Judge Robreno has done a heroic job of resolving the “elephantine mass” of asbestos litigation stuck in the federal system (MDL 875) but his attempt to resolve an ancient Greek paradox came up short. In a memorandum opinion (Mortimer v. A.O. Smith Corp., et al.) addressing Ford’s motions to exclude Plaintiff’s experts intent on opining that his renal cell cancer was caused by exposure to asbestos, the judge tries to draw a distinction between “any exposure” (a/k/a “every breath”) and cumulative exposure yet misses, I think, the point. Meanwhile, Ford decided to run the risk factor play – by which I mean that it wants to assert as alternate causes those risk factors for renal cell cancer gleaned from plaintiff’s medical records (e.g. hypertension) while denying that asbestos isn’t really a risk factor for renal cell cancer and so cannot be a cause. When everyone agrees that a risk factor is the same thing as a cause a lot of unfortunate pronouncements about science usually follow and that’s very much what happened here.
First though the Sorites paradox. A grain of sand is not a heap of sand. Add a second grain and it’s still not a heap. Add a third and still no heap. Thus adding a grain of sand to something that isn’t a heap won’t make it one. Similarly take a heap of sand. Remove one grain and it remains a heap. Remove another and it’s still a heap. Thus removing a grain of sand from a heap won’t make it a non-heap. Swap asbestos fiber for grain of sand and you get the point of this post.
When you don’t require plaintiff to quantify a range of exposure but instead create a rule whereby plaintiffs win with a heap but lose with just grains you wind up with competing arguments about heaps and grains that cannot be rationally resolved. Here Plaintiff’s experts claim to have solved the problem of discerning when sand goes from grains to heap calling their theory “cumulative exposure” and further that plaintiff experienced a heap of it. Ford argued that it was still just a bunch of grains of sand. Judge Robreno sided with plaintiffs.
After carefully reviewing the opinion of Dr. Frank (and that of Dr. Bralow), the Court notes that, as stated by Plaintiff, the opinions are “cumulative exposure” opinions, which are – in substance and, by definition – different from the “any exposure” opinion often proffered by experts in asbestos litigation and rejected by the Pennsylvania Supreme Court. For this reason, the Court declines to accept Defendant’s argument that the experts’ opinions are inadmissible on grounds that they are the same as the “any exposure” opinion.
Apparently the court was persuaded in part by the fact that Ford “does not dispute that there is evidence of frequent, regular and proximate exposure to asbestos from brakes for which it is liable” and the fact that Ford’s own data demonstrates that “the number of asbestos fibers to which Plaintiff would have been exposed from Ford brakes would be at least in the millions and possibly in the billions.” The problem is that neither frequency, regularity nor proximity to a billion asbestos fibers does a cumulative exposure heap make.
A single breath while resting is about 500 cc of air. The mid-range for an average person is 15 breaths per minute. That comes to about 4 billion cc of air per year. Using the typical asbestos background level of 0.0001 fibers/cc in non-industrial urban/suburban areas that means 400,000 fibers per year, and nobody thinks that’s a heap. Using 0.04 f/cc, which is below not only OSHA’s Permissible Exposure Level (PEL) but also below its “action level” yields 35 million fibers over the course of 240 8-hour work days, over a billion fibers in a typical work life and not even OSHA thinks that’s a heap.
The only sensible course is to stop arguing about whether the fibers alleged constitute a few or a heap and to instead make plaintiffs quantify a reasonable range of exposures, compare those to reliable risk estimates for the disease in question given the putative causal agent and see if plaintiff has a causal claim that can be justified. The proposed “cumulative exposure” theory is not in fact an answer to the Sorites paradox; it’s actually just another version of the Small Glasses approach whereby plaintiffs try to change the conversation (or at least their analogies) when people start to ask whether their new causal argument isn’t really just their old tautology.
Well, this post has gone on long enough already but I want to make one other point and that has to do with Ford’s embrace of risk factor epidemiology. Risk factor epidemiology it must be remembered is not science. Don’t take my word for it, re-read The Emptiness of the Black Box. I understand completely why Ford wants to talk about obesity, high blood pressure, age and smoking – they’re all risk factors for renal cell cancer, and they’re all either under Plaintiff’s control, unavoidable, or at least not Ford’s fault. The problem is that once you play the risk-factors-are-causes game you wind up playing by plaintiffs’ rules. You forfeit the argument that observational epidemiology studies cannot demonstrate causation when you rely on observational epidemiology studies for your defense.
You also wind up with opinions like the one in Mortimer in which a court holds that a risk factor is the same thing as a cause, that Plaintiff’s experts have two reliable studies that say asbestos is a risk factor for renal cell cancer, that injuries may have more than one cause so that the problem of multiply present risk factors is no obstacle to recovery and that Plaintiff’s experts reliably reasoned their way to their opinions from these foundations. The problems with this are many but here are the main ones: (1) By definition the crowing of a rooster is a risk factor for the sun’s rise, so remember that correlation is NOT causation; (2) the vast majority of studies of renal cell cancer show that all of the proposed risk factors combined account for less than half of all cases; (3) the vast majority of renal cell risk factor epidemiology studies have failed to suggest asbestos is a risk factor thus Plaintiff’s two studies are no more “reliable” than a broken watch that’s accurate twice a day; (4) the multiple sufficient causes idea as presented here is fatally flawed – if you found in your closet a shirt that had been cut and on your dresser a knife, scissors and a razor it wouldn’t even cross your mind that they all, each and every one, caused the cut; and, (5) relying on observational epidemiological studies demonstrating weak effects is actually not a reliable way to reason about causation – if it were we wouldn’t be in the midst of a reproducibility crisis in biomedical science and billions wouldn’t have been wasted on theories arising out of nothing more than statistically significant findings – read Scientific Method – Statistical Errors again if you have any lingering doubt.
So in closing, remember that if you lie down with risk factor dogs you’ll get up with risk factor fleas.