holding that because appellant failed to actually offer testimony into evidence, appellant could not complain on appeal about its exclusion
How later courts described this case
- holding that because appellant failed to actually offer testimony into evidence, appellant could not complain on appeal about its exclusion
- rejecting Daubert ⅛ “scientific methodology” approach as the controlling standard of evidence in Texas negligence cases and in suits brought under the Jones Act, 46 U.S.C.App. § 688
- rejecting Daubert's "scientific methodology" approach as the controlling standard of evidence in Texas negligence cases and in suits brought under the Jones Act, 46 U.S.C.App. § 688
Written by the judges who cited it.
The opinion
ROBERTSON, Justice,
concurring and dissenting.
Maritime Overseas Corporation appeals from a judgment rendered in favor of appel-lee for more than $12.6 million in damages. Appellant raises fifteen points of error challenging the sufficiency of the evidence supporting the award of damages and challenging the amounts of the awards of actual damages, the awards of punitive damages, and the exclusion of certain evidence.
This case was argued before a panel of this court in June 1992. The panel consisted of Justices Junell, Robertson, and Draughn. On December 31, 1992, a majority opinion was issued, joined in by Justices Junell and Robertson, in which we found insufficient evidence to support the damages award. Justice Draughn dissented without an opin *800 ion. Justice Junell, not having sought reelection, retired that day. Subsequently, appel-lee’s motion for rehearing en bane was granted and over fourteen months ago this case was re-argued before the court en banc, Chief Justice Brown not sitting because of his recusal. Since then, Justice Bowers (who was a member of the court on rehearing) has passed away. This case is ripe for resolution.
I concur in three holdings of the majority: (1) that punitive damages are not recoverable in a general maritime case, (2) that there is no evidence that appellant arbitrarily denied maintenance and cure justifying an award of punitive damages, and (3) that prejudgment interest was wrongfully awarded. However, instead of the extended discussion by the majority, I merely note that as a matter of substantive federal law, prejudgment interest is simply not recoverable when a damage award is based on a jury verdict finding both Jones Act negligence and unseaworthiness, without providing any basis for determining which portion of the damage award, if any, is attributable to the unseaworthiness rather than the Jones Act negligence. Colburn v. Bunge Towing, Inc., 883 F.2d 372, 378 (5th Cir.1989). This is true even though neither party suggests “that the jury be requested to allocate damages between the Jones Act and unseaworthiness claims.” McPhillamy v. Brown & Root, Inc., 810 F.2d 529 (5th Cir.1987). Further, McPhillamy holds that unless “there is an evidentiary footing for separating the damages caused by unseaworthiness and Jones Act negligence, the jury cannot be asked to apportion the damages.” Id. at 532 . In that case there was a single harm from a single cause and the court stated that “even if he [the plaintiff] had asked for apportionment, he would not have been entitled to it.” Id. The same facts are present in this ease.
I dissent to the holding of the majority opinion that there is sufficient evidence to support the jury’s finding that appellee suffered $8,576,000 in actual damages. Finally, I dissent to the summary disposition of appellant’s points of error 13, 14 and 15 complaining of the awards for past and future medical expenses, past and future physical pain and mental anguish, and past and future physical impairment.
Appellee was a steward’s assistant aboard the S/T OVERSEAS ALASKA. On August 27,1982, the chief steward sprayed undiluted diazinon in the galley, pantry, and dry storeroom. The next morning, crew members noticed a strong odor of insecticide and the captain ordered cleaning of the sprayed areas. Appellee participated in the clean-up for approximately five hours without any protective gear to prevent inhalation or dermal contact. Subsequently, appellee began complaining of a headache and eye irritation. When the ship reached port in New Orleans two days later, appellee received treatment at the New Orleans General Hospital emergency room.
Testimony indicated that exposure to orga-nophosphates can lower the levels of an enzyme called acetylcholinesterase, also called cholinesterase, which is essential to the normal transmission of messages from one nerve to another. Diazinon is an organophosphate. Cholinesterase levels are measured by testing the red blood cells and the blood serum. Blood tests performed at the emergency room revealed that appellee’s level of choli-nesterase was depressed. Appellee’s red blood cell level of cholinesterase was .40, while the average range for men of appellee’s age is .44 to 1.09. Appellee’s serum level of cholinesterase was .53 or .54, while the average range is 1.90 to 3.80, The examining physician, Dr. Velma Campbell, concluded that appellee suffered organophosphate exposure but determined that this exposure was not serious enough to hospitalize appellee or to administer antidote medications. Appellee received medication for eye irritation and was advised to return for a follow-up visit. Appellee returned to work and served as a crew member for appellant for the rest of that year.
In June 1983, appellee filed suit against appellant under 46 U.S.C.AApp. § 688 (the Jones Act) alleging gross negligence, and under general maritime law alleging unseaworthiness. Appellee claimed that he was suffering from delayed neurotoxic effects caused by the exposure to diazinon. Appel-lee’s deposition testimony and the testimony *801 regarding his medical records indicate that appellee continued to suffer from eye problems, that he had trouble sleeping, that he was depressed, anxious, and had memory problems, that he had high blood pressure, and that he suffered gastrointestinal problems. Appellee’s wife testified that appellee is depressed, is more irritable, has headaches, muscle weakness, memoxy problems, and has been unable to hold a job.
The jury found in favor of appellee on both claims and awarded appellee approximately $12.6 million including $1 million in punitive damages, and $1 million in exemplary damages for failure to pay maintenance and cure. The trial court awarded appellee an additional $1,871,728.00 in prejudgment interest.
In point of error one, appellant contends the trial court erred in denying appellant’s motion for a new trial because there is insufficient evidence to support the jury finding that appellee suffered $8,576,000.00 in actual damages. Appellant concedes that appellee suffered short-term effects from the exposure to diazinon. Thus, appellant does not contest damages for the medical treatment appellee received in New Orleans in 1982 or for the loss of two days of work. Appellant does contest damages awarded for appellee’s claim of delayed neurotoxicity on the ground that appellee’s expert testimony was speculative and not based on reasonable medical probability.
A trial court has wide discretion in granting a motion for new trial. Champion Int'l Corp. v. Twelfth Court of Appeals, 762 S.W.2d 898, 899 (Tex.1988). We must uphold the trial court’s decision absent a showing of a manifest abuse of discretion. Id. Because appellant contends there was factually insufficient evidence to support the award of damages, we must consider, weigh, and examine all of the evidence. Plas-Tex., Inc. v. United States Steel Corp., 772 S.W.2d 442, 445 (Tex.1989). We may set aside the verdict only if the evidence is too weak to support the finding, or if the finding is so against the overwhelming weight of the evidence that it is manifestly unjust and clearly wrong. See Garza v. Alviar, 395 S.W.2d 821, 823 (Tex.1965).
Appellant asserts that we must apply federal law to this case because appellee’s causes of action are both federal causes of action. The Texas supreme court has stated:
Where applicable and properly invoked, general maritime law preempts state causes of action and remedies, consistent with the longstanding desire of Congress and the judiciary to achieve uniformity in the exercise of admiralty jurisdiction.
Texaco Refining & Marketing v. Estate of Dau Van Tran, 808 S.W.2d 61, 64 (Tex.1991), cert. denied, 502 U.S. 908 , 112 S.Ct. 301 , 116 L.Ed.2d 245 (1991). In Texaco, the court was determining whether a plaintiff could recover mental anguish damages, allowed under state law, but prohibited under general maritime law. Id. at 63. Because the court found that the plaintiff had properly invoked remedies under general maritime law, the court reversed the award of damages for mental anguish. Id. at 64. In American Dredging Company v. Miller, — U.S. -, 114 S.Ct. 981 , 127 L.Ed.2d 285 (1994), the supreme court made it clear that in exercising in personam jurisdiction in a maritime case, a state court may adopt such remedies and attach to them such incidents as it sees fit so long as it does not attempt to make changes in the “substantive maritime law.” There, the court held that the doctrine of forum non conveniens concerned procedural as opposed to substantive law and that, therefore, the federal law on the subject did not preempt state law. Id. — U.S. at -, 114 S.Ct. at 983 . See also Exxon Corporation v. Chick Kam Choo, 881 S.W.2d 301 (Tex.1994). Since the question of causation is one of substantive law, our review of the case law convinces me that federal case law regarding evidence of causation should control in this case.
Generally, however, Texas law is consistent with federal law regarding expert testimony on causation. To recover damages, a plaintiff must prove by competent evidence a causal nexus between the event sued upon and the injuries alleged. See Morgan v. Compugraphic Corp., 675 S.W.2d 729, 732 (Tex.1984). “Causal connection ... must rest in reasonable probabilities; otherwise, *802 the inference that such actually did occur can be no more than speculation and conjecture.” Insurance Co. of North America v. Myers, 411 S.W.2d 710, 713 (Tex.1966). See also Gideon v. Johns-Manville Sales Corp., 761 F.2d 1129, 1137 (5th Cir.1985). Whether the evidence rests in reasonable probabilities depends upon the substance of the expert’s testimony. Myers, 411 S.W.2d at 713 . “Expert testimony that the event is a possible cause of the condition cannot ordinarily be treated as evidence of reasonable medical probability except when, in the absence of other reasonable causal explanation, it becomes more likely than not that the condition did result from the event.” Lenger v. Physician’s Gen. Hosp., 455 S.W.2d 703, 706 (Tex.1970).
Toxic tort cases such as this present juries with questions upon which medical or scientific experts may disagree. See Brock v. Merrell Dow Pharmaceuticals, Inc., 874 F.2d 307, 309 (5th Cir.), modified on reh’g, 884 F.2d 167 (5th Cir.1989), cert. denied, 494 U.S. 1046 , 110 S.Ct. 1511 , 108 L.Ed.2d 646 (1990) (hereinafter referred to as Brock I and Brock II). Whether a substance caused an injury is a scientific question that requires the testimony of expert medical professionals. See Insurance Co. of North America v. Myers, 411 S.W.2d 710, 713 (Tex.1966). An expert’s testimony “must be based upon ‘reasonable medical probability', as opposed to a mere ‘possibility', since almost anything is ‘possible’ in the field of medicine.” Duff v. Yelin, 721 S.W.2d 365, 370 (Tex.App.—Houston [1st Dist.] 1986), aff'd 751 S.W.2d 175 (Tex.1988). Thus, if the proof consists of mere medical possibilities, it is insufficient to establish a causal connection. Duff, 751 S.W.2d at 176 .
Confronting a challenge to the evidence of causation in a toxic tort case, the Fifth Circuit held that courts should “critically evaluate the reasoning process by which the experts connect data to their conclusions in order for courts to consistently and rationally resolve the disputes before them.” Brock I, 874 F.2d at 310 . In Brock, the Fifth Circuit analyzed the types of evidence regarding causation typically offered in a toxic tort case. The court noted that the most useful and conclusive type of evidence is the epidemiological study which attempts “to define a relationship between a disease and a factor suspected of causing it....” Id. at 311. Regarding such studies, the court added:
To define that relationship [between a disease and its alleged cause], the epidemiologist examines the general population, comparing the incidence of the disease among those people exposed to the factor in question to those not exposed. The epidemiologist then uses statistical methods and reasoning to allow her to draw a biological inference between the factor being studied and the disease’s etiology.
Id. As the court also mentioned, epidemiological studies do not necessarily exclude other possible causes for the same disease. Id. Two epidemiological studies of the effects of the drug Bendectin were admitted into evidence in Brock. See id. at 312. One study did not support a causal connection between Bendectin and birth defects. Id. The other study found a greater risk of birth defects, but that the risk was not statistically significant. Id. Because the plaintiffs did not present any statistically significant epidemiological proof that the drug causes birth defects, the court held that the evidence was insufficient to enable a trier of fact to make a reasonable inference as to causation. 1 See id. at 315; Brock II, 884 F.2d at 167 .
In a later case, the Fifth Circuit again addressed questions about an expert’s testimony regarding causation in a toxic tort case. See Christophersen v. Allied-Signal Corp., 939 F.2d 1106 (5th Cir.1991), cert. denied, — U.S. -, 112 S.Ct. 1280 , 117 L.Ed.2d 506 (1992). In Christophersen , the trial court had excluded an expert’s opinion that exposure to certain chemicals at a plant caused cancer. Id. at 1109 . In determining whether the trial court erred in excluding this testimony, the Fifth Circuit set forth three threshold requirements for the admissibility of expert testimony: (1) whether the *803 witness is qualified to express an expert opinion on the topic at issue, (2) whether the data upon which the expert relies are of the same type other experts in the field reasonably rely upon in forming their opinions, and (3) whether in reaching his conclusion, the expert used a “well-founded methodology or mode of reasoning, one ‘sufficiently established to have gained general acceptance in the particular field in which it belongs’.” Id. at 1110-11 . Even if the testimony meets these three requirements, it may still be excluded if the testimony’s “potential for unfair prejudice substantially outweighs its probative value.” Id. at 1110 . See also Fed. R.Evid. 403.
The trial court in Christophersen had criticized the expert’s testimony on the grounds that the facts and data underlying the opinion were inaccurate and incomplete and that the expert offered no scientific methodology to support his conclusion. Id. at 1113-15 . In reviewing these criticisms, the Fifth Circuit first found that the expert over-estimated the duration of the decedent’s exposure to certain chemicals and had no accurate data regarding the chemical composition of the fumes in the plant where the alleged exposure occurred. Id at 1113. Thus, the court agreed that the trial court could properly reject expert opinions founded on critical facts that are untrustworthy. Id. at 1114 . The expert in question also testified that the kind of evidence most often used to establish causation are epidemiological studies, animal testing, and in vitro testing. Id. at 1115 . Despite his testimony regarding the main methodologies, this expert offered no methodology to support his conclusion that the types of chemicals used at the plant were associated with the form of cancer found in the decedent. Id. Because the expert offered no well-founded methodology to support his opinion regarding causation, the Fifth Circuit concluded that the expert’s opinion was no more than a scientific hunch and was inadequate to support a judgment in favor of the plaintiff. Id.
Appellee contends that Christophersen has lessened the Brock requirements for evidence supporting causation in toxic tort cases. I disagree. Neither Brock nor Christophersen holds that epidemiological studies are required to establish causation in toxic tort cases; however, both cases note their importance. See Brock I, 874 F.2d at 313 ; Christophersen, 939 F.2d at 1115 . Furthermore, both cases indicate that expert opinions unsupported by some type of well-founded scientific reasoning or methodology constitute mere speculation, insufficient to support a judgment. See Brock I, 874 F.2d at 315 ; Christophersen, 939 F.2d at 115 . Both Brock and Christophersen have now been strengthened by Daubert v. Merrell Dow, Inc., — U.S. -, 113 S.Ct. 2786 , 125 L.Ed.2d 469 (1993).
Based on the standards set forth in Brock and Christophersen , and now Daubert , appellant contends the conclusions of appellee’s experts amounted to speculation because they were unsupported by scientific studies or other well-founded methodologies establishing a link between diazinon exposure and delayed neurotoxicity. My review of the evidence leads me to agree. Appellee’s syllogism, 2 which appears to have been adopted by the majority, is:
Some organophosphates can cause delayed neurotoxicity;
Diazinon in an organophosphate;
Diazinon, therefore, must cause delayed neurotoxicity.
*804 This is a fallacy. The issue, as framed by the majority, is not whether organophos-phates cause delayed neurotoxicity; the issue is simply: does exposure to diazinon, one of many organophosphates, cause delayed neu-rotoxicity?
While the United States Supreme Court was faced with the question of the admissibility of evidence in Daubert , the same principles the court there announced apply to weighing the sufficiency of the evidence. Indeed, in approving Brock v. Merrell Dow Pharmaceuticals, referred to above, the Daubert court sanctioned the reversal of the judgment for insufficient evidence of causation “rather than wholesale exclusion under an uncompromising ‘general acceptance’ test,” noting that devices such as reversal of a judgment or direction of judgment are “the appropriate safeguards where the basis of scientific testimony meets the standards of Rule 702.” (emphasis supplied). — U.S. at -, 113 S.Ct. at 2798 .
The Daubert court held that the subject of an expert’s testimony must be “scientific knowledge.” Id. — U.S. at -, 113 S.Ct. at 2795 . “Scientific,” the court said, “implies a grounding in the methods and procedures of science;” and that the word “knowledge” “connotes more than subjective belief or unsupported speculation.” Id. Finally, in order to qualify as “scientific knowledge,” “an inference or assertion must be derived by the scientific method.” Id.
Daubert commands that in determining whether the reasoning or methodology underlying “expert testimony” is scientifically valid, “many factors will bear on the inquiry.” Id. — U.S. at -, 113 S.Ct. at 2796 . While not setting forth a “definitive checklist or test,” the supreme court stated that the key question to be answered is “whether it can be (and has been) tested.” Id. Other considerations are: (1) whether the theory or technique has been subjected to peer review and publication; (2) the known or potential rate of error; and (3) whether the conclusion has been generally accepted in the scientific community. Id. — U.S. at -, 113 S.Ct. at 2797 . While the court recognized the inquiry is a flexible one, “[t]he focus of course, must be solely on principles and methodology, not on the conclusions that they generate.” Id. (emphasis supplied)
Appellee offered the testimony of four experts on the issue of causation. Dr. Edward Ezrailson, who holds a Ph.D. in biochemistry, testified that he has studied the effects of certain organophosphates on humans, using animal tests, for the Environmental Protection Agency. Dr. Ezrailson admitted that his EPA study was of the effects of malathion and parathion on the skeletal muscle protein metabolism in rats. No paper was published as a result of this study. Based on the amount and duration of appellee’s exposure to diazinon, Dr. Ezrailson concluded that ap-pellee’s symptoms were caused, in reasonable medical probability, by this exposure.
On cross-examination, Dr. Ezrailson agreed that his research involved a review of the scientific literature. He testified that he relied, to some extent, upon the opinions of the authors writing the chapters in a textbook entitled “Toxic Effect of Pesticides.” Dr. Ezrailson agreed with a statement in this text that individual compounds within a similar chemical class may range from extremely toxic to practically nontoxic. He also agreed with the statement that red blood cell choli-nesterase, rather than that in blood plasma, provided a more accurate reflection of the inhibition of acetylcholinesterase in the nerve cells. Dr. Ezrailson testified that the average time for restoration of acetylcholinester-ase in a person with diazinon exposure was two weeks to three months.
Dr. Ezrailson testified that he based his conclusion, at least in part, on his review of the scientific literature. Although Dr. Ezrailson testified about fourteen different scientific articles regarding the effects of exposure to organophosphates, 3 the record eon- *805 tains only two articles that were actually admitted into evidence. 4 A review of the testimony indicates that only two articles addressed the effects of diazinon exposure, and these concerned fatal ingestion or poisoning. None of the articles concludes that diazinon causes delayed neurotoxicity. Testimony about the conclusions of some of the articles indicated that symptoms of delayed neurotoxicity caused by certain organophos-phates usually occur within one to three weeks after exposure.
Another expert witness for appellee was Dr. Alfred R. Johnson, a Doctor of Osteopathy, who works at the Environmental Health Center of Dallas, Inc. This center provides health care to the public emphasizing the health effect and treatment of environmental exposure. Dr. Johnson testified that he has treated appellee and other patients suffering from exposure to diazinon or other similar chemicals. Dr. Johnson’s diagnosis was “or-ganophosphate toxic exposure with relating damage in the form of delayed toxicity reaction and permanent nerve damage,” but that he had not seen anyone, other than Ellis, who had delayed neurotoxicity from diazinon exposure. Dr. Johnson testified that exposure to diazinon can cause delayed central nervous system symptoms and that the length of time before such symptoms appear can vary with the individual from a couple of weeks to a few months. Dr. Johnson testified that, in his opinion, based upon reasonable medical probability, appellee’s current problems were caused by the August 1982 exposure to diazinon. Dr. Johnson based this diagnosis on his examination of appellee and on a review of appellee’s medical records showing exposure to diazinon and depressed levels of cholinesterase. Dr. Johnson testified that he was familiar with the literature regarding organophosphate poisoning, but he could not recall any studies dealing only with *806 diazmon and the long-term effects of diazinon exposure on humans.
Appellee also called Dr. Francis J. Waiek-man as an expert witness. Dr. Waiekman’s area of specialty is pediatrics, but he has taken postgraduate courses in many areas, including allergy, toxicology, and clinical immunology. He is board certified in pediatrics, allergy, clinical immunology, utilization review and quality assurance, and environmental medicine. Dr. Waickman evaluates and treats people who have chemical sensitivities and who have been exposed to pesticides. In his examination of appellee, Dr. Waickman found symptoms of central nervous system involvement. Specifically, Dr. Waickman found slow verbal responses and below normal reasoning and recall. Based on his examination, Dr. Waickman testified that appellee’s problems are delayed neuro-toxic effects from diazinon exposure. Dr. Waickman testified that he is familiar with the scientific literature regarding diazinon and organophosphates and he has no doubts that these chemicals can cause long-term effects on human beings. Dr. Waickman, however, offered no case histories or studies of any kind, nor any personal experiences with patients or research, linking diazmon with delayed neurotoxicity.
Finally, appellee offered the testimony of Dr. Richard Austin, a clinical psychologist who has had experience treating people who have been poisoned by various chemicals. Dr. Austin personally examined and evaluated appellee, gave him a battery of psychological tests, reviewed the medical records of doctors who had treated appellee, elicited historical information from appellee’s family and friends, and reviewed scientific literature regarding organophosphate poisoning. Dr. Austin concluded that appellee suffered nervous system damage resulting in emotional problems caused by the chemical poisoning in 1982. Dr. Austin was familiar with a study, admitted into evidence, that was performed on behalf of the EPA by Drs. Savage, Keefe, and others, entitled “Chronic Neurological Sequelae of Acute Organophosphate Pesticide Poisoning.” This study involved testing of individuals chronically exposed to a variety of pesticides, not including diazinon. Dr. Austin agreed that appellee suffers from many of the same impairments and exhibits similar test results to those discussed in the literature resulting from organophosphate poisoning. Dr. Austin testified that there are authoritative studies showing that orga-nophosphate poisoning can cause delayed neurotoxic effects. The testimony regarding these studies indicated no conclusion that diazinon causes delayed neurotoxicity.
Finally, the majority relies upon the testimony of Dr. James Carter, described as “a family doctor” from Ellis’ hometown. Dr. Carter, however, never treated Ellis until almost two years after his diazinon exposure. While Dr. Tim Lee Carter (Dr. James Carter’s uncle) purportedly saw Ellis five or six months after his exposure, there is no documentation of that visit in any medical records. The first indication of a visit even to Dr. Tim Lee Carter is a letter Tim Lee Carter wrote to appellee’s counsel in August of 1983. That letter does not describe any of the symptoms Dr. James Carter later claimed Ellis had; instead, it merely asks appellee’s counsel to keep him apprised of any progress in the litigation. There is then a record of three visits in 1984. Dr. Tim Lee Carter prescribed an antibiotic in February, associated with a complaint of fever, another antibiotic for a cold in May, and later prescribed Tagament, used in treating peptic ulcers, in October. Dr. James Carter saw Ellis briefly for the flu in May 1984 and did not see Ellis again until 1986. Other than visits for an ingrown toenail and bronchitis, Dr. Carter’s medical records are unremarkable.
Unlike the expert in Christophersen , the expert witnesses here based their opinions on accurate underlying facts, such as estimation of the duration of appellee’s exposure to diaz-inon. Thus, we should turn to whether there was sufficient evidence supporting the experts’ testimony that, in reasonable medical probability, diazinon caused the injuries alleged by appellee. Brock and Christophersen require that an expert’s conclusions regarding causation rest upon a well-founded scientific methodology. See Brock I, 874 F.2d at 315 ; Christophersen, 939 F.2d at 1115 . Daubert requires that an expert’s con- *807 elusions regarding causation rest upon “scientific knowledge.” — U.S. at -, 113 S.Ct. at 2795 . Appellee’s experto all testified that they based their conclusions on past experience treating patients exposed to orga-nophosphates and/or on published scientific studies showing a connection between exposure to organophosphates and delayed neuro-toxicity. These experts admitted, however, that none of the published studies documented a connection between delayed neurotoxicity and exposure to diazinon. Only one study referenced by appellee’s experts addressed diazinon and this study concerned a fatal ingestion of the pesticide and not whether a less than fatal exposure can cause delayed neurotoxicity. Testimony also indicated that the effects of exposure to compounds within a similar chemical class can vary widely.
Appellant presented the testimony of three doctors, Dr. Velma Campbell, Dr. Eric Corn-stock, and Dr. Francisco Perez. Dr. Campbell treated appellant in the emergency room at the New Orleans General Hospital. Campbell testified that some pesticides can cause delayed neurological symptoms, but that to her knowledge, diazinon is not one of these.
Dr. Perez is a clinical psychologist specializing in neuropsychology and behavioral medicine. Perez did not examine appellant, but reviewed his medical and psychological records and reviewed the literature regarding organophosphates. Perez testified that a worsening of a patient’s psychological condition is not a typical symptom caused by exposure to diazinon. Perez concluded, based on his review of the records and literature, that appellant’s symptoms are most likely unrelated to the diazinon exposure.
Dr. Erie Comstock, a medical toxicologist, testified that he had experience treating persons exposed to toxic substances, 80-100 of which involved diazinon. Comstock also reviewed appellant’s medical records and the literature about organophosphates, but did not examine appellant. Comstock agreed that appellant initially exhibited mild acute effects from the exposure, including eye irritation, slight weakness, diarrhea, headaches, and vomiting, but based on his experience and review of the records and literature, Comstock concluded that appellant has suffered no delayed effects related to the diazi-non exposure.
Comstock testified that diazinon is an “unrestricted use” pesticide, which means that it does not cause or has not been shown to cause severe, impairing long-term effects. Comstock noted that his personal experience treating persons exposed to diazinon has not indicated that diazinon causes delayed neuro-toxicity. Furthermore, Comstock testified that diazinon has been widely used by the public for many years and that, if it caused delayed neurotoxicity, this would have been identified. Finally, Comstock testified that none of the literature supports the conclusion that diazinon causes delayed neurotoxicity, and that there is literature concluding diazi-non does not cause delayed neurotoxicity. 5
Even if expert testimony rests upon a well-founded methodology, it will nevertheless be insufficient to support a finding of causation if the studies or tests fail to show a statistically significant relationship between exposure to the substance and the kind of injury alleged. See Brock I, 874 F.2d at 315 ; Brock II, 884 F.2d at 167 . Although the studies relied upon by appellee’s experts support a conclusion that certain pesticides falling within the organophosphate classification can cause delayed neurotoxicity, these studies do not establish any relationship, statiscally significant or otherwise, between diazinon and delayed neurotoxicity. Absent a well-founded scientific methodology showing some connection between exposure to diazinon and the kind of injuries alleged by appellee, the conclusions of appellee’s experts regarding causation were speculative and insufficient to enable the jury to make a reasonable inference as to causation. See Brock I, 874 F.2d at 315 ; Brock II, 884 F.2d at 167 . None of appellees experts had ever seen or treated a single person with “delayed neurotoxicity” due to diazinon poisoning. Despite over thirty years of diazinon’s wide use, including use
*808 as a common household pesticide, the appel-lee’s experts could not point to a single case history, animal study or in vitro study— much less any epidemiological study on humans — to link diazinon as a cause of delayed neurotoxicity. The majority has not undertaken the review commanded by Daubert of the “reasoning or methodology underlying the testimony” to assess its scientific validity. Because there is no “scientific knowledge,” as commanded by Daubert , concluding that diazinon causes delayed neurotoxicity, appel-lee’s damages should be limited to those resulting from short-term exposure. Consequently, appellant’s first point of error should be sustained.
The majority dismiss appellant’s complaints on the amounts of damages awarded for past and future medical expenses, past and future physical pain and mental anguish, and past and future physical impairment with the bare conclusion that all the evidence has been considered and we “find it sufficient to support the jury’s findings.” I disagree.
The jury awarded $38,000 for past medical expenses and $850,000 for future medical expenses. In point of error 13, appellant sought a new trial or a remittitur based upon insufficient evidence. I believe appellant is entitled to a remittitur as to future medical expenses for two reasons. First, there is insufficient evidence, as discussed in the first point, that appellant’s injuries resulted from exposure to diazinon. However, there is the further reason that the award of $850,000 is excessive. Dr. Johnson, an osteopath, testified appellant’s future medical expenses would probably be $600,000, 6 based upon a $10,000 a year program of vitamin C injections, regular doctor visits, clean living, and sauna-type therapy. This award is shockingly excessive.
The jury awarded $228,000 for past physical pain and mental anguish and $4,000,000 for future physical pain and mental anguish. In point of error 14, appellant sought a new trial or a remittitur based upon insufficient evidence. In addition to the reasons discussed in the first point, I believe appellant is entitled to a remittitur.
Appellee did not testify at trial. His mother testified that “at times he feels better but he has a lot of headaches and so much chest pain but has times he has felt better for a short period.” Other than headaches and chest pain, appellee complains of stomach aches, insomnia, muscle aches and memory loss. This 4 million dollar award is shockingly excessive. Further, appellant argues and I agree, the awards for physical pain and suffering and for physical impairment (point of error 15) are cumulative. These awards compensate appellee for an identical injury. The only “physical impairment” that appellee can assert is the impairment due to physical pain — aches and pains and nausea. In the same vein, the only “suffering” appellee can assert is due to these very same symptoms. This is not a ease of an appellee suffering actual physical damage or disfigurement, for there is no evidence of either in the record. Thus, the injuries in this case — pain and suffering and physical impairment — are indistinguishable, and to award damages for both permits a double recovery. I believe appellant is entitled to a remittitur.
The jury awarded $250,000 for past physical impairment and $1,000,000 for future physical impairment. In point of error 15 appellant sought a new trial or a remittitur because of insufficient evidence.
In addition to the reasons discussed in the first point of error, there are additional reasons why appellant’s point is well-taken. Ap-pellee offered no evidence that he has suffered or will suffer actual physical impairment. The only medical tests ever conducted on appellee, including neurological tests such as EEG and peripheral nerve tests, have been normal. The evidence offered— limited to appellee’s descriptions of his symptoms, and opinions that his verbal responses are “slow,” and that he “looks older than his chronological age,” — is insufficient to support an award for physical impairment. To recover for past and future impairment
*809 [the] injured party must sustain the burden of proving that the effect of his physical impairment extends beyond any impediment to his earning capacity and beyond any pain and suffering to the extent that it produces a separate and distinct loss that is substantial and for which he should be compensated.
Allen v. Whisenhunt, 603 S.W.2d 242, 243 (Tex.Civ.App.—Houston [14th Dist] 1981, writ dism’d) (emphasis added). In this case, Ellis has not proved that the effect of his impairment extends beyond any pain and suffering and loss of earning capacity. See also Valdez v. Church’s Fried Chicken, 683 F.Supp. 596, 615 (W.D.Tex.1988) (no recovery for physical manifestations — avoidance of stimuli, difficulty sleeping, etc. — related to the mental anguish). I believe appellant, at the very least, is entitled to a remittitur.
For all the reasons discussed, I respectfully dissent.
MURPHY, J., concurs in this opinion.
. In Brock I, the Fifth Circuit found "the lack of conclusive epidemiological proof to be fatal to the Brock's case.” 874 F.2d at 313 . On rehearing, the court changed this sentence and others indicating a requirement of conclusive epidemiological studies to a requirement of "statisticaEy significant epidemiological proof." Brock II, 884 F.2d at 167 .
. Appellee asserts and the majority seems to agree that because diazinon is an organophos-phate, a scientific study that links any organo-phosphate to neuropathy or neurotoxicity should be sufficient to link diazinon to neurotoxicity. This rationale runs contrary to all commonly understood scientific principles. "Organophos-phate" is a broad chemical family name that encompasses a diverse group of compounds. For example, ATP (adenine triphosphate) is also an organophosphate. ATP, however, occurs naturally in the human body, and relatively large amounts of ATP are essential for our metabolism and energy production. Exposure to ATP certainly does not cause neurotoxicity; however, under the majority’s rationale, simply because ATP is an organophosphate and scientific studies have linked some organophosphates to neurotox-icity, ATP must also be linked to neurotoxicity.
Diazinon is a distinct chemical compound, one of many different organophosphates, and is itself marketed under a variety of brand names (e.g., "Spectricide”). In fact, appellee’s exhibit 63 lists over 30 different organophosphate pesticides in an appendix, each with its unique chemical name and composition.
. Dr. Ezrailson's testimony referenced the following articles: (1) "Sequelae of Acute Organo-phosphate Poisoning” by Dr. I.R. Tabershaw, which concluded that exposure to certain orga-nophosphates can result in delayed symptoms (did not list diazinon as one of the organophos-phates studied); (2) "Delayed Neurotoxicity and Other Consequences of Organophosphates Ester-ase,” by Ronald Baron, not admitted into evidence, noting that certain organophosphates have been shown to cause a delayed neurotoxic effect, but that this neuropathy is always pro *805 ceeded by a period of approximately 7-14 days (article did not mention diazinon); (3) "Correlations Between Recovery Rate of Neurotoxic Est-erases and Sensitivity of the Organic and Phosphate Induced Delayed Neurotoxicity,” by Car-rington, not admitted into evidence but does not even mention diazinon; (4) "Long Term Effects of the Organophosphate Sarin on EEG in Monkeys and Humans,” by Duffey and Burchfiel, not admitted into evidence, stating that many, but not all organophosphates have been found to cause delayed neurotoxicity; (5) two articles by Finklestein entitled, "Brain Acetylcholinesterase After Acute Parathion Poisoning,” and "CNS Involvement in Acute Organophosphate Poisoning: Specific Pattern of Toxicity, Clinical Correlates, and Antidotal Treatment,” both of which concerned parathion and neither were admitted into evidence but does not consider or discuss diazi-non; (6) "Anxiety Associated with Exposure to Organophosphate Compounds,” by Levin, not admitted into evidence, which concerned effects on farm workers who received chronic exposure to organophosphates and found no relationship between exposure and depression; (7) "Behavioral Effects of Organophosphate Pesticides in Men" by Levin and Midski, not admitted into evidence; (8) “Spatial Memory Impairment and Central Muscarinic Receptor Loss Following Prolonged Treatment with Organophosphate” by McDonald, not admitted into evidence, which studied the effects following daily exposure to two insecticides, not including diazinon, over a fourteen-day period; (9) “Delayed Neurotoxic Effects of Some Organophosphorous Compounds," by Johnson, not admitted into evidence, delayed neurotoxicity manifests itself 7-14 days after exposure but not all organophosphates induce delayed neurotoxicity; (10) "Evidence of Necrosis in Human Intercostal Muscles,” by Wecker, Mrak, and Dettbam, not admitted to evidence, which concerned a study of a man who received a fatal dose of malathion and diazinon but did not link diazinon to delayed neurotoxicity; (11) “Fatal Diazinon Poisoning in Man,” by Hendricks, not admitted into evidence, which concerned a person who committed suicide by ingesting diazinon but did not link diazinon with delayed neurotoxicity; (12) “Central Actions of Organophosphate Agents,” by Karczmar, not admitted into evidence, which studied the mental effects of exposure to certain organophosphates, not including diazinon; (13) "Organophosphate Polyneuropathy,” by Lotty, not admitted into evidence, that concluded symptoms of organo-phosphate induced delayed neurotoxicity usually begin one to three weeks after acute exposure and lists six chemicals that cause delayed neuro-toxicity but does not list diazinon.
. The two studies admitted into evidence include: (1) "Chronic Neurological Sequelae of Acute Or-ganophosphate Pesticide Poisoning," by Savage, Keefe, Mounce, Heaton, Lewis and Burear, offered into evidence by appellee which evaluated the latent neurological effects of organophosp-hate poisoning on 100 patients, none of which had been exposed to diazinon; and (2) “Pesticides & brain-function changes in a controlled environment” by Rea, Butler, Laseter, and De-Leon, offered into evidence by appellant, which studied whether environmentally controlled conditions improve the symptoms of patients who have been exposed to pesticides, other than diazi-non.
. Comstock specifically noted that the article entitled ‘‘Poisoning Due to Organophosphate Insecticides,” (author unknown) concluded that diazi-non, as well as certain other insecticides, did not produce neuropathy.
. Dr. Austin, the psychologist, estimated appel-lee’s future psychological treatment costs to be $250,000.