Yesterday, in celebration of the first day of summer, the Fifth Circuit handed down a decision in a case that looks like a laundry list of expert witness fallacies. Fortunately, the district judge and two of the three appellate judges kept their analytical faculties intact. Johnson v. Arkema Inc., Slip op., 2012 WL ___ (5th Cir. June 20, 2012) (per curiam) (affirming exclusion of expert witnesses).
The plaintiff had worked in a glass bottling plant, where on two occasions in 2007, he was in close proximity to the defendant’s ventilation hood, designed to be used with a chemical, Certincoat, composed of monobutyltin trichloride (MBTC), an organometallic compound. Plaintiff claimed that the ventilation was inadequate and that as a result he was exposed to MBTC as well as hydrochloric acid.
The plaintiff sustained some acute symptoms and ultimately was diagnosed with a “chemical pneumonia,” by his treating physician. The plaintiff further claimed that his condition progressively worsened, and that he was ultimately diagnosed with “pulmonary fibrosis,” a “severe restrictive lung disease.” The plaintiff filed reports from two expert witnesses – Richard Schlesinger, a toxicologist, and Charles Grodzin, a pulmonary physician – in support of his claim that his pulmonary fibrosis was caused by overexposure to MBTC and hydrochloric acid (HCl).
Plaintiff’s claim led to defendant’s Rule 702 challenge, which the trial court sustained, and the appellate court affirmed.
A basic problem faced by plaintiff is that there was virtually no evidence that MBTC or HCl causes pulmonary fibrosis. Undaunted, the plaintiff and his expert witnesses pushed on, but the lack of epidemiologic evidence associating MBTC or HCl with pulmonary fibrosis proved reliably harmful to plaintiff’s case.
General Acceptance
Plaintiff could point to no evidence that MBTC or HCl causes pulmonary fibrosis. Slip op. at 7. Given the delay in manifestation of the fibrosis after the plaintiff’s rather limited, discrete exposures, the court recognized that epidemiologic evidence was important, if not essential, to plaintiff’s case. Without epidemiology, the plaintiff retreated to generalities – the chemicals cause lung irritation, lung injury, etc. One concurring judge was taken in, but the majority of the panel saw through the dodge.
Anecdotal Evidence
Without epidemiologic evidence, the plaintiff invoked anecdotal evidence that other employees sustained similar lung injuries. The problem, however, for even this low-level evidence was that other employees experienced only transitory symptoms, which quickly resolved. Id. at 4 -5, 27.
Post Hoc, Ergo Propter Hoc
Focusing only on himself as an anecdote with n =1, the plaintiff, and his expert witnesses, argued that temporal sequence of his exposure and his pulmonary fibrosis was itself evidence of causality. Neither the trial court nor the appellate court found this much of an argument. Id. at 16 n.13, 18.
Mechanism in Search of Data – Schlesinger’s irritant theory
Schlesinger argued that both MBTC and HCl are pulmonary irritants, which can cause inflammation, and pulmonary fibrosis results from inflammation. Id. at 8. True, but not all irritants cause pulmonary fibrosis. Chronicity and dose are important considerations. Whether these chemicals, under exposure conditions experienced by plaintiff, were capable of causing pulmonary fibrosis, cried out for evidence.
The Material Safety Data Sheets (MSDS)
The plaintiff argued that the MSDS for HCl established that this chemical was “severely corrosive to the respiratory system.” Id. at 11-12. The defendant’s own MSDS for MBTC stated that MBTC “causes respiratory tract irritation.” Id. at 16. The courts saw these arguments as transparently absent evidence. None of the MSDS identified pulmonary fibrosis; nor did they specify (1) the underlying scientific support, or (2) the relevant duration and exposure needed to induce any particular adverse outcome.
Animal Studies
For both MBTC and HCl, plaintiff adverted to animal studies, but the courts found that the animal studies failed to support the plaintiff’s expert witnesses’ opinions and the plaintiff’s claims. The studies were readily distinguishable in terms of dose, duration, and disease outcome. In particular, none of the studies showed that the chemicals caused pulmonary fibrosis. Id. at 7, 12 (baboon study of HCl showed impairment but not fibrosis at 10,000ppm for one year, quite unlike plaintiff’s exposure), 16-17 (rat inhalation study of MBTC, six hrs/day, five days/wk, up to 30 mg/m3, with toxicity but no mention of lung fibrosis).
Regulatory Limits
Plaintiff argued that HCl levels were multiples of the OSHA limits, but the courts would not credit regulatory exposure limits are evidence of harmfulness because of the precautionary nature of many regulations. Id. at 14. Furthermore, the disease outcomes of regulatory concern did not appear to be pulmonary fibrosis for the chemicals involved.
Res Ipsa Loquitur
The plaintiff argued that causation was a matter of common sense and general experience. Even if his expert witnesses did not have valid, reliable evidence, the jury could make the causal determination without scientific evidence. Id. at 26. Rejected.
Chemical Analogies
The defendant’s expert witness acknowledged that tin oxide can cause pulmonary fibrosis. Id. at 28. This admission, however, came without any qualification about what exposure or duration data might be needed to support a conclusion about specific causation in the plaintiff. Id. Furthermore, tin pneumoconiosis, or stannosis, is known as a benign lung disease, unassociated with impairment or disability. Like simple silicosis, stannosis is a picture change on chest radiograph, without diminution of performance on pulmonary function tests. Agency for Toxic Substances and Disease Registry, A Toxicological Profile for Tin and Tin Compounds at 30 (2005).
Differential Diagnosis
Plaintiff’s pulmonary expert witness, Dr. Grodzin, tried to bootstrap specific causation by assuming general and putting it in the “differentials” for him to embrace. Id. at 19. A fallacious form of reasoning, but the courts here were on top of it.
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The panel did reverse the trial court’s grant of summary judgment. The gate closed a little too fast to permit scrutiny of plaintiff’s claim of acute injuries and symptoms, which were less dependent upon epidemiologic evidence.
