maladies laid at the feet of inhaled particulate matter smaller than 2.5 micrometers (thus PM2.5) is long and growing. You can add diabetes to the list thanks to "Association Between Fine Particulate Matter and Diabetes Prevalence in the United States" and lung function deficits in early childhood too ("Effect of Prenatal Exposure to Fine Particulate Matter on Ventilatory Lung Function of Preschool Children of Non-Smoking Mothers").

Is it a certain type of ultrafine particle that's responsible? Some studies say yes and others say no. In vitro toxicity testing tends to suggest that altered function is due simply to particle size while epidemiology studies tend to cast blame on one sort of particle rather than another though the findings vary from study to study and often conflict (a common problem when looking for weak effect associations). Do the observed effects meet the so-called specificity criterion for causal inference? At first the reported ill effects of exposure were said to be cardiovascular but now everything's in play especially since several studies have linked PM2.5 and Premature Death - All Causes.

So, is PM2.5 a universal toxicant and among the leading causes of death? Or could it be that people who live in urban areas with higher PM2.5 levels tend to have higher rates of unhealthy living? Is there anything good to be said about PM2.5? For example, why do farmers, who are often exposed to high levels of PM2.5, especially from endotoxins (think bits of bacteria), often have lifelong protection from many allergies that afflict those exposed to lower doses?

There's also the question of what's to be done about PM2.5. Farmers produce lots of it what with their gravel roads, grain bins, diesel tractors and plowed fields. EPA intends to regulate PM2.5 down on the farm and much more strictly than in the past but at what cost? And for those who don't like cost-benefit analyses what if the changes needed to reduce farm PM2.5 simply causes generation of ultrafine dust to be shifted elsewhere; and to increased markedly? See "The Environmental Cost of Reducing Agricultural Fine Particulate Matter Emissions".

Finally, of course, there's the issue of whom shall be sued. The finding that a speck of cotton dust from your shirt is as toxic (or as non-toxic, depending on how things shake out) as soot from combusted diesel fuel is an obvious impediment to to the diesel litigation plus there's a new study of truck drivers demonstrating that their presumed PM2.5 mortality may not be due to their work but rather can be, at least in part, explained by ultrafine dust exposures in and around the home: "Long-Term Ambient Multi-Pollutant Exposures and Mortality". Efforts to target other deep pockets will have to wait until science produces more definitive answers about what's to blame and how it can be determined that the PM2.5 in question was the cause in fact of the plaintiff's demise - likely an impossible task since causation in such circumstances is almost certainly the result of a constellation of factors; a constellation to be explored by something called eco-epidemiology. More on that another day.

• Email This
• Print
• Share Link