Full opinion text
ORDER RODRIGUEZ, District Judge. On this date, the Court considered Defendants’ Motion to Exclude Expert Testimony of Dr. Malin Dollinger (docket no. 196), Plaintiffs’ Response (docket no. 232), and Defendants’ Reply (docket no. 250). In addition, the Court has reviewed voluminous additional material submitted by both sides, including but not limited to, Defendants’ Memorandum of Science and Law in Support of Motions to Exclude Expert Testimony (docket no. 198), both sides’ responses to the questions posed by the Court at the December 2003 status conference (including two volumes of appendices filed by Plaintiffs), submissions filed after the Daubert hearings, and the various other motions and affidavits filed by the parties. After careful consideration of the submitted briefs, the evidence, and the applicable legal principles, the Court GRANTS Defendants’ Motion to Exclude Expert Testimony of Dr. Malin Dollinger (docket no. 196). Because Dr. Dollinger’s testimony is the Plaintiffs’ sole evidence regarding specific causation, the Court also GRANTS Defendants’ Motion for Summary Judgment Based on Plaintiffs’ Lack of Admissible Proof (docket no. 191) and DISMISSES this case WITH PREJUDICE. All other pending motions are dismissed as moot. Background This is a toxic tort case with federal jurisdiction under the Price-Anderson Act, 42 U.S.C. § 2210. See Acuna v. Brown & Root, Inc., 200 F.3d 335, 339 (5th Cir.2000). The Plaintiffs include fifty-three individuals who have or have had various forms of cancer and numerous related claimants. The individuals with cancer resided or worked in or around Karnes County, Texas, where the Defendants engaged in uranium mining and milling activities. Uranium was discovered in Karnes County in 1954 and the first uranium mill began operating in 1961 near Falls City. The uranium was removed from the ground and transported to the mills, where the natural uranium was extracted from the ore to produce yellowcake. The waste material, called tailings, was placed in tail-ings piles or ponds around the facility. The uranium mills were decommissioned in the early 1980s and the tailings ponds were capped and closed by the early 1990s. Plaintiffs allege that their exposure to ionizing radiation from the uranium ore and its decay products caused their cancers. Natural uranium is primarily U-238 (99.27%), and thus Plaintiffs’ primary exposure from the uranium ore is exposure to U-238 and its decay products. The half-life of U-238 is 4.5 x 10 years, which results in a low decay rate. Although natural uranium is radioactive, it is considered weakly radioactive. ATSDR 1999, Toxicological Profile for Uranium (“Natural uranium is radioactive but poses little radioactive danger because it gives off very small amounts of radiation.”) Uranium emits ionizing radiation. Plaintiffs suffer from many different types of cancer, including lung, bladder, colorectal, pancreatic, kidney, skin, breast, uterine, esophageal, liver, stomach, bone, brain, and leukemia. Plaintiffs contend that they were exposed to uranium primarily as a result of Defendants’ hauling ore from the mine to the mill in uncovered trucks, allowing the uranium ore to fall from the trucks and uranium dust to blow off the trucks. Plaintiffs further contend that, with each additional vehicle that passed over the road, the ore was crushed and the resulting particles were suspended in the air. Due to this resuspension of particulates in the air with each passing vehicle, Plaintiffs allege that uranium and its progeny were dispersed in their community and that, as a result, Plaintiffs were exposed to ionizing radiation through inhalation and ingestion of the ore dust and contaminated food and water, which caused their cancers. They also attribute additional exposure to direct gamma radiation from the haul roads, facilities’ tailings pile, and from the uranium at the facilities themselves (for workers and plant visitors). Under the Price-Anderson Act, any public liability action arising out of a nuclear incident is deemed to arise under the Act. However, the substantive rules of decision are governed by state law to the extent it does not conflict with the Act. 42 U.S.C. § 2214(hh). The Plaintiffs’ burden under Texas law is to prove to a reasonable degree of medical certainty, based on a reasonable medical probability and scientifically reliable evidence, that their exposure to ionizing radiation from the natural uranium ore and its progeny was a cause of their injuries. Black v. Food Lion, Inc., 171 F.3d 308, 310 (5th Cir.1999). In toxic tort cases such as this one, causation is often discussed in terms of general and specific causation. See Merrell Dow Pharmaceuticals, Inc. v. Havner, 953 S.W.2d 706, 714 (Tex.1997). General causation deals with whether a substance is capable of causing a particular injury or condition in the general population, and specific causation deals with whether a substance caused a particular individual’s injury. Id. Plaintiffs have designated five experts in this case, all of whom have been challenged by the Defendants. On March 1 and 2, 2005, this Court held a hearing to consider Defendants’ challenges to four of those experts. Dr. Dollinger is the only expert offered to testify on the issue of specific causation, and exclusion of his testimony would necessitate a grant of summary judgment in favor of Defendants. Thus, because the Court concludes that the testimony of Dr. Malin Dollinger is not admissible under Daubert and the Federal Rules of Evidence, the Court need not consider the other Daubert challenges to Plaintiffs’ experts. Applicable Law Regarding Expert Testimony In 1993, the United States Supreme Court issued its seminal decision, Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579, 113 S.Ct. 2786, 125 L.Ed.2d 469 (1993), in which it established the standard for admitting expert scientific testimony in a federal trial. In Daubert, the Court abandoned Frye’s “general acceptance” test as the dominant standard for determining admissibility, noting that it had been superseded by the adoption of the Federal Rules of Evidence. Id. at 587-89, 113 S.Ct. 2786. The Court noted that, “under the Rules the trial judge must ensure that any and all scientific testimony or evidence admitted is not only relevant, but reliable.” Id. at 589, 113 S.Ct. 2786. Thus, the Court held that, “[f]aced with a proffer of expert scientific testimony, then, the trial judge must determine at the outset ... whether the expert is proposing to testify to (1) scientific knowledge that (2) will assist the trier of fact to understand or determine a fact in issue.” Id. at 592, 113 S.Ct. 2786. “This entails a preliminary assessment of whether the reasoning or methodology underlying the testimony is scientifically valid and of whether that reasoning or methodology properly can be applied to the facts in issue.” Id. at 592-93, 113 S.Ct. 2786. Ordinarily, “a key question to be answered in determining whether a theory or technique is scientific knowledge that will assist the trier of fact will be whether it can be (and has been) tested.” Id. at 593, 113 S.Ct. 2786. Another pertinent consideration is whether the theory or technique has been subjected to peer review and publication; however, publication is not a sine qua non of admissibility. Id. In the case of a particular scientific technique, the court should ordinarily consider the known or potential rate of error and the existence and maintenance of standards controlling the technique’s operation. Id. at 594, 113 S.Ct. 2786. Finally, “ ‘general acceptance’ can yet have a bearing on the inquiry.” Id. Widespread acceptance can be an important factor in ruling particular evidence admissible, and “ ‘a known technique that has been able to attract only minimal support within the community’ may properly be viewed with skepticism” Id. (citation omitted). The inquiry is a flexible one, and its focus must be solely on principles and methodology rather than the conclusions generated. Id. at 594-95, 113 S.Ct. 2786. However, conclusions and methodology are not entirely distinct from one another. General Elec. Co. v. Joiner, 522 U.S. 136, 146, 118 S.Ct. 512, 139 L.Ed.2d 508 (1997). Nothing in 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. Id. A court may conclude that there is simply too great an analytical gap between the data and the opinion proffered. Id. Federal Rule of Evidence 702 embodies these reliability principles. It requires the district court to consider: (1) whether the knowledge will assist the trier of fact to understand the evidence or to determine a fact in issue; (2) whether the witness is qualified as an expert by knowledge, skill, experience, training, or education; (3) whether the testimony is based upon sufficient facts or data; (4) whether the testimony is the product of reliable principles and methods; and (5) whether the witness has applied the principles and methods reliably to the facts of the case. Fed.R.Evid. 702. The party seeking to have the district court admit expert testimony must demonstrate that the expert’s findings and conclusions are based on the scientific method, and, therefore, are reliable. Moore v. Ashland Chem. Inc., 151 F.3d 269, 276 (5th Cir.1998). This requires some objective, independent validation of the expert’s methodology. Id. The Fifth Circuit has directed that, “[i]n the vast majority of cases, the district court first should decide whether the factors mentioned in Daubert are appropriate. Once it considers the Daubert factors, the court then can consider whether other factors, not mentioned in Daubert, are relevant to the case at hand.” Black v. Food Lion, Inc., 171 F.3d 308, 311-12 (5th Cir.1999). “[Wjhether Daubert’s suggested indicia of reliability apply to any given testimony depends on the nature of the issue at hand, the witness’s particular expertise, and the subject of the testimony.” Seatrax, Inc. v. Sonbeck Int’l, Inc., 200 F.3d 358, 372 (5th Cir.2000). It is a fact-specific inquiry. Id. The district court’s responsibility “is to make certain that an expert, whether basing testimony upon professional studies or personal experience, employs in the courtroom the same level of intellectual rigor that characterizes the practice of an expert in the relevant field.” Id. Further, “the law cannot wait for future scientific investigation and research. We must resolve cases in our courts on the basis of scientific knowledge that is currently available.” Moore, 151 F.3d at 276. Applicable Law Regarding Causation Burden of Proof Under Texas law, the Plaintiffs’ burden of proof on causation is as follows: The two elements of proximate cause are cause in fact (or substantial factor) and foreseeability. Id.; Travis v. City of Mesquite, 830 S.W.2d 94, 98 (Tex.1992). These elements cannot be satisfied by mere conjecture, guess, or speculation. Doe v. Boys Clubs of Greater Dallas, Inc., 907 S.W.2d 472, 477 (Tex.1995). Cause in fact is established when the act or omission was a substantial factor in bringing about the injuries, and without it, the harm would not have occurred. Id.; Union Pump Co. v. Allbritton, 898 S.W.2d 773, 775 (Tex.1995); Travis, 830 S.W.2d at 98. In Lear Siegler, Inc. v. Perez, [819 S.W.2d 470 (Tex.1991)], we found the Restatement (Second) of Torts to be instructive on this point: In order to be [the proximate cause] of another’s harm, it is not enough that the harm would not have occurred had the actor not been negligent. ... [T]his is necessary, but it is not of itself sufficient. The negligence must also be a substantial factor in bringing about the plaintiffs harm. IHS Cedars Treatment Ctr. of Desoto, Tex. v. Mason, 143 S.W.3d 794, 798-99 (Tex.2004). Thus, Plaintiffs must establish that it is more likely than not that Plaintiffs would not have suffered from their various cancers but for the Defendants’ activities related to the uranium mining and milling and that their exposures were a significant factor in bringing about their cancers. See Southwest Key Program, Inc. v. Gil-Perez, 81 S.W.3d 269, 275 (Tex.2002) (reversing jury verdict for plaintiff because evidence did not establish that it was more probable than not that plaintiff would not have been injured but for defendant’s failure to provide ordinary protective gear); see also Restatement (Third) of Torts § 26 cmt. 1 (“[A] plaintiff must prove that it is more likely than not that, if the defendant had not acted tortiously, the plaintiffs harm would not have occurred. Consistent with Comment c, plaintiff need not prove that defendant’s tortious conduct was the predominant or primary cause of the harm. So long as the defendant’s tor-tious conduct was more likely than not a factual cause of the harm, plaintiff has established the element of factual cause.”)- Toxic Torts & Epidemiology In toxic tort cases, direct human experimentation cannot be done, and generally there will be no direct evidence of causation. Havner, 953 S.W.2d at 715. In such cases, claimants may attempt to demonstrate that exposure to the substance at issue increases the risk of their particular injury. Id. One method of demonstrating an increased risk is through epidemiological studies, which examine existing populations to determine if there is an association between a disease or condition and a factor suspected of causing that disease or condition. Id. The Fifth Circuit has noted that, in toxic tort cases, “the most useful and conclusive type of evidence ... is epidemiological studies.” Brock v. Merrell Dow Pharms., Inc., 874 F.2d 307, 311 (5th Cir.1989), modified by 884 F.2d 166 (5th Cir.1989). Thus, although the Fifth Circuit has not held that “epidemiologic proof is a necessary element in all toxic tort cases, it is certainly a very important element.” Id. at 313. This is especially true when the only other evidence is of questionable applicability, such as animal studies. Id. As the Texas Supreme Court has recognized, there is some disagreement over the use of epidemiological studies to establish causation in the litigation context. Havner, 953 S.W.2d at 717. The Texas Supreme Court has concluded that “properly designed and executed epidemiological studies may be part of the evidence supporting causation in a toxic tort case and that there is a rational basis for relating the requirement that there be more than a ‘doubling of the risk’ to ... the more likely than not burden of proof.” Id. Courts adopting such a requirement have found that the requirement of a more than 50% probability means that epidemiological evidence must show that the incidence of an injury or condition in the exposed population was more than double the incidence in the unexposed or control population. Id. at 716. This may be reflected as a “relative risk” of greater than 2.0. Even if an epidemiological study satisfies the doubling of the risk criteria, however, other factors must still be considered. Id. at 718-19 (noting that conclusions about causation should not be drawn until other criteria, such as the Bradford-Hill or Hen-le-Koch-Evans Postulates are considered). As the Court noted, the Bradford-Hill criteria and the Henle-Koch-Evans Postulates “are part of sound methodology generally accepted by the current scientific community.” Id. at 719. Particularly where direct experimentation cannot be done, it is important that any conclusions about causation be reached only after an association is observed in studies among different groups and that the association continues to hold when the effects of other variables are taken into account. Id. at 727. In addition, to support causation, an epidemiological study must be statistically significant at the 95% confidence level and the confidence interval may not include I.0. Id. at 723-24. The Texas Supreme Court left open the question “whether epidemiological evidence with a relative risk less than 2.0, coupled with other credible and reliable evidence, may be legally sufficient to support causation.” Id. Applicability of Havner Because federal procedure and state substantive law govern this case, the parties disagree over the controlling effect of the Texas Supreme Court’s decision in Havner. Plaintiffs are correct that the admissibility of expert testimony is a procedural issue, and this Court agrees that the admissibility of the proffered experts is governed by federal law. However, the Court disagrees with Plaintiffs regarding the controlling effect of Havner. Plaintiffs repeatedly argue that Havner “is not substantive law and is not controlling on this Court because it was decided on evidentia-ry grounds.” However, Havner was not concerned with the admissibility of expert testimony, but the legal sufficiency of that evidence, although the inquires are conflated under Texas law in the context of expert testimony. The Court concludes that whether a Plaintiffs proffered evidence amounts to some evidence (or, in other words, legally sufficient evidence) of causation is a question of Texas substantive law, and thus Havner controls on that issue. If evidence is admissible under federal procedural law but fails to constitute “some evidence” under Texas substantive law, the Plaintiffs’ victory on the admissibility question would be a hollow one, as the evidence would be deemed insufficient as a matter of law to survive summary judgment. Moreover, whether expert testimony will assist the trier of fact is governed in part by whether the testimony is relevant to the plaintiffs burden of proof under the substantive law, and testimony that will not assist the trier of fact by advancing an element of the plaintiffs case should be excluded. See Daubert v. Merrell Dow Pharms., 43 F.3d 1311, 1320 (9th Cir.1995) (“In assessing whether the proffered expert testimony ‘will assist the trier of fact’ in resolving this issue, we must look to the governing substantive standard .... ”); Norris v. Baxter Healthcare Corp., 397 F.3d 878, 884 n. 2 (10th Cir.2005) (“Under the relevance prong of Dau-bert, the court must ensure that the proposed expert testimony logically advances a material aspect of the case.”). Thus, the Court concludes that Havner controls the issue of what evidence is required to establish causation in a toxic tort case and therefore what evidence is relevant. In Havner, the Court was considering whether the Plaintiffs had introduced legally sufficient evidence that Bendectin caused the plaintiffs birth defect. Plaintiffs arg-ue that Havner does not apply to this case because it is limited to the Ben-dectin context. In Havner, the Court was deciding whether the plaintiffs proof of causation was sufficient in an area in which the harmful nature of Bendectin was quite unsettled and available epidemiological evidence failed to support causation. In contrast, Plaintiffs contend, the harmful nature of ionizing radiation and its potential to cause cancer is well accepted by the medical and scientific community, and has been recognized by the courts. See, e.g., In re TMI, 193 F.3d 613 (3d Cir.1999). Although Havner was a Bendectin case, the Court spoke generally about the use of epidemiological evidence and how the doubling of the risk standard relates to the “more likely than not” burden of proof, and the Court does not read the opinion to limit those principles solely to the Bendec-tin context. Plaintiffs rely not on Texas cases, but on federal cases dealing with causation in the radiation context—In re TMI, 193 F.3d 613 (3d Cir.1999), amended by 199 F.3d 158 (2d Cir.2000), which dealt with litigation resulting from the Three Mile Island nuclear reactor accident, and In re Hanford Nuclear Reservation Litigation, 292 F.3d 1124 (9th Cir.2002) and In re Berg Litigation, 293 F.3d 1127, 1129 (9th Cir.2002), which dealt with the radiation release from the Hanford Nuclear Reservation. In In re TMI, 193 F.3d 613 (3d Cir.1999), the court considered the claims of area residents who allegedly developed radiation-induced neoplasms as a result of ionizing radiation released into the environment as a result of the Three Mile Island nuclear reactor accident in 1979. Specifically, the plaintiffs alleged that their conditions were caused by gamma ray exposure from radioactive iodine, xenon, and krypton. Id. at 659. The Third Circuit held that, to recover for their injuries, the plaintiffs had to show that the defendants released radiation into the environment in excess of the federal regulatory limits, that plaintiffs were exposed to this radiation (although not necessarily at levels prohibited by the regulations), that the plaintiffs were injured, and that the radiation exposure was the cause. Id. The court held that the “exposure element requires that plaintiffs demonstrate they have been exposed to a greater extent than anyone else, i.e., that their exposure levels exceeded the normal background level.” Id. The Third Circuit also rejected the district court’s holding that all plaintiffs had to present evidence that they were exposed to 10 rem or more of ionizing radiation in order “to establish causation on the basis of a specific radiation exposure level.” Id. at 726. The court noted that, at exposure levels below 10 rem, cancer risks are based on extrapolations from risks seen at higher exposure levels, but the fact that risks of cancer from exposure at low doses are based on extrapolations from higher doses does not mean that the scientific community believes that there is no causal connection between a low-level exposure and cancer induction. Id. On the contrary, the court noted, it is possible that very low doses of ionizing radiation may deposit sufficient energy into a cell to adversely modify it and scientists assume no threshold for cancer induction. Id. Thus, the court concluded that the “non-trial” plaintiffs “ought to be able to attempt to establish that doses below the [10 rem] threshold ... has induced their neoplasms.” Id. In In re Hanford Nuclear Reservation Litigation, 292 F.3d 1124 (9th Cir.2002), the district court established a threshold for generic causation — proof would meet the more-likely-than-not standard only if it established a doubling of the risk. Expert testimony indicating only that the radiation was capable of causing a disease was excluded as irrelevant unless it also passed muster under the “doubling of the risk” standard. Id. at 1132. The Ninth Circuit reversed, stating that “the appropriate understanding of generic causation is ... whether exposure to a substance for which a defendant is responsible, such as radiation at the level of exposure alleged by plaintiffs, is capable of causing a particular injury or condition in the general population.” Id. at 1133. The court further stated that cases dealing with substances for which there was no scientific evidence of capacity to cause the plaintiffs’ injuries (and for that, reason statistical epidemiological evidence was necessary) are inappo-site. Id. at 1136. In contrast, the court held, “[rjadiation is capable of causing a broad range of illnesses, even at the lowest doses.” Id. at 1137. Thus, to show generic causation, plaintiffs had to establish by scientific evidence only that radiation was capable of causing the types of injuries plaintiffs suffered, and the district court erred in requiring epidemiological evidence that would require a plaintiff to prove exposure to a specific threshold level of radiation that created a relative risk of greater than’2.0 at the general causation stage. Id. The Ninth Circuit affirmed this conclusion in In re Berg Litigation, 293 F.3d 1127, 1129 (9th Cir.2002): “As we explained in Hanford, reliance on [the doubling dose] standard was error because the ‘doubling of the risk’ is a measure courts use to determine whether a substance is capable of causing harm in the absence of any evidence other than epidemiological evidence of toxicity. Here, we deal with a substance, radiation, that is known to be capable of causing harm. Indeed, there is no threshold harmful dosage level for radiation because it can cause harm at any level.” Hanford and Berg’s, rejection of the doubling of the risk standard was in the context of the court’s discussion of general causation — whether ionizing radiation is capable of causing the plaintiffs’ injuries. In Hanford, the plaintiffs offered expert testimony to show the generic capacity of levels of radiation emitted from the Han-ford facility to cause the illnesses experienced by the plaintiffs, and the Ninth Circuit held that evidence sufficient for general causation. Id. at 1137. It did not discuss the sufficiency of evidence to establish specific causation. In re TMI did not reject the doubling of the risk requirement; rather, it rejected the district court’s imposition of a 10 rem threshold because it was inconsistent with scientific thinking. The Court finds TMI, Hanford, and Berg instructive and agrees with Plaintiffs that the generic capacity of ionizing radiation to cause cancer is well accepted. However, regardless of whether one accepts the premise that ionizing radiation is generally capable of causing cancer, Plaintiffs must still prove that their particular exposures to ionizing radiation from the uranium ore contamination was the cause of their particular cancers. Whether they can do so will depend in large part on the strength of the epidemiological evidence, which, although establishing generally that various exposures to ionizing radiation from various sources may cause the forms of cancer involved here, is “mixed and inconclusive” (to use Dr. Dollinger’s words) with regard to a causal link between exposure to natural uranium ore and cancer. Given that cancer is a common phenomenon with many causes, both known and unknown, without epidemiological evidence demonstrating a relative risk of greater than 2.0, Plaintiffs will have a more difficult time reliably establishing that an individual’s cancer was, more likely than not, caused by Defendants’ conduct. In addition, to establish specific causation, a claimant must not only introduce sufficient epidemiological evidence, he must also show that he is similar to those in the studies, which includes “proof that the injured person was exposed to the same substance, that the exposure or dose levels were comparable to or greater than those in the studies, that the exposure occurred before the onset of injury, and that the timing of the onset of injury was consistent with that experienced by those in the study.” Havner, 953 S.W.2d at 720. Consistent with these requirements under Texas law, the Eighth Circuit has held that a plaintiff in a toxic tort case must “prove the levels of exposure that are hazardous to human beings generally as well as the plaintiffs actual level of exposure to the defendant’s toxic substance” before he may recover. Wright v. Willamette Industries, Inc., 91 F.3d 1105, 1106 (8th Cir.1996). “It is not enough for a plaintiff to show that a certain chemical agent sometimes causes the kind of harm that he or she is complaining of. At a minimum, ... there must be evidence from which the factfinder can conclude that the plaintiff was exposed to levels of that agent that are known to cause the kind of harm that the plaintiff claims to have suffered. We do not require a mathematically precise table equating levels of exposure with levels of harm, but there must be evidence from which a reasonable person could conclude that a defendant’s emission has probably caused a particular plaintiff the kind of harm of which he or she complains before there can be a recovery.” Id. at 1107. Though the plaintiffs proved they were exposed to defendant’s emissions, they failed to produce evidence that they were exposed to a hazardous level of formaldehyde, and thus their case failed. Id. In Allen v. Pennsylvania Engineering Corp., 102 F.3d 194 (5th Cir.1996), the Fifth Circuit considered whether the plaintiff had produced sufficient evidence that ethylene oxide caused the plaintiffs brain cancer. The court noted that “the fact that EtO has been classified as a carcinogen by agencies responsible for public health regulations is not probative of the question whether Allen’s brain cancer was caused by EtO exposure.” Id. at 195-96. Citing Wright, the Fifth Circuit stated that “[s]cientific knowledge of the harmful level of exposure to a chemical, plus knowledge that the plaintiff was exposed to such quantities, are minimal facts necessary to sustain the plaintiffs burden in a toxic tort case.” Id. at 199 (cited with approval in Curtis v. M & S Petroleum, Inc., 174 F.3d 661, 670 (5th Cir.1999)). Just last year, in Burleson v. Texas Department of Criminal Justice, 393 F.3d 577 (5th Cir.2004), the Fifth Circuit considered the admissibility of expert opinion testimony in a case alleging that a prison inmate’s cancer was caused by his exposure to radioactive particles in thoriated tungsten rods used during his prison welding operations. The plaintiff worked as a welder and performed tungsten inert gas welding activities using 2% thoriated tungsten steel welding electrodes. These electrodes were radioactive and the warning on the box indicated that exposure to them may cause cancer. The thorium in the welding rods was present in the form of thorium dioxide, a naturally occurring radioactive compound that is distributed in the air during the welding and grinding processes, and which has been classified by the Department of Health and Human Services as a carcinogen. Burleson developed throat and lung cancer, as did four other individuals employed as welders. The Court noted, however, that Burleson also had a forty-five year, two-pack-per-day history of smoking and both his parents and maternal grandparents died of cancer. To support his causation claim, Burleson presented the expert witness testimony of Dr. Arch Carson, a well-credentialed toxicologist and expert in occupational medicine, who opined that Burleson inhaled hazardous radioactive particles while engaging in welding operations, in turn exposing him to a significant risk for the development of respiratory tract cancers, and that that risk exceeded Burleson’s other risk factors. Dr. Carson espoused a “radiation hot spot” theory according to which the primary risk factor for cancer is the local microscopic dose of radiation that is received by the one cell that transforms into cancer, not the total dose of radiation to the body, and asserted that this theory has been proven in practice and that published scientific and epidemiological studies show that patients who received Thoro-trast — a form of thorium dioxide used as a medical imaging dye — during its thirty-year use developed multiple types of cancer. Burleson attempted to distinguish the Fifth Circuit’s prior Allen opinion on the basis that there are epidemiological studies that clearly link thorium dioxide, a known carcinogen, with cancer, and there are no such studies disproving the theory that welding with thoriated tungsten welding rods causes lung or throat cancer. He further argued that there is no legal requirement that a plaintiff produce epidemiological studies concerning a specific use of the same known carcinogen in order to create a genuine issue of material fact concerning the causal relationship between lung and throat cancers and thorium dioxide in welding electrodes. The Court rejected these arguments, noting that Dr. Carson offered “no studies which demonstrate a statistically significant link between thorium dioxide exposure in dust or fumes and Burleson’s type of lung or throat cancer. The U.N. report relied upon by Dr. Carson only reports that liver, spleen and bone cancers were associated with Thorotrast.... Additionally, one of the few, if not the only, epidemiology study which examined the cancer risk to welders from thoriated welding electrodes was a Danish study that showed no statistically significant link between the exposure to thoriated welding electrodes and cancer. Here, as in Allen, there are no epidemiological studies supporting a correlation between the suggested causative agent and the type of cancer experienced by the plaintiff. Accordingly, we find Allen un-distinguishable.” The Court went on to criticize Dr. Carson’s failure to determine the dose, and eventually concluded that “[s]ince Dr. Carson cannot show that the welding electrodes are more or less probable to be the cause of Burleson’s cancers, the testimony is irrelevant under the Federal Rules of Evidence.” With these legal standards in mind, the Court now turns to a specific examination of Plaintiffs’ proffered expert witness Dr. Malin Dollinger. Dr. Malin Dollinger, M.D., F.A.C.P.’s Opinions and the Parties’ Arguments Plaintiffs seek to introduce Dr. Dolling-er’s testimony to show that Defendants caused the Plaintiffs’ cancers (specific causation). Dr. Dollinger is a well-credentialed clinical professor of medicine at the Univei"sity of Southern California School of Medicine. He received his undergraduate and medical degrees at Yale, and completed a residency in internal medicine, with a three-year fellowship in medical oncology. He is currently in the private practice of medical oncology in California. Dr. Dol-linger states that, on the basis of his education, training, and experience, he is familiar with the risk factors and causes for the various types of cancer in man, in particular those cancers caused by radiation, as well as the natural history, diagnosis, treatment, and prognosis of the different types of cancer in man. August 2002 report According to his 2002 report, in reaching his conclusions, Dr. Dollinger reviewed the plaintiffs’ medical records. He also reviewed various studies and literature concerning ionizing radiation, including uranium, and Dr. Resnikoffs August 2002 dose reconstruction report. Dr. Dollinger made two visits to Karnes County to conduct independent medical examinations on available Plaintiffs or he conducted interviews with relatives when the case subjects were not available for examination. Referring to Dr. Resnikoffs report, Dr. Dollinger states that “estimates were made regarding exposures to various radioactive and non-radioactive materials, for each of the various subjects.... The findings outlined appear to be and are considered accurate.” Dollinger 2002 Report at 15. He further asserts that “plaintiffs have been exposed to radioactive decay products, which include alpha radiation, gamma rays, radon and radon daughters, and other products of radioactive decay, as well as radioactive dust, radioactive particles, heavy metals, and other contamination caused by the uranium mining and milling activities.” Id. He also states that Resnikoffs “reports and conclusions appear to be conducted in a reasonable, sound, logical, and scientific manner, and [he has] assumed that these studies, measurements, and data furnish accurate and reliable information on radiation exposures of each individual to the various contaminants. Excessive exposure to sources of ionizing radiation was demonstrated and documented.” Id. at 16. Dr. Dollinger states that in his interviews with plaintiffs, he confirmed their employment, location of homes, proximity to haul roads, and in general obtained a first-hand knowledge of conditions as they existed at the time of exposure, and though he did not attempt to repeat the details of each plaintiffs exposure, his discussions did confirm certain information as provided in Resnikoffs report. Thus, his report “assume[s] that such contamination by radioactive materials did in fact occur, at dosage levels higher than background radiation.” Id. at 17. Dollinger’s report “is primarily concerned with the questions of specific causation of the various plaintiffs’ specific cancers by such radiation/radioactive material, and toxic material exposure. In other words, was their exposure to ionizing radiation and toxic materials resulting from the activities of defendants a cause or a substantial contributing factor in the production of subjects’ cancers?” Id. at 17-18. Dr. Dollinger states that the radioactive materials of concern produce ionizing radiation, which produces damage in biological systems through ionization of molecules. Id. at 18. With regard to DNA damage, he states that ionizing radiation is much more likely to produce double-strand breaks with impaired ability to repair, compared to single-strand breaks (for example, from chemical carcinogens). Id. at 19. In the case of exposure to ionizing radiation, Dr. Dollinger states that there is no minimum threshold of exposure that is required to produce genetic mutations that may lead to abnormalities, including cancer. Id. He points out that the effects of ionizing radiation are “stochastic,” which means that: (1) there is no threshold; even a very small dose (for example, a single radiation track) can produce a key genetic mutation leading to cancer; (2) increasing doses of radiation produce a higher risk of genetic damage (at least two “hits,” and usually more, are required to produce a cancer mutation, and thus prolonged exposure would favor the occurrence of several hits); and (3) once the key genetic damage occurs, the effect is independent of the dose required to produce it. Id. at 19-20. Thus, regardless of the dose, once a cell is damaged, it is permanent in that cell and cancer will develop if not controlled by the body. Id. Dr. Dollinger cites Fairlie for the proposition that, “for the majority of tumor types, a single mutational event in a single target cell in vivo [in the body] can create the potential for neoplastic [cancer] development. On this basis, a single radiation track (the lowest dose and dose rate possible) traversing the nucleus [central point] of an appropriate target cell has a finite possibility, albeit low, of generating the specific damage that results in a tumor initiating mutation.” Id. at 20. Thus, because even a single ionization event is capable of producing critical DNA damage leading to cancer mutation, there is no threshold dose of ionizing radiation that is “safe.” Id. Dr. Dollinger states that industry guidelines serve as convenient parameters, but do not define a “safe” dose. Id. at 20-21. Even the industry standard of “as low as reasonably achievable (ALARA)” is still an amount of ionizing radiation capable of producing biological effects that lead the cancer. Id. at 21. Dr. Dollinger also states that there are two additional factors of importance. First, the health effects on humans of more than one toxic material or exposure may be additive or synergistic, and thus it is “quite likely” that the risk of chromosomal damage from ionizing radiation may be increased due to repeated exposures over time as well as the presence of multiple sources of ionizing radiation. Id. “Specifically, exposures like those experienced by these subjects in Texas, that is exposure to multiple radioactive sources, various isotopes, by various routes and at various times, over a prolonged interval of time, are more like to produce genetic (DNA) mutations, with the resulting risk of cancer. During the time interval during which exposure occurs, other exposures to radiation or other carcinogens may add and amplify the initial genetic damage.” Id. Dr. Dollinger concludes that a “defined” and precisely monitored exposure by a worker during his shift may in fact be less worrisome regarding cancer induction than a continuous chronic exposure of unknown intensity, location, involvement of varying portions of the body, and degree of exposure internally, to an individual in the contaminated community who is exposed for long periods of time. Id. at 22. In addition, the genetic damage caused by ionizing radiation may take years to develop into cancer and thus the damage may not be apparent for a long time. For example, the studies of Japanese atomic bomb survivors showed that solid tumors may not develop for forty years, and thus surveys done at shorter time intervals may miss detection of many solid tumors. Id. Dr. Dollinger states that the second additional important factor relates to the pathway of exposure. Id. at 23. Dr. Dollinger notes that regulators apply the linear non-threshold hypothesis, and states that “[t]his model is widely accepted” and “accurately reflects the mechanism by which ionizing radiation induces cancer and other damaging effects.” Id. He cites Fairlie and Resnikoffs 1996 mortality study of the Japanese atomic-bomb survivors as showing a statistically significant upward trend of risk with doses in the region of 50 mSv, which reinforces the validity of the no-threshold concept. Id. at 25. Further, Dr. Dollinger asserts that “Straume points out that high energy gamma rays (e.g. the Japanese exposure) are expected to be substantially less effective in producing biological damage compared with lower energy radiation.” Id. Thus, he asserts, “[a]eute leukemia was clearly evident as a result of radiation exposure in those cities in Japan, and it would be expected that the lower energy [gamma rays] produced in the present situation would be even more effective biologically than the high energy gamma rays in the Japanese exposure.” Id. at 25-26. Dr. Dollinger states that many sources of data verify and document that existence of radiation-induced cancers. Id. at 23. Further, ionizing radiation has the ability to produce cancer regardless of the particular source of the ionizing radiation. Id. at 26. Dr. Dollinger states that the “harmful effects of ionizing radiation on the blood and blood-forming organs (hema-topoietic system) has been known for many decades.” Id. at 27. The effects of ionizing radiation have been intensively studied. Id. Dr. Dollinger states that because of the latency period and high incidence of naturally occurring cancers, the more common ones in particular, the increase in cancer incidence that is caused by radiation exposure is difficult to detect in epidemiological studies of large exposed populations. Id. at 29. This does not mean, however, that each exposed individual’s risk was not significantly increased. Id. Rather, [specifically, for those individuals who do develop cancer, the ionizing radiation resulting from the environmental contamination was a substantial contributing factor and a cause of the cancer which developed. The increase in risk of each exposed individual increases linearly with the increase in dose. For each individual, the development of cancer is an “all or nothing” phenomenon. For each exposed individual who did develop cancer, the risk for that person was 100%. Id. Dr. Dollinger states that ionizing radiation has been invoked as a causative factor for acute leukemia, chronic myelogenous leukemia, thyroid cancer, breast cancer, lung cancer, stomach cancer, colorectal cancer, esophageal cancer, bladder cancer, ovarian cancer, multiple myeloma, and pancreatic cancer, and less frequently, kidney cancer, lymphoma, skin cancer, rectal cancer, bone cancer, uterine cancer, and connective tissue cancer (sarcomas). Id. at 29. Further, “radiation exposure has also been implicated in tumors of the central nervous system (brain).” Id. Di\ Dollinger further states that because the genetic changes that result in cancer production are microscopic, and since each cancer is caused by a series of “hits” to various genes, it is not possible, in almost all cases, to determine which environmental insult or which radiation (or other) “hit” caused a specific genetic mutation that resulted in the first cancer cell. Id. at 30. The cancer that results from one cause (such as smoking) are the same types of cancer that may result from another cause, such as radiation exposure. Id. Indeed, many cancers in the general population are likely caused by “background” ionizing radiation, but it is not possible to know which person’s cancers are so-caused, and which may have other causes. Id. In fact, since a series of genetic mutations is responsible for most cancers, there may be several or multiple causes of an individual’s cancer, and the chromosome changes and mutations from one cause are not distinguishable, with rare exception, from those induced by another cause. Id. Epidemiologists attempt to determine if a certain population that has been exposed to a carcinogenic substance such as ionizing radiation has a higher incidence of cancer than an unexposed control population. Id. Dr. Dolling-er states that detecting a real effect from ionizing radiation through epidemiological studies is difficult in both small and large populations. In large populations, the increase in cancer incidence caused by radiation contamination may be too small to detect by comparison to naturally occurring cancers, making it “inappropriate, therefore, to conclude that because an increase in cancer incidence is difficult to detect in population studies, that the risk of developing cancer in certain individuals has not increased.” Id. at 32. With regard to each specific plaintiff, Dr. Dollinger reviewed their personal and health information and medical records. He conducted an independent medical examination when possible. He determined each plaintiffs specific type of cancer and the relationship of that type of cancer to causation by ionizing radiation contaminating their environment. He also included data from Resnikoffs report concerning presence and degree/dose ranges of radiation exposure, and organ doses in some cases. He then created individual reports for each plaintiff. His expert medical opinion is that “[i]t is medically probable that ionizing radiation from radioactive materials, via contamination of the personal environment of these various individual subjects, was a substantial contributing factor and was a cause of the various cancers in these individuals that have occurred in the past or which are present now.... The development of these cancers is directly related to exposures of these subjects to various substances and materials produced by the defendants, said substances and materials producing ionizing radiation that contaminated their general and specific environment. The location and periods of residence in this community and their exposures to such ionizing radiation has been well documented. Within reasonable medical probability, the ionizing radiation produced as a result of the contamination acted as a carcinogen (a cause of cancer), and such exposure to ionizing radiation resulting from the environmental contamination was a cause and a substantial contributing factor in the development of these cancers, and the signs and symptoms, required treatment, and outcome that did result.” Id. at 33-35. Each of the reports that specifically pertain to individual Plaintiffs are brief (less than one page), and indicate the Plaintiffs cancer diagnosis and treatment, whether the form of cancer has been associated with exposure to ionizing radiation, details regarding family history and exposure, the total effective radiation dose (and occasionally organ dose), and the conclusion that the ionizing radiation resulting from the contamination was a cause of the Plaintiffs cancer. With respect to the four children Plaintiffs, Dr. Dollinger concluded that exposure of the subject’s mother or father to ionizing radiation, either in isolation or in conjunction with the child’s exposure, was a cause and substantial contributing factor in the development of the subject’s cancer. For example, CarylAnn Hernandez was born in 1983 and developed an osteogenic sarcoma of her leg in September 1993. Dr. Dollinger noted that her total effective radiation dose was 328-869 mrem, that of her father David Hernandez was 836-2,004 mrem, and that of her mother Helen Hernandez was 357-1,259 mrem, and that “such exposure of this subject and her parents to such ionizing radiation was a cause and a substantial contributing factor in the development of this subject’s cancer.” Dollinger 2002 Report at 53. Crystal Yanta was born in 1982 and was diagnosed with leukemia in 1996. Similarly to CarylAnn Hernandez, Dr. Dollinger appears to have based his causation opinion on both Crystal’s total effective radiation dose of 10-26 mrem and her father Paul’s dose of 461-1,693 mrem. Id. at 74. With regard to two of the children, Dr. Dollinger’s report indicates that he based his cancer causation opinion solely on parental exposure. Jose Hernandez IV was born in 1997 and was diagnosed with a brain tumor in 2001. Dr. Dollinger noted that the total effective radiation dose of his mother, Bridget Hernandez, was 4,489'— 11,547 mrem and “[w]ithin reasonable medical probability, the ionizing radiation resulting from the contamination acted as a carcinogen (a cause of cancer), and such exposure of this subject’s mother to such ionizing radiation was a cause and a substantial contributing factor in the development of this subject’s cancer.” Id. at 54. Similarly, Thomas Molina was diagnosed with leukemia. Dr. Dollinger concluded that “[wjithin reasonable medical probability, the ionizing radiation resulting from the contamination acted as a carcinogen (a cause of cancer), and such exposure of this subject’s father [Gary Molina, whose total effective radiation dose was 4,875 — 11,237 mrem] to such ionizing radiation was a cause and a substantial contributing factor in the development of this subject’s cancer.” Id. at 59. The 2003 Report Dr. Dollinger submitted a supplementary and rebuttal report in April 2003. It included an additional appendix that listed additional data on cancers from exposure to ionizing radiation, which he claims “further lists and documents the relationship of ionizing radiation exposure as a cause of various types of cancer, such as seen in these plaintiffs.” Dollinger 2003 Report at 3. In the listing of materials reviewed in making his report, Dr. Dollinger added references to the “supplemental listing of cancers from exposures to ionizing radiation,” an April 2003 study by Rothkamm et al. entitled “Evidence for a lack of DNA double-strand break repair in human cells exposed to very low x-ray doses,” Resni-koffs April 2003 Supplementary and Rebuttal Report, and an additional forty-six articles. Id. at 14-17. The supplementary and rebuttal report also considers Resni-koff s April 2003 supplementary and rebuttal report, which addresses resuspension doses, fifty-year versus shorter time-period committed doses, and calculation of organ-specific doses. Id. Dr. Dollinger states that “[t]his new data, TEDE [total effective dose equivalent] and Organ Dose, should be used to replace the earlier data given and reproduced from my prior report of August 18, 2002.... [T]he new data of Resnikoff and Hinterman should be used in each plaintiffs case instead of the ‘total effective radiation dose’ values listed in the prior report.” Id. at 3-4. Daubert hearing Dr. Dollinger testified at his Daubert hearing on March 2, 2005. He again emphasized his reliance on the “stochastic” effects of ionizing radiation in cancer production and the importance of the linear no-threshold hypothesis, which he testified has now been validated. Much of the testimony at the hearing was the same as that presented at Dollinger’s two depositions and in his reports and affidavit. However, Dr. Dollinger also set forth a new methodology he had developed for determining whether the exposure resulting from Defendants’ conduct was a “predominant factor” (as opposed to merely “a” factor) in causing the Plaintiffs’ cancers. Dr. Dollinger acknowledged that he had previously declined to rank contributing factors by relative importance, but Plaintiffs’ counsel asked him: Q. However, if you have a situation, for example, where you know what the background level of radiation is and you know what the average dose is from perhaps x-rays and you also know what the dietary contribution might be, but you also have an external source that is a multiple of all of those sources, can you make probabilistic statements about what sources are the most likely or most dominant that would contribute to mutations that ultimately lead to a cancer? A. Yes. That would go to the stochastic principle, which I outlined or the model which I outlined earlier, that the higher the dose, the more the risk. Dr. Dollinger testified that, though he was “confident” that the exposure was a cause of the cancers, he “sought to consider whether [he] could further subdivide the group and [see whether] some of these in which radiation could be thought of as the predominant or principal cause, as compared to a cause.” Daubert hearing at 314. Boiled down, Dr. Dollinger sought to compare the average organ dose for an individual, based on Dr. Resnikoffs calculations, with the natural background radiation rate to determine whether the exposure due to Defendants’ activities was the predominant cause of a plaintiffs cancer. Dr. Dollinger testified that his first step was to select the mean organ dose because that number was “most likely to represent the true number.” Daubert hearing at 313. He clarified that it seemed to be a “reasonable representation of the dose” and it would be hard to deny that was a valid number because although the high end of the range might be too high and the low end of the range might be too low, “you really can’t argue that [the mean] in this case is not in the general vicinity of the dose.” Id. Thus, he stated, in a range, “the average is most likely to represent the true number” and “represents the best estimate for purposes of thinking.” Id. The second step was to determine the background radiation for Karnes County, which he did by asking Dr. Resnikoff. Id. at 314. The remainder is set forth as follows: A. So I took that data of 250 milli-rem as being the average background radiation from all of the various sources, celestial and in the body, potassium 40, carbon 14, whatever. And I took that 250, and I said let’s multiply it by four, make it four times greater. Q. Four times greater than background? A. Background. Certainly, if somebody was exposed to cancer — I’m sorry — radiation, of course, one develops cancer, exposed to radiation, and the extra radiation above background which, of course, increases the risk; whatever the risk of background is, if you get more radiation, you increase the risk. That’s the stochastic model. So if it were four times greater, that is, 1,000 millirem as background in that area, it certainly must be the principal and predominant cause compared to the other sources. When I went through that analysis of the 49 people on these two pages in which we have an organ dose, 33 of the 49 had an average above 1,000. That’s 67 percent or two-thirds of them- — • THE COURT: Doctor, I am not sure I understand your basis for selecting four. Why four, rather than six, rather than ten, rather than two? THE WITNESS: Thank you, Your Honor. I initially thought about selecting two or three, but the reason for selecting four, it is sort of arbitrary, in that I wanted to be sure I had a number high enough no one that could question it. If I selected two or three, one might say: Well, there is some inherent uncertainty about some of the numbers, similarly, like a few minutes ago I explained why I picked the average. There is some uncertainty about every number, but four times the dose of radiation, I was sure that if I picked four times 250, or 1,000, I was absolutely sure that it wasn’t 250; even with the inherent errors in measurement, you could not get back down to just background. It had to be above background, and most likely significantly above background, but I allowed room for the inherent error in the measurement, and Dr. Resnikoffs or anyone’s calculations may not be exactly precise, but our best scientific estimates, but I wanted to allow that there could be no error in the estimation. Q. Now, at background levels that you have described, there would be a certain number of mutations that would be attributable to ionizing radiation in a given population; is that correct? A. Yes. Q. And when you multiply the background level, let’s say, by a factor of four, what are you doing in terms of the risk or the probability of increasing the number of mutations? A. Again, according to the stochastic model, if the risk of a cancer mutation from background is a number X, it is four X, four times greater. Q. And is that because of the linearity of the no-threshold model that has been empirically validated? A. Absolutely, yes. Q. And you feel confident that when you have persons, for example, in Karnes County that have exposures to the ionizing radiation as a result of living next to the haul routes, and perhaps as a result of being in the area, that those exposures will increase the frequency of mutations relative to what exists at the background level? A. Yes. Q. And from that, are you able to deduce that the most probable cause of the cancers for those persons who are at the 1,000-millirem level, external dose from ionizing radiation were more likely to develop their cancers as a result of the ionizing radiation, rather than other factors? A. That is correct. I am absolutely sure that that dose over 1,000, that is the most likely cause. Dr. Dollinger continued: A. Next, I considered the fact that there is another group of people who have more than background, but less than 1,000. And I considered that one of the pathways of thinking that has been used is doubling the risk of cancer from any cause, radiation being an example. Well, if the risk of background is X and the risk of giving additional radiation is twice background, then you have doubled the risk. Whatever the risk background was, if you get twice as much as background, you have doubled the risk. Well, the background is 250, and then you get 250 more from ionizing radiation, let’s say from the contamination in this situation, then you have doubled the risk. So I have gone through the same set of numbers, and these penciled — let me see if I can make the laser work. Yes. These lines right here are the second part of the analysis. These represent people, represent people who have had at least 250 or more; in other words, these people have at least twice the risk of getting cancer as a result of the radiation, because the background dose has been doubled. Q. And when you double the background dose, do you double the risk in terms of increased number of mutations that may result in a manifested cancer? A. Yes. That is again because of the linear relationship in the stochastic model. You double the number of ionizing radiation effects, and you double the risk of their causing cancer. Q. Do you believe over the past few years the literature has evolved to the point where there is no longer any question about the validity of the linear no-threshold model? In other words, you can go below 5,000 millirems, which is the extent of resolution of epidemiological studies, and go down to zero, from the molecular biological experimentation that has been done to date? A. No question about the validity of those studies. Q. And are these articles appearing in very, very recent journals, 2004, 2005? A. Yes. And 2003 as well. Q. And as a result of this recent literature, has your thinking evolved where you are now able to define more probable causes than perhaps you were at the time when you gave your deposition when you indicated that as long as there was an excess above background, it would be a substantial contributing factor? A. Yes. I might — if it would be okay to finish up the last part of this discussion. If we take the people, as I told you earlier, the people over 1,000, or two-thirds, 33 out of 49 or 67 percent, if we add the people over 250, which is at least doubling the dose and, therefore, doubling the risk, 41 of 49 apply