Opinion ID: 76908
Heading Depth: 2
Heading Rank: 1

Heading: Application of Broad Scientific Principles

Text: 24 O'Donnell testified that ephedrine belongs to a family of drugs called the sympathomimetics. These drugs stimulate the cardiovascular system by raising heart rate and blood pressure. He drew key conclusions about ephedrine's toxicity from its classification as a sympathomimetic. A close examination of his testimony, however, shows that he dramatically dilutes the value of these conclusions, which in turn, impugns his methodology. About ephedrine's family or drug class connection and effects, he left a trail of equivocation by making the following statements at various points in his testimony: Sympathomimetics can constrict blood vessels. And when you constrict blood vessels, you may raise blood pressure. Sympathomimetics stimulate the heart and increase the pulse, increase the heart rate. If you stimulate the heart, you may cause an abnormal heart rate or an abnormal heart rhythm. If you constrict blood vessels, if it happens in a cerebral vessel in the brain, it may cause vasospasm which may lead to a stroke. If you stimulate or cause a constriction in the coronary blood vessel that can cause vasospasm and it may lead to chest pain, angina, arrhythmia, or myocardial infarction. He also testified that aggravation of blood pressure is something that the ephedrine and caffeine in Metabolife or any product containing those drugs can do.  He further explained that the ephedrine/caffeine combination  can elevate blood pressure and stimulate the heart, and it has been reported to be associated with strokes and heart attacks. Or as O'Donnell stated: this may be dangerous for some patients.  O'Donnell's equivocation about the effects of sympathomimetics exposes a tenuous basis for his opinions about Metabolife's profound toxicity — that any level of caffeine combined with ephedrine poses an unreasonable risk of harm. 25 O'Donnell likewise offered nothing specific about how Metabolife affects individuals. When asked how one tablet of Metabolife might increase heart rate, he could not give an answer and explained that it would vary from patient to patient. He also could not say how much it might elevate a patient's blood pressure. He agreed that effect would vary from patient to patient and admitted that it might not raise a person's blood pressure at all. He further said that aerobic exercise impacts blood pressure and heart rate more than the maximum recommended dosage of Metabolife. 26 Although he agreed that a drug's effect is dose-driven, he offered no testimony about the dose of Metabolife required to injure Plaintiffs or anyone else. He could not say how much is too much. In explaining his opinion about the extreme danger of Metabolife, while at the same time offering no opinions about dose, he said: [t]hat's why I always answer with potential, may, or could. On the other hand, he admitted that the amount of ephedrine in Metabolife 356 does not exceed the amount of ephedrine in the hundreds of over-the-counter products available to the public. Likewise, he conceded that many people take drugs containing ephedrine at the same time they ingest large amounts of caffeine from coffee, and that the recommended dose of Metabolife 356 contains 72 milligrams of ephedrine, roughly half the FDA allowable limits on ephedrine. His lack of testimony about the dose-response relationship combined with his vague testimony about significant individual variations leaves a muddle of ambiguity that undermines his opinions. 27 Because of this ambiguity, O'Donnell laid no reliable groundwork for determining the dose-response relationship for either ephedrine or ephedrine and caffeine. This signals a methodology problem. In toxic tort cases, [s]cientific knowledge of the harmful level of exposure to a chemical plus knowledge that plaintiff was exposed to such quantities are minimal facts necessary to sustain the plaintiff's burden.... Allen v. Pennsylvania Eng'g Corp., 102 F.3d 194, 199 (5th Cir.1996). Or, as the Court of Appeals for the Tenth Circuit explained in Mitchell v. Gencorp, 165 F.3d 778, 781 (10th Cir.1999), to carry the burden in a toxic tort case, a plaintiff must demonstrate `the levels of exposure that are hazardous to human beings generally as well as the plaintiff's actual level of exposure to the defendant's toxic substance before he or she may recover,' (quoting Wright v. Willamette Indus., Inc., 91 F.3d 1105, 1106 (8th Cir.1996)); see also Moore v. Ashland Chem. Inc., 151 F.3d 269, 278 (5th Cir.1998) (excluding expert testimony which offered no scientific support for his general theory that exposure to toluene solution at any level would cause RADS.). 6 28 Although Plaintiffs can testify about how much Metabolife 356 they took, O'Donnell could not provide any opinions about the general dose-response levels for Metabolife's toxicity, i.e., the dose or level of exposure at which it causes harm. O'Donnell opined that any level is too much, but this statement conflicts with the importance of individual responses to toxins — [b]ecause of individual variation, a toxic agent generally will not cause disease in every person exposed. Green, supra, at 392. 29 When analyzing an expert's methodology in toxic tort cases, the court should pay careful attention to the expert's testimony about the dose-response relationship. The dose-response relationship is [a] relationship in which a change in amount, intensity, or duration of exposure to an agent is associated with a change — either an increase or decrease — in risk of disease. Id. at 390. The expert who avoids or neglects this principle of toxic torts without justification casts suspicion on the reliability of his methodology. 30 To help federal judges deal with Daubert issues in toxic tort cases, the Federal Judicial Center published several articles in the Journal of Law and Policy under the title Science for Judges I: Papers on Toxicology and Epidemiology. 12 J.L. & POL'Y 1 (2003). 7 The article entitled Scientific Judgment and Toxic Torts — A Primer in Toxicology for Judges and Lawyers by Dr. David Eaton provides valuable insight for understanding how to assess Daubert issues in these cases. Id. at 5. Dr. Eaton, Ph.D., is a toxicologist and Professor of Environmental and Occupational Health Sciences at the University of Washington. Id. He also serves as Associate Dean for Research, School of Public Health and Community Medicine at the University. Id. 31 In his article Eaton describes some key principles of toxicology that a court should consider in any attempt to establish whether a chemical exposure was causally related to a specific adverse effect or disease in an individual. Id. at 9. Foremost among these principles is the dose-response relationship. 32 Dr. Eaton explains that the relationship between dose and effect (dose-response relationship) is the hallmark of basic toxicology. Id. at 15. Dose is the single most important factor to consider in evaluating whether an alleged exposure caused a specific adverse effect. Id. at 11. Often low dose exposures — even for many years — will have no consequence at all, since the body is often able to completely detoxify low doses before they do any damage. Id. at 13. Furthermore, for most types of dose-response relationships following chronic (repeated) exposure, thresholds exist, such that there is some dose below which even repeated, long-term exposure would not cause an effect in any individual. Id. at 16. 33 These essential principles of toxicology directly contradict several of what O'Donnell calls the broad principles of pharmacology upon which he bases his opinions. But more importantly, it shows something about O'Donnell's methodology: he does not follow the basic methodology that scientists use to determine causation — the dose-response relationship. 34 Beyond explaining the importance of the dose-response relationship, Dr. Eaton offers four scientific criteria for proving causation between a chemical exposure and a particular illness in an individual. First, the toxic substance in question must have been demonstrated to cause the type of illness or disease in question. Id. at 38. This focuses on the issue of general causation. O'Donnell has failed to show that Metabolife 356 causes either strokes or heart attacks. Furthermore, the medical literature does not support this opinion. O'Donnell has simply substituted his own ipse dixit for scientific proof on this essential issue. 35 Second, the individual must have been exposed to a sufficient amount of the substance in question to elicit the health effect in question. Id. at 39. This requires not simply proof of exposure to the substance, but proof of enough exposure to cause the plaintiff's specific illness. This focuses on the issue of individual causation. 36 As already shown, O'Donnell offers no opinion about the dose of Metabolife that caused ischemic strokes in three Plaintiffs and a heart attack in the other. He only said that any amount of Metabolife is too much, which clearly contradicts the principles of reliable methodology delineated by Eaton. 8 37 Third, the chronological relationship between exposure and effect must be biologically plausible. Id. On this point Eaton explains that if a disease or illness in an individual preceded the established period of exposure, then it cannot be concluded that the chemical caused the disease, although it may be possible to establish that the chemical aggravated a pre-existing condition or disease. Id. at 39-40. This also focuses on individual causation. 38 The issue of the chronological relationship leads to another important point — proving a temporal relationship between taking Metabolife and the onset of symptoms does not establish a causal relationship. In other words, simply because a person takes drugs and then suffers an injury does not show causation. Drawing such a conclusion from temporal relationships leads to the blunder of the post hoc ergo propter hoc fallacy. 39 The post hoc ergo propter hoc fallacy assumes causality from temporal sequence. It literally means after this, because of this. BLACK'S LAW DICTIONARY 1186 (7th ed.1999). It is called a fallacy because it makes an assumption based on the false inference that a temporal relationship proves a causal relationship. As the Court of Appeals for the District of Columbia explained in a similar context: [i]n essence, the requirement of `adequate documentation in scientific literature' ensures that decision makers will not be misled by the post hoc ergo propter hoc fallacy — the fallacy of assuming that because a biological injury occurred after a spill, it must have been caused by the spill. Ohio v. U.S. Dept. of the Interior, 880 F.2d 432, 473 (D.C.Cir.1989). 40 Fourth, and finally, the likelihood that the chemical caused the disease or illness in an individual should be considered in the context of other known causes. Eaton, supra, at 40. This refers to the background risk of a specific disease — the risk that everyone faces of suffering the same malady that a plaintiff claims without having exposure to the same toxin. 41 A reliable methodology should take into account the background risk. The background risk is not the risk posed by the chemical or drug at issue in the case. It is the risk a plaintiff and other members of the general public have of suffering the disease or injury that plaintiff alleges without exposure to the drug or chemical in question. The background risks include all those causes of a disease, whether known or unknown, excluding the drug or chemical in question. So, the background risk for heart attack is very high because heart disease is the leading cause of morbidity and mortality in America. See Heart Attacks, Nat'l Heart, Lung, & Blood Inst., at http://www.nhlbi.nih.gov (last visited Dec. 27, 2004). Likewise, stroke is the third leading cause of death in America and the leading cause of disability. See Jeffrey L. Arnold, Ischemic Stroke, emedicine, at http://www.emedicine.com (last visited Dec. 27, 2004). Ischemic strokes, like three Plaintiffs suffered in this case, account for 80% of all stroke cases. Id. Thus, in evaluating the reliability of the experts' opinions on general causation, it would help to know how much additional risk for heart attack or ischemic stroke Metabolife consumers have over the risks the general population faces. If ephedrine or an ephedrine/caffeine combination do not increase the incidence of heart attack and ischemic stroke in persons who ingest it, as opposed to all those who do not and still have heart attacks and strokes, that fact would reduce the likelihood that Metabolife harmed Plaintiffs. Likewise, if Plaintiffs could show that taking Metabolife increases the risk of heart attack and ischemic stroke beyond the usual incidence of these common diseases, that would support their methodology in this case. O'Donnell offered no evidence of additional risk. The court must assume that it does not exist. (Indeed, O'Donnell testified that he did not know the background risk for stroke and heart attack.) 42 Toxicologists and medical doctors doing research commonly assess risks posed by drugs, chemicals and other agents. A quick internet search of TOXNET for risk assessment or background risks will show thousands of articles about risks for various drugs and chemicals — Plaintiffs' experts offered no such evidence. See generally, Thomas v. Hoffman-LaRoche, Inc., 949 F.2d 806, 816 (5th Cir.1992); Norfolk & W. Ry. Co. v. Ayers, 538 U.S. 135, 156, 123 S.Ct. 1210, 155 L.Ed.2d 261 (2003). 43 Now as to these four criteria for proving causation, O'Donnell failed to demonstrate a link between Metabolife and the types of injuries Plaintiffs suffered as required by the first criteria. He also failed to show that Plaintiffs had sufficient individual exposure to Metabolife to cause the medical problems as required by the second criteria, and he further failed to show evidence of an increased incidence of strokes and heart attacks from Metabolife 356 over the background risk as required by the fourth criteria. There is evidence in the case supporting the third criteria, the chronological relationship between exposure and effect, but this does not overcome the failure of proof on the other three propositions. 44 Finally, on the speculative nature of his testimony, O'Donnell attempts to anoint his opinions by claiming that he based them on the broad principles of pharmacology. In the Daubert context, such phrases have little value. They are not shibboleths that distinguish those experts that offer reliable science from those who foist junk science on the court. The expert's assurances that he has utilized generally accepted scientific methodology [are] insufficient. See Moore, 151 F.3d at 276. Such statements can spring just as quickly from the ipse dixit of the expert as some ultimate opinion about causation or toxicity. As the Supreme Court explained in Joiner: nothing in either Daubert or the Federal Rules of Evidence requires a district court to admit opinion evidence that is connected to existing data only by the ipse dixit of the expert. 522 U.S. at 147, 118 S.Ct. 512. Moreover, [t]he trial court's gatekeeping function requires more than simply `taking the expert's word for it.' Fed.R.Evid. 702 advisory committee's note (2000).