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At a Glance:
Austin v. Kerr Mcgee Refining Corp.
June 29, 2000
25 S.W.3d 280
Published Opinion

Austin v. Kerr Mcgee Refining Corp.

Court of Appeals of Texas,


Tara AUSTIN, et al., Appellants,


KERR–McGEE REFINING CORP., et al., Appellees.

No. 06–99–00087–CV.


Submitted May 16, 2000.


Decided June 29, 2000.

Attorneys & Firms

*282 Steve R. Baughman, Baron & Budd, P.C., Dallas, for appellants.

Thomas B. Taylor, Taylor & Eggleston, Houston, for appellees.

Before GRANT and ROSS, JJ.

*283 O P I N I O N

Opinion by Chief Justice CORNELIUS.

Tara Austin and other aligned parties appeal from the trial court’s ruling excluding their experts’ scientific evidence of medical causation. They contend that the trial court erred in applying Havner. After carefully reviewing the record, we conclude that the trial court did not abuse its discretion in excluding the evidence. Accordingly, we affirm the trial court’s judgment.

From 1983 to 1991, Richard Alan Austin worked in the pipe inspection industry near Lone Star, Texas, readying pipes for use on oil rigs. From 1983 to 1985, Austin worked for Tuboscope Vetco, International, cleaning pipes for inspection. From 1985 to 1986, he worked for A.D. Surratt Pipe Inspection Company, where he also cleaned pipes. To clean the pipes, he placed them in a waist-high vat of cleaning solvents, generically called “mineral spirits.” In 1986, Austin left Surratt and returned to Tuboscope where, in addition to cleaning pipes, he inspected pipes for imperfections by spraying them with mineral spirits and examining them under a florescent light in an enclosed inspection booth. In 1991, Austin left the pipe inspection industry to work elsewhere.

In 1994, Austin was diagnosed with chronic myelogenous leukemia (CML). He died from the disease within four months of the diagnosis. In 1996, Austin’s wife, Tara Austin, individually and as executrix of Austin’s estate, and as next friend of Austin’s parents and two minor children (collectively, the Austins), brought a wrongful death action against Kerr–McGee Refining Corp., Irvin Enterprises, Inc., Basis Petroleum, Inc., and Delta Distributors, Inc. (collectively, Kerr–McGee), asserting claims of negligence, gross negligence, strict liability, and breach of implied warranties. The Austins alleged that the mineral spirits the defendants manufactured and distributed, to which Austin was exposed while working at Tuboscope and Surratt, contained benzene, a harmful chemical that caused Austin’s CML and death.

In January 1999, Kerr–McGee moved to exclude the Austins’ experts’ scientific and medical testimony, contending that the testimony was unreliable under Havner. Based on its decision to exclude the Austins’ experts’ testimony and on the parties’ stipulation, the court granted summary judgment for Kerr–McGee.

The Austins first contend that the trial court properly relied on Robinson but abused its discretion in relying on Havner as a basis for excluding their experts’ testimony. They contend that Robinson prescribes factors for evaluating the reliability of expert testimony for purposes of determining its admissibility, while Havner prescribes additional “statistical-significance” requirements for evaluating reliability for purposes of determining its legal sufficiency. The Austins recognize that both Robinson andHavner require courts to evaluate the reliability of evidence, but *284 they argue that a determination of reliability for separate and distinct purposes calls for the application of separate and distinct standards. Because the evidence was excluded, the Austins contend that the trial court should have determined reliability based on the test for reliability as set out in Robinson only.

Although overlapping, in that both types of analyses examine the reliability of the evidence, in theory the admissibility and sufficiency reviews are distinct because they involve the resolution of different issues: Admissibility involves whether the evidence makes a fact more probable or less probable than it would be without the evidence, whereas legal sufficiency involves whether the evidence amounts to more than a scintilla. However, Havner requires that both reviews be governed by the same test of reliability; therefore, the distinction between the two reviews has little practical effect.

Robinson and Havner are both toxic tort cases. In Robinson, the plaintiffs claimed that a fungicide damaged their pecan orchard; in Havner, the plaintiff claimed that her use of an anti-nausea drug during pregnancy caused her child’s birth defects. The plaintiffs in both cases presented experts testifying that the chemical at issue caused injuries. See Havner, 953 S.W.2d at 709. On appeal, the issue in Robinson was whether the court abused its discretion in excluding the testimony, while in Havner the issue was whether the admitted testimony was sufficient to show causation.

In Robinson, the Texas Supreme Court addressed the proper standard for the admission of expert testimony under Rule 702 provides,

If scientific, technical, or other specialized knowledge will assist the trier of fact to understand the evidence or to determine a fact in issue, a witness qualified as an expert by knowledge, skill, experience, training, or education may testify thereto in the form of an opinion or otherwise.

TEX.R. Rule 702: 1) the extent to which the theory has been or can be tested; 2) the extent to which the techniques rely on the subjective interpretation of the expert; 3) whether the theories have been subjected to peer review and/or publication; 4) the techniques’ potential rate of error; 5) whether the underlying theories or techniques have been generally accepted as valid by the relevant scientific community; and 6) the nonjudicial uses which have been made of the theories or techniques.

In Havner, the Texas Supreme Court addressed whether the evidence at issue in that case was legally sufficient, i.e., some evidence, to support the jury’s finding of causation. See Id. at 714.

We know from Havner that a determination of reliability is appropriate for both admissibility and legal sufficiency. See Atterbury, 978 S.W.2d at 192. If the defendant objects to the reliability of the evidence before or at trial, as he should to preserve a no-evidence objection, and the trial court excludes the evidence, the reviewing court views the trial court’s decision by the lenient abuse of discretion standard. If the trial court overrules the defendant’s objection, the defendant may seek review of the trial court’s decision in a sufficiency of the evidence point of error to an appellate court. Id.

The distinction between the legal sufficiency standard and the admissibility standard is blurred because both standards are governed by the same test for reliability. If the testimony is admitted as reliable evidence, an appellate court may overturn the jury verdict, not on the ground that the trial court erred in admitting unreliable expert testimony, but on the ground that the evidence, under the same standard, is unreliable for legal sufficiency purposes. Despite the overlap between these standards, if certain evidence is admitted because wholesale exclusion of the evidence is inappropriate, the totality of causation evidence may nonetheless be legally insufficient to support a verdict. Daubert, 509 U.S. at 596, 113 S.Ct. 2786. But Havner failed to explain how the same evidence could be admissible as reliable but still be insufficient, since courts are to apply the *286 same Robinson factors in evaluating reliability for both admissibility and sufficiency.

The debate primarily has been over whether theHavner ‘s statistical-significance requirements when determining whether evidence is admissible under Robinson. Having carefully considered the facts and holdings of Robinson and Havner, we are unable to conclude that Havner requires a standard separate and distinct from that in Robinson that a trial court must ignore in determining admissibility.

In Havner, before applying the Robinson factors to the evidence, the court was concerned with “arm[ing] [itself] with some of the basic principles employed by the scientific community in conducting studies....” id. at 718.

The Austins contend that Havner, 953 S.W.2d at 715–16.

We cannot conclude, where the evidence the proponent seeks to have admitted is the proponent’s only evidence of causation, that a court evaluating the reliability of the evidence for admissibility must *287 apply a different test than the court evaluating the reliability of the evidence for legal sufficiency. Instead, we conclude that a trial court could not properly review the reliability of scientific testimony based on epidemiological studies if it were required to ignore the basic principles articulated in Havner that the scientific community employs in conducting such studies. Thus, we conclude that a trial court’s determination of admissibility requires application of the Robinson factors as well as application of Havner ‘s statistical-significance requirements in determining the reliability and admissibility of causation evidence admitted at trial).

In the trial court’s final judgment excluding the Austins’ experts’ testimony, the court stated that it was excluding the evidence on the basis of both Havner and Havner ‘s epidemiological, statistical-significance requirements.

The Austins overlook the fact that the court’s letter also stated that the motion to exclude would be granted under the guidelines of both Havner and Robinson. But even if we assume the letter indicates the court found that the evidence satisfied Kates v. Smith, 556 S.W.2d 630, 632 (Tex.Civ.App.-Texarkana 1977, no writ). The final judgment excluded the evidence on the basis of both Havner and Robinson. The Austins contend that the trial court erred only in excluding their evidence of causation on the basis that it failed to satisfy the statistical-significance requirements of Havner.

The decision to admit evidence rests within the sound discretion of the trial court. In re Perritt, 973 S.W.2d 776, 780 (Tex.App.-Texarkana 1998, no pet.)

*288 In determining reliability, the trial court is not to determine the truth or falsity of the expert’s opinion. Rather, the trial court’s role is to determine whether the expert’s opinion is relevant and whether the methods and research underlying the opinion are reliable.Robinson, 923 S.W.2d at 557.

Teitelbaum’s theory of general causation is that exposure to benzene increases the risk for the development of all types of myeloid leukemia.

Kerr–McGee contends that Teitelbaum’s conclusion is based on a reliable foundation only if the epidemiological evidence shows a relationship between benzene exposure and CML specifically. We disagree. Teitelbaum’s conclusion may be reliable if it is supported by evidence that shows what Teitelbaum contends it shows, that there is an association between benzene exposure and the development of all types of leukemia equally, including CML.

In forming his opinion that exposure to benzene causes all types of cancers have been reported, but are in need of further evaluation.” (Emphasis added.) Importantly, in the abstract preceding the study, the study was noted as having concluded, “Analyses by work area, duration of exposure, and cumulative dose index did not show patterns suggestive of a causal association between exposure to benzene and any particular category of death.”

Teitelbaum also based his theory in part on the “Decoufle” study, a study conducted of 259 employees of a chemical plant where benzene was used.5 Four leukemia following occupational exposure to benzene.

Teitelbaum also relied on the “Paxton” article, an update of an earlier study that reported a statistically-significant number of leukemogenesis. A part per million year is the number of parts per million per year multiplied by the number of years of exposure.

The Travis study7 concluded there was a statistically-significant increase in all lymphohematopoietic disorders. Eighty-two patients with chronic granulocytic leukemia (CGL), which Teitelbaum testified is a description previously used for CML, were observed. The others were nonleukemia. The study *290 stated that preliminary analysis indicates that the age and sex-adjusted relative risk of all confirmed lymphohematopoietic disorders was statistically significant.

The Yin study8 identified excess mortality and incidence of lymphohematopoietic malignancies, which includes many malignancies including lymphocytic leukemia and CML was not statistically significant.

The Austins also relied on two studies from Italy and France, whose findings were similar to the other studies.

Thus, no study on which Teitelbaum relies has recognized or posited that exposure to benzene causes CML specifically. Some find specific relationships between benzene and AML that reach the level of statistical significance. A few conclude that exposure to benzene causes leukemia generally.

As we stated, Teitelbaum must further show that all types of leukemia, including CML, derive.

The Austins point to the testimony of Teitelbaum, who testified that benzene causes genetic mutations in the pluripotential stem cell, the cell from which all bone marrow cells through division derive. Teitelbaum said that benzene causes the stem cell to mutate and when this cell divides, the new cells carry the mutation. He testified that when these mutated cells receive additional “hits” from exposure to carcinogens, such as from further exposure to benzene or exposure to radiation, the cells further mutate and eventually a leukemia develop at least as a result of the initial exposure to benzene.

As support for Teitelbaum’s explanation, the Austins cite a flow chart they created for purposes of trial that illustrates the concept Teitelbaum described. They also point to a paper written by Dr. Philip Fialkow, on which Teitelbaum relied. They cite a passage in which Fialkow states the following:

CML and at least one form of AML develop clonally in stem cells that have multipotent differentiative expression.... [M]yeloid leukemia.

Philip J. Fialkow, leukemia are so closely related in terms of how and why they develop that they can be treated interchangeably. The Austins have not indicated whether Tietelbaum’s theory can be or has been tested and have not directed us to any location in the record where other scientists espouse this theory.

*291 The Austins cite the testimony of Kerr–McGee’s toxicology expert, Dr. Gary Krieger, who testified that benzene can affect the pluripotential stem cell. However, Krieger testified that benzene can attack at a variety of places and that benzene-related Philadelphia Chromosome may cause CML independently of other possible causes.

The Austins also contend that the epidemiological studies’ authors’ grouping choices demonstrate that the different leukemias are derived from the same source. In one study, the author, recognizing that very few studies reviewed medical records or histologic data to ensure correct categorization of diseases, expressed a need for more accurate categorization. Travis, supra, at 92.

Additionally, we find persuasive the rulings on a similar issue in two cases tried in the federal courts. In the cases of Chambers, 81 F.Supp.2d at 664–65.

The Austins concede that there is insufficient reliable data to establish an association between exposure to benzene and CML. In their brief to this Court, they state that CML is a relatively rare disease and “there simply are not enough cases of the disease for epidemiologists to generate a statistically-significant relative risk. .... [N]o benzene-exposed population is significantly large to generate the numbers ... required to create statistical significance.” *292 A similar concession was made by the plaintiffs in Havner, 953 S.W.2d at 728. The lack of reliable scientific evidence cannot be an excuse for imposing liability without proof of causation.

Likewise, the Austins did not offer scientifically reliable evidence of specific causation, i.e., that Austin was exposed to benzene at all, or if he was, to what degree or level. Specific causation requires that a plaintiff show that the injured person is similar to those in the epidemiological studies, that he was exposed to the same substance, and that the exposure or dosage levels were comparable to or greater than those in the studies. Mitchell, 165 F.3d at 781.

The Austins must show that benzene probably, or more likely than not, caused Austin’s CML. See Robinson, 923 S.W.2d at 558.

Before he worked at Tuboscope and Surratt, Austin held a job where he was a bystander to pipe inspection activities involving radiographic techniques. The job required that Austin wear a radiation badge that monitored the levels of radiation he received. Teitelbaum requested data regarding Austin’s radiation exposure from his employee badge.

Teitelbaum suggested that radiation exposure could not have been an independent cause of Austin’s CML, stating, “[T]he contributing cause [benzene exposure] stands whether we model it [radiation] or not.” However, he also suggested that radiation may have been an alternative cause. He stated that he did not find any alternative cause, “other than the radiation issue,” and he further testified, “Because radiation is always ... or potentially a ‘one-hit’ kind of experience, single ionization could cause a genetic change and remains a viable possibility....” Teitelbaum went on to opine that radiation exposure was unlikely or less likely than benzene to have caused Austin’s CML because of the size of the dose of radiation that Austin received. However, like the Austins’ treatment of the Philadelphia Chromosome as an alternative cause of Austin’s CML, the record does not contain a full explanation of the dose-size or the duration of Austin’s radiation exposure, or a full explanation of the reason for Teitelbaum’s decision to exclude radiation as a cause. Teitelbaum stated that he received Austin’s badge but did not have data from which to model a radiation dose, suggesting at best that the dose of radiation was insignificant.

We conclude that the Austins’ scientific evidence does not adequately exclude exposure to radiation as a cause of CML. The Austins concede that exposure to radiation is a recognized cause of Id. at 781.

After thorough and careful review of the Austins’ contentions, as well as the record testimony and exhibits they cite, we conclude that the Austins have failed to demonstrate the reliability of their scientific evidence as to either general or specific causation. They also have failed to exclude other plausible causes with reasonable certainty. We conclude that the trial court acted within its discretion in excluding the Austins’ causation evidence on the basis that it failed to satisfy the requirements of Robinson and Havner. Accordingly, we affirm the judgment.



Daubert v. Merrell Dow Pharm., Inc., 509 U.S. 579, 113 S.Ct. 2786, 125 L.Ed.2d 469 (1993).


953 S.W.2d 706 (Tex.1997).


The Austins ask that we apply the no-evidence standard because in excluding the evidence the trial court, they contend, relied only on Havner,a case that applied the no-evidence standard. The trial court relied on both Robinson and Havner, and because Havner involved a challenge to the legal sufficiency of admitted evidence, the no-evidence standard was appropriate in Havner, but it is inappropriate here.


G.G. Bond, et al., An Update of Mortality Among Chemical Workers Exposed to Benzene, BRITISH JOURNAL OF INDUSTRIAL MEDICINE 685 (1986).


Pierre Decoufle, et al., Mortality Among Chemical Workers Exposed to Benzene and Other Agents, 30 ENVIRONMENTAL RESEARCH 16 (1983).


Mary B. Paxton, et al., Leukemia Risk Associated with Benzene Exposure in a Pliofilm Cohort: I. Mortality Update and Exposure Distribution, 14 RISK ANALYSIS 147 (1994).


Lois B. Travis, et al., Hematopoietic Malignancies and Related Disorders Among Benzene–Exposed Workers in China, 14 LEUKEMIA AND LYMPHOMA 91 (1994).


Song–Nian Yin, et al., A Cohort Study of Cancer Among Benzene–Exposed Workers in China: Overall Results, 29 AMERICAN JOURNAL OF INDUSTRIAL MEDICINE 227 (1996).


O. Wong, An Industry–Wide Mortality Study of Chemical Workers Occupationally Exposed to Benzene, 44 BRITISH JOURNAL OF INDUSTRIAL MEDICINE 365 (1987).

End of Document